c 
DM 
AAV 
AAV 
DM 
c 
Photograph of heart showing sclerosis of the coronaries (C) and of the artery of the 
auriculo-ventricular node (A.A.V.). The artery is surrounded by a zone of degenerated 
musculature (D.M.). 
For details with electrocardiogram, see Case 108, Cardiovascular Clinics. 
* (Frontispiece) THE HEART 
ITS PHYSIOLOGY, PATHOLOGY AND 
CLINICAL ASPECTS 
BY 
DR. SELIAN NEUHOF, B. S., M. D. 
i • • 
VISITING PHYSICIAN, CENTRAL AND NEUROLOGICAL HOSPITAL; CONSULTING CARDIOLOGIST, 
BROAD STREET HOSPITAL; ASSOCIATE ATTENDING PHYSICIAN, LEBANON HOSPITAL; 
FORMER CLINICAL PROFESSOR OF CARDIOLOGY, FORDHAM UNIVERSITY 
NEW YORK 
WITH v300 ILLUSTRATIONS 
PHILADELPHIA 
P. BLAKISTON’S SON & CO. 
1012 WALNUT STREET Copyright, 1923, by P. Blakiston’s Son & Co. 
P R I NTED IN U. S. A. 
BV THE MAPLE PRESS YORK PA TO MY WIFE 
IN TRIBUTE TO HER CONSTANT INSPIRATION AND HELP 
THIS BOOK IS AFFECTIONATELY DEDICATED PREFACE 
The rapid epoch-making advances in cardiology in recent years, with 
consequent broadening scope of the subject have inevitably resulted in a very 
voluminous literature. As a result, considerable confusion has arisen as 
each writer stressed the particular points he wished to bring out, but without 
sufficient correlation with the larger clinical and practical aspects of cardiology. 
The importance of some of the valuable contributions to the knowledge of the 
subject has sometimes been lost sight of because couched in highly technical 
terms incomprehensible to readers not especially trained in cardiology. The 
time is therefore ripe for a monograph that shall completely embrace this 
special field, critically weigh the value of the newer contributions to cardi- 
ology, and at the same time present the subject in a manner that can be clearly 
grasped by the general reader.' These have been the main purposes of the 
author in this book. It was with this in view, that the author has combined 
the many graphic phases of the subject such as electrocardiography, polyg- 
raphy and orthodiascopy with the older and customary methods of clinical 
examination. Realizing that the necessary instruments are not always at 
hand for the student or practitioner, and that the necessary technical knowl- 
edge for the use of such instruments may not have been acquired, the author 
has attempted to express in simple language the fundamental principles 
upon which these instruments are based, together with a sufficiently detailed 
description of their use. Similarly the meaning of the graphic curves that 
are obtained is presented in a readily comprehensible manner. The author 
lays special emphasis throughout on his view that as soon as the basic 
principles underlying graphic registration and fluoroscopy have been grasped 
by the reader, proper diagnosis of the cardiac arrhythmias as well as physical 
diagnosis can usually be arrived at even without the newer instrumental 
methods. Furthermore the author holds that the clinical value of lessons 
derived from graphic curves is often less than that to be obtained from the 
older time-honored non-instrumental methods. 
As may be seen by the Table of Contents, many practical questions con- 
tinually arising in the practitioner’s and student’s daily routine are considered 
in this work, and an effort is made to meet many of his perplexing problems 
in cardiology. Therapeusis, diagnosis with and without instruments, 
graphic methods, arrhythmias, physiology, cardiac disease (including syph- 
ilis), cardiac neurosis, the heart in various extra-cardiac conditions, diet, 
exercise, etc., are fully dealt with. Embryology, physiology, pathology 
and the conduction system are given proper emphasis. The newer view- 
points of cardiac function in terms of respiration, blood oxygenation and 
blood chemistry have also been incorporated. 
ix X 
PREFACE 
An original feature of this book is its series of Cardiovascular Clinics 
in the form of Case Histories. In this manner the every-day phases of the 
cardiovascular field are covered. These Clinics were given as a course 
of clinical conferences to senior students of medicine. At first, simple 
cardiac cases are presented, and the methods and reasons for arriving at the 
diagnoses are explained. As the conferences proceed more complex cases are 
discussed, and those questions having a direct bearing upon the cases are 
given, as well as the author’s views as indicated in his responses. Thus the 
student and practitioner learn how cases should be analyzed and the means 
by which the diagnosis is made at the bedside. Treatment and the reason for 
the choice of drugs are given equal consideration. In this manner the 
practical and clinical side of the cases is presented. Where possible, several 
similar cases are grouped and discussed, and similarities as well as differences 
both in physical signs and symptoms are explained. 
The aim of this volume has been to present the entire subject of cardiac 
and cardiovascular disturbances and diseases in a clear, well-balanced manner 
from the clinician’s rather than from a highly specialized viewpoint, and the 
author hopes that this work will therefore supply a practical, comprehensive 
reference book for both practitioner and student, as well as for those especially 
interested in the subject of cardiovascular diseases. TABLE OF CONTENTS 
PART I 
Chapter Page 
I. Embryological and Anatomical Considerations—The Conduction 
System—The Coronary System—Systemic, Portal and Pulmonary 
Circuits—Cardiac Nerve Supply—Weight and Size of the Heart— 
Position of the Valves i 
II. Fetal Circulation—Congenital Malformations, Defects and 
Anomalies 25 
III. Physiological Considerations—Normal Spread of the Wave of 
Excitation—Extrinsic Cardiac Nerves—Cardio-inhibitory Center 
•—Myogenic or Neurogenic Impulse 34 
IV. Cardiac Histology and Pathology 44 
V. Etiology of Heart Disease 63 
VI. Dynamic and Mechanical Considerations—Cardiac Dilatation ... 73 
VII. Graphic methods—Sphymographs and Sphymograms—The Ink Poly- 
graph—Polygraphic Curves—Radial Curves 78 
VIII. The Electrometer—The Electrocardiograph—Electrocardiograms 94 
IX. Variations in the Muscular Mass of the Heart that Influence the 
Rhythmic Electrocardiogram—Ventricular Hypertrophy and Dila- 
tation—Split Waves—Wide R Waves—Variations of the T Wave— 
Summary of Clinical Interpretations 106 
X. The Arrhythmias—Their Polygraphic, Electrocardiographic and 
Clinical Recognition 130 
XI. The Arrhythmias—Their Clinical Etiology and Therapy 193 
XII. Teleroentgenography, Orthodiascopy and Fluoroscopy 210 
XIII. History Record—Normal Heart Sounds—Physical Examination of 
the Heart—Abnormal Sounds and Murmurs 240 
XIV. General Signs and Symptoms ofCardiac Decompensation in Organic 
Cardiac Disease—The Neurotic Element in Organic Cardiovascular 
Disease—Cardiac Strain—Functional Efficiency Tests 271 
XV. Rheumatic and Bacterial Endocarditis:—Prevalence, Clinical Phe- 
nomena, Symptomatology, Prognosis, Therapy—Dynamic Considera- 
tions 289 
XVI. Cardiac Syphilis—Aneurismal Dilatation of the Aorta—Saccu- 
lated Aortic Aneurisms—Non-syphilitic Aortic Aneurisms 311 
XVII. Acute Myocarditis—Symptomatology, Physical Signs, Diagnosis and 
Prognosis of Chronic Myocarditis and Cardiosclerosis—The Heart 
in Chronic Emphysema—The Fatty Heart 325 
XVIII. Cardiac Neurosis — General Considerations — “Weak Heart” — 
Irritable Heart in Civil and Military Practice, with Comparative 
Observations—The Goitrous Heart 338 
XIX. Congenital Heart Disease 353 
XX. Drug and other Therapy in Circulatory Disease 360 
XXI. Tobacco—Diet—Renal and Blood Tests in Cardiovascular Disease 389 
xi xii 
TABLE OF CONTENTS 
Chapter Page 
XXII. Sociological Aspects of Heart Disease—Focal Infection—Prophy- 
laxis—General Management—Occupation for “Cardiacs”— 
Cardiac Clinics 396 
XXIII. Precordial Pains of Cardiovascular Origin—Angina Pectoris— 
Coronary Disease:—Etiology, Pathology, Clinical Complexes and 
Therapy 407 
XXIV. Precordial Pains of Extra-cardiac Origin 420 
XXV. Arterial Blood Pressure—Venous Pressure—Capillary Circula- 
tion 426 
XXVI. The Heart and Circulation in Special Diseases—The Heart in 
Diphtheria—The Tobacco Heart—The Aviator’s Heart—The 
Circulation in Surgical Shock—Surgery and the Arrhythmic Heart, 
WITH AND WITHOUT DECOMPENSATION—SURGERY AND HYPERTENSION—THE 
“Fibroid Heart” 444 
XXVII. The Heart in Pneumonia—Therapy from the Circulatory Stand- 
point 455 
XXVIII. Cardiac Disease in Marriage and Pregnancy 463 
XXIX. Cardiovascular Examination of War Recruits. . 471 
XXX. The Role of the Heart in Life Insurance Examinations 476 
XXXI. Graphic Methods—Heart Sound Registration—Phonocardiograms . 482 
XXXII. Clinical Significance of the Abnormally W7ide Ventricular Devia- 
tion in the Electrocardiogram 491 
XXXIII. Mathematical Considerations Underlying the Electrocardiogram. . 498 
PART II 
Cardio-vascular Clinics 505-668 
Index 669 PART I 
THE HEART- 
HS PHYSIOLOGY, PATHOLOGY AND 
CLINICAL ASPECTS 
CHAPTER I 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS—THE 
CONDUCTION SYSTEM—THE CORONARY SYSTEM—THE 
SYSTEMIC, PORTAL AND PULMONARY CIRCUITS—CARDIAC 
NERVE SUPPLY—WEIGHT AND SIZE OF THE HEART- 
POSITION OF THE VALVES 
Embryology as applied to the development of the human heart is impor- 
tant not only because of its intrinsic interest but also because it aids in 
explaining the vast majority of congenital malformations. 
As will be shown later (p. 5), the human heart is essentially a muscular 
pump made up of intricate systems of fibers and muscular bands, and of 
valves. The first rudiment of the embryonic heart consists of a simple tube 
formed by the fusion of two straight tubes on either side of the body; this 
fusion occurs as the ventral cleft of the embryo closes. The septum of the 
fused tube disappears so that a simple straight tube constitutes the primary 
propulsatory apparatus. The tube is lined by a collapsed endothelial lining 
suspended from the tube wall by fine fibrils. The latter seem constant in the 
embryo and are regarded by some as the source of the future connective 
tissue of the endocardium and valves (Mall). The simple muscular 
cylinder undergoes two simultaneous changes: one, of growth, with elonga- 
tion, bending and rolling of the cylinder upon itself; the other, of differentia- 
tion into cavities. In this process, there is gradually developed an important 
embryonic construction, the bulbo-ventricular groove. When the’embryo 
reaches 3.5 mm. in length, the heart becomes separated from the mesoderm, 
the middle layer of the embryo, and is seen as a completed heart tube. By 
continued growth, twisting and elongation, the cardiac tube becomes 
S-shaped and is turned on itself in such fashion that the atrial and venous 
ends are brought close together; what had been the caudal end becomes the 
left limb of the twisted tube, and the cranial end becomes the right limb 
(Tandler). At this stage of growth, the heart tube consists of but two 2 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
chambers—a single ventricle and a single auricle. The anterior lower part of 
the twisted cardiac tube consists of the common ventricle (Fig. i, C. V.) with 
its aortic bulb (Fig. i, A. B.); the latter, an important embryological struc- 
ture, passes upward and to the left, giving off the aortic trunk at right angles. 
The upper part of the common tube consists of 
a one-chambered auricle (Fig. i, C. A.), with the 
sinus venosus behind and to its left. The common 
auricle is lined throughout with endothelium com- 
posed of a solid strand of cells suspended by the 
delicate fibrils already mentioned. In the later 
stages of embryonic development the single atrial 
(auricular), as well as the single ventricular cavity 
become markedly constricted; septa also begin 
to form then, thus gradually dividing each 
common cavity into its respective two chambers. The bulbo-ventricular 
and interventricular grooves become well marked at this time. 
The embryonic aortic bulb (bulbus cordis) leads from the right end of the 
common ventricle to the aortic arches. In the embryo from 4-6 mm. 
long, the bulb is a thick walled muscular tube passing to the left and upward. 
It is lined with endothelium presenting certain endocardial thickenings. 
These are the so-called proximal and distal bulbar swellings, rudiments of the 
semilunar cusps and of the lower part of the aorta-pulmonary septum. Thus 
the human bulbus arteriosus represents developmentally an independent 
chamber with muscular walls and 
valves. Later the bulbus disappears, 
the proximal portion fusing with the 
ventricular wall. The distal portion 
becomes elongated and loses its 
musculature, to become the primitive 
aortic trunk. 
Fig. 1.—Heart of the hu- 
man embryo 5 mm. long. 
Front view. X 30. 
(Modified from His.) 
DEVELOPMENT OF THE INTER- 
AURICULAR AND INTERVEN- 
TRICULAR SEPTA 
The interauricular septum is 
formed partly by the fusion and 
partly by the disappearance of two 
separate partitions. The one—the 
septum primum —at about the fourth week begins from the upper and 
posterior wall of the auricle; it projects downward and forward toward the 
ventricular cavity but does not completely divide the one-chambered 
auricle. The hiatus thus formed in the rudimentary interauricular septum 
is called the ostium primum. Later, another opening is formed by the thin- 
ning of the septum primum itself: this is called the ostium secundum. Thus 
from the primary septum (.septum primum), which only partially divides 
Fig. 2.—Formation of the fetal septa 
{After Aschoff.) EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
3 
the common auricle, two ostia are formed. A second partial partition— 
the septum secundum—arises much later; this also springs from the upper 
right auricular wall and is parallel to the septum primum. In its downward 
growth, the septum primum partially covers the ostium secundum, thus 
giving the latter a valvular character and forming the foramen ovale of 
fetal life. The persisting portion of the ostium secundum found in the adult 
heart is known as the annulus ovalis (Fig. 12). The depression in the 
septal wall of the left auricle of the adult known as the valvida foraminis 
ovalis (Fig. 12) represents the remains of the fetal septum primum. 
The interventricular septum begins at about the fourth week; it springs 
from the inferior wall of the ventricle. With continued growth, the posterior 
portion of the septum fuses with the corresponding walls of the ventricle, its 
anterior projection with the anterior ventricular wall, and the medial part 
with a projection of the aortic septum (q. v.). It is this partition which 
finally divides the common trunk into the aorta and pulmonary artery. 
At about the same time, a constriction appears upon the ventricular surface 
of the heart. This—the interventricular groove—is at first more prominent 
at the apex and becomes shallower as it courses upward. It marks the 
external division between the right and left ventricles, and corresponds to the 
development of the interventricular septum. In this manner, the ventricles 
and their respective vessels are finally separated into right and left chambers 
with their corresponding venous and arterial ostia. The junction of the 
prolongation of the aortic with the interventricular septum forms the pars 
membranacia or the undefended space of the adult heart. It is situated 
immediately beneath the aortic cusps. As its name indicates, it is membrane- 
ous, thin and transparent, and contains no musculature. It is best demon- 
strated in the adult heart by opening both ventricles of the isolated organ, 
and then holding the heart suspended by its great vessels: the undefended 
space then becomes visible as a thin transparent membrane beneath the 
aortic cusps, and forms the upper part of the interventricular septum in this 
organ. 
THE AORTIC SEPTUM 
The study of the development of the aortic septum is important because 
congenital malpositions and malformations of aorta and pulmonary artery 
occur comparatively frequently. The truncus arteriosus—the original 
common embryonic efferent vessel of the common ventricle—becomes 
divided into aorta and pulmonary artery by the formation of the aortic 
septum. Three components are concerned in the formation of this septum— 
the septum aorta-pidmonale (the aorto-pulmonary septum proper), and 
endocardial elevations in the aortic bulb (bulbus cordis) grouped and; known 
as the distal and proximal bulbar swellings. These bulbar swellings later 
develop into the bulbar septa. The truncus arteriosus is thus for a time 
subdivided as follows: distally by the septum aorta pidmonale; mesially by 4 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
the distal bulbar septum, and proximally by the proximal bulbar septum. 
Finally the three septal components—the septum aorta—pulmonale and the 
two bulbar septa coalesce to form the aortic septum. In this manner the 
truncus arteriosus (common arterial trunk) is separated into the two great 
arterial trunks—the aorta and pulmonary artery. This occurs at about the 
seventh week of fetal life, at which time the heart is also divided into its 
various future chambers. 
D uring the period in which the various partitions and septa are being formed 
in the cardiac cavities and in the common arterial trunk, tissue differentiation 
is also proceeding by the continued growth of myocardium (especially of the 
ventricles) and of endocardial thickenings. The myocardium in the spurious 
or false interauricular septum forms a stray bundle. Muscular ridges—the 
rudiments of the future musculi pectinati (Figs. 11, 12) also form at this 
period. Musculature likewise forms in the horns and transverse portions of 
the right and left sinus. The auricular and ventricular musculature is still 
continuous at this period. In the ventricular musculature, two layers can 
be distinguished at this stage; a peripheral cortical, and a central trabecular 
layer. The development of the various muscular layers of the heart will be 
taken up later. 
DEVELOPMENT OF THE VALVES 
The epithelium lining the heart consists of a single layer of epithelial cells. 
The entire ring of the primary foramen ovale is likewise covered by an endo- 
thelial layer. The atrial (auricular) endocardial cushions continue their 
growth downward. At the same time, however, they become gradually 
undermined by the ingrowing trabecular musculature of the ventricle: they 
thus become sharp-edged and finally project freely into the ventricular cavity. 
In the aortic bulb, a similar process proceeds in its bulbar swellings, struc- 
tures which resemble the endocardial cushions histologically. Here also, 
at about the level of the atrial canal, there develops a muscular trabecular 
structure which becomes thicker in texture as it approaches the ventricle. 
Hence at this stage of their formation, all the rudimentary valves are com- 
posed of endocardial projections and cushions, and of musculature. Gradu- 
ally there is differentiation into valve cusps, chordae tendinae, and papillary 
muscles in the auriculo-ventricular valvular structure, and less marked 
differentiation in the formation of the semilunar valves. 
After the division of the heart into its respective chambers, and after 
the formation, of the aortic septum, the right horn of the sinus venosus 
becomes fused with the right auricular wall, and the valvula venosa sinistra 
disappears. The persisting portion of the valvula venosa dextra remains as 
the Eustachian valve (Figs, n, 12) which, corresponding to its origin, is 
continuous above and behind with the crista terminalis (Figs, n, 12) and 
ends below at the coronary sinus. The pulmonary veins are constituted from 
the original single venous trunk. EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
5 
Development of the Cardiac Musculature.—For the understanding of the 
complicated muscular architecture of the adult heart, it will be necessary 
to follow in 'some detail its embryonic development. Most of the bundles 
of the heart in the young embryo run circularly; this circular arrangement, 
however, does not apply to the ventricular apex. The anterior circular 
group, starting at the bulbo-ventricular groove, passes from the bulb, 
to run circularly and penetrate the medial side of the left ventricle; this 
is the sino-spiral bundle. The posterior circular muscle fibers leave the 
surface of the ventricle and enter the rudimentary inferior septum: this 
posterior bundle is known as the bulbo-spiral. Even at this stage of develop- 
ment (embryo io mm. long) the bundle layers, as they sweep over the apex of 
the heart, run in such a direction that they form a vortex at the apex. In 
early embryonic life the circular bundles (the sino- and bulbo-spiral)—are 
found at the base of the heart. With the downward growth of the ventricles 
these bundles are pushed downward, so to speak, and the direction of the 
muscle bundles become more complicated. There are posterior fibers which 
cross diagonally to the apex of the left ventricle anteriorly, thus forming the 
anterior face of the apical whorl or vortex. Beneath the sino-spiral bundle 
are loops encircling the left ventricle, to end posteriorly. They enter the 
septum from behind and constitute the bulbo-spiral fibers. 
Thus, to recapitulate, the simple heart tube is composed chiefly of circu- 
lar fibers. With the bending of the heart tube upon itself somewhat later, 
the muscular bundles at the base retain their circular arrangement. The 
muscle bundles in the apical region undergo changes corresponding in direc- 
tion to changes in the contour of the cardiac tube. The anterior fibers 
originating in the bulbo-ventricular groove in front, pass around the anterior 
surface of the left ventricle to the ventricular septum high up posteriorly, 
immediately beneath the interventricular foramen. The posterior bundles 
originating in the bulbo-ventricular groove encircle the right ventricle and 
pass into the heart in front of the anterior longitudinal sulcus. With the 
continued growth of the ventricles downward, these two encircling strands 
are also pushed downward, and finally interlace at the apex of the left ven- 
tricle. The fibers from the bulb constitute the bulbo-spiral band and the 
posterior horn of the apical vortex; those arising from the sinus side form the 
sino-spiral band and the anterior horn of the apical vortex (Mall). 
Muscular Architecture of the Adult Heart (Fig. 3).—In the auricular 
musculature there is a superficial muscular layer which runs transversely and 
encircles both auricles. Each auricle also possesses a relatively independent 
system of fibers which runs at right angles to the superficial layers. 
The course of the ventricular fibers and layers is quite complex and is as 
yet a matter of uncertainty. According to the most reliable studies, the 
fibers on the ventral surface arise from tendinous rings and membranes at 
the base of the heart; here they form a vortex, pass into the interior of the 
left ventricle to the septum, and connect with the papillary muscles. They 6 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
thus turn on themselves toward the base and form spiral loops, which, when 
contracting, approximate base and apex, and at the same time rotate the 
apex clockwise from left to right. Mall divides these “superficial fibers” 
into two groups: the superficial bulbo-spiral and the superficial sino-spiral. 
The former belong chiefly to the left ventricle. They arise from the conus 
to the left of the aorta and left ostium venosum, proceed spirally, penetrate the 
anterior aspect of the left ventricle and end in the septum and posterior aspect 
of the ventricle, at that point they connect with the posterior papillary mus- 
Fig. 3.—A and B. Muscular architecture of the human heart. Exact reproduction 
from Tractatus de Corde, by Richardo Lower, M.D., published in 1649, showing the general 
arrangement of the layers (A) and the arrangement of the special fasciculi B. 
cles. Some of the deeper fibers of this layer encircle the lower part of the 
ventricle and pass upward, to end at the base of the heart. The superficial 
sino-spiral fibers arise mainly from the posterior aspect of the heart in the 
neighborhood of the right ostium venosum, proceed spirally (though more 
transversely than the first group) to the apex across the anterior surface of 
the right ventricle. They penetrate the interior of the left ventricle arid 
terminate on its anterior surface and in the papillary muscles, especially the 
anterior. Beneath the superficial layers of the bulbo- and sino-spiral systems 
lie similar deep layers which run more transversely or circularly. The deep 
bulbo-spiral layer encircles the left ventricle and ends by way of the septum 
on the dorsal side of the aorta. Some fibers make a circular loop around the 
conus at the base of the pulmonary artery. The entire layer makes a strong 
circular system whose contraction tends to diminish the lumen of the left 
ventricle. The deep sino-spiral layer originates from the posterior aspect 
of the left ostium venosum, passes transversely to enter the interior of the right 
ventricle, and then turns upward toward the base. Here some strands pass 
circularly around the base of the heart and left ostium. EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
7 
THE CONDUCTION SYSTEM 
Because most of the advance in modern cardiology is based upon our 
comparatively recent exact knowledge of what is known as the junctional 
tissue, the bundle of His or the conduction system—a subject to be often 
alluded to—it is important to study in detail its embryonic beginnings as 
well as its structure and distribution in the adult heart. Former embry- 
ologists regarded the atrio-ventricular conduction system as a new formation. 
According to Mall, however, it is to be regarded as 
the remnant of the wall of the atrial canal after its 
anterior and lateral sides have been broken in the 
formation of the tricuspid and mitral valves. 
In various sections of the human embryo, the 
bundle can be followed as a definite structure 
commensurate with the breaking down of the atrial 
wall. The conduction system is plainly visible in 
an embryo 20 mm. long (Fig. 4). Not only does 
the growth of the endocardial cushions previously 
described play a part in the final breaking down 
of the atria but there is also decided ingrowth of 
the connective tissue of the epicardium in the 
neighborhood of the atrio-ventricular groove; 
connective tissue prolongations extend into the 
anterior and posterior longitudinal sulci and into the auriculo-ventricular 
valves. Posteriorly this circular connective tissue surrounds the atrio- 
ventricular bundle so that the latter becomes wedged between the posterior 
Fig. 4.—The atrio-ven- 
tricular conduction system 
in the fetus. {After Mall.) 
r * - \/ Mooe 
- - M aim «S T6rt 
. 0 qb/Tato»? 
8^no 
PoftKl 
Fig. 5.—Right ventricle of ox heart, showing the auriculo-ventricular node (A-V node) 
and the main stem. The right branch is seen running along the “ moderator band.” 
{Modified, from Tawara, ‘ Das Reitzleitungssystem des Sdugethierherzens.”) 
endocardial cushion and the outer connective tissue. This, the survival 
of the embryonic muscular connection between the auricles and ventricles, 
represents the future atrio-ventricular conduction system (the bundle of 8 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
His)—later to become differentiated and innervated. Its embryonic position 
corresponds to its position in the adult. 
In order to have a definite conception of many of the physiological func- 
tions of the heart, as well as of its patho-physiology, it is important to have 
a clear picture and even a visual image of what constitutes the conduction 
system in the adult heart. The conduction system has been variously 
named the atrio-ventricular conduction system, the auriculo-ventricular 
conduction system and the junctional tissues. But no matter how called, 
the outstanding fact to be remembered is that the conduction system forms 
a continuous strand of specialized fibers encased within special sheaths and 
Hr AofTA*- COSPy 
__P0 6T AOHTAL C OIP 
AWTt'»l*(T / 
HMAKf / 
Po«TeRi*ir 
MU»C*-e. 
Pur k'imse. . 
runKiMje 
Fig. 6.—Left ventricle of ox heart, showing conduction system. {Modified from Tawara.) 
having special attributes. The entire system may perhaps be likened to a 
slender uprooted and inverted Y-shaped tree stripped of its leaves (slender, 
for the width of the main stem in the adult heart is approximately i mm.). 
The tree root-clod would then represent the node of Tawara, the origin of the 
conduction system: the tree trunk before its division, the main bundle of 
the conduction system (the bundle of His); the two limbs of the Y, the main 
branches that go to the right and left ventricles, respectively; and the 
smaller branches and twigs of the tree, the twigging branches and final 
aborizations of the conduction system. 
In the adult, for purposes of anatomical identification, the various parts of 
the conduction system (Figs. 5, 6, 7, 8) are differently named, but as already 
stated, they together form one continuous strand. The node of Tawara 
—the beginning of the junctional tissue—and the bundle of His constitute 
the major part of the conduction system before its division. The node and 
bundle lie immediately beneath the endocardium in the lower part of the 
right auricle, slightly above the level of the ventricle, and about midway 
between the opening of the coronary sinus and the fibrous tissue beneath the 
aortic cusps (the aortic vestibule or “undefended space” (Figs. 11,12). The 
further continuation of the conduction system is called the main stem; this 
soon makes a hairpin-like division into its two main branches—the right 
and left (Figs. 5, 6, 7, 8). These branches course respectively on either side 
of the interventricular septum in a direction roughly parallel to the axis of the EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
9 
respective ventricular cavities. The right branch is thin and spreads out in a 
somewhat fan-shaped fashion; the left is more compact, thicker and club- 
like. In their upper portions both branches are superficial and subendo- 
cardial, becoming deeper as they course downwards. At the same time they 
split into secondary and minor twigs and twiglets as they spread toward the 
apex (Figs. 5, 6, 7, 8). In the human adult heart, the main stem and main 
Fig. 7.—i-Branch to base of right ventricle; 2-Tricuspid valve; 3-Conus arteriosus; 
4-Right division of A-V Bundle; 5-Branch to conus arteriosus; 6-Branch to apex. 
{Courtesy of Nelson’s Loose-Leaf Living Medicine.—After A. E. Cohn, injection specimen 
of conduction system on the ox-heart.) 
branches of the conduction system are sometimes dimly discernable through 
the shimmering endocardium as separate, paler, non-glistenings tructures. 
In the ox heart the main branches can be studied macroscopically by first 
hardening' the heart in formalin and then carefully teasing off the overlying 
endocardium with forceps. If this be done, the left branch will be found to 
have three main divisions—one to the apex, and one each to the anterior and IO 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
posterior papillary muscles. The right branch of the ox heart has one divi- 
sion that goes to the large papillary muscle and venous base, the other forms 
the “moderator band” (Fig. 5) which supplies the septal papillary muscle and 
the arterial base (conus arteriosus); from both of these, a division to the 
Fig. 8.—i-Aortic valve; 2—Mitral valve; 3-Left division of A-V bundle; 4-Branch to posterior papillary muscle; 
5—Branch to apex; 6—Branch to anterior papillary muscle. {AfterA. E. Cohen.) {Courtesy of Nelson'sLoose-Leaf 
Living Medicine.) 
apex is formed from separate heads. In both human and mammalian hearts 
the branches finally divide into terminal aborizations (known as Purkinje 
fibers in the mammal), which ramify throughout the papillary muscles and 
probably throughout the entire ventricular musculature. Some of these 
terminal aborizations run free across the apical portion of the ventricular EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
11 
cavities; they were formerly regarded as aberrant tendinous strands. All are 
not purely tendinous, however. Microscopically, they may be distinguished 
from tendinous connective tissue structures by their paler and finer texture 
and non-glistening appearance; and microscopically, final aborizations are 
found to consist of fine, pale, delicately staining cells. 
The main branch and the various subsidiary branches and fasiculi of 
the conduction system are enveloped in special sheaths of connective tissue. 
The smaller enveloping sheaths are fairly constant in structure. The main 
sheath varies somewhat, the connective tissue being at times condensed; at 
others, looser and almost areolar in texture. The main sheath contains the 
blood and lymph vessels, and nerves. 
Dissection and Demonstration of the Conduction System.—In order to 
dissect out the conduction system, the endocardium over the site of the 
auriculo-ventricular (A-V) conduction system is gently teased off with for- 
ceps after the heart has been washed in water and hardened in a formaldehyde 
solution. The conduction system is most readily dissected in the ox or calf 
heart, less readily in the human. After hardening, the heart is first incised 
with a scalpel near the margin of the interventricular septum. The ven- 
tricles are then cut parallel to the latter. In this manner they can be turned 
back flapwise, and the septal walls of the auricle and the ventricular septum 
exposed without injury to the conduction system. In oxen the main branch 
on the right side exists as a separate strand—the moderator band. After 
exposure by teasing in the manner above described, the structure of the 
atrio-ventricular (commonly abbreviated A-V) conduction system will be 
found paler, softer, and more delicate than that of the surrounding muscula- 
ture. Another method of gross demonstration of the conduction system is 
by subendocardial injection of the main branches with a fine hypodermic 
needle and syringe containing a 50 per cent, solution of India ink (Figs. 7, 8). 
If carefully performed, not only the main branches but the subsidiary divi- 
sions as well stand out prominently as darker strands. In this manner, also, 
corroborative evidence is derived that ventricular contraction begins at the 
papillary muscles, for the ink may be seen to reach the latter first, and then 
the base and apex of the heart. For purposes of injection, a No. 1 Luer 
hypodermic syringe with the finest steel needle is used. By careful multiple 
small injections of various fasciculi, a complete picture of the main branches 
with their ramifications and distribution is possible. It can thus be seen 
that in the left ventricle of a beef heart there are two main strands coursing 
along the interventricular septum; these form two subsidiary branches which 
cross the left ventricular cavity and form a network at the base of the papil- 
lary muscles; the interlacing fibers however reach only halfway to the apices 
of these muscles. The network then spreads upward to an area of the ven- 
tricles situated beneath the mitral cusps and near the fibrous ring of the 
mitral orifice. The posterior ventricular wall is also richly supplied by simi- 
lar superficial interlacing fibers. The septal wall itself is not as abundantly 12 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
covered with the superficial network as are the ventricular regions just 
described. The main left branch at its point of emergence beneath the aortic 
cusp is flat and superficial. As it forks, the branches become more oval or 
cylindrical; these course in the trabecular muscular bridges of the ventricular 
musculature and link together the septal and posterior ventricular walls. 
Most of the so-called false or aberrant tendinous fasciculi found in the ven- 
tricular cavity are actually the final threadlike ramifications of the conduc- 
tion system. The tendinous-like threads may be divided into three classes: 
(i) Those containing both the ordinary cardiac muscular fibers as well as 
the special fibers of the conduction system; these form a majority of the 
strands. (2) Those made up of connective tissue alone. (3) Those made 
up of fibers of the conduction system alone (DeWitt). 
The main right branch of the atrio-ventricular conduction system of the 
beef heart also divides and subdivides freely, so that the right ventricle is 
likewise plentifully supplied with subsidiary branches, networks and anasto- 
moses. The right branch, more deeply embedded subendocardially than 
the left, is usually cylindrical in form. It courses along the right of the 
septum and reaches the moderator band, along which it runs until it reaches 
the anterior papillary muscle. To judge from specimens studied by the 
injection method, apparently the right branch does not subdivide until it 
reaches the base of the anterior papillary muscle. 
The injected atrio-ventricular node resembles somewhat in form the 
semilunar ganglion. Besides its continuation into the main stem, and right 
and left branches already described, there are in the beef heart apparently 
two other prolongations of the node; one passing upward going in the direc- 
tion of, and seemingly connected with the sino-auricular node (the node of 
Kieth-Flack), and the other passing in the direction of the coronary sinus. 
The main arterial supply of the auriculo-ventricular conduction system 
(for convenience called the A-V system) is derived from a special branch of 
the right coronary. The junctional tissue is supplied and intertwined with 
medullated nerve fibrils and ganglia. There are numerous ganglion cells— 
(mono-, bi-, and multipolar)—whose processes pass to adjacent ganglion 
cells, to nerve fibers in the bundle or through the A-V system, and end in 
ganglia cells of the bundle or in the muscle plexus. There is an intricate 
plexus of varicose fibrils around, and in close relation to, the muscle fibers of 
the bundle. Thus the A-V system, like the sino-auricular node, is a neuro- 
muscular structure. Although the exact distribution of the extrinsic cardiac 
nerves to the nodes is not known, it appears probable that, regarding the 
vagus distribution, the sino-auricular (or S-A) node is supplied chiefly by 
branches of the right vagus, and the A-V by those of the left. There appears 
to be a similar distribution to the S-A and A-V nodes by the right and left 
accelerators, respectively. 
The Rhythm Center or Pacemaker (Fig. 9).—It has required much 
patient experimentation, and the combined work of physiologist, histologist, EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
13 
pathologist and electro-physiologist to finally determine the exact site and 
minute structure of the rhythm center (also called the pacemaker) of the 
mammalian heart. It may now be definitely set down that the rhythmic 
periodic impulses which normally excite the mammalian heart have their 
origin in the sino-auricular node (also called from their discoverers, the node 
Fig. 9.—Sino-auricular node of pig’s auricle. (After Lewis.) 
of Keith-Flack), and that this node constitutes the normal rhythm center 
or pace-maker. This bit of specialized cardiac tissue is histologically a 
neuromuscular structure. It is irregularly pear-shaped with a larger upper, 
and a somewhat tapering lower end; it is situated in the sinus region, in 
the groove at the junction of the superior vena cava and right auricle (the 
sulcus terminalis (Fig. 12)) immediately beneath the epicardium. The 
node is surrounded by branches of the vagus and sympathetic: it contains a 
plexus of moniliform nerve fibrils and a few ganglionic cells; it is, therefore, 
histologically considered, a neuro-muscular structure. Its blood supply is 
derived from a special artery. The structure, arrangement and composition 
of the node differ materially from the remainder of the cardiac musculature 
(Fig. 9): the cells are smaller, stain more delicately and are paler; the cross 
striations are indistinct or may be absent; the nuclei are pale: there is a 
relative richness of perinuclear sarcoplasm. The cells contain more glycogen 14 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
than those of the non-specialized muscle. They do not follow any orderly, 
layer-like arrangement, but are placed irregularly in a rich stroma of fine 
connective tissue. A f small specialized muscle band connecting the sino- 
Fig. io.—Roentgenogram of the blood supply of the average heart. (After Gross.) 
The coronary arteries and their branches. 
auricular node with the remainder of the conduction system has been 
described (Thorel), but its presence has not been corroborated by other 
observers. 
In early fetal life, the heart lies immediately under the head and is of 
relatively large size. Later, it becomes a thoracic organ, lying at first 
vertically, then gradually assuming a more oblique position. The auricular 
portion with its intercommunication (the foramen ovale) is at first larger EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
15 
than the ventricle. By means of the ductus arteriosus (ductus Botalli), 
the blood from the right ventricle and pulmonary artery passes mainly to 
the aorta instead of to the lungs. To carry on this circulation, the wall of 
the right ventricle is correspondingly muscular and as thick as that of the 
left. Toward the end of fetal life, the left ventricle becomes thicker and 
heavier than the right, and remains so throughout life. 
Coronary Circulation.—The intra-cardiac blood supply demands detailed 
consideration, for disease of this arterial system is very common and accounts 
for many of the symptoms and cardiac changes found in certain types of 
heart disease. The heart itself derives its arterial supply from the right and 
left coronaries (Fig. io). Each arises from the corresponding aortic sinus. 
The right coronary courses at first between the right auricle and conus arterio- 
sus; it finally runs along the posterior longitudinal sulcus, and, as the posterior 
descending ramus, almost reaches the apex of the heart. Branches of the 
right coronary supply the right ventricle, the right atrium and to a lesser 
extent the left ventricle. 
The left coronary is usually the larger of the two. It almost immediately 
divides into a right descending and a circumflex branch. The former soon 
runs along the anterior longitudinal sinus toward the apex of the heart; 
it supplies the interventricular septum, the left ventricle and to a slight 
extent, the right ventricle. The circumflex branch supplies the left ventricle 
and auricle. 
Contrary to older opinions, anatomical investigations by Spalteholz 
and more recently by Gross have demonstrated that the coronaries are not 
end arteries and that they anastomose freely by means of minute branches; 
the latter are usually found in the cardiac muscle itself, more rarely upon the 
surface of the heart. The fact that the coronaries anastomose is extremely 
important, for it explains upon anatomical grounds how some patients with 
occlusion of even comparatively large coronary branches may continue to 
live by the establishment of collateral circulation. Gross’s research has also 
established some interesting and suggestive facts regarding the size and dis- 
tribution of the coronary systems in the various decades of life. Thus in 
early life, there is not much difference between the right and left coronary 
distributions, as shown by injected specimens. With advancing years the 
left gradually gains the ascendancy in the number and distribution of its 
branches. Finally in the old, there is gradual restriction of the distribution 
of both coronaries, but particularly that of the right coronary artery. Such 
anatomical studies may perhaps account for the more serious clinical symp- 
toms occurring in occlusions and disease of that coronary system which is 
already undergoing retrogression. 
The veins of the heart accompany the coronary arteries and their 
branches, and empty into the right auricle. 
The lymph vessels of the heart are very abundant; they are formed from 
radicals derived .from the lymph spaces in the clefts between the muscle 16 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
fibers; they accompany the blood vessels in their course and terminate in 
the thoracic and right lymphatic ducts. 
Regarding the systemic circulation mechanically and as a whole (Figs. 
ii, 12, 13) the primary source of power is of course the heart. But the heart 
may after all be regarded as a means to an end. The central pumping station 
A 
_PV 
PA 
RA 
J LA 
MV Gf) 
RV_ 
MV(pf) 
LCA 
.PM 
XC 
Ms-llone e.'ii. 
Fig. ii.—The adult heart, left side. (After Gray.) 
A, Aorta; P.A., pulmonary artery; R.A., right auricle; R.V., right ventricle; L.C.A., 
left coronary artery; P.V., pulmonary veins; I.L.A., interior of left auricle; M.V. (a.f.), 
anterior flap of mitral valve; M.V. (p.f.), posterior flap of mitral valve; P.M., detached 
papillary muscle; C.C., columnae carneae. 
is designed to carry the blood especially to and through the capillaries, 
by means of which the growth, nutrition and chemical change of life go on; 
for the capillaries come into immediate and direct contact with the tissue cells. 
It is interesting to recall the significant structural adaptation of various parts 
of the cardio-vascular system to their special purposes. Thus, the larger 
arteries consist chiefly of elastic tissue; they are readily distensible, can 
accommodate large quantities of blood, and by their elastic recoil, they propel 
the blood after cardiac systole has ceased. The arterioles contain many 
smooth muscle fibers under the control of the vaso-motor system; this com- EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
17 
bination acts to control the amount of blood flow to the capillary bed. The 
capillaries consist of cells and basement membrane, so that there is ample 
opportunity for the exchange between blood and tissue. The veins are 
thin-walled and distensible, so that, if necessary, they can accommodate 
large quantities of blood; this is especially true of the splanchnic area. 
Some of the larger veins have valves in order to assist the return circulation 
to the right heart. 
vcs 
_A 
_PA 
FT 
TL 
„hp 
A p 
i RA 
sv 
CA 
ACT 
-LA 
FO_ 
CV_ 
_LCA 
E V_ 
TV (af) 
XT 
_PM 
CC_ 
IVC_ 
XV 
RV. 
r'Ullonee.'a.x 
Pig. 12.—The adult heart, right side. (After Gray.) 
V.C.S.- vena cava superior; P.T., foramena Thebesii; T.L., tuberculum Loweri; I.R.A., 
interior right auricle; A.O., annulus ovalis; P.O., fossa ovalis; E.V., Eustachian valve; 
C.V., coronary vein; C.C., columnae carneae; I.V.C., inferior vena cava; R.V., right ven- 
tricle; A, aorta; S.V., semilunar valves; L.C.A., left coronary artery; T.V. (a.f.), anterior 
flap of the tricuspid valve; C.T., chordae tendinae; P.M., papillary muscle; L.V., left ven- 
tricle; P.A., pulmonary artery; A.P., appendix; C.A., corpus Arantii. 
Two subsidiary systems—the portal and pulmonary—(Fig. 13)—remain 
to be briefly considered. The portal vein collects the blood from the venous 
radicals of the intestinal walls and villi. This blood, with its elaborated food 
products as the result of intestinal digestion, is re-distributed through the 
liver by means of a second set of hepatic capillaries, to be again collected into 
the inferior vena cava. In the pulmonary circuit, the venous blood is dis- 
tributed to the alveoli in the lungs, so that the venous blood loses its surplus 18 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
1- canal; 
2- ventricle; 
3- auricle; 
4- auricle; 
5- ventricle; 
6- 
Fig. 13.—Schematic view of systemic, pulmonary and portal circulations. EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
19 
of carbon dioxide and receives oxygen in exchange. The freshly oxygenated 
blood is finally returned to the left auricle by means of the pulmonary veins. 
Thus the pulmonary circuit is completed. 
The Cardiac Nerve Supply (Figs. 14, 15).—It is necessary to describe in 
some detail the nerve supply of the heart because of its importance both from 
the physiological and clinical standpoints. The extrinsic nerve supply is an 
extremely complicated one. It is rendered more so by the presence of 
numerous plexuses which themselves intercommunicate and decussate. 
The extrinsic cardiac nerves are those derived from the vagus and from the 
sympathetic system. The vagus arises by several roots in the medulla in 
the furrow behind the olivary body and below the origin of the glosso- 
pharyngeus (Figs. 14, 15). It contains not only motor and sensory, but also 
vegetative fibers. It sends afferent branches to the heart, pharynx, esopha- 
gus and stomach, and possibly also to other viscera. The chief physiological 
function of the vagus on the heart is inhibition. The depressor nerve, the 
efferent nerve of the heart, has branches which are grouped chiefly about the 
root of the aorta. It runs as part of the vagus and forms the viscero-sensory 
tract of the latter nerve. Experimental stimulation of the central cut end 
of the depressor causes a fall of blood pressure by reflex action upon the 
medulla. The chief sympathetic afferent nerve of the heart is the accelerator. 
In mammals, the two most constant branches of the sympathetic system 
are those which surround the subclavian arteries to form the plexus known 
as the annulus of Vieussens (ansa subclavia). Situated at the base of the 
heart are the superficial and deep cardiac plexuses. The superficial plexus 
lies in the concavity of the aortic arch; the deep plexus, between the trachea 
and aorta. The latter is composed of nerves derived from the sympathetic 
cervical ganglia, and from the cardiac branches of the recurrent laryngeal 
and vagus. The branches from the right side of the plexus go to form parts 
of the anterior and posterior coronary plexuses; they also send a few filaments 
to the right auricle. The branches from the left side are distributed to the 
left auricle and compose a large part of the posterior coronary plexus. The 
superficial cardiac plexus forms the chief part of the anterior coronary plexus. 
The posterior and anterior coronary plexuses surround and accompany 
the branches of the right and left coronary arteries, respectively, and dis- 
tribute filaments to the ventricular musculature. The coronary plexuses as 
well as their muscular filaments are richly supplied with ganglia. 
Intracardiac ganglia have been found in the auricular wall, at the mouths 
of the superior and inferior vena cava, and at the origin of the coronary sinus. 
They have also been found at the level of the auriculo-ventricular junction, 
especially about the aorta and the pulmonary artery. Scattered ganglia, 
either as single cells or in small groups, have likewise been observed practi- 
cally throughout the entire heart. As has already been pointed out, 
impulses normally originate in the pacemaker (the sino-auricular node), and 
not, as previously thought, in other ganglionic groups. 20 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
Pyramis 
Gang/.jugu/are 
- Oliva 
Gang!, 
jug u /are 
Gang/, petrosum' 
R. auric. 
,/va3' 
R. anastomot/cus _ 
cum 
Gang/. 
nodosum 
N. g/ossopharyngTg/ 
R. auricu/ar/'s -— 
R. pharyngeus - 
Ai./aryngeus superior 
Gang/, sympath. 
supremum 
//. Vagus 
N Vagus 
Sympath, 
cervica/is 
P/exu.sW 
phar/ngeus 
Gang/, 
ste! latum 
Truncus sympathicus thoracai is 
fjGang/. < 
lY/risbergii 
P/ex. 
pu/mona/is 
Plexos oesophageos 
Gang/, so/a re 
Fig. 14.—Extrinsic nerves of the heart. (After Muller.) 
P/ex. Gastricus EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
21 
Nucleus vagi 
| viscera! is 
'Fasciculus so/tlanus 
\ (Nucleus vagi sensibi/is ) 
'jug u! are 
vd$' 
Ganglion 
nodosum 
Nervus 
gssiricus 
Fig. 15.—Schematic view of the vagus and its branches, and their connection with the 
sympathetic. (After Muller.) 22 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
Of special clinical importance and interest is the connection between the 
extrinsic nerves with the sino-auricular node and the atrio-ventricular 
conduction system. These two specialized structures are supplied by, and 
intertwined with, nerve fibrils and ganglia. Regarding the atrio-ventricular 
conduction system, as already stated, they contain numerous ganglion cells, 
with one, two or several polar processes; these processes pass either to adja- 
cent ganglion cells, to nerve fibers in the bundle, or directly to the conduc- 
tion system. Some nerve fibers end in ganglia cells of the bundle or in the 
muscle plexus. There is also an intricate plexus of varicose fibrils around, and 
in close relation to, the muscle fibers of the bundle, making the auriculo-ventrlc- 
ular conduction system, like the sino-auricular node, a neuro-muscular 
structure. Although the exact distribution of the extrinsic cardiac nerves 
to the nodes is not known, it appears probable that, regarding the vagus dis- 
tribution, the sino-auricular (S-A) node is supplied chiefly by branches of the 
right, and the atrio-ventricular (A-V) node by those of the left vagus. 
There appears to be a similar distribution to the S-A and A-V nodes by the 
right and left accelerators, respectively. 
P.v. 
-A.V. 
-TV. 
'H-V. 
tfti- 
Fig. 16.—Diagrammatic position of the cardiac valves. 
P.V., Pulmonary valves; A.V., aortic valves; T.V., tricuspid valves; M.V., mitral valves 
Weight and Size of the Heart—Position of the Valves.—The average 
normal adult heart weighs, in the male, from 280 to 360 grams to 12 oz.); 
in the female, from 240 to 330 grams (9 to n oz.); its proportion to body 
weight ranges approximately from 1:160 to 1:170. Although hearts vary 
considerably in size within normal limits, the average length of the adult 
heart on its longest axis is from 12 to 15 c.m. to 6 inches); its greatest 
breadth, 9 to n c.m. to inches); thickness, 5 to 8 c.m. (2 to 3 
inches). The normal circumference of the various valvular orifices is as 
follows: the tricuspid, n to 13 c.m. (5 to inches); the mitral 9 to n c.m. EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
23 
(4T4 to 5 inches): the pulmonary, 8 to 9 c.m. (about 3)4 inches); the aortic, 
7 to 8 c.m. (about 3)4 inches). The adult heart lies behind the lower two 
thirds of the sternum. The methods for determining the position of the 
valves with the heart in situ by frozen sections, and also by coating the 
valvular surface with lead and subsequently taking radiographs, have not 
Fig. 16A.—Exact location of the heart, etc. See Legend on Photo. (Courtesy of Dr. 
L. T. Le Wald.) 
given uniform results. According to Piersol, the aortic valves lie behind 
the left half of the sternum, a little below and to the right of the pulmonary 
valves; the latter are situated behind the sternal end of the third left costal 
cartilage. The tricuspids are situated behind the midsternum, opposite the 
fourth interspace and the fifth chondro-sternal articulation; the mitral valves 
are opposite the sternal end of the third left interspace (Figs. 16, 16A). 
REFERENCES 
Abbott in Osier & McRae: Vol. IV, p. 330. 
Aschoff, L.: Referate ueber die Herzstoerungen der specifischen Muskelsystems des 
Herzens; Verhandlungen der deutschen pathologischen Gesellschaft, 1910. 
Born: Beitraege z. Entwickelung d. Saeugethierherzens, Arch. f. Mikro. Anatom., 1889, 
XXXIII, p. 284. 24 
EMBRYOLOGICAL AND ANATOMICAL CONSIDERATIONS 
Cyon, E. de: Les Nerfs du Coeur. 
Cohn, A. E.: Differences in the effects of stimulation of the two vagus nerves on rate and 
conduction in the Dog’s Heart. Journal Experimental Med., 1912, XVI, 732. 
Cohn, A. E., Kessel, L., and Mason, H. H.: Observations on the functions of the Sino- 
auricular Node in the Dog; Heart, 1911-1912, III, 311. 
Cohn, A. E.: Observations on Injection Specimens of the Conduction System in Ox Hearts; 
Heart, 1912-1913, IV, 225. 
Cohn, A. E., and Lewis, T.: The Predominant Influence of the Left Vagus on Conduction 
between Auricle and Ventricle in the Dog; Journal of Experimental Medicine, 1913, 
XVIII, 739- 
Dogiel: Das Verhaeltnis des Nervensystems, beim Hunde, Kalbe und Menschen, Archiv. f. 
ges. Physiologie, Vol. 142, 19x1. 
Keibel & Mall’s Human Embryology, 1912, II, 534-570. 
King: The Sino-ventricular system as demonstrated by the injection method. 
American Journal Anatomy, 19x6, XIX, p. 149. 
Keith, A., and Flack, M.: The form and nature of the Muscular Connections between the 
Primary Divisions of the Vertebrate Heart; Journal of Anatomy and Physiology, 
1907, XLI, 172. 
Lewis, T.: Lectures on the Heart. 
Lewis, T., Oppenheimer, B. S., and Oppenheimer, A.: The site of origin of the Mammalian 
Heart Beat; The Pacemaker in the Dog; Heart, 1910-1911, II, 147. 
Lhamon, R. M.: The sheath of the Sino-ventricular Bundle; American Journal of Anatomy 
1912, XIII, 55. 
Mall: American Journal of Anatomy, 1911, XI, 211; 1912, XII, 264; 1913, XIV, 249. 
McCallum, J. B.: On the Histogenesis of the Striated Muscle Fibre and the Growth of the 
Human Sartorius Muscle: Johns Hopkins Bulletin, 1918, IX, 208. 
Monckeberg: Verhand, d. Deut. Path. Gesellsch, 1913, XVI, 228. 
Muller, L. R.: Beitraege zur Anatomie, Histologie und Physiologie des Nervus vagus, etc. 
Deut. Arch. f. Klin. Med., 19x0, Cl, 423, 437. 
Tawara, S.: Das Reitzleitungssystem des Saeugethierherzens. 
Thorel, C.: Vorlaeufige Mittheilung ueber eine besondere Muskelverbindung zwischen der 
Cava Superior und dem Hissischen Buendel; Muenchener Med. Wochenschrift, 1909, 
LVI, 2159. 
Wilson, J. G.: The nerve of the Atrio-ventricular Bundle; Proceedings of the Royal Society 
1909, B, LXXXI, 151. CHAPTER II 
FETAL CIRCULATION—CON GENITAL MALFORMATIONS, DEFECTS 
AND ANOMALIES 
Fetal Circulation.—It will simplify the understanding of some of the 
congenital anomalies by recalling the salient features of the fetal circulation. 
The blood for the fetus is collected from the placenta by the umbilical vein. 
This vein enters the fetal abdomen through the umbilicus and courses along 
the suspensory ligaments of the liver to the under surface of that organ. 
Here the blood of the umbilical vein is divided into three channels: (i) the 
greater quantity passes by means of the hepatic veins through the liver with 
the portal venous blood before the latter enters the inferior vena cava; (2) 
some blood goes directly to the liver, to be also returned to the inferior vena 
cava by the junction of the ductus venosus and left hepatic vein; (3) a small 
quantity goes directly into the vena cava by the junction of the ductus 
venosus and left hepatic vein. 
Congenital Malformations, Defects and Anomalies.—Although it had 
been formerly held that maternal impressions, injuries to the mother, and 
fetal endocarditis were the usual causes of congenital anomalies, malfor- 
mations and defects, modern research has shown that practically all con- 
genital defects are of developmental origin. Maternal impressions and 
injuries may now be entirely discarded as etiological factors. Regarding 
fetal endocarditis, an occasional rare case of sclerosis, especially of the 
pulmonary valve, may be exceptionally caused by a severe infection, particu- 
larly rheumatism, in the pregnant mother. 
Developmental defects may be subdivided into: (1) those due to com- 
pletely arrested developments; (2) abnormal developments; (3) abnormal 
septal deviations. All occur in early fetal life before the affected structures 
are fully grown. In a fair proportion of cases, other congenital anomalies, 
such as imperforate anus, absence of the fibula and complete or partial 
transposition of the viscera are found. Indeed, such more striking 
anomalies alone may direct attention to the heart as another possible con- 
genitally defective organ. 
It should be remarked that septal defects, complete absence of the septum 
and other anomalies do not often occur as “pure” cases; there is very 
frequently an admixture of anomalies in the same heart. 
25 26 
FETAL CIRCULATION—CONGENITAL MALFORMATIONS 
SEPTAL DEFECTS 
Although septal defects have been variously subdivided, it will be suffi- 
cient for our purposes to adopt the following simple classification to indicate 
the usual types. 
Fig. 17.—Patent foramen ovale with cornua of the embryonic valves still remaining apart 
Pulmonary stenosis is also present. {After Peacock.) 
1. Defects of the Interauricular Septum. Patent Forman Ovale (Fig. 
17).—It is very common to find that the foramen ovale in the adult has 
not been entirely closed, leaving a small slit-like opening. Referring however 
to appreciable sized foramina, patent foramen ovale is not only by far the 
most frequent defect of the interauricular septum, but it is the most common 
of all congenital defects (191 out of 631 defect cases—Abbott). The size 
of the opening varies considerably, from one admitting an ordinary lead 
pencil to one several centimeters in diameter. 
Other malformations of this septum consist in defects of its upper pos- 
terior, and of its lower portion. The latter are probably due to failure of 
closure of the septum primum (q. v. Chapter I). Another septal deformity 
consists of multiple foramina in the interauricular wall. 
2. Defects of the Interventricular Septum.—These are not uncommon 
(189 out of 631 defect cases—Abbott). Almost all of these defects occur 
at the base of the septum (Fig. 18); rarely elsewhere. Such basal defects 
are most commonly combined with pulmonary stenosis and a right sided 
aorta. It has already been pointed out that in the embryo, the aortic 
septum is pushed downward to form part of the upper interventricular 
septum (q. v. Chapter I) at the pars membranacea (Figs. 11,12). It would 
therefore appear that basal interventricular defects are probably due to 
arrest or non-development of the downward prolongation of this embryo- 
logical aortic septum. In most of the defects of the interventricular septum, FETAL CIRCULATION—CONGENITAL MALFORMATIONS 
27 
it is rather surprising to note that the conduction system (Chapter I), 
although it lies in close proximity to the undefended space (pars membrancea) 
and hence to the basal defect, is little if at all disturbed in its course. 
3. Aneurism of the Undefended Space.—Several observers (especially 
Rokitansky) have recorded instances of this interesting anomaly (Fig. 19). 
It has occasionally been found as the site of malignant endocarditis. It 
Fig. 18.—Patent interventricular septum. (After Farre.) 
has therefore been held by some that endocarditis is the cause of such aneu- 
risms. According to Mall, however, the cause lies in malposition of the 
inferior septum (q. v. Chapter I); as a consequence, the membraneous septum 
develops in a horizontal plane and thus becomes subject to undue mechanical 
strain and impact from the circulating blood, with the final result of the 
development of an aneurism. 28 
FETAL CIRCULATION—CONGENITAL MALFORMATIONS 
4. Gross Defects or Entire Absence of Interauricular and Interventricu- 
lar Septa.—Septal defects so large that only rudiments of the septa persist 
give rise to various types of two or three chambered (bi- and tri-loculated) 
hearts {cor biloculare, cor triloculare). There may co-exist atresia of the 
mitral or tricuspid valves, and, in addition, an abnormal origin or rudimen- 
tary development of either the aorta or pulmonary artery, or of both. 
PiG. 19.—a, Aneurism of the undefended space. (After Rokitansky.) 
A curious septal anomaly consists in the presence of an interauricular 
septum and the absence of an interventricular one, i.e. a three-chambered 
heart: two auricles with a common ventricle (cor biatriatrum triloculare). 
In rare instances there exists another type of triloculated heart: the inter- FETAL CIRCULATION—CONGENITAL MALFORMATIONS 
29 
auricular septum is absent and the interventricular one is present; there are 
thus two ventricles and a common auricle {cor biventriculare triloculare). 
5. Defects of the Septum of the Aorta and of the Truncus Arteriosus.— 
The embryological formation of the aorta and pulmonary artery by the 
growth of the aortic septum has already been described (Chapter I). If 
there be entire absence of the aortic septum, there results a persistent truncus 
arteriosus; the latter, as the common arterial trunk, then usually receives the 
blood from both ventricles and gives off a pulmonary artery branch, in 
addition to supplying the usual branches of the aorta. A persistent truncus 
arteriosus is frequently combined with bi- or triloculated hearts, or with single 
interventricular defects. 
6. Valvular Stenoses and Atresias.—There are varying degrees of con- 
genital stenosis which may affect the cardiac valves. When there is complete 
obliteration of the canal, the condition is called atresia. Although most 
valvular stenoses and atresias are regarded as of developmental origin, some 
of the stenoses, especially where they form the only anomaly, are believed to 
be of inflammatory origin, the result of fetal endocarditis. 
Stenosis or atresia of the ascending aorta is quite rare. 
Stenosis and Atresia of the Pulmonary artery form alarge and very impor- 
tant class of the cardiac defects. Either anomaly may affect the vessel at its 
cardiac insertion (the conus), at the level of the valves, or, finally, the calibre of 
the artery beyond the valves. In rare instances a large part of the pulmonary 
artery from and including its insertion may be involved. A developmental 
triad that forms a common associated picture consists of pulmonary stenosis, 
defect at the base of the interventricular septum and a rightsided aorta 
receiving blood from both ventricles. 
Atresia and stenosis of the auriculo-ventricular valves are exceedingly 
rare anomalies. To judge from associated pathological changes, some of the 
cases seem to be the result of fetal endocarditis, the others of developmental 
origin. Atresia and stenosis affect the tricuspid oftener than the mitral 
valve. 
7. Septal and Valvular Anomalies.—Anomalous intra-auricular septa 
have been reported. Those occurring in the right auricle consist of a weblike 
reticulum stretching across the auricular chamber (Chiari). They are 
ascribed to mal-development of the septum spurium (q. v. Chapter I) or of the 
venous valves (Chiari). Cases have been reported in which the left auricle is 
divided into two chambers by the formation of a membrane; the latter is 
perforated so as to allow the blood from the upper chamber (into which the 
veins empty) to flow into the lower chamber and thence to the mitral orifice. 
This developmental anomaly is regarded as due to a misplaced septum 
spurium (Borst, quoted by Abbott). 
The auriculo-ventricular valve may be duplicated by a similar supernu- 
merary valvular apparatus with its papillary muscles, chordae tendinae and 
valve leaflets, thus forming a double auriculo-ventricular opening. Semi- 30 
FETAL CIRCULATION—CONGENITAL MALFORMATIONS 
lunar cusps may be increased or decreased in number as the result of develop- 
mental defects; the largest number described has been five; the smallest two 
In the latter instance, it is probably the result of fusion in fetal life of the 
rudiments of the individual leaflets. 
Occasionally fenestra of larger or smaller size occur in the semilunar 
valves (Aschoff) i 
So-called false tendons may traverse either ventricular cavity. It is 
now known that in the majority of cases these anomalous structures are not 
tendinous in nature but are large, coarse, aberrant ventricular branches of 
the auriculo-ventricular conduction system (q. v.). 
8. Defects and Anomalies of the Ductus Arteriosus (Ductus Botalli).— 
As is known, the ductus arteriosus is a short, patent, fetal vessel connecting, 
the aorta and pulmonary artery. Normally it becomes impermeable within 
two or three weeks after birth. When patency persists—a comparatively 
frequent congenital anomaly—it is usually combined with pulmonary atresia 
or stenosis. The lumen of a patent ductus arteriosus varies considerably in 
size, from a scarcely perceptible opening to one admitting a pencil or even 
larger. Occasionally, the persistent duct becomes dilated. This condition 
has been called aneurism by some observers, but the name is apparently not 
justified, for no change in the vessel wall comparable to that of an actual 
aneurism has been found. 
9. Deviations and Transpositions of the Arterial Trunks.—Rokitansky 
has described in great detail his theory of the causes of deviations and trans- 
positions of the aorta and pulmonary artery. Briefly expressed, he attributes 
the phenomena fundamentally to varying degrees of congenital deviations 
of these vessels. He conceives the anomaly as a fault in the development of 
the aortic septum. If, for example, the concavity of the aortic septum be 
deviated so that it faces anteriorly, it would give rise to an anterior left aorta 
and a posterior right pulmonary artery. This exactly reverses the normal 
relationship of the aorta and pulmonary artery, for the pulmonary artery 
normally originates anterior to, and to the left of the aorta (Figs, n, 12), and 
passes backward underneath the aortic arch. Ihe normal aorta at its 
origin lies to the right of, and in a plane posterior to the root of the pulmonary 
artery. 
By means of various deviations and transpositions of the fetal aortic 
septum in the primitive aortic bulb (Figs. 1, 2), combined with mal-union of 
the aortic and fetal interventricular septa, several types and combinations of 
anomalies can be readily conceived. For example, a deviated aortic septum 
(and with it, the aorta) could fuse with a normally placed or with a misplaced 
interventricular septum. In the former instance, the aorta and pulmonary 
alone are transposed; the aorta then surmounts the right ventricle, and the 
pulmonary artery, the left ventricle. The ventricles retain their normal posi- 
tions. This represents complete transposition of the arterial trunks. With 
fusion of aortic and interventricular septa—both misplaced—there is cor- FETAL CIRCULATION—CONGENITAL MALFORMATIONS 
3i 
responding transposition of position of right with left ventricle, so that the 
transposition of the vessels may be regarded as “corrected;” that is to say, 
the transposed (now right sided aorta) arises from a transposed (now right 
sided) “left” ventricle. Such transpositions are therefore classified as 
“corrected” transposed arterial trunks. 
Other arterial transpositions consist of double implantation of aorta and 
pulmonary artery from a common ventricle, either right or left, with a 
normal or transposed relationship of pulmonary artery to aorta (Abbott). 
The semilunar cusps in almost all instances of these transpositions show 
various deformities, such as being of unequal size or being bicuspid. The 
valves become rotated in accordance with the abnormal position taken by the 
arterial trunks; the degree of rotation and deviation may be determined by 
observing, for example, the position of the non-coronary cusp of the aorta. 
Although the theory of Rokitansky as already given seems to cover the 
facts, it should be observed that Keith believes the various transpositions 
can be best accounted for by assuming a fetal atrophic process affecting one 
arterial trunk, and an expansion of the remaining vessel; the final effect would 
thus also bring about various abnormal relationships of the aorta to the 
pulmonary artery. 
10. Co-arctation of the Aorta.—This, a comparatively frequent congenital 
anomaly, consists of various degrees of narrowing of the aorta near the inser- 
tion of the ductus Botalli. The narrowing may vary from slight constriction 
to complete obliteration. The area of the aorta affected is the isthmus (the 
portion lying between the ductus arteriosus and the origin of the subclavian 
artery), which in fetal life is normally of smaller calibre than the remainder 
of the aorta. 
11. Aortic hypoplasia consists of congenital general narrowing of the 
entire aorta and its branches. The vessel walls are usually thinner and 
finer in texture than the normal. With this condition there may also be 
similar diminution in the size of the heart. 
12. Anomalies of the Aortic Arch.—The aorta and its chief branches are 
subject to various anomalous positions. These include vicarious insertions 
and courses of the aortic branches. The fundamental reason for the anomaly 
lies in the fact that in fetal life, the aorta represents a double tube with six 
embryonic arches (Figs. 20, 21). Several of these normally disappear, while 
those that persist form the carotids, the aorta, the subclavians, and the 
pulmonary artery with the ductus arteriosus. 
13. Anomalies Affecting the Entire Heart.—If the embryonic process 
affecting the heart be interfered with in early fetal life, the heart may be 
merely a rudimentary organ (hemicardia), or indeed there may be no cardiac 
organ at all (acardia). As an exceedingly rare finding in man, more than one 
heart may be present. The apex of the heart may be bifid, due to persistance 
of the fetal interventricular groove (q. v. Chapter I). Such a bifid apex may 32 
FETAL CIRCULATION—CONGENITAL MALFORMATIONS 
occur as the only anomaly. The heart may be congenitally displaced outside 
of the thorax, either through a fissure in the sternum (ectopia cordis pectoralis) 
or through an opening in the diaphragm. In the latter instance, it becomes 
External carotid 
Internal carotid 
Common carotid 
Ventral aorta- 
Aortic arch. 
Right 
subclavian 
artery "" 
.Ductus Arteriosus 
Artery 
Right 
pulmonary 
artery 
% Subclavian - 
artery left pul- 
monary artery 
Trunk 
of pulmonary 
artery 
Dorsal aorta 
Fig. 20.—Diagram showing aortic arches and their derivatives in the human embryo 
(After Prentiss.) 
Aortic arch 3 
'nt. carotid artery. 
Aortic arch 2. 
Aortic arch 4 
Aortic arch 6— 
Aortic arch 5 
Pulmonary artery 
Butbus cord 
Dorsal aorta 
Pig. 21.—Aortic arches of human embryo of 7 mm. (After Tandler.) 
an abdominal organ (ectopia cordis abdominalis); this condition is not neces- 
sarily incompatible with life. 
14. Congenital Dextrocardia.—There may be no actual transposition but 
a simple vertical rotation in an anti-clockwise direction, so that the apex is FETAL CIRCULATION—CONGENITAL MALFORMATIONS 
33 
directed to the right, with the result that the left ventricle comes to lie more 
anteriorly, and the right ventricle more posteriorly than is normal. Most 
cases of congenital dextrocardia are of this type. 
In another—a rare group—there is “mirror” transposition—(Abbott) 
—all rightsided structures become left, and vice versa. The apex, directed 
to the right, is formed, as normally by the left ventricle. Congenital dextro- 
cardia is often accompanied by transposition of other viscera; for example, 
of the gastro-intestinal canal, the testes, liver, etc. The diagnosis of con- 
genital dextrocardia by means of electrocardiograms will be discussed later 
in another connection (Chapter IX). 
REFERENCES 
Abbott in Osier and McCrae: Vol. IV. 
Aschoff: Pathologische Anatomie. 
Carpenter: On Congenital Heart Affections. British Journal Child. Dis., 1909, Vol. VI, 
PP- 337, 385, 433- 
Farre: On Malformations of the Human Heart, London, 1814. 
Gerard: De la persistance simple de la canal arteriel., Rev. de med. 1900, pp. 645 and 837; 
Jour, de l’Anat et de la Physiologique, 1900, pp. x and 323. 
Kaufman: Pathologische Anatomie. 
Keith: Malformation of the Heart, Lancet, 1909, Vol. II, 359, 433, 519. 
Lebert: Schrotter in Ziemssen’s Handbuch der spec. Path, et Ther., Vol. VI. 
Morison: The auriculo-ventricular nodes in malformed hearts. Jour. Anat. and Physiol., 
1913, XLVII, 459. 
Moussous: Maladies Congenital du Coeur. 
Peacock: Malformations of the Human Heart, 1858 and 1866. 
Rauchfuss (1878): Gerhardt’s Handb. d. Kinderkrankheiten, IV, part I. 
Rokitansky: Defekte der Scheidewand des Herzens, Vienna, 1875. 
Theremin: Etudes sur les affections congenitales du coeur. 
Thorel: in Lubarsch and Ostertag’s Ergebnisse, XIV (2), 268. CHAPTER III 
PHYSIOLOGICAL CONSIDERATIONS—NORMAL SPREAD OF THE 
WAVE OF EXCITATION—THE EXTRINSIC CARDIAC NERVES— 
THE CARDIO-INHIBITORY CENTER—MYOGENIC OR NEURO- 
GENIC IMPULSES? 
It has long been known that certain fluids appropriately introduced into 
the isolated frog’s heart will keep that organ beating for a long time; such 
artificial circulation consists essentially in a method of perfusing the heart 
by introducing the fluid through the veins. Blood and lymph were originally 
used. Later, various solutions were employed, and their effect upon the 
contractility of the isolated frog’s heart was studied. Ringer discovered that 
a perfusion solution containing a mixture of sodium, potassium and calcium 
chlorid would keep a frog’s heart beating for many hours. An effective 
Ringer’s solution for experimentation purposes upon the frog or turtle heart 
should contain 0.7 per cent, sodium chlorid, 0.03 per cent, potassium chlorid 
and 0.025 Per cent, calcium chlorid (Howell). A physiological salt solution 
alone (sodium chlorid, 0.7 per cent.), if perfused, produces rhythmical con- 
tractions for a comparatively short time; the contractions gradually become 
weaker and finally stop. In order to keep an isolated mammalian heart 
alive, Locke’s solution is preferable; it contains sodium chlorid, 0.024 Per 
cent.; potassium chlorid, 0.042 per cent.; bicarbonate of soda, 0.01 to 0.03 
per cent., and dextrose 0.1 per cent. The dextrose, while not essential, 
increases the effectiveness of the mixture. The mammalian heart is perfused 
under an atmosphere of oxygen. 
The results of much experimentation have shown that, in order to main- 
tain cardiac contractility of the isolated heart most efficiently, the salts of 
sodium, potassium and calcium must be employed, and these in certain 
definite proportions. If, for example, a turtle’s heart be perfused with blood 
serum from which the calcium salts have been removed by precipitation with 
sodium oxalate, the heart comes to a standstill, to again contract normally 
when the proper proportion of calcium chlorid has been added to the oxalated 
blood. While it is evident that the ions just mentioned have an intimate 
and necessary connection with the maintenance of cardiac contractility, and 
while it seems probable that each metal has an individual and specialized 
function relating to cardiac systole and diastole, it is as yet unknown what 
their definite correlation is to the contractile substance of the heart or to the 
fundamental ‘‘inner stimulus”—be it chemical, neurogenic or otherwise—• 
which produces the heart beat (Howell). On the whole, it seems probable 
that the calcium, sodium and potassium salts act antagonistically, that the 
34 PHYSIOLOGICAL CONSIDERATIONS 
35 
calcium promotes contractility, while sodium and potassium salts produce a 
state of relaxation. 
Engelmann and Gaskell, by careful experimentation about forty years 
ago, established certain attributes of the cardiac musculature, namely, irrita- 
bility, contractility, rhythmicity and conductivity. These have been 
respectively designated by Engelmann as bathmotropic, inotropic, chronotro- 
pic, and dromotropic functions; he has qualified them as positive or negative, 
depending upon influences which act favorably or unfavorably upon the 
individual functions. This nomenclature, however, has not found its way 
into the general literature of cardiology. To the four attributes of cardiac 
musculature, Gaskell has added a fifth—tonicity. As will be seen later, 
various portions of the heart are differently endowed with these five special 
attributes. 
Rhythmicity.—Thorough experimental and electrocardiographic inves- 
tigations in mammals, and histological and pathological studies in man and 
animals, have proven, as already stated (Chapter I), that the primwn movens 
—the center for rhythmicity—the normal impulse center in the human being 
—exists in what is variously known as the pacemaker, the sino-auricular node 
(the S-A node), or the node of Keith-Flack. The classical ligature experi- 
ment of Stannius (first ligature of Stannius) many years ago proved that in 
cold blooded animals, the rhythm center is situated in the region of the 
sinus venosus. He ligated the heart in the sinus region: The auricle and 
ventricle ceased beating; the sinus continued to beat. Other more recent 
corroborative evidence that the sino-auricular node is the normal pace- 
maker is the fact that experimental excision of the node usually causes the 
auricle to stop beating entirely or to beat very slowly; and, further, the 
electrocardiographic observation that the node becomes electrically negative 
(that is, it shows activity) before the remainder of the sinus region. 
While the node is the normal pacemaker, it is well to emphasize here that 
clinical conditions occur in which the normal pacemaker does not act but 
that other portions of the heart—usually other portions of the auricle— 
take up the pacemaking function, and become for the time being the 
rhythm center. These abnormal clinical conditions will be described later 
(Chapters X, XI). 
As the result then, of all these different investigations, it may be definitely 
stated that the normal excitation processes, the normal center from which 
impulses in the human heart start, originate in the pacemaker, the sino- 
auricular node. 
Conductivity.—This property of the cardiac musculature deals with the 
manner in which impulses starting from the pacemaker spread throughout 
the remainder of the heart muscle, that is, through the auricles and ventricles. 
In these observations of the respectively excited portions of the cardiac 
musculature, use has been made almost entirely of electrocardiographic 
tracings. These will be described in detail in their proper connections 36 
PHYSIOLOGICAL CONSIDERATIONS 
(Chapters VIII-X). For the better understanding of the spread of the 
excitation wave, it will suffice to state at this time that every muscle in 
contracting produces a small amount of electricity; that this electricity can 
be conducted (led off) from the contracting muscle by means of non-polari- 
zable electrodes. In animal experiments such electrodes can be placed directly 
in contact with the various portions of the heart whose excitation and con- 
tracting processes one wishes to study: This constitutes the direct method of 
electrocardiography (Figs. 59-69). For other purposes the indirect method 
is employed. It consists of different types of non-polarizable electrodes 
which are placed around each forelimb and left leg of the animal, correspond- 
ing to the electrodes placed upon the forearms and left leg (Figs. 64, 65) 
when a human electrocardiogram is taken. In either case, the muscle 
(Figs. 59, 60) (in this instance, the heart) becomes electro-negative during 
contraction; indeed, electro-negativity and muscular contractility are syn- 
onymous and interchangeable terms. This wave of electric excitation is 
led off by means of wires which connect the electrodes to the electrocardio- 
graphic apparatus (Figs. 59-69) with its “string”—a very fine silvered quartz 
fiber. The string becomes activated and moves as the result of the electrical 
excitation produced by cardiac contraction. The movements of the string 
are magnified and photographed (Figs. 67, 69). The resultant picture con- 
stitutes the electrocardiogram. 
In order to study the paths taken by impulses arising from the sino- 
auricular node, non-polarizable electrodes were placed in contact with 
various appropriate parts of the cardiac musculature, and those portions 
which first became electrically negative (and therefore which first contracted) 
as compared with other parts, were recorded by means of electrocardiograms. 
In this manner it was demonstrated that the excitation wave spreads ripple- 
like over the auricles from the sinus node as a center at a rate of about 1000 
millimeters per second. The excitation wave follows the chief auricular 
muscle bands which radiate from the sinus region, and spreads thus throughout 
the auricular musculature and auricular septum to reach the junctional tissue 
(the auriculo-ventricular or A-V conduction system (Chapter I). 
After the excitation impulse reaches the A-V node, its spread through the 
ventricles does not follow the anatomical arrangement of that musculature 
(Chapter I). From the A-V node, the excitation wave first spreads almost 
simultaneously to those areas supplied most directly by the right branch of 
the A-V bundle, that is, the part of the right ventricular wall which lies over 
the large anterior papillary muscle; later, the remainder of the right ventri- 
cle becomes excited and contracts. In the left ventricle the wave also 
follows a definite course. The earliest point to be excited is the muscular 
vortex of the left ventricle near its apex or the extreme apex itself; about one 
hundredth of a second later the neighboring points are activated; excitation 
of the remainder of the left ventricle is almost simultaneous. The cardiac 
base and the region of the conus are usually the last to receive the excitation PHYSIOLOGICAL CONSIDERATIONS 
37 
impulse. Since some areas of the ventricular musculature are excited practi- 
cally simultaneously, the ventricular wall must presumably be reached by 
simultaneous impulses traveling along a large number of paths; by experi- 
ments, these have been shown to be the Purkinje fibers (Chapter I). But 
some parts of the ventricular musculature not supplied by free, branching 
Purkinje strands (e.g. the conus region beneath the pulmonary valves) are 
activated very early. This has been demonstrated experimentally to be due 
to the thinness of the ventricular musculature in such regions. In other 
words, the excitation wave is conceived as traveling not only along the surface 
of the interior of the ventricular chambers but also as piercing the muscula- 
ture. The varying thickness of the musculature also explains the reason for 
the excitation wave reaching the thinnest area first and later the thicker left 
ventricular areas. Excitation is found to travel extremely rapidly through 
the conduction system; the rate is about 5000 mm. per second. Through 
the muscle itself, however, it is much slower, namely about 500 mm. per second. 
In brief, then, the excitation wave appears almost simultaneously along the 
interior of both ventricles. The activation of the ventricular surface is only 
partly dependent upon its distance from the Purkinje fibers; it is mainly 
controlled by the time required for the excitation wave to pierce the thicker 
musculature overlying the latter fibers. 
To Summarize.—From a study of the physiological and anatomical 
distribution of the specialized tissues, as well as from experimental electro- 
cardiographic investigations, it is evident that the normal impulse arises 
in the S-A node; it spreads thence through the auricles, following, as far as 
known, no especially differentiated path in the latter. It then reaches the 
junctional tissue (that is, the A-V conduction system), and by way of its 
right and left branches and its terminal aborizations (the Purkinje system), 
the normal impulse spreads to the papillary muscles and throughout the 
entire ventricular musculature. 
Contractility.—A characteristic of the systolic contraction of the heart 
muscle which distinguishes it from skeletal musculature is that each systole is 
of maximum intensity. This property—the so-called all or none reaction—■ 
means that the heart muscle answers any stimulus sufficient to cause any 
response at all by a maximal contraction; that is to say, any stimulus pro- 
duces either a maximal contraction or none at all. As is well known the 
contractility of skeletal and plain muscle varies with the degree of the stimu- 
lation, a law which is entirely different from that applying to the heart. 
Cardiac contractility therefore does not depend upon the strength of the im- 
pulse. It does vary considerably, however, with the state of irritability 
(q. v.) of the heart muscle, so that despite the fact that artificial stimulation 
of the mammalian heart produces maximal contraction, the resultant systoles 
are by no means necessarily alike, for the state of irritability of cardiac 
muscle may vary considerably, depending for example, upon the state of 
nutrition of the muscle at the time of stimulation. 38 
PHYSIOLOGICAL CONSIDERATIONS 
This so-called “all or none law” or law of maximal contraction of cardiac 
muscle seems to depend upon the difference in the histological structure 
between skeletal and cardiac fibers. In the former, muscle bundles are 
encased in, and are separated by, sarcolemmal sheaths. In cardiac muscula- 
ture such sheaths are absent. Hence stimulation of skeletal muscle may vary 
and produce sub-maximal contractions because all the fibers cannot partici- 
pate at one time; in the case of the heart however, the whole muscle can, so to 
speak, contract as one fiber because of its histological continuity. Further- 
more, the intricate intertwined muscle layers of the heart, already described 
(Chapter I) also tends to make the heart act physically as one continuous 
muscle. 
Irritability.—The heart is not irritable during the entire time of its systole, 
that is to say, if an electric stimulus be applied to the heart during its stage of 
contraction, it has no effect upon, the contraction. This is termed the refrac- 
tory period of the heart beat. In consequence of this, the heart is irritable 
only during its diastolic or resting period. A stimulus applied during 
diastole produces an extra or premature contraction, called technically an 
extrasystole (q. v.). The heart therefore is different from skeletal muscula- 
ture in that it cannot be tetanized like the latter. There is an experimental 
exception to this law; hearts that have been poisoned by muscarine, alcohol, 
chloral, etc., may have a shortened refractory phase and hence may be 
brought into tetanic contraction by proper stimuli. 
The irritability of the heart returns gradually during its diastolic period. 
It would therefore seem that the return of cardiac irritability is intimately 
associated with some as yet unknown metabolic change or changes going on in 
the cardiac musculature. 
Tonicity or Tonus.—This property is similar to that found in ordinary 
skeletal musculature, which, in the case of the heart, keeps it in a slight state 
of contracture even during diastole. Tonicity is a term which is perhaps used 
too loosely and indiscriminately, and is often confused with the contractile 
power of the heart. Tonicity is the attribute about which few clinical or 
experimental facts are known. It is apparently intimately connected with 
various degrees of cardiac dilatability—an important clinical complex—yet 
tonicity is in so far an individual property in that it may be present even 
when the heart is dilated. Furthermore the degree of tonicity does not 
necessarily vary proportionately with the amount of cardiac dilatation. It 
would thus seem that tonicity is a property apart from contractility. This 
has received some verification from Porter’s experiments. These demonstrated 
that tonus contractions vary with the strength of the stimulus and have no 
refractory period, and that tonus tetanus can be produced by proper stimuli. 
As has been pointed out, the characteristics of cardiac contractility are just 
the reverse, for the heart muscle has a refractory period, contraction does not 
vary with the strength of the stimuli and heart muscle cannot ordinarily be 
tetanized. PHYSIOLOGICAL CONSIDERATIONS 
39 
The Physiological Action and Influences of Cardiac Nerves.—The 
anatomical distribution of the cardiac nerves and the relationship of the vagi 
and sympathetics to the conduction system—the sino-auricular node and the 
bundle of His—have already been described (q. v.). The heart is often pro- 
foundly influenced by impulses which reach it from these nerves. The vagi 
contain the inhibitory fibers. If, in the experimental animal, the vagi be 
cut in the neck, the cardiac rate will be increased. If the peripheral ends of 
the cut vagi be stimulated, there will be slowing or stoppage of the heart, or a 
condition in which the auricles beat more rapidly than the ventricles, with no 
rhythmic relationship between the two (complete heart block) (Chapters X 
and XX). In warm-blooded animals . there is not only a diminution of 
cardiac rate, but also of the strength of auricular and ventricular contractions, 
until finally the heart stops in diastole. On the other hand, stimulation of 
the cut end of the sympathetic produces a varying degree of cardiac acceler- 
ation. Depending upon the degree of stimulation of vagus and sympathetic, 
the one or other nerve has a predominant influence upon the cardiac rate. 
Although antagonistic, this antagonism cannot be measured purely arith- 
metically for if vagus influence predominates during the course of the experi- 
ment, with cessation of stimulation a typical accelerator influence results. 
This fact in itself indicates that a certain amount of “tone” is present in both 
nerves. Nerves of sensation have not been discovered in the heart. How- 
ever, since the lower cervical and upper dorsal nerves supplying the integu- 
ment of the neck, chest and upper extremity also send filaments to the deep 
and superficial cardiac plexuses, painful skin areas of varying degrees of 
intensity and extent are found; such painful areas are the result of reflex 
excitation originating in some pathological process or function of the heart 
itself. 
As stated, stimulation of the vagus sometimes has as its most marked 
effect not slowing of the pulse rate, but diminution of the strength of the 
auricular and ventricular contractions. The latter, for example, may be 
considerably weakened and lessened in amplitude. Vagus stimulation, how- 
ever, seems to have a more marked influence upon auricular than upon 
ventricular systoles. Indeed, it is questionable whether the effect upon the 
ventricle is not secondarily caused by the inhibitory action of the vagus on the 
sinus region, particularly upon the sino-auricular node (thepacemaker), thus 
causing inhibition of normal impulses passing from auricle to ventricle. As 
an occasional result of vagus stimulation the ventricles may either continue 
beating or may stop entirely when the auricles are brought to a standstill. 
The cause for these occasional variations is not clear; they may possibly be 
due to varied distribution of branches of the vagi to the sino-auricular and 
atrio-ventricular nodes (Chapter I), or to differences in vagal and accelerator 
nerve tone. Other reasons adduced for these occasional variations of ven- 
tricular action following vagal stimulation are increased ventricular diastole 
produced by slowing of the heart rate, and differences in the strength of the 40 
PHYSIOLOGICAL CONSIDERATIONS 
stimuli applied in the various experiments Despite these 
contradictions it seems probable that the vagus has a decided influence, 
directly or indirectly, on cardiac rate and contractility, as well as on 
conductivity. 
Because of dissimilar distribution of the right and left vagus nerves 
(Chapter I), it has been shown experimentally in the dog’s heart that stim- 
ulation of the right vagus usually brings the heart to a standstill: that, 
because of its predominant distribution to the auriculo-ventricular conduction 
system, stimulation of the left vagus influences and interferes with conduc- 
tion from auricle to ventricle. Such interference may vary from simple pro- 
longed conduction time from auricle to ventricle (Chapters X, XI), to 
incomplete heart block (Chapters X, XI); or in more marked instances it may 
end in a condition in which the auricles beat but no impulses pass to the 
ventricles; hence the latter finally 'cease beating (A. E. Cohn). These 
experimental observations have definite clinical application, especially in 
attempting to control paroxysmal tachycardia by pressure over the vagus 
in the carotid sheath (Chapter XI). 
The primary effect of experimental stimulation of the accelerator is 
an increase of cardiac rate; this increase may be slight or marked. Com- 
bined with the acceleration there may or may not be increased amplitude of 
the cardiac contractions. Because of such possible differences in amplitude, 
some physiologists believe that there are augmentor as well as accelerator 
fibers in the accelerator nerve. There seems to be a distribution of right 
and left accelerators to the sino-auricular and auriculo-ventricular nodes 
comparable to that of the vagi, that is, the right accelerator supplies pre- 
dominantly the sino-auricular, and the left accelerator, the auriculo-ven- 
tricular node. 
Regarding the ganglia, stimulation of the right stellate ganglion causes 
an increased auricular and ventricular rate, but no change in conduction 
time. Stimulation of the left stellate ganglion produces similar acceleration, 
in addition to shortening of the auriculo-ventricular conduction time (Roth- 
berger and Winterberg); this suggests increased irritability of the auriculo- 
ventricular node and bundle of His, probably corresponding to a preponder- 
ant nerve supply from the left accelerator. 
The Cardio-inhibitory and Accelerator Centers—Reflex Excitation.— 
The location of the accelerator center—whether in the medulla or elsewhere—- 
has not been accurately defined. It is known that the center must be in the 
brain, for stimulation of the cervical region of the spinal cord produces 
acceleration. As for the cardio-inhibitory center, it is definitely known to be 
in the medulla (Figs. 14, 15). 
There is much clinical and experimental evidence that the cardio-inhibi- 
tory center as well as the vagi themselves can be reflexly stimulated and 
influenced in many ways. Thus centripetal (afferent) nerves from the skin, 
from the heart itself, from the gastro-intestinal canal, lungs and the special PHYSIOLOGICAL CONSIDERATIONS 
4i 
sense organs can affect the cardio-inhibitory center. In addition, such 
central influences as sorrow and joy can have a decided action upon the 
cardiac rate. 
The classical example of reflex inhibition is that of Goltz who, 
by continued light tapping upon a frog’s abdomen, brought the heart to a 
standstill: with the vagi out, cardiac standstill was not obtained. 
In man, the afferent (centripetal) impulses—whether from skin, muscle or 
organ.—are carried by means of the central nervous system to the cardio- 
inhibitory center in the medulla; from there the efferent (centrifugal) inhibi- 
tory impulses pass along the vagi. In addition, the center in the medulla 
may be directly affected by pressure of new growths or by neighboring inflam- 
matory reactions, and especially by changes in the composition of the blood 
supply of the center. It is important to recall that, as with other centers, 
the cardio-inhibitory when influenced by afferent impulses, may be either 
excited or inhibited. When inhibited the cardiac rate is accelerated. If 
when excited the center be already active, then the cardiac rate is retarded. 
Myogenic or Neurogenic Impulse?—I have already indicated the prob- 
able course of the normal impulse in the mammalian heart and have also 
emphasized the rich nerve supply of the sino-auricular node and of the auri- 
culo-ventricular conduction system. These facts lend renewed interest to 
the old question in dispute for many years, especially among physiologists, 
whether the “inner stimulus” is of neurogenic or myogenic origin. It will 
perhaps be advisable to set forth the salient features of the myogenic theory 
(at present the more popular among physiologists), and to give the objections 
thereto from the standpoint of the neurogenic theory. 
1. Those favoring the myogenic theory point out that the heart of the 
embryo chick pulsates before it contains nerve cells (His, Jr.). This is one 
of the strong basic observations upon which the myogenic theory is founded. 
The antagonists state that it is open to the usual objections of negative 
findings (Cyon), for with better technique and further progress in neuro- 
embryology, nerve structure may be discovered in the early embryonic 
chick’s heart. 
2. Haphazard strips cut from hearts of coldblooded animals, when placed 
in proper solutions, will continue to beat. This argues for inherent rhyth- 
micity in the muscle fiber, for it does not appear probable that every bit of 
cardiac tissue thus haphazardly cut off has its own arrangement of nerve 
tissue acting as a motor center. The neurogenic theory holds that such nerve 
structures as are found in the isolated strips of cardiac muscle tissue are 
sufficient to induce rhythmic contractions. 
3. If a zig-zag preparation of the frog’s heart be cut so that there are in 
places only slight, frail muscular bridges (Engelman), and the preparation be 
stimulated at any point, the whole muscle preparation will contract. The 
objection offered by the neurogenists to this experiment is that there are 
innumerable nerve anastomoses along which the excitation wave may travel. 42 
PHYSIOLOGICAL CONSIDERATIONS 
4. The discovery of the sino-auricular node, and the propagation to the 
ventricles of impulses by muscular continuity (the bundle of His, its two 
chief branches, and their aborizations) argues strongly for a primary myo- 
genic impulse. The counter-argument (Cyon) is that it does not seem prob- 
able that so small a muscular bridge can carry all the impulses from auricle 
to ventricle. 
5. Section of the auriculo-ventricular bundle, by breaking muscular con- 
tinuity, interferes with conduction of impulses and produces heart block 
(Chapters X, XI), that is, dissociation between normal auricular and ven- 
tricular contraction. The counter argument is that the bundle also con- 
tains nerve structures which are likewise demolished by the experimental 
section of the bundle, hence the interference with conductivity. 
6. Isolated heart muscle cells of a chick embryo, placed in a plasma 
medium, may be kept alive and continue to beat (Burrows). The answer to 
this argument is that even in the absence of nerve cells, an embryonic function, 
originally muscular, need not necessarily continue so. For example, Carlson 
has shown that in the heart of the limulus, the embryonic impulse, originally 
muscular, later becomes neurogenic. 
The intimate and intricate relationship existing between the muscle and 
nerve structure in the nodal regions demonstrates how difficult must be the 
final determination of this question of neurogenic and myogenic impulse. 
It is known clinically that the rhythm center is readily influenced by purely 
neurogenic impulses; these can indeed upset the normal cardiac control and 
give rise to abnormal rhythms. How far such clinical observations can be 
applied to the question of the normal control of the rhythm center it is 
impossible to state. All in all, it seems probable that the sino-auricular node 
is activated by both neurogenic and myogenic influences, although we have 
at present no means of discovering under which circumstances the one or the 
other becomes the controlling factor. 
Whether myogenic or neurogenic, however, the important question to 
decide is the primary nature of the automatic, intrinsic stimulus (the “inner” 
stimulus) which fundamentally excites the heart beat. The prevailing 
opinion at present is that its cause lies in the chemical composition of the 
blood, particularly in the sodium, calcium and potassium content of the 
plasma. 
REFERENCES 
Burrows: Science, 1912, XXXVI, 90. 
Burrows: Muenchener Med. Wochensch, 1912, 1473. 
Carlson: Am. Journal Physiology, 1906, XVI, 67. Am. Journal Physiology, 1907, XVIII, 
n- 
Cohn, A. E.: On the Differences in the Effects of Stimulation of the Two Vagus Nerves on 
Rate and Conduction in the Dog’s Heart. Journal Expt’l Med., 1912, XVI, 732. 
Cohn, Kessel and Mason: Functions of the Sino-auricular node of the dog. Heart, 
1911-12;III, 311. PHYSIOLOGICAL CONSIDERATIONS 
43 
E. de Cyon: Les Nerfs du Coeur, p. 203. 
Engelmann: Bijrage tot de Kennis vagus ophet hart. 
Gaskell: On the Tonicity of the Heart and Bloodvessel. 
Howell’s Physiology. 
Lewis: Mechanism and Graphic Representation of the Heart Beat. 
Lewis, Oppenheimer and Oppenheimer: The Site of Origin of the Mammalian Heart 
Beat, the Pacemaker in the Dog. Heart, i9io-n;'lI, 147. 
Marey: Methode Graphique, p. 4x7. 
Nagel: Handbuch der Physiologie. 
Porter: American Journal of Physiology, 1905, XV, 1. 
Rothberger and Winterberg: Ueber die Beziehungen der Herznerven zur Form des Elek- 
trokardiogramms, Arch. f. ges. Physiologie, 1910, CXXXV, 506. 
Tigerstedt: Lehrbuch der Physiologie des Menschen. 
Wiggers: Circulation in Health and Disease. CHAPTER IV 
CARDIAC HLSTOLOGY AND PATHOLOGY 
The structure, distribution and histology of the sino-auricular node and 
of the junctional tissue have already been described (Chapter I). 
The heart is composed of three layers: The endocardium, the epicardium 
and the myocardium. 
The endocardium, the serous membrane of the heart, lines all the cardiac 
chambers and both sides of all the valves. It is continuous with the intima 
of the veins and arteries at the various cardiac orifices and is composed of two 
layers: A superficial single layer of endothelial cells; a deeper layer of loose 
areolar tissue containing fibrous and elastic tissue, and some smooth muscle 
cells. This deeper layer is continuous and merges with the intermuscular 
connective tissue septa of the myocardium, and is intimately attached to the 
latter. Strong fibrous rings (annuli fibrosi) consisting of fibrous and elastic 
tissue line the auriculo-ventricular openings. Rings of similar structure 
surround the openings of the aorta and pulmonary artery. The cardiac 
valves are composed of fibrous and elastic connective tissue covered by 
endocardium; they contain muscle fibers at their attached margins, which in 
turn are attached to the annuli fibrosi. The ventricular valves—the mitral 
and tricuspid—are thinner than the aortic and pulmonary valves. 
The epicardium forms the visceral layer of the pericardium. It is com- 
posed of connective tissue, with comparatively few elastic fibers or fat 
cells, and of a single layer of squamous epithelium. It is closely applied 
to the underlying myocardium or subpericardial fat. 
The pericardium is the closed sac in which the heart is suspended. It 
is a fibro-serous structure. Its inner visceral layer is the epicardium. The 
parietal layer contains much elastic and connective tissue, and is rich in 
lymphatics, nerves and blood vessels. At certain parts it becomes thicker 
and tougher so as to form pericardial ligaments. These ligamentous pro- 
longations extend and become attached to the aorta and pulmonary artery 
at the base of the heart; to the upper and lower portions of the sternum; 
to the diaphragm near the inferior cava; and to the vertebra by merging with 
a mediastinal extension of the deep cervical fascia. The pericardial liga- 
ments are mechanically important because they help to fix various portions 
of the heart during its systolic contractions. 
The myocardium—the muscular layer of the heart—is made up histologi- 
cally of a special type of involuntary muscle cell (Fig. 22) not found elsewhere 
in the body. The cells are striated and anastomose by means of short lateral 
44 CARDIAC HISTOLOGY AND PATHOLOGY 
45 
processes. Each heart muscle cell usually contains but one nucleus, centrally 
placed. A cell membrane, the sarcolemma, if at all present, is extremely 
delicate. The cells contain a large amount of sarcoplasm. The striations 
of heart muscle are finer and more delicate than those of skeletal musculature. 
The longitudinal striations represent fibrillae in 
the sarcoplasm. The transverse striae indicate 
light and dark discs. Through the middle of 
the former is found the so-called Krause mem- 
brane. Of special histological interest are inter- 
collated discs or cement lines of irregular length 
which may or may not completely transect the 
fiber. Seen in longitudinal section, they appear 
as dark lines running transversely across the 
main fibers and side branches. The impor- 
tance and significance of these discs or cement 
lines lies in the question as to whether they 
do or do not represent actual cell boundaries; 
for if they do, it would clinch the fact that 
cardiac musculature is composed of separate 
cells, and not as some suppose, of synticium—a 
structure in which there are no actual cell 
boundaries. Views regarding the interpretation 
of the discs are still at variance. The most 
recent interpretation is that the discs do not 
represent actual cell boundaries, and hence that 
heart muscle is not a cellular structure. The 
blood vessels, veins and lymphatics of the heart 
have already been described (Chapter I). 
PATHOLOGY OF THE ENDOCARDIUM AND 
MYOCARDIUM—CARDIOSCLEROSIS 
Pig. 22.—Muscle cells from 
the human heart showing 
longitudinal and transverse 
striations, and lines of union 
between cells. X 500. 
(After Bailey.) 
Degenerative Changes of the Endocardium. 
The endocardium is subject to the following 
degenerative changes: 
Fatty Degeneration (Fig. 23).—Microscopically, pure white or yellowish 
white areas are found in the endocardium, especially on the mitral valves in old 
people. Such degenerative areas usually represent retrogressive senile 
changes; they are, however, occasionally the result of anemia, toxemia and 
infections. The connective tissue cells in the degenerated areas contain more 
or less numerous large and small fat droplets. 
Amyloid degeneration of the endocardium occasionally occurs. It is 
rarely the predominant pathological change. 
Sclerosis.—The affected endocardium takes on a white, thickened, hyaline 
appearance. An entire valve (especially the mitral), or its free border, or parts 46 
CARDIAC HISTOLOGY AND PATHOLOGY 
of the mural endocardium may be involved; in addition to these changes 
there may be calcareous deposits. Occasionally the sclerotic areas undergo 
mucoid degeneration. Microscopically, the sclerotic patches are found to 
consist of strands of connective tissue which have undergone hyaline 
degeneration. 
Atheromatous Degeneration (Fig. 24).—This consists of focal necrosis in 
the valvular tissue and may include any of the changes already mentioned. 
The above degenerative types (sometimes 
called arteriosclerotic endocarditis when 
sclerosis is marked) are as a rule found in 
elderly people, and may be regarded as senile 
or retrogressive in nature. They are occasion- 
ally encountered in the middle aged, very 
rarely in the young. The valves especially 
attacked by these degenerative processes are 
those previously inflamed. The result is that 
the free surface of the valvular endocardium 
becomes roughened; adherent thrombi may 
form which may later become partially or 
totally organized as the result of a slow pro- 
ductive inflammation. Thickened patches are 
thus formed. The end result of all these 
changes is an irregular, more or less diffuse, 
sclerotic and atheromatous thickening of 
the valves, with consequent profound change in their structure, shape and 
function. They can no longer close the cardiac orifices properly, thus giving 
rise to various abnormal blood currents and consequently to murmurs 
(Chapter XIII). The arteriosclerotic type of endocarditis is especially apt 
to involve the aortic valves, usually at their bases. It is at times difficult 
to differentiate this primary sclerosis and atheroma from chronic fibrous and 
infectious endocarditis. 
Inflammation of the Endocardium—Endocarditis. Acute Simple Endo- 
carditis.—It is now generally believed that all types of acute endocarditis— 
rheumatic, mycotic, etc. are due to bacteria or to their toxins. Since bacteria 
have not yet been demonstrated in the blood of patients with simple, acute 
rheumatic endocarditis, the term simple acute endocarditis will here be 
applied to the pathological changes in the endocardium accompanying the 
latter condition. However, even this limitation is artificial for, as will be 
shown, the simple may be combined with other more destructive changes. 
Acute endocarditis is also termed verrucous, productive or rheumatic endo- 
carditis. The valves are usually affected along their free borders of closure. 
According to our present knowledge these portions of the valves do not 
possess blood vessels, hence the assumption is that the valves are damaged by 
bacteria or bacterial toxins flowing in the blood stream. The damage is 
hear^musclet1:7(After 1 a"aw/wtan ) CARDIAC HISTOLOGY AND PATHOLOGY 
47 
Fig. 24.—Atheromatous degeneration of the aorta due to syphilis. (Courtesy of Dr. J. 
Larkin.) 48 
CARDIAC HISTOLOGY AND PATHOLOGY 
occasionally so mild and superficial that the only sign of a previous inflamma- 
tion is a small amount of scar tissue. The only pathological change may be 
simple swelling of the valves with tumefaction of the basement substance; 
the valve surfaces then retain their glistening appearance, there is only 
slight production of new connective tissue. In more severe cases, the growth 
Fig. 25.—Ulcerative endocarditis showing large vegetations (V). (Courtesy of Dr. J. 
Larkin.) 
of new connective tissue becomes the predominant feature. The basement 
substance splits, making way for fungoid projections of connective tissue 
masses. These are the so-called vegetations, hence also the name verrucous 
endocarditis. If cluster and deposits of fibrin adhere to the vegetations, the 
latter may reach enormous proportions. In other instances, production of 
new tissue and degeneration with ulceration go on simultaneously in different 
parts of the affected valve; the result—vegetation and loss of substance—is CARDIAC HISTOLOGY AND PATHOLOGY 
49 
characteristic of what is termed simple acute ulcerative endocarditis (Fig. 
25). Since the verrucous and ulcerative varieties of endocarditis are not 
always distinct and do indeed merge at times, both may occur together as a 
mixed process. A shrinkage of this granulomatous connective tissue pro- 
duces what is known as chronic fibrosis or fibroplastic endocarditis. 
Fig. 26.—Malignant endocarditis affecting the aortic valves. V = vegetations. (Courtesy 
of Dr. J. Larkin.) 
As shown by autopsies, these varying types or degrees of simple endo- 
carditis—including even the simple ulcerative form—may occasionally 
regress so completely that there is scarcely any, or indeed no resultant valvu- 50 
CARDIAC HISTOLOGY AND PATHOLOGY 
lar deformity. In such fortunate cases there is full recovery and restoration 
of all cardiac functions. In other instances the valves remain permanently 
damaged. 
Acute endocarditis, either by recrudescence or as a continuing non- 
quiescent inflammatory lesion, may develop into chronic endocarditis. 
Acute Mycotic or Malignant Endocarditis (Fig. 26).—Malignant, myco- 
tic, ulcerative and septic endocarditis are the various names for that type of 
acute endocarditis in which the infective exciting agent is a bacterial organism 
recoverable from the blood. In the autopsy specimen the infective bacteria 
in large quantities can often be recovered from the damaged valve. 
Malignant ulcerative endocarditis may occur as a primary process but 
it is usually an accompaniment of acute infectious diseases, or of pyemia. 
The common sequence of the pathological process affecting the valves is 
as follows: The bacteria form clumplike deposits which appear as very fine 
grayish granules. Beneath these, there is destruction and necrosis of the 
endothelial, and finally of the deeper layers of the valvular structure. The 
extent of the destructive process apparently depends on the virulence of 
the invading bacteria. If the endothelial layer is not entirely destroyed, it 
shows only cloudy swelling. Thrombi from the circulating blood, consisting 
of platelets, fibrin, and white and red blood cells become adherent to the 
damaged surface. With the washing off of the bacterial clumps by the blood 
stream, there remains a small defect with a necrotic base to which thrombi 
again become attached. Where blood vessels are present in the valves at 
their bases, an exudative inflammation surrounds the necrotic areas. Where 
the vascular supply is absent there is a growth of connective tissue cells and 
an increase in lymphocytes; later, there may be formation of new blood 
vessels. In widespread, progressive mycotic disease, large reddish or dirty 
gray thrombotic masses may occupy large areas of the infected valves. The 
process may finally result in perforation of the valve and even of the chordae 
tendince, with consequent production of loud, musical murmurs. The 
impingeing blood is also apt to break and carry off small friable masses, causing 
septic infarcts and abscesses in the lungs, kidneys and other viscera. 
Subacute Bacterial Endocarditis.—This may be regarded as a special 
type of mycotic endocarditis, longer in its course than the acute variety 
and caused chiefly by the streptococcus viridans, exceptionally by the 
influenza bacillus. The pathological picture is practically that of mycotic 
endocarditis. For many reasons, the clinical picture of subacute bacterial 
endocarditis is of great importance and interest (Chapter XV). 
Chronic Endocarditis.—As in the verrucous form, there are two distinct 
pathological processes found either separately or in combination. 
The mural endocardium, but especially the valves of the left side of the 
heart, become thickened, rigid and covered with small, firm vegetations 
and infiltrated with lime salts. Or there may be simultaneous connective 
tissue growth and degeneration with ulceration and fibrin deposition on the CARDIAC HISTOLOGY AND PATHOLOGY 
SI 
ulcerated roughened surface; shrinkage and lime salt deposits finally result 
(Fig. 27). The mural myocardium may also be affected by the spread and 
infiltration of the endocardial process. 
Verrucous endocarditis is usually found in the left heart in adults. The 
ulcerative type is seen fairly frequently in the right side of the heart. In the 
new born, the site of predilection for verrucous endocarditis is also the right 
heart. 
The verrucse and the formation of fibrous tissue give rise to stenosis of 
the valvular orifices (stenotic lesion); or the valves no longer properly close 
Fig. 27.—Chronic endocarditis with calcification of the thickened valves. Aortic insuffi- 
ciency. (Courtesy of Dr. J. Larkin.) 
the orifices, they become incompetent and allow the blood to flow back into 
abnormal cardiac chambers (regurgitant lesion). 
It is of importance to correlate, where possible, the pathological picture 
•of endocarditis with valvular disease as encountered clinically. Thus, in 
acute endocarditis, the usual change consists in the production of ulcers with 
thickening of the cusps and in healed areas and granulations. Valvular 
deformity is slight or absent. In the longer-continued, subacute cases of 
endocarditis, verrucse along the margins of the valves represent the promi- 
nent, pathological change. Valvular deformity is moderate. In chronic 
endocarditis, there is production of new tissue affecting not only the valves 
but also the chorda tendina; the latter become stiff, the valves hard and 
inelastic. The result of both of these changes is marked deformity; in the 52 
CARDIAC HISTOLOGY AND PATHOLOGY 
case of the mitral valves, there is lengthening and funnel-like formation of 
the mitral opening, accompanied by varying degrees of stenosis. 
In a general way, it may be stated that the mitral valve is usually affected 
in simple, chronic endocarditis, and that the aortic valve is commonly 
involved in arteriosclerotic endocarditis and in syphilis (Chapter XVI). 
Myocardial Degenerations.—The following are the chief pathological 
changes occurring in degenerative changes affecting the myocardium. 
Simple and Brown Atrophy.—In both, the cardiac fibers become smaller 
and the entire heart is decreased in size. In addition, in brown atrophy, 
pigment is found in the form of small granules in the sarcoplasm. The 
entire heart is brownish in appearance. Both types occur in inanition and 
in various cachectic states. Brown atrophy is regarded as a senile change. 
Pig. 28.—Fatty infiltration of heart muscle. (After Kaufman.) 
Parenchymatous or Albuminous Degeneration.—Microscopically this 
condition is marked by cloudy swelling, with a varied number of albuminous, 
usually minute granules in the musculature. On gross section the cardiac 
musculature presents an opaque, dark red, somewhat spotted appearance, 
and is softer and more friable than the normal muscle. This degenerative 
change is a frequent accompaniment of infectious fevers, and of biological and 
chemical poisons. It is also found in severe anemia. 
Fatty Degeneration.—This exists either as a primary process or it may 
represent a later development of parenchymatous degeneration. Depending 
upon its severity, the myocardium is studded with fat droplets of various 
size (Fig. 23). The musculature on section shows patchy or diffuse 
yellowish areas. When the damage is extreme, the muscle is flabby, friable CARDIAC HISTOLOGY AND PATHOLOGY 
53 
and grayish in color. Very many factors, especially those that alter the 
quantity and quality of the blood, may cause fatty degeneration. For 
example, it is found in severe primary anemias, in anemia following hemor- 
rhage, in infectious diseases, in chemical intoxications (especially from phos- 
phorous, arsenic and alcohol), in coronary disease, in cardiac hypertrophy and 
in chronic nephritis. 
Fatty Infiltration.—The “Fatty Heart” (Fig. 28). This lesion must be 
distinguished from fatty degeneration. In the ‘‘fatty heart” the organ is 
covered by more or less extensive fat pads. Sometimes these lipomatous 
masses insinuate themselves between muscle bundles and appear as fat 
clumps or fatty spots under the endocardium. “Fatty hearts” are usually 
found in those obese, thick set individuals who have fat accumulations in 
other parts of the body. The subpericardial fat is sometimes considerably 
increased in quantity, so that the entire organ may be encased in the fat 
layer. The “fatty heart” is also occasionally found as a secondary change 
in the cardiac atrophy which accompanies cachexia. 
Coronary Lesions.—Lesions of the coronary arteries are of supreme 
importance because of the prominent role played by disturbances of the 
intra-cardiac circulation in the etiology of myocarditis. 
Infections such as typhoid fever, scarlatina and pyemia may so affect 
the media and intima of the coronaries that these coats undergo necrotic and 
hyperplastic changes, finally leading to patchy arterio-sclerosis of these 
vessels. Coronary endarteritis may give rise to extreme intimal thickening 
or calcareous deposits, with the deposition of thrombi on the denuded, 
roughened, intimal surface. 
Whatever the underlying pathological process in the coronaries, the 
narrowed calibre of these vessels with consequent partial or complete coro- 
nary occlusion causes lessened arterial supply to the cardiac musculature. 
As a result, various degrees and kinds of myocardial changed may result. 
Such changes depend largely upon the amount of coronary occlusion, the 
rapidity of its formation and the infectious nature of the process; they may 
vary from anemia and myocardial degeneration to fibrous hyperplasia and 
even cardiac aneurism. 
Coronary thrombosis occurs most frequently as an accompaniment of 
coronary arteritis and sclerosis. Occlusion and thrombosis of the coronaries 
at their orifices may also occur as the result of a neighboring aortitis, or 
from vegetations and clots on the aortic cusps. 
Local anemia is the simplest primary change that results because of 
interference of the coronary circulation from emboli in the main coronaries 
or their subsidiary branches. 
With complete obliteration of one of the smaller coronaries, the 
corresponding cardiac area becomes ischemic and pale, and undergoes coagu- 
lation necrosis, a process sometimes termed anemic necrosis or anemic 
infarct. The infarcted area may become myomalaceous, that is, the entire 54 
CARDIAC HISTOLOGY AND PATHOLOGY 
affected musculature may become softened. In rare instances, such softened 
areas develop into aneurisms of the cardiac wall which may finally rupture. A 
more frequent outcome is organization of the anemic infarct; the necrotic 
material becomes absorbed, and granulation tissue with the production of 
new vessels takes place. This ends in fibrous or fibroplastic myocarditis, 
and finally, in scar tissue formation. If the process is widespread, the 
ventricular musculature appears striped on section. It presents a somewhat 
checkered appearance when older scars are found in conjunction with fresh 
necrotic areas. 
Myocardial Inflammation. Myocarditis.—The primary inflammatory 
process involves the blood vessels and interstitial tissue, the musculature 
becomes secondarily affected by atrophy and degeneration. 
Acute Interstitial Suppurative Myocarditis.—When occurring as a diffuse 
process from severe infections or from ulcerative endocarditis, there is wide- 
spread purulent infiltration of the cardiac musculature. Acute interstitial 
myocarditis is, however, more frequently a localized rather than a diffuse 
process, with single or multiple foci. The most common etiological factors 
are pneumonia, bacterial endocarditis and severe general infections. 
As the result of bacterial infection in which a clump of bacteria forms 
the inflammatory nidus, an area of cloudy swelling, necrosis and fatty degen- 
eration of the musculature is developed. If the leucocytes penetrate the 
necrotic zone, an abscess results. These abscesses are usually minute, 
though by confluence they may sometimes be readily seen with the naked 
eye. Small abscesses may occasionally end in scar tissue formation by 
destruction of bacteria, and by liquefaction and absorption of the pus cells. 
The defect is then covered by granulation tissue coming from the surrounding 
musculature. On the other hand, such abscesses may cause purulent 
pericarditis, emboli, ulcerative myocarditis and cardiac aneurisms. Any of 
these sequelae can directly or indirectly cause death. In those instances in 
which the inflammation stops short of abscess formation, the process may 
end in the production of granulation tissue and of young connective tissue; 
finally scar tissue is formed. 
Chronic Fibrous Interstitial Myocarditis—Myocardial Fibrosis.—This is 
a secondary productive process resulting in the formation of fibrous areas 
containing elastic and connective tissue. It largely originates as the conse- 
quence of disturbances of the intracardiac circulation from coronary disease. 
Other less frequent causes of this fibrotic change are chronic endocarditis and 
pericarditis, and bacterial and other infections. Experimental injections 
of bacterial toxins in animals have also been followed by the production of 
dense, fibrous connective tissue. Injection of adrenalin into the ear veins of 
rabbits has been followed by similar results. Depending upon the amount 
and type of coronary occlusion, coronary disease as already stated may give 
rise to degeneration or necrosis of the cardiac musculature with the produc- 
tion of fibrous tissue. This production of new connective tissue is therefore CARDIAC HISTOLOGY AND PATHOLOGY 
55 
not inflammatory in the more recent acceptation of the term, but is actually 
a (replacement) fibrous hyperplasia following atrophy of the muscle fibers; 
for atrophy is the primary effect on the heart of impaired circulation and 
nutrition either from coronary disease or from such others causes as decom- 
pensated valvular lesions. The new fibrous tissue may be present as small 
scattered foci or in larger, irregular patches (Fig. 29). 
Fig. 29.—Chronic interstitial myocarditis. (After Delafield and Prudden.) 
Rheumatic Myocarditis.—Interstitial fibrous myocarditis to a varying 
degree is also present as a concomitant of rheumatic endocarditis. Another 
type of myocardial change occasionally found in rheumatic endocarditis is 
the so-called Aschoff body or nodule (Fig. 30). The cells composing the 
nodules are epitheloid in character and contain large pale nuclei. Some of 
the cells resemble, and are of the size of plasma cells; others are much larger, 
resembling the giant cells of the lymph nodes in Hodgkin’s disease. Inter- 
mingled with these cells there is occasionally a sprinkling of lymphocytic and 
eosinophilic leucocytes. The Aschoff bodies, when present, are particularly 
numerous in the interventricular septum and at the base of the left ventricu- 
lar wall. Their presence in the former location is apt to involve the conduc- 56 
CARDIAC HISTOLOGY AND PATHOLOGY 
tion system and therefore may cause heart block during the rheumatic 
attack. After the rheumatic attack has passed the Aschoff bodies change to 
fibrous tissue. 
Cardiosclerosis.—Of late years there have appeared in the literature of 
clinical medicine the generic terms cardiosclerosis, cardiovascular disease, and 
cardiorenal disease. These are convenient although somewhat inexact terms 
which are meant to describe and group certain clinical conditions. There 
is no single pathological picture which accurately describes these groups. 
Fig. 30.—Nodules in the perivascular connective tissue in fresh rheumatic myocarditis. 
A. Aschoff nodula. (After Aschoff.) 
As the names denote, the pathological change in the myocardium and endo- 
cardium is an exceedingly variable one. It depends to a great extent upon 
the amount and type of the other concomitant diseases affecting the kidneys 
and general arterial structure. The usual underlying factor is a general 
degenerative change of the entire vascular system, but especially of the 
smaller arterioles (capillary fibrosis of Jores) of the heart and kidneys. 
The heart then presents changes corresponding to this widespread cause, in 
addition to that wrought by renal disease. The heart is either atrophic, 
witl\ sclerosed and calcareous endocardium, and with indurated 
scars in the myocardium; or it is enlarged, the coronaries showing signs of 
mild or widespread disease varying from slight thickening to extreme calci- 
fication and obliteration of the arterial lumen. This arterio-sclerotic process CARDIAC HISTOLOGY AND PATHOLOGY 
57 
may involve the smallest coronary branches. The aorta is dilated, its 
intima thickened and atheromatous, containing calcareous deposits. A 
similar process affects the semilunar valves which, as a consequence, become 
incompetent (aortic regurgitation) or stenotic (aortic stenosis). The ven- 
tricular endocardium shows various patches of fibrotic thickening. Similarly 
when the process is widespread, the mitral valves are infiltrated with fibrous 
patches on their surface or along their free margins. The valves may even 
be incrusted with calcareous deposits. The myocardium presents indurated 
areas of scar tissue formation, or the entire musculature is riddled by massive 
formation of this character. Engrafted upon these commoner changes are 
those which frequently accompany hypertension and renal disease, i.e., 
massive hypertrophy usually of the left but sometimes of both ventricles. 
Cardiac Syphilis. Spirochetal Infection.—The immense strides in the 
detection of syphilis made possible by the discovery of the causative organ- 
ism (spirocheta pallida) and by the use of the Wassermann reaction, have 
enhanced our knowledge of the frequency of lues as a cause of cardiac disease 
(Chapter XVI). The relation of syphilis to valvular disease, especially to 
disease of the aorta, although not proven, had long been suspected. Syphilis 
has now also been demonstrated as a fairly common cause of disease of the 
heart muscle itself; in fact, myocarditis is occasionally present in the secon- 
dary (Chapter XVI), as well as in the tertiary, stages of lues. By special 
staining methods, spirocheta have been found in the aorta and in the cardiac 
musculature. The most marked, and probably the earliest pathological 
involvement consists in a periarteritis of the arterioles of the coronary system, 
resulting in various types of muscle degeneration (fibrosis, fatty degeneration, 
brown atrophy). As a later involvement, gumma and gummatous infiltra- 
tion also occur. The valves and walls of the aorta are, however, the site of 
predilection of cardiac syphilis. The picture varies from mild arteriosclerosis 
to extreme cicatrization with calcification. Thickening of the mitral cusps 
is less frequent; but it is occasionally sufficient to produce actual mitral 
regurgitation. Endocardial changes varying from slight opacities to exten- 
sive degeneration may coexist. 
As a rare complication in the secondary stage of syphilis, it has been 
found, pathologically, that the myocardium alone may be occasionally 
involved. Such involvements are sometimes sufficient to produce symptoms 
of myocardial insufficiency:—dyspnoea on exertion, indefinite precordial 
distress and pain, precordial sensitiveness to pressure, slight pretibial edema, 
sometimes also a faint systolic murmur at the apex. 
In occasional cases, isolated luetic valvulitis of the mitral or tricuspid has 
been found. In a vast majority of instances, however, the aortic valves, as 
stated, bear the brunt of the endocardial infection. In addition to the cusps, 
there is often widespread destruction of the aortic walls, finally resulting in 
aneurismal dilatations and in true aneurisms (Chapter XVI). Accompany- 
ing these are changes affecting the myocardium, the remainder of the endo- 58 
CARDIAC HISTOLOGY AND PATHOLOGY 
cardium, and the coronaries. Together, they comprise a composite picture 
often similar to that found in non-luetic cardiosclerosis (Chapter XVII). 
AneurismaL Dilatations of the Aorta.—The pathological process in dilata- 
tions of the first and second parts of the aorta consists of a mesaortitis, with 
perivascular infiltrations of the vasa-vasorum, small-celled or granulomatous 
infiltration in areas of the media, and splitting and destruction of the muscu- 
lar and elastic tissue layers. Diffuse dilatation of the entire thoracic aorta 
from its root to the diaphragm is occasionally seen. I have observed three 
such cases: One was an autopsy finding and included severe myocarditis 
and coronary sclerosis, the other two were diagnosed by physical signs in 
conjunction with fluoroscopy. 
While syphilis is the chief cause of aneurismal dilatations there are 
undoubted cases in which syphilis can be etiologically excluded by means of 
serological and clinical examinations (Chapter XVI). I have seen a number 
of patients—chiefly older individuals—in whom the Wassermann test was 
negative, who gave no history of rheumatism or syphilis, and in whom X-ray 
plates, fluoroscopic and clinical examination showed undoubted evidence of 
marked aneurismal aortic enlargement. These are probably examples of 
marked sclerotic changes found in the old in which the intimal coat is first 
affected; later the process may extend to the middle aortic coat (mesaortitis) 
and weaken it to ultimately produce aneurismal enlargement. 
True Aortic Aneurism.—As in aneurismal dilatation, the chief patho- 
logical change is in the media. When the intima is also involved, it usually 
shows no atheromatous placques, but shallow, bluish tinted depressions, or 
the intima is pitted and puckered in small longitudinal or transverse ridges. 
There is perivascular infiltration of the vasa vasorum, and scattered leuco- 
cytic infiltration of the media. There is, further, destruction and separation 
of the elastic and muscular fibers; in other words a productive mesaortitis. 
Pathological Features of Streptococcus Viridans Infection.—Of the 
chronic bacterial infections of the heart, that by the streptococcus viridans 
has been most exhaustively studied. The process is almost always engrafted 
upon a chronic rheumatic infection. Occasionally congenital lesions form 
the nidus. The pathological process consists of vegetative proliferative 
masses of grayish, greenish or pink color. Their main site is the mitral 
valves. Here they form a few soft, friable masses, or the valve may be 
encrusted with large polyoid lesions. The latter may then extend along the 
left auricular wall above, and the chorda tendina below. The process on 
the chorda tendina occasionally leads to ulceration and rupture of these 
structures. Similar sequelae are sometimes found as the result of vegetations 
on the mitral. Proliferative lesions on the aortic cusps and walls are less 
common and less extensive than on the mitral. Mycotic aneurisms of the 
valves are also occasionally found. 
Characteristic changes in the kidney depend chiefly on the presence of 
infarcts. When pyogenic, they give rise to numerous small congested areas CARDIAC HISTOLOGY AND PATHOLOGY 
59 
containing minute purulent foci; these are readily seen when the capsule 
is stripped from the kidney. Non-pyogenic bland infarcts occasionally 
occur; they show the changes usual to anemic necrosis; the infarcted areas 
are wedge-shaped and may be several centimeters in depth. When they are 
recent, the cut surface is yellow; the color becomes paler with the process 
of organization. Another type of infarct, sometimes assumed as pathogno- 
monic of chronic streptococcus viridans, is embolic focal nephritis. Char- 
acteristic changes are then found in the glomeruli; a part of, or an entire tuft 
may be involved. The capillaries are congested, the glomeruli contain a 
fibrinous exudate, the glomerular epithelium becomes swollen and finally 
desquamates. The adjacent parietal layers of Bowman’s capsule are often 
involved in the necrotic process, so that the entire necrotic area becomes 
semilunar in shape. The mass eventually organizes. There is a growth of 
epithelial cells from the healthy adjacent Bowman’s capsule, finally covering 
the lateral surface of the mass. When healing is complete, the result is a 
hyaline area of pyramidal shape. 
Cerebral lesions consist chiefly of areas of softening following emboli. 
Occasionally cerebral hemorrhages from rupture of embolic aneurisms of 
the cerebral vessels have been observed. 
Cardiac Hypertrophy—Etiological Considerations—Physiological 
Hypertrophy.—True physiological hypertrophy of any muscle consists in an 
increase in the size of the normal cells. The process is probably intimately 
connected histologically with hyperplasia (increase simply in the number of 
normal cells) and with physiological hyperemia. 
Based on our experience with skeletal muscles, we assume that the 
increased activity of the normal heart within certain limits will be accom- 
panied by physiological hypertrophy of that organ. The assumption of 
physiological hypertrophy in man is also partly based on experimental 
observations, chiefly that in which the dog’s heart was found considerably 
increased in weight as the result of working the dog steadily in a treadmill 
(Kulbs). The hypertrophy in these experiments was concentric, that is to 
say, about equally divided among the various chambers. 
Increased cardiac activity can be aroused by various stimuli. The most 
obvious stimulus is one from the nervous system, for, as has been shown 
(Chapter III) there exists intimate correlation between nerve excitation and 
the various physiological cardiac functions. Another important stimulus to 
cardiac activity is a mechanical one, for simple stretching of the cardiac 
musculature by its contained blood incites the heart to contraction. Chem- 
ical changes produced by such drugs as digitalis and adrenalin, and chemical 
irritants assumed to be present in the blood of patients with exophthalmic 
goitre or renal disease may also act as excitants to cardiac contraction. 
It is popular belief that physical work itself, such for example as is usual 
in athletics and laborers, can lead to physiological hypertrophy of a normal 
heart. Such assumption does not seem to take sufficient account of the 60 
CARDIAC HISTOLOGY AND PATHOLOGY 
possible role of hypertension occurring during the actual performance 
of hard work as a causative factor of hypertrophy. Nor does it apparently 
emphasize sufficiently the possible incidence of infectious diseases (even 
old and long forgotten ones) as the nidus and primary cause of so-called 
“physiological” hypertrophy. In addition to the above considerations, most 
observations of “physiological” hypertrophy have been made upon the living, 
and unless controlled by modern methods it is now commonly conceded by 
students of cardiology that physical examination, even by the most expert 
clinicians, is open to gross errors and cannot vie with the much more exact 
roentgen and fluoroscopic examinations (Chapter XI). It is, for example, 
well known that percussion (Chapter XIII) as a criterion of the size 
of the heart is faulty, especially when we are dealing with slight or moderate 
hypertrophy in which it is assumed that there is no great increase in the 
size of the heart. Furthermore, all types of abnormalities such as accentua- 
tions, thrills and even diffuse apex beats—signs upon which the diagnosis of 
hypertrophy is commonly based—can be found in various forms of irritable 
heart (Chapter XVIII), in which that organ is of normal size. In this con- 
nection the following observation has an important bearing. A careful 
teleroentgenographic study of a series of soldiers’ hearts who had undergone 
the exertions and physical strain incidental to warfare showed that the hearts 
were not larger than those of normal individuals (A. E. Cohn). Another 
observer, (Karson) who weighed the hearts of soldiers who died from septic 
infection, tentatively concluded that long-continued active service probably 
leads to an increase in the weight of the heart. It should be added however 
that arteriosclerosis, although mild, was present in nineteen out of the 
twenty-four hearts weighed; and the average weight of the enlarged hearts 
was 300 grammes, not much more than the normal. 
Another cause of physiological hypertrophy emphasized especially by the 
German and French schools is the so-called hypertrophy of adolescent growth. 
It is claimed by these observers that in a certain number of such growing 
individuals, there is a physiological hypertrophic increase in the size of the 
heart. I have not been able to corroborate this assumption, for in many 
hearts of growing and large children, X-ray examination showed no inordinate 
or disproportionate enlargement as compared with the height and weight of 
the individuals. I would here except a few tall, young, rapidly growing boys 
from 13 to 16 years of age, of large bony frame, in whom I found by fluoro- 
scopic examination that the heart was larger than the normal for such type of 
chest and for the size of these individuals. My impression of such enlarged 
hearts is, however, not that they are “hypertrophied” but that they are 
examples of organs which have grown larger and more quickly than the 
remainder of the skeletal musculature and hence stand out disproportion- 
ately. Whether these are to be classed as instances of “physiological hyper- 
trophy” will of course depend on the conception of that term. These 
hearts in any case do not seem to become enlarged as a physiological reaction CARDIAC HISTOLOGY AND PATHOLOGY 
61 
to any assumed hyperemia or cardiac overstrain. In this connection, it is 
of interest to note that careful X-ray examination (the teleroentgenographic 
method (Chapter XII) by means of plates taken at a distance of seven feet) 
of a number of college oarsmen, some of whom had been rowing for several 
years, did not disclose enlargement of the heart beyond the normal for adults 
of that physique. 
It is necessary to emphasize here that caution should be exercised in 
diagnosing cardiac enlargement by the usual physical signs. Such ab- 
normal physical signs as an overacting apex (a condition often giving the 
impression of hypertrophy (Chapters XIII, XVIII) or over-vigorous cardiac 
activity are often due to unstable nerve equilibrium common to youth, a 
condition which may conceivably affect cardiac nerve control, and with it, 
cardiac activity. 
Although based upon clinical observations which in their nature are 
not susceptible to proof, it seems probable to me that nerve exhaustion 
rather than physical exhaustion from expended physical energy is the con- 
trolling limit of physiological activity of the heart, and that physiological 
hypertrophy due to cardiac circulatory strain alone in a normal individual 
is probably a very rare occurrence. 
Cardiac Hypertrophy as the Result of Disease.—According to Cohnheim’s 
old classification, the types of hypertrophy were divided into the general 
concentric hypertrophy (equal distribution of the hypertrophic process to all 
the cardiac chambers), local concentric hypertrophy, and local excentric 
hypertrophy. This classification was based to a great extent upon the 
mechanical theories of overwork and of back pressure as the chief causes of 
ventricular hypertrophy. With the more modern conception of the etiology 
of cardiac hypertrophies, and because it has been found that the hypertro- 
phic process by no means regularly follows the assumed overwork of a 
chamber consequent upon circulatory work and strain, the classification of 
Cohnheim has fallen into clinical disuse. 
It has already been pointed out that varying degrees of myocarditis very 
frequently accompany valvular disease; this, however, does not necessarily 
imply hypertrophy. 
Although subject to many exceptions, the following are types of hyper- 
trophy to be found in the well-marked chronic cases of the respective valvu- 
lar lesions. In mitral regurgitation, the prominent hypertrophy effects the 
left auricle; in mild cases, there is slight hypertrophy of the right ventricle, 
and slight or no hypertrophy of the left ventricle. In mitral stenosis, there 
is hypertrophy of the left auricle and of the right ventricle. In aortic 
insufficiency, tremendous hypertrophy of the left ventricle {cor bovinum) is 
the predominant enlargement, while in aortic stenosis, in the rare instances 
in which it is the only lesion, moderate left ventricular hypertrophy is the 
rule. Recent observations in which the ventricles were carefully separated 
by an exact method and were then weighed individually, have shown that 62 
CARDIAC HISTOLOGY AND PATHOLOGY 
the normal weight relationship of right to left ventricle is as 1:1.7. By the 
same method of weighing, it was found that ventricular hypertrophy 
in mitral regurgitation was frequently general. In mitral stenosis it 
seemed that the back pressure theory had some justification, for in the pure 
uncomplicated stenotic cases, right ventricular hypertrophy was the rule. 
Cardiac hypertrophy following chronic renal lesions with hypertension 
is an almost constant finding. The hypertrophy, however, is by no means 
constantly predominant in the left ventricle, as is commonly supposed, for 
the hypertrophy may be general; indeed, predominant right ventricular 
hypertrophy is by no means rare. 
It is well to emphasize here that in valvular lesions the probable reason 
for frequent absence of the usually assumed predominant chamber hypertro- 
phies is the accompanying myocardial disease, for the latter ultimately acts 
as the nidus for hypertrophy; that the myocardial (and hence hypertrophic) 
process may be scattered, or it may extend along and through the original 
complicated anatomy of the muscular cardiac layers (Chapter I) rather than 
follow the anatomy of the individual chambers; and finally, that back pres- 
sure, especially in mitral stenosis, less in aortic regurgitation, may play an 
important etiological part when the myocardium has first been attacked 
and affected by a diseased process. 
REFERENCES 
Aschoff, L.: Pathologische Anatomie, 3rd Edition. 
Bailey, F. R.: Text Book of Histology, 4th Edition. 
Brooks, H.: The Heart in Syphilis; New York State Journal of Medicine, 1916, XVI,185. 
Brooks, H.: Myocarditis, American Journal of the Medical Sciences, 1911, CXLII, 781. 
Delafield and Prudden, T. M.: Textbook of Pathology, nth Edition. 
Kaufmann, E.: Lehrbuch der Speziellen Pathologischen Anatomie. 
Krehl, L.: Ueber Fettige Degeneration des Herzens; Deutsches Archiv fuer Klinische 
Medizin; LII, 416. 
Langly, J. N., and Sherrington, C. S.: Journal of Physiology, 1891, XII. 
Lee, R. I.: Effect of Rowing on the Heart; Boston Medical and Surgical Journal, 1915, 
CLXXIII, 499. 
Rokitansky, von C.: Lehrbuch der Pathologischen Anatomie, nth Edition, 1861. 
Stoehr, P.: Textbook of Histology. 
Warthin, A. S.: Transactions of the Association of American Physicians, May 15, 1914. CHAPTER V 
ETIOLOGY OF HEART DISEASE 
Classification.—In the following enumeration, aortic disease will be 
included because histologically the intima of the aorta is a continuation of the 
endocardial endothelium; and disease affecting the one often affects the other. 
Any classification adopted at this time must in a measure be arbitrary 
and tentative; for example, diseases now grouped as toxic alone may later be 
found to be of bacterial origin. Further studies may isolate specific factors 
in cases now grouped generically. With these limitations, the etiology of 
endocarditis and of cardiovascular disease may be conveniently tabulated 
as follows: * 
(a) Metallic and industrial poisons 
(b) Alcohol 
(c) Tobacco 
(d) Diabetes 
(e) Gout 
(/) Products of food metabolism 
1. Chemical agents 
2. Bacterial agents • 
(a) Diphtheria—pneumonia—typhoid—typhus 
(b) Rheumatism—tonsillitis 
(c) Pyorrhea—mouth infections—focal infections 
(id) Pyogenic abscesses. 
3. Bacterial endocarditis 
4. Spirochetal infection—cardiovascular syphilis 
5. Endocrine disturbances 
6. Senility 
i. CHEMICAL AGENTS 
(a) Metallic Poisons.—Of metallic poisons, the action of lead is best 
known. Lead poisoning (plumbism) formerly occurred principally in 
painters who worked with pigment containing much lead. In modern pig- 
ments, however, the amount of lead has been reduced to a minimum. Die 
workers and those working in fumes in which lead is used now form the chief 
susceptible class. Lead poisoning may affect the endocardium and aorta. 
In rare instances, the coronaries and their branches also become diseased. 
The renal arterioles are often involved, and nephritis results. Depending 
on the severity and location of the arteriolar disease, the symptoms 
and physical signs may be those of aortitis, nephritis, cerebral endarteritis, 
coronary disease or of endocarditis; or there may be a clinical picture com- 
* The clinical phases of these various poisons and factors of heart disease are described 
in their appropriate chapters. (See Table of Contents.) 
63 64 
ETIOLOGY OF HEART DISEASE 
bining these pathological entities in varying proportions. The patient’s 
occupation, a history of colic, peripheral neuritis, the presence of a lead line 
on the gums, microscopic examination of the blood, and the chemical examina- 
tion of the feces and of the total urine of several successive days for lead are 
data which are of aid in the search for lead as the etiological factor. These 
examinations, however, are of use chiefly during the time the individual is 
still working at his lead trade; for it must be remembered that cardio-vascular 
disease originating in lead poisoning may insidiously progress long after the 
patient has given up his original occupation. Whether myocardial degenera- 
tion, when present, is primary, or is secondary to disease of the coronary 
system is still an unsettled question. However, the selective action of lead 
on the arterial system seems to indicate that myocarditis results secondarily 
from the vascular disease. 
Severe phosphorous poisoning can produce fatty degeneration of the heart 
and of the arterial intima. Other metallic poisons—copper, mercury, arsenic 
■—have a much greater selective action upon the gastro-intestinal canal, and 
upon nervous, osseous, and renal, rather than upon the cardiac structures. 
Except for the action of mercury upon the kidneys, it is questionable whether 
copper, mercury and arsenic produce cardiac damage that is clinically 
recognizable. 
“Industrial” Poisons.—I am applying this term to possible other poisons, 
non-metallic in nature, which may have some as yet practically unknown 
effect upon the cardio-vascular system. Thus the fumes of some aniline 
dyes, some of which in acute poisoning cause marked blood and other destruc- 
tion may also insiduously change the chemical composition of the blood, 
and finally cause disease of the myocardium by interference with its proper 
nutrition. These and other similar questions are still problems of the future 
in the study of the possible effect of industrial poisons upon the heart. 
(b) Alcohol.—The degree of damage to the cardiovascular system by 
alcohol is still a matter of dispute. Like other poisons, it affects the cardio- 
vascular structures to a variable extent, so that necropsy reports showing 
absence of cardiovascular damage in chronic alcoholism are not necessarily 
evidence of its innocuousness. It is probably true, however, that the impor- 
tance and frequency of alcohol as a cardiac poison have been overestimated. 
Alcohol attacks particularly the cardiac musculature; the result is myocardial 
disease varying from slight fatty degeneration to scar-tissue formation. The 
arterial system, when affected, presents various grades of thickening of the 
intima as well as calcareous deposits; in exceptional cases, there is also 
degeneration of the remaining arterial coats. 
The clinical symptoms referable to alcoholism are usually those of myo- 
carditis and myocardial insufficiency. The heart is moderately hypertro- 
phied. As a clinical syndrome of moderate myocarditis may be cited that 
due to constant drinking of large amounts of beer (the “Munchener Bier- 
herz”). In severe cases of alcoholic myocarditis, cardiac hypertrophy may ETIOLOGY OF HEART DISEASE 
65 
be extreme. In one case that I observed at necropsy, a man of 45 who was 
an inveterate wine drinker, the ventricular musculature consisted mainly of 
scar tissue, the heart weighed twice the normal. Symptoms and clinical 
signs due to aortitis—an impure first, and an accentuated second sound at 
the right base, and hypertension—are also occasionally due to alcoholism. 
(c) Tobacco Poisoning.—It is the general belief that tobacco users are 
particularly prone to aortic disease, coronary sclerosis and myocardial 
degeneration, and that these pathological changes are caused by nicotine, the 
main tobacco alkaloid. This view is based chiefly on the result of experi- 
ments on rabbits in whom nicotine solutions were injected; as a result, 
various degrees of aortitis were produced. Before conclusions from such 
experiments can be regarded as comparable to tobacco poisoning in the 
human being, it should be remarked that these injections were repeated at 
frequent intervals over a long period before aortitis resulted. As further 
objections to inferences drawn from these nicotine injection experiments, it 
must be stated that others have found no abnormal aortic change following 
nicotine injections; indeed, one observer found spontaneous changes in the 
aorta in a certain proportion of normal rabbits. Moreover, when the 
attempt was made to produce parallel conditions by forcing rabbits to inhale 
fumes on successive days from measured amounts of burning tobacco, no 
definite changes in the aorta were found. One observer who made a careful 
pathological study of the hearts of heavy smokers dying of various diseases 
found only a slight change in the papillary muscle; this he attributed to the 
rapid heart action usually found in smokers. From the experimental and 
pathological sides, therefore, it must be concluded that no incontrovertible 
proof has as yet been adduced that smoking in itself produces cardiovascular 
disease. On the other hand, as the result of physiological and pharmacological 
experiments, it is known that nicotine has a strong affinity for nervous struc- 
tures (neurotropic action), particularly upon the sympathetic nervous 
system (Chapter X). Many of the symptoms complained of by patients 
with so-called “ tobacco heart” (Chapter XXVI)—tachycardia, arrhythmias of 
various types (especially extrasystoles), syncope, precordial pains and distress 
—can be more readily and rationally explained, I believe, by the selective 
action of nicotine upon the sympathetic nerves and ganglia (Fig. 210) than 
upon the assumption of organic cardiovascular disease. In the majority of 
cases, when tobacco is withdrawn, cardiac irregularities and pain cease, and 
patients examined months or years later show no evidence of organic damage 
to the heart or arteries. I believe, however, that if from any other cause a 
symptomless aortitis exists, the lesion may become activated and produce 
symptoms as the result of tabagism. Even this statement is only surmise, 
for it is not susceptible of clinical proof. 
(d) Diabetes is frequently accompanied by arteriosclerosis and nephritis. 
In chronic cases the myocardium may show advanced fatty degeneration. 
The rather marked tendency to arteriosclerosis—and therefore to coronary 66 
ETIOLOGY OE HEART DISEASE 
disease—may be a primary cause of myocardial change found in some diabe- 
ties. The clinical symptoms and signs of the resultant cardiovascular 
disease, when not marked or complicated by diabetes itself, are high blood 
pressure; thickening of the palpable arteries; sugar, albumen and casts in 
the urine, and aortitis. Therapy should be directed to both diseases— 
diabetes and cardiosclerosis; relief or cure of the former is often followed by 
beneficial results in the latter. 
(e) Gout is very frequently accompanied by arteriosclerosis, nephritis 
and hypertension. Aortitis and coronary disease are also very common in 
gouty individuals, and as a consequence, myocardial changes of various degrees 
and extent are often present. An abnormal amount of uric acid in the blood 
and in the tissues may be the cause of these pathological changes, or both 
the latter and gout may be the expression of some common, as yet unknown, 
underlying factor or diathesis. The problem of therapy directed to the 
cardiorenal disease is rarely complicated by the presence of gout. 
(/) Products of Food Metabolism, Amino Acids, etc.—The study of 
metabolism and of blood chemistry has shown the presence of amino-acids 
and other protein derivatives in the blood. Experiments have demonstrated 
that protein feeding can produce changes in the cardiovascular and renal 
apparatus of animals. Although clinical proof is lacking, these investiga- 
tions suggest that protein overfeeding in man may be followed by arterial 
disease, and that therefore protein can act as cardiovascular poisons. 
2. BACTERIAL AGENTS 
In the production of disease, bacteria act directly or by the elaboration of 
chemical poisons, that is, of toxins. Chemically the latter are at present 
regarded as extremely complex poisons of nitrogenous nature. It should be 
emphasized that the various bacterial agents possess special predeliction for 
various parts of the cardiac structures and hence cause disease of varying 
degrees (e.g., of heart muscle, endocardium, conduction system, etc.). 
(a) Diphtheria.—The heart muscle in severe diphtheritic myocarditis 
undergoes fatty and parenchymatous degeneration; the valves and endo- 
cardium are rarely affected. When the poison attacks the heart more 
slowly, there is in addition, leucocytic infiltration (inflammatory myocardi- 
tis). Occasionally the conduction system is attacked, with the consequent 
production of various types of heart block (Chapters X, XI). The clinical 
syndrome of the heart in diphtheria is described in another connection 
(Chapter XXVI). 
Pneumonia.—Endocarditis due directly to an invasion by pneumococci 
is by no means rare; this type will be discussed later. The pathological 
damage is comparable to that found in bacterial endocarditis (Chapter IV). 
Regarding the effect of pneumonic toxins on the heart, many pathological 
examinations of the cardiac musculature have been reported. Slight paren- ETIOLOGY OF HEART DISEASE 
67 
chymatous degeneration (cloudy swelling) is the rule; occasionally more 
severe damage has been described. When widespread, these degenera- 
tive changes can undoubtedly cause death. But there is no evidence that 
slight cardiac degeneration, the usual damage in pneumonia, is in itself 
sufficient to produce death; nor have attempts been made to correlate the 
amount and degree of pathological damage with the clinical or bacteriological 
evidence of toxicity. Experimental evidence pertaining to this subject 
indicates that pneumonia usually acts as a poison upon the functional power 
of the heart; for example, pneumonic blood perfused into a healthy dog’s 
heart is immediately followed by greatly weakened contractility. The con- 
tractions become normal when healthy blood is subsequently perfused. 
At present the conclusion seems warranted that death from pneumonia in 
the majority of cases is not due to demonstrable changes in the myocardium. 
On the other hand, damage to the cardiovascular apparatus as a late sequel 
of pneumonic infections has been insufficiently emphasized. Such sequalae 
produce symptoms only some months or years after pneumonia has run its 
course, so that the connection between the two diseases is usually entirely 
overlooked. In some instances the pneumonic poison seems to light up a 
dormant cardiovascular process; in others, it is the prime factor. Case 
reports illustrating these statements are given elsewhere (Cardio-vascular 
Clinics). 
The action of diphtheria and of pneumonia as cardiovascular poisons has 
been described in some detail because similar observations apply in varying 
degrees to other infectious diseases. Typhoid fever deserves special 
mention in this connection, for it occasionally causes areas of necrosis in the 
musculature. 
All these various toxic causes of myocarditis show the importance of a 
careful search for infectious disease as an etiological factor, especially when 
the etiology of cardiac impairment is obscure. 
(b) Rheumatism—Tonsillitis.—Of all diseases, rheumatism is the most 
frequent source of valvular disease. Although the etiology of rheumatism is 
not yet known, recent experimental research and clinical observation indicate 
that it is of bacterial (probably of streptococcic) origin. For the present, 
however, until the specific organism has been isolated, it is here classified 
under toxemias. Valvular endocarditis is the most frequent sequel of a 
rheumatic infection. Varying degrees of myocarditis, and, occasionally, the 
formation of submiliary inflammatory nodes (Aschoff’s bodies) are frequent 
accompaniments of rheumatic endocarditis. Permanent damage always 
results from rheumatic valvulitis and myocarditis; but here, as else- 
where in the body, if the infective process stops early, scar tissue may form 
(Chapter IV); hence clinical signs of myocardial or valvular disease may 
never appear. Necropsy alone gives evidence of cardiac damage in such 
instances. In some cases, even if clinical manifestations of valvular disease, 
particularly of mitral regurgitation be present, the process may heal, the 68 
ETIOLOGY OF HEART DISEASE 
valvular leakage may stop and the patient remain clinically well. Such 
observations at the bedside have been substantiated by necropsy. 
Tonsillitis is grouped with rheumatism in the etiology of cardiac disease, 
for, like rheumatism, it may also give rise to joint manifestations and to endo- 
carditis. Even without joint involvement, tonsillitis frequently causes endo- 
carditis. In fact, exceedingly mild and apparently harmless tonsillar and 
pharyngeal attacks, accompanied by a few spots on the tonsils or pharynx, 
can be the source of an endocardial infection. As one instance, a vigorous 
young man of twenty-one developed mild pharyngeal grippe lasting three 
days; the highest temperature was 101.50. Within one week typical signs of 
a mitral regurgitant lesion were present. Similarly so-called “colds” (acute 
pharyngeal and nasal catarrh)—can occasionally, although rarely, be the 
infectious nidus for endocarditis. (See Cardio-vascular Clinics.) 
• (c) Pyorrhoea Alveolaris—Mouth Infections—Focal Infections.—Much 
experimental and clinical work has recently been done to show that the 
various pyorrhoea-producing organisms harbored in the mouth may, by 
systemic absorption, cause myocarditis and endocarditis. Among other 
bacteria, the streptococcus viridans has been especially accused. However, 
it has been shown that this organism is a fairly frequent inhabitant of the 
normal mouth; hence not only demonstration of the pyogenic organism is 
required but also definite clinical evidence that it bears an etiological relation- 
ship to the cardiac disease. In the face of negative blood cultures and 
in view of the other well-known causes for endocarditis, several procedures are 
necessary in order to prove the correlation between pyorrhoea alveolaris 
and cardiac disease. Thorough examination of the mouth for carious teeth 
and for periostitis by radiographic examination of the jaws and of the roots 
of the teeth constitutes the first step. Then a careful search of the entire body 
must be made for other possible infective foci which may cause cardiovascular 
disease. Cholecystitis, cystitis, deep-seated bone abscess and pyelitis are 
some of these inflammatory conditions. So that even should roentgen- 
ography disclose root abscesses, and the mouth harbor pathogenic bacteria, 
it is for the clinician to decide from the clinical history, the type and probable 
duration of the cardiovascular disease, and from a complete examination 
for all other possible sources of infection, what weight, etiologically, should be 
given to the presence of root abscesses or pyorrhea as the causative agents of 
endocarditis. Thus studied, it appears to me that the claims now made for 
the extremely frequent connection between oral infections and heart disease 
are unwarranted. This statement indeed fits in with general clinical experi- 
ence. For instance, very many children with endocarditis have healthy 
teeth and mouths, and again many with carious teeth have normal hearts. 
In those patients with cardiovascular disease observed by me, in whom 
extraction of teeth had been done because of root abscesses, extraction had no 
effect upon the cardiovascular process or upon the clinical signs. In general, 
one would not expect that the small amount of toxins presumably elaborated ETIOLOGY OE HEART DISEASE 
69 
and absorbed from a small dental focus could be a frequent cause of endo- 
carditis; one would expect sufficient antibodies to be developed to prevent 
cardiac mischief in the great majority of cases. On the other hand, it cannot 
be denied that, given an extremely susceptible individual, general systemic 
damage and especially cardiac disease can occasionally, though I believe very 
rarely, be caused by diseased teeth or diseased gums acting as foci of infection. 
It is therefore necessary for the clinician to weigh all factors and not to 
conclude too hastily that because pus, pathological bacteria, or small root 
abscesses are found in the mouth, they are necessarily the cause of the 
cardiovascular disease in that individual. We are greatly indebted to the 
dental profession for indicating the teeth as a “focus” for endocarditis, but 
the physician must finally judge all the evidence in every case before he can 
decide whether the cause of endocarditis lies in the mouth or elsewhere. 
None of the statements here made of course militate against the fact that 
purulent mouth conditions should receive proper dental attention in order to 
remove that source of a possible endocarditis. My main object has been 
to refute the usual accepted opinion that diseased teeth commonly cause 
disease of the heart. In those exceptional cases under my observation in 
which alveolar pyorrhea might have been the cause of the existent 
cardiovascular disease, the pyorrhea was frank and usually severe even at 
the time the patients presented themselves for examination because of 
cardiac symptoms. There was usually a long history of foul breath, and 
of decaying and loose teeth. The patients were of middle age or past 
middle age. Questioning elicited that the pyorrhea was severe and of several 
years duration. Of interest and importance is the fact that, in my own ob- 
servation, at least symptomatically and pathologically, the picture is one of 
cardiosclerosis (Chapter XVII). It seems as if the poison acts, if at all, 
primarily upon the arterioles of the cardiovascular system, affecting in varying 
degrees the vessels of the heart and kidneys. Its final effect upon these 
organs often closely resembles, indeed sometimes coincides with, the patho- 
logical picture of senile cardiosclerosis (Chapter XVII). 
Regarding the relation between diseased teeth and valvular endo- 
carditis in children, with the exception of cases of widespread and gross oral 
sepsis developing into bacterial invasions of the blood, there is as yet no 
definite evidence that diseased teeth have actually caused endocarditis. 
Such a possibility cannot of course be denied, particularly perhaps in valves 
already damaged by rheumatism or other infections. The warning lies in 
accepting possibilities for probabilities, and in assuming that because diseased 
teeth occasionally produce rheumatism of a certain type, they therefore 
can act as commonly and as virulently upon the endocardium in the 
production of valvular disease. Each case must be carefully studied indi- 
vidually, and although thorough modern dental care should be given abscessed 
teeth, we should not lean to unnecessary wholesale extraction in our efforts 
to rid the mouth of “foci of infection.” 70 
ETIOLOGY OE HEART DISEASE 
The clinical aspects of “foci of infection” are described in other connec- 
tions. (See Table of Contents.) 
(d) Pyogenic Abscesses.—These may occasionally produce endocarditis 
by the production of a bacteremia or from toxins. In endocarditis where 
a frank etiological factor cannot be found, careful search should be made 
for hidden abscesses as possible foci of infection. 
Bacteria were demonstrated in valvular vegetations by Heilberg as early 
as 1869. Since then many type of organisms have been recovered from such 
vegetations, and more recently, isolated from the blood. 
The question of systemic bacterial infection in rheumatic fever is still 
unsettled, although, as already indicated, there are good clinical and experi- 
mental grounds for considering it a bacterial disease. 
The known organisms found in the blood which produce endocarditis 
are grouped, according to Simon’s modification of Litten’s classification, as 
follows: 
3. BACTERIAL ENDOCARDITIS 
x. Ordinary streptococcus. 
Streptococcus viridans (Schottmueller). 
Endocarditic cocci (Libman). 
Modified pneumococci (Rosenow). 
Saprophytic streptococci (Horder). 
Streptococcus tenuans (Hastings). 
2. Small streptococcus. (Probably all alike, but 
variously named by different observers.) 
3. Staphylococcus albus and aureus. 
4. Pneumococcus. 
5. Gonococcus. 
6. Meningococcus. 
7. Bac. coli. 
8. Bac. influenzae. 
9. Bac. pyocyaneus. 
As gathered from the statistics of various authors, the most common 
invaders in acute bacterial infections are, in order of their frequency, the 
streptococcus pyogenes and the staphylococcus aureus; next in frequency are 
the pneumococcus and gonococcus; the streptococcus viridans is very rare. 
The other bacteria—staphylococci, meningococci, bac. coli., bac. pyocyaneus, 
and bac. aerog. capsulat.—are only occasionally found. The chronic invaders 
are, in the order of frequency, the streptococcus viridans (common), the 
streptococcus pyogenes, pneumococcus, bac. influenzae, and the gonococcus. 
It is thus seen that the gram-positive chain cocci are the chief causes of bac- 
terial endocarditis. 
Regarding the relative frequency of bacterial invasions of the various 
valves, the mitral is the most frequently affected alone; next is the aorta. 
Bacterial infection of the pulmonary or tricuspid valves alone is exceedingly 
rare. The most common combination of a multiple infection is the mitral ETIOLOGY OF HEART DISEASE 
7i 
and aortic; the next, the tricuspid and mitral. Vegetations on the walls of 
the auricle and ventricle have also been described, but they do not occur 
without vegetations on the valves as well. 
4. SPIROCHETAL INFECTION 
As already noted, and as is well known, the etiological factor is the spiro- 
cheta pallida. The pathological changes in the heart produced by this 
organism have already been described (Chapter IV). 
5. ENDOCRINE DISTURBANCES 
Because of our incomplete knowledge of the endocrines, there are at 
present no exact data of the effect of disturbances of the ductless glands upon 
the etiology of cardiac disease. An exception is the thyroid gland. Here there 
is definite evidence that in addition to the symptoms caused by hyperthyroid- 
ism (Chapter XVIII) there may be not only functional myocardial distur- 
bances but occasionally actual myocarditis maybe present. There is another 
fairly frequent distinctive picture of cardio-vascular disease; that found in 
women at the menopause. Such patients may have hypertension for years 
(Chapter XXV); the disturbance seems mainly vaso-motor in origin. The 
question arises whether such types of hypertension—often innocuous in the 
beginning—may finally produce actual cardio-renal disease. Until autopsy 
reports of such conditions have been offered, the question must remain 
sub judice. 
6. SENILITY 
It is commonly assumed that old age as such forms part and parcel of the 
chronic diseases and changes of the heart and arteries so frequent in the old. 
The general trend of this thought, so far as it can be translated, is that the 
“wear and tear of life”-—-especially from the physical standpoint—has finally 
caused “senile” cardiac changes. This view seems incomplete and inexact; 
in particular, it does not reckon sufficiently with factors of infection, perhaps 
present many years before and long since forgotten, which can ultimately 
bring about definite pathological changes in old age. This phase of the sub- 
ject will probably not be cleared up until we can obtain experimental or 
clinical evidence of the slow, insidious progress of the effects of infection long 
after the infection itself has completed its acute course. Perhaps then se- 
nility as far as the arterial tree is concerned may be translated into the insidi- 
ous results of the long-continued “wear and tear of life” acting upon arteries 
already affected, no matter how minutely, by some actual pathological 
change, a minor effect of any one of the commoner, universal infections. 
REFERENCES 
Adler, I.: Syphilis of the Heart, 1898. 
Adler, I. and Hensel, 0.: Intravenous Injections of Nicotine and Their Effects upon the 
Aorta of Rabbits; Journal of Medical Research, N. S. X, 229. 72 
ETIOLOGY OE HEART DISEASE 
Baehr, G.: Glomerular Lesions of Subacute Bacterial Endocarditis; Journal of Experi- 
mental Medicine, 1912, xv, 330. 
Bamberger, H. von: Lehrbuch der Krankheiten des Menschen. 
Brooks, H.: The Tobacco Heart; New York Medical Journal, 1915, Cl, 830. 
Cohn, A. E.: On Investigation of the Size of the Heart of Soldiers by the Teleroentgen 
Method—Archives of Internal Medicine, 1920, XXV, 499. 
Cotton, T. F.: Cardiac Hypertrophy; Journal Canadian Medical Association, 19x4, N. S., 
XLIII, 709. 
Fleming, G. B. and Kennedy, A. M.: A Case of Complete Heart Block in Diphtheria with 
* an Account of Post-mortem Findings; Heart, 1910-1911, II, 77. 
Flexner, S.: The Pathology of Toxalbumin Intoxication; John Hopkin’s Hospital Report, 
1897, VI, 259. 
Gy, A.: L’Intoxication Tabagique chez l’Homme; Paris Theses, 1908-1909, 203. 
Hartzell, T.: The Clinical Type of Arthritis Originating about the Teeth; Journal of 
American Medical Association, 1915, LXV, 1903. 
Hecht, A. F.: Der Mechanismus der Herzaction im Kindesalter; Ergebnisse der Innerc 
Medizin und Kindesheilkunde, 1913, XI. 
Heiberg, H.: Ein Fall von Endocarditis Ulzerose, etc.; Virchow’s Archiv fuer Pathologische 
Anatomie und Physiologis, 1872, LVI, 407. 
Horder, T. J.: Infectious Endocarditis; Quarterly Journal of Medicine, 1908-1909, II, 289. 
Hume, H. E. and Clegg, S. J.: A Clinical and Pathological Study of the Heart in Diph- 
theria; Quarterly Journal of Medicine, 1914-1915, VIII. 
Jochmann: Ueber Endocarditis Septica; Berliner Klinischer Wochenschrift, 1912, XLIX, 
1, 436. 
Jores, L.: Wesen und Entwickelung der Arteriosklerose; Weisbaden, 1903. 
von Juergensen, T.: Endocarditis; Nothnagel’s Encyclopedia, American Edition, 1908. 
Karsen, T. K.: Acute Endocarditis Following War Wounds Including Notes on Heart- 
Weight and Arterio-sclerosis in Soldiers; Heart, 1918. 
Krehl, L.: Disease of the Myocardium, Nothnagel’s Encyclopedia of Practical Medicine. 
Kulbs: Experimentelles ueber Herzmuskel and Arbeit. Archiv f. Experimentelle Pathologie 
und Pharmakologie, 1906, LV, 288. 
Lewis, T.: Observations upon Ventricular Hypertrophy, with Especial Reference to Pre- 
ponderance of One or Both Chambers; Heart, 1913-1914, V, 367. 
Libman, E.: A Study of the Endocardial Lesions of Subacute Bacterial Endocarditis, etc.; 
American Journal of Medical Sciences, 1912, CXIV, 313. 
Litten, M.: Die Endocarditis und ihre Beziehungen zur anderen Krankeiten; Verhand- 
lungen d. Kongresses fuer Innere Medizin, 1900, XVIII, 97. 
Longcope, W. T.: The Effect of Repeated Injections of Foreign Protein on the Heart 
Muscle. Archives of Internal Medicine, 1915, XV, 1079. 
Lucien et Parisot: Quoted by Vaquez; Archives des Maladies de Coeur, 1915, VIII, 678. 
Newburg, L. H. and Porter, W. T.: The Heart Muscle in Pneumonia; Journal of Experi- 
mental Medicine, 1915, XXII, 123. 
Osier, W. in Osier & McCrae: Modern Medicine, Vol. IV. 
Pearce, R. M.: Experimental Myocarditis: A Study of the Histological Changes Following 
the Injection of Adrenalin. Journal of Experimental Medicine, 1906, VIII, 400. 
Poyton & Paine: Researches on Rheumatism. 
Romberg, E.: Ueber die Erkrankungen des Herzmuskels bei Typhus und Scharlach; 
Deutsches Archiv fuer Klinische Medizin, 1891, XLVIII, 369. 
Rosenau, E. C.: Elective Localization of Streptococci; Journal of American Medical 
Association, 1915, LXV, 1687. 
Smith, B.: Teleroentgen Measurements of Hearts of Normal Soldiers. Archives Internal 
Medicine, 1920, XXV, 522. 
Welsh, E. W.: Adaptation in Pathological Processes, Transaction of Congress of American 
Physicians and Surgeons, 1897, IV, 284. CHAPTER VI 
DYNAMIC AND MECHANICAL CONSIDERATIONS—CARDIAC 
DILATATION 
Valve Closure.—The valves guarding the mitral and tricuspid orifices 
are slightly muscular at their origin but are otherwise membraneous (Chapter 
I). They are attached by means of the chorda tendina to the apices of the 
papillary muscles (Figs, n, 12). The tendinous cords and papillary muscles 
serve to keep the valves under a certain amount of tension so that they cannot 
become inverted into the auricles during any phase of the cardiac cycle. 
During cardiac systole, the chorda tendina become taut, chiefly as the result 
of contraction and shortening of the papillary muscles. The semilunar 
valves guarding the pulmonary and aortic orifices form a complete membrane- 
ous closure at these openings, the small fibrous nodules at the center of each 
cusp (the corpora Arantii, Fig. 12) helping to make the closure perfect. The 
valves of the great vessels and of the ventricles very probably do not flap 
back during diastole sufficiently to touch the arterial or ventricular walls, 
respectively. Such approximation is presumably prevented by eddies occur- 
ring during diastole which tend to float the valve leaflets away. 
The usually accepted view regarding the mechanism of valve closure is 
that with the inrush of blood, these diastolic eddies not only float up the valves 
to prevent their touching cardiac structures but in addition they co-apt 
the various valve leaflets to bring about valve closure. A more modern 
conception assumes that accompanying the diastolic inrush of blood immedi- 
ately after systole, negative pressure is momentarily induced; it is this nega- 
tive pressure which tends to draw in blood behind the valve leaflets; as a 
consequence the valves close. It seems probable that this action permits 
of perfect closure because it begins at the attached border of the valve leaflets 
and thus tends to hermetically seal the various valve openings. 
Pressure in the Cardiac Chambers.—Various instruments—optic man- 
ometers, cardiometers, etc.—have been devised for the study of pressure curves 
as they exist in the chambers of the animal’s beating heart. As a result of 
these studies, it has been determined that the pressure in both ventricles is 
practically the same. The initial rise in intraventricular pressure (Fig. 57) 
is initiated by a very slight rise in presystole due to auricular contraction. 
After this there occurs a sharp rise in intraventricular pressure. This takes 
place during what is called the isometric period of the cardiac cycle—that 
brief interval during which both the auriculo-ventricular and semilunar valves 
are closed, and the cardiac fibers are in a state of tension before actual ventricu- 
73 74 
DYNAMIC AND "MECHANICAL CONSIDERATIONS 
lar systole begins. During ventricular systole and with the opening of the 
semilunar valves, the intraventricular pressure curve reaches its peak. 
With the onset of ventricular diastole, the intraventricular pressure rapidly 
falls, to again reach its base line with the onset of auricular systole. 
There is a sharp rise of pressure in the aorta and pulmonary artery as the 
blood is ejected with the onset of ventricular systole (Fig. 57); this pressure 
is sustained during the entire period of ventricular contraction. With the 
onset of ventricular relaxation and diastole, the arterial pressure rapidly falls. 
As in the ventricles, so also in the auricles there is no appreciable difference 
in the pressure curves of the right and left sides. There is a sharp rise of 
auricular pressure due to auricular systole, followed by a fall caused by 
auricular relaxation and diastole. With the onset of, and during ventricular 
systole (at which time the auricles are filling with blood), there is a steady 
slight rise of intra-auricular pressure as the result of stasis. 
Volumetric Ventricular Curves.—For the experimental observation of 
volumetric curves in various phases of the cardiac cycle, a cardiometer is 
employed. This is a glass vessel containing a rubber dam or diaphragm 
which can be snugly closed around the auriculo-ventricular groove. The 
projecting end of the cardiometer is placed in circuit with a tabular recorder 
and revolving drum. Thus a graphic study may be made of the systolic 
output as well as of the volumetric changes occurring during diastole. With 
the ejection of blood from the ventricular chambers during systole, there is 
naturally a great diminution in their size. The period of ventricular empty- 
ing and filling may be divided as follows: (1) the stage of blood ejection: 
the systolic period. This is followed by (2) the early diastolic filling, called 
also the active diastole or diastasis (Henderson); during this period, filling 
proceeds rapidly; finally there is (3) the late diastolic filling period (passive 
diastole). As shown by experiments, the entire diastolic period (both active 
and passive) is profoundly influenced by variations in venous pressure and 
cardiac tone, and by the cardiac rate, that is, by the number of cardiac cycles 
per minute. These three factors are by no means interdependent although 
each by itself can markedly affect the ventricular volumetric curve. Regard- 
ing the influence of rate, the maximal systolic output is seen when the heart 
beats at the rate of 75 or 80 per minute. At higher speeds, especially with 
extreme cardiac acceleration, the diastolic period (especially active diastole) 
becomes considerably shortened, and the systolic output markedly reduced. 
The output per minute may still increase but not proportionately to cardiac 
acceleration. 
Regarding the influence of venous pressure on the volumetric curve, no 
“critical” pressure has been discovered which will always deleteriously 
effect the volumetric curve. However, an amount of venous pressure can be 
induced during which the cardiac output no longer maintains its level, but 
decreases, and with it, the heart dilates. Muscular exercise (that is, the 
action of skeletal muscles as an accessory pump in forcing the blood through DYNAMIC AND MECHANICAL CONSIDERATIONS 
75 
the systemic veins) exerts a great influence in filling up the right auricle, 
thus enabling the right ventricle to receive its proper quota of blood. 
Finally, regarding the influence of cardiac tonus on the volumetric curve, 
it must be remembered that tonus (Chapter III)—that state of partial 
contraction in which variations in size of the heart are resisted—is difficult to 
determine experimentally. It seems probable, however, that cardiac tonus 
must exert a decided influence on systolic output and volumetric filling. 
Thus, with high tonus, the systolic output is quite effective but diastolic filling 
is interfered with, while with low tonus, there is rapid diastolic relaxation and 
filling. 
Acute Cardiac Dilatation.—The importance of the physiological and 
experimental considerations just described lies in the attempt to correlate 
them with what actually occurs in the human heart in health and disease. 
Some facts regarding the effect of exercise upon the size of the heart are 
pertinent in this connection. Previous attempts at exact studies of the heart 
by means of X-rays have not given any conclusive evidence as to the size of 
heart during actual exercise or work, partly because pictures were not taken 
during the exercise and partly because the phase of respiration during which 
the roentgenogram was taken was not considered. A roentgenogram taken, 
for example, with the diaphragm in the act of rising will naturally push up 
the heart and show a much broader cardiac shadow than if the heart picture 
is taken with a descending diaphragm (Chapter XII). Exact teleroentgeno- 
graphic study of hearts immediately before, and about 20 seconds after exercise 
with the respiratory phase taken into consideration, showed slight diminution 
in the size of the heart in 29 out of 33 normal subjects. Attacking the 
problem of cardiac output from the physiological standpoint by a study of 
the tension of nitrous oxide experimentally inhaled, and measurement of the 
quantity exhaled, it has been demonstrated that the cardiac output in the 
resting state is 3 to 5 liters per minute and that during heavy muscular 
work, the cardiac output per minute may reach 20 liters. This of itself 
shows the tremendous “factor of safety” of the human heart. Other physio- 
logical observations have demonstrated that there exists a normal physio- 
logical dilatation of the heart during exercise, and that its limit is fixed by 
that amount which fills the pericardial sac during diastole (Bainbridge). 
Naturally it is a very difficult process to determine actual dilatation 
clinically with any exactitude, so that we are often limited to inferences alone. 
Indeed one observer (Williamson) who made very careful teleroentgeno- 
graphic studies of both normal and decompensated hearts during exercise, 
categorically states that even by this refined, objective method the amount of 
dilatation of decompensated hearts after exercise is so small (3 mm.) that it 
is obviously all but impossible to detect it objectively at the bedside. The 
cardiac fibers possess the property of shortening during, and of lengthening 
after, contraction. In health this function is perfect. Fundamentally, it 
is this ability to contract and expand which indicates what is known as the 76 
DYNAMIC AND MECHANICAL CONSIDERATIONS 
“cardiac reserve.” As the result of valvular disease, there is a varying amount 
of change in the ventricles and their chambers; this consists of myocarditis, 
hypertrophy and dilatation. These abnormal factors compromise to a 
varying degree the underlying function of lengthening and shortening of the 
cardiac fibers, and hence interfere with the reserve power of the heart. In 
consequence, the cardiac power is decreased and signs of decompensation 
(Chapter XIV) appear. There is also evidence that differences in tone may 
play a part in the symptomatology. For example, patients may complain 
of dyspnoea, of vaso-motor symptoms, and even of precordial distress with- 
out any physical or clinical evidence of cardiac dilatation. These symptoms 
may appear suddenly, remain for a few hours or a day, and then disappear 
without any signs of decompensation. 
Several pertinent questions arise. To what extent in the living do such 
experimental factors as venous pressure and cardiac rate increase or lessen 
output? If output is lessened, does it cause the gradual or rapid onset of 
cardiac dilatation? What is the role of that much misused term, tonus, in 
cardiac dilatation? The matter is further complicated by the fact that it is 
by no means easy to diagnose cardiac dilatation by the usual, or indeed by 
refined methods of examination. In fact, I believe that cardiac dilatation in 
the sense of mechanical stretching of the heart is often assumed when its 
actual presence is, to say the least, purely inferential. An exception to this 
statement, however, must be made with paroxysmal tachycardia (Chapter 
X). In some of these patients the heart actually swells, so to speak, so that 
the presence of dilatation can usually be diagnosed by the ordinary methods 
of examination. The heart occupies an abnormally large area in some 
individuals during the tachycardial seizure, and recedes in size when the 
paroxysm ceases. 
A further perplexing clinical aspect of the problem of cardiac dilatation 
is the fact that we possess no data as to the amount of acute dilatation a 
diseased heart can stand, for cardiac disease in itself can presumably decrease 
heart tone and thus establish a vicious circle. Again, a heart already inured 
in a way to rapid heart action, may be able to withstand more dilatation 
without serious results than one in which the tachycardia is sudden and 
unexpected. I believe that the subject of cardiac dilatation in its clinical 
sense—especially its diagnosis and degree—presents very many perplexing 
phases, each of which has to be carefully weighed, and indeed often 
only inferred in order to arrive at the proper diagnosis in the case at 
hand. 
Cardiac dilatation and cardiac reserve power are also intimately con- 
nected with the involved question of so-called cardiac strain. The subject 
will be dealt with more fully in other connections (Chapter XIV). Here it 
is sufficient to indicate that in normal hearts, the neurogenic nerve control 
and cardiac inhibitory centers are the safeguards and checks that probably 
prevent abnormal cardiac dilatation. That is to say, before the cardiac DYNAMIC AND MECHANICAL CONSIDERATIONS 
77 
chambers became greatly overdistended, a degree of nerve exhaustion super- 
venes which prevents further overaction, tachycardia, etc. 
To sum up the dynamics of a normal cycle and its clinical application to 
cardiac dilatation: The presssure in the ventricles rises with ventricular 
systole and falls with the beginning of ventricular relaxation (diastasis). 
When the auricular exceeds the ventricular pressure, the auriculo-ventricular 
valves open and blood flows from auricle to ventricle. The rate of ventricu- 
lar filling depends on the degree of ventricular relaxation and on the 
venous “head” (venous pressure). As the pressure of the auricle becomes 
increased by the venous flow and tends to equal that of the ventricle, the 
flow becomes less rapid until auricular diastole is finally completed and the 
auriculo-ventricular valves close. Cardiac dilatation unless extreme is not 
readily diagnosticated. Among important factors in its causation are the 
cardiac rate, venous pressure and tonus. In a majority of instances, it is 
impossible to weigh these factors categorically. Often a shrewd analysis is 
the only clinical solution of the problem. Until we possess more knowledge 
and are able to diagnose slight and moderate dilatations, and their effects 
on normal and diseased hearts, the term cardiac dilatation should be used 
cautiously. 
REFERENCES 
Bainbridge, F. A.: The Physiology of Muscular Exercise. 
Baumgartern: Ueber den Mechanismus . . . venosen Herzklappen; Arch. f. Anat. u. 
Physiologic, 1843, 463. 
Frank (Francios): Les effets de la systole des oreillettes sur la pression ventriculaire et 
arterielle. Arch, de Physiologie, 1890, 395. 
Frank, Otto: Zur Dynamik des Herzmuskels. Zeitsch, f. Biol. 1895, XXXII, 370. 
Henderson & Johnson: Closure of the Heart Valves. Heart, 1912-13, IV, 69. 
Henderson and Prince: Relative Systolic Discharges of the Right and Left Ventricles; 
Heart, 1914, V, 217. 
Marey: Methode graphique. 
Patterson, Piper & Starling: Regulation of the Heart Beat. Journal of Physiology, 1914, 
XLVIII, 465. 
Tigerstedt: Physiologie des Menschen. 
Wiggers: Circulation in Health and Disease. 
Williamson, C. S.: Effect of Exercise on the Normal and Pathological Heart. American 
Journal of Medical Sciences, 1915, CXLIX, 492. CHAPTER VII 
GRAPHIC METHODS—SPHYGMOGRAPHS AND SPHYGMOGRAMS 
—THE INK POLYGRAPH—POLYGRAPHIC CURVES—RADIAL 
CURVES. 
For purposes of exact graphic study of the time relationships of arterial 
and venous pulsations, various instruments have been devised. Among 
the first to construct and employ an instrument for the registration of the 
flow of blood through the heart and arteries was Marey. He, together with 
his colloborator, Chauveau, constructed special sounds armed with rubber 
capsules at one end; these were introduced into the arteries at the base of the 
heart and into the heart cavities. The other ends of the sounds were con- 
Fig. 31.—Apparatus for experimental curves in animals and for registering pressure 
curves as well as the time relationship of the events in the cardiac cycle. Sounds were 
placed in various cardiac chambers; the movements of the lever were registered upon the 
paper covering the revolving drum. (After Marey, one of the early experimental 
investigators.) 
nected with rubber tubing which was connected with tambours and writing 
levers. The levers rested against a revolving drum covered with blackened 
paper (Fig. 31). In this manner, movements imparted to the capsule were 
transmitted to the lever and were thus transcribed on the revolving paper. 
78 GRAPHIC METHODS 
79 
In the various experiments undertaken upon the horse, the sounds were 
placed into the right auricle, or into the right and left ventricles. Thus 
curves were obtained that were measures of the pressure as it actually 
existed in the cardiac chambers; in addition, the time relationships of the 
events occurring in auricle and ventricle were transcribed. In some experi- 
ments, the sounds were withdrawn from the ventricular cavities and were 
allowed to rest in the aorta, thus registering both the arterial pressure, and 
the onset and velocity of the blood current in that vessel. An instrument 
that transcribes arterial records is called a sphygmograph. Among the first 
instruments for direct sphygmography in man was that constructed by 
Marey (Fig. 32). The instrument is strapped on the wrist. A button with 
its spring is placed over the radial; the pulsations of the latter are transmitted 
Fig. 32.—Marey’s sphygmograph, illustrating an early type. 
to a lever and transcribed upon a blackened surface. This instrument and 
the principle upon which it depended was later improved upon by Dudgeon, 
von Jacquet, Frank and Petter, Uskoff and others. The Uskoff sphygmo- 
graph transcribes the arterial pulsations more accurately than the older 
models because of the sensitiveness of its spring arrangement. For pur- 
poses of more accurate and detailed registration, Frank employed an optica] 
device, a segment capsule as the recording member. The capsule is not 
circular but has an oblated, straight side forming the chord of the circle. 
Over the capsule a rubber membrane is stretched. A small trapezoidal plate 
is glued upon the straight chord side of the membrane. Upon this plate, at 
its free edge, is cemented a tiny mirror. The entire segment capsule with 
its mirror is so placed that it can readily be moved in a vertical and hori- 
zontal direction by thumb screws. The light is supplied by an arc or 
incandescent light which throws its beams upon the mirror of the capsule by 
means of a focusing lens. The light is then reflected from the mirror upon 
a moving photofilm apparatus, which is supplied with a motor for turning, 
and a shutter for exposing, the film. Each capsule has its separate focusing 8o 
GRAPHIC METHODS 
lens so that various tracings (arterial and venous) may be simultaneously 
reflected and photographed. When used with a wrist sphygmograph, the 
segment capsule is put in circuit with the wrist pelotte and tambour by 
means of elastic tubing. Thus connected, the radial pulsations are trans- 
Presystolic 
Systolic 
Diastolic 
Fig. 33.—Upper tracing—supraclavicular venous pulse. Lower tracing—subclavian 
pulse. The letters a, c and v have the same significance as in the ink polygraphic tracings 
to be described later. (After Wiggers.) 
mitted to the mirror capsule, the reflections from which are photographed 
as just indicated. In this manner, very accurate arterial and venous pulse 
tracings may be obtained (Fig. 33). The chief objections to the common 
use of the Frank mirror capsule are its intricacy and the time required for 
photography. GRAPHIC TRACINGS 
81 
In addition to the sphygmographs already alluded to, many others have 
at various times been used. Brief mention may be made of the onycho- 
graph (used on the nail bed), the tachograph (depending on the variations 
of a gas flame, placed in circuit with the pulse by tubing), the capillary sphyg- 
mograph, the sphygmopalpeur, the sphygmoscope: The names are suffici- 
ently descriptive to explain their special applications and uses. Tracings 
may also be made by introducing a sound in the esophagus, by which means 
pulsations of the left auricle can be transcribed. 
Instruments that simultaneously transcribe arterial, cardiac and jugular 
pulsations are called polygraphs. For clinical use I have found the Mackenzie 
Cl, Clockwork; Ti, time-marker; S, screw which regulates speed of time-marker; S.B., 
1 and 2, keys for winding the driving gear and time-marker; Le, lever for starting and stop- 
ping the driving mechanism; SI, slot for support of the paper roll (P.R.); Ar, arm for the 
support of the two transmitting tambours to the receiving apparatus; P, writing pens; 
E.T., elastic tubing connecting the transmitting tambours to the receiving apparatus; 
Cu, cup for receiving venous or cardiac pulsations; L.S., leather strap for buckling over the 
radial artery; Bu, button for receiving the radial pulsations; Sp, screw for regulating 
the pressure of the button upon the radial; W.T., wrist tambour. 
Fig. 34.—Mackenzie ink polygraph. 
Ink Polygraph satisfactory. Its compact size, the comparative simplicity 
and ease of operation, the fact that if necessary very long records can be 
taken, and the use of ink and a paper roll instead of smoked paper, make it 
suitable for clinical work. 
The Mackenzie polygraph (Fig. 34) consists essentially of a clock work 
(Cl) encased in a metal container. The clock is fitted with a time-marker 
(Ti) which ticks and marks fifth seconds by means of a small pen. The 
speed of the time-marker is regulated by a small screw (S). There are two 82 
GRAPHIC METHODS 
separate keys (S.B.i, S.B. 2), one for winding the driving gear, the other for 
the time-marker. There is also a small lever (Le) which starts and stops the 
driving mechanism. Attached to one side of the case is a slot (SI) into which 
is fitted a support for a paper roll (Pr). On the opposite side is a smaller 
slot into which fits a long, narrow arm (Ar) for the support of two transmitting 
tambours (TT); the latter are so arranged that they can move in any direc- 
tion. To the tambours are attached long writing pens (P); the pressure of 
the points upon the paper may be regulated by manipulating the tambours. 
Elastic tubing (ET) connects each tambour separately with the receiving 
apparatus that is placed over the venous and arterial pulse in order to tran- 
scribe their pulsations. The receiver for the jugular is a small circular 
metal cup (Cu): This may also be used for registering cardiac pulsations by 
placing it over the apex. For transmitting radial pulsations, a perforated 
leather strap (LS) is buckled about the wrist and so adjusted that the 
button (Bu) or pelotte rests upon the most prominently pulsating part of the 
radial; the pressure of the pelotte upon the latter is regulated by a small flat 
spring (Sp). There is a broad wrist tambour (WT) which rests upon the 
button and transmits radial pulsations to the writing pens through the trans- 
mitting tambour. 
Method of Use of the Mackenzie Polygraph.—The polygraph is used as 
follows: The driving mechanism and time-marker are first wound, the paper 
roll is set in place, the pens thoroughly inked and lightly adjusted upon the 
paper. After palpating the radial, its most pulsatile point is marked by an 
ink spot, or preferably by two rectangular lines ([ _), one along the radial, 
the other across the wrist; these serve as guides for the proper position of the 
pelotte and wrist strap. The best position of the wrist is -with the hand in 
moderate extension or hyperextension, because this tends to make the 
radial artery more superficial. This position can be conveniently maintained 
by firmly pressing the extended hand against some stable object like a table. 
The upper strap of the wrist attachment is put on loosely so as not to obliter- 
ate the artery; the lower is buckled on firmly. The spring regulating the 
pressure of the pelotte is then pressed down sufficiently to make the latter 
bob vigorously with the radial pulsations. The wrist tambour is slipped in 
position with its screw support loose, so that the metal tip on the under 
surface of the tambour rests fully upon the bobbing button; it is then screwed 
and held in this position. Thus through the receiving and transmitting air 
system of tambours and their connecting elastic tubing, the radial pulsations 
are transmitted to the writing pens. 
To transmit and transcribe venous pulsations the metal cup is placed 
over the jugular bulb (Fig. 35), preferably on the right side, because the 
vein is usually more prominent on that side. The neck of the cup is grasped 
between the fore and middle fingers, the rim by the thumb, and the cup slid 
along the outer border of the sterno-mastoid muscle until it touches the clavi- 
cle. It thus rests over the triangle area formed by the jugular vein (with its GRAPHIC METHODS 
83 
bulb), the inner end of the clavicle, and the sterno-mastoid muscle. The 
patient is made to lie as flat as possible; he should breathe quietly, for 
stertorous breathing interferes with proper registration. Rigidity of the 
neck muscles also mars pulsations. Superabundance of fat and respiratory 
dyspnoea are other factors which may interfere with or vitiate accurate 
registration. 
After the wrist tambour and venous cup have been satisfactorily adjusted, 
the pens are separately slid across the paper, so as to establish vertical lines 
JUG O CAR, v) e i*j .... 
Po».ycRAPv* Receive*-/; 
■3 OUL.S.. 
.C/M’of'0 
4oPeff»o* KEMm CAV*. 
&lHb AOtfiUM-AR H60C/ 
Fig. 35.—Schematic view of the a-c-v waves and of the jugular bulb, 
(coincident ordinates) for measurement of the curves. These lines need not 
necessarily be continuous, for simultaneous venous and arterial pulsations 
may be measured off and standardized by means of calipers. The driving 
mechanism is now released, and arterial and venous pulsations simultaneously 
registered. 
As already stated, early experimentors gained information regarding 
auricular pressure curves by inserting sounds directly into the auricles of 
dogs and horses; they found that auricular contractions were accompanied 
by increased auricular pressure, that is, by positive pressure waves (Figs. 
36,57). While there is a general correspondence between such pressure curves 
and human jugular tracings obtained by the polygraph, it must be remem- 
bered that the latter tracings primarily depend upon differences in volume 
created in the confined air space of the cup resting over the jugular bulb. 
These volumetric differences are transmitted to the tambour and the pen is 
then correspondingly deflected. Hence differences in auricular pressure 
are not necessarily transmitted and transcribed as corresponding differences 
in the volumetric waves by the cup over the jugular bulb; and as a corollary, 
one can rarely predicate and estimate auricular pressure by the excursion and 
direction of the “venous” polygraphic waves. 
The Waves of the Normal Jugular Pulse. The Normal Phlebogram. 
Frequent observations have shown that, corresponding to the first auricular 
pressure curve coincident with auricular systole, there exists normally 84 
GRAPHIC METHODS 
a venous pulse beat seen in the venous trunks at the root of the neck. In 
man, for each radial beat, there are in the normal jugular tracing three waves 
or elevations; each elevation is accompanied by a corresponding depression 
(Fig. 37). We shall follow the simple nomenclature usually adopted in 
Fig. 36.—Simultaneous tracings from the right auricle (I); the right ventricle (II) and 
systolic shock of the ventricle (III) of the horse; a—auricular systole; v—ventricular systole; 
c, ventricular shock. According to Marey, the smaller undulations h, h', h" are due to 
closure of the auriculo-ventricular valves; the vertical divisions measure 41 o seconds. 
(After Marey.) 
the literature and call the elevations the a-c-v. waves. The a refers to the 
auricular, c to the carotid, and v to the ventricular filling wave. The rise 
(Figs. 35, 37) and fall (Figs. 35, 37) of the first wave a are caused by the reflex 
wave produced in the veins of the neck by auricular systole. In rhythmically GRAPHIC METHODS 
85 
beating hearts, the a wave comes before the advent of ventricular systole (c 
wave). Absence of the a elevation in those types of arrhythmia in which 
experimental and electrocardiographic evidence shows absence of normal 
rhythmic auricular contractions (auricular fibrillation, Chapter X), 
and abnormal position of the 
a wave in arrhythmias affect- 
ing relationship between auric- 
ular and ventricular contrac- 
tions (heart block, Chapter 
X)—these constitute con- 
firmatory evidence that the a 
wave is in the main, if not 
entirely, due to auricular 
systole. If the jugular tracings 
corresponded to the experi- 
mental auricular pressure 
curves, they would show but 
two waves, that is, the a wave marking auricular systole, with its fall (Fig. 37, 
1-2) and the v (ventricular filling) wave with its fall (Fig. 37, 2-3). The post- 
auricular fall, however, is interrupted by the advent of another elevation, the 
c wave. For the present disregarding the latter, the chief cause of the post- 
auricular fall of pressure (Figs. 35, 37 1-2) is undoubtedly auricular relaxation 
following auricular systole; ventricular systole influences and increases this 
relaxation mainly by dragging down the interventricular septum, and to a 
lesser degree by producing diminished intrathoracic pressure. The physio- 
logical limit of the duration of the a wave as measured at its base line is one 
fifth of a second. 
The cause of the carotid (c) wave is still a matter of dispute. Its occa- 
sional appearance one twentieth of a second before the onset of carotid pulsa- 
tion, and its presence after experimental ligation of the carotids have been 
offered as evidence that the c wave is not due to carotid pulsation. However, 
those who have worked with the cup receiver over the jugular bulb will have 
observed how the venous tracing is often vitiated by placing the receiver too 
close to the carotid, in consequence of which the usual polygraphic c wave 
will often obtrude itself upon the venous tracing. Although there exists 
some dispute as to its cause, the practical importance of the incidence of the c 
wave in the study of the human phlebogram rests upon the fact that its foot 
point (its beginning) is coincident with the onset of carotid pulsation. The 
determination of the foot point of c therefore, becomes an important land- 
mark in the study of the polygram. Since the pulse wave reaches the wrist 
approximately one tenth of a second after its arrival at the carotid artery, 
and since the onset of the individual radial beats is readily discernible in the 
arteriogram, the foot point of the c wave may be determined and distinguished 
from the a and v waves in the phlebogram by measuring with calipers from coin- 
. 3 u c u u a R 
Na 
Fig. 37.—Diagrammatic representation of the 
normal polygraphic curve. 
a, auricular wave; c, carotid wave; v, ven- 
tricular filling wave. 86 
GRAPHIC METHODS 
cident ordinates in the radial and venous tracings. These ordinates are 
derived by stopping the driving mechanism for a moment and sliding both 
pens across the paper (Fig. 38). They need not necessarily form a continu- 
ous line; in fact, they rarely do because the pens are often not in alignment. 
Calipers are then taken to measure from the ordinate to the foot point of 
any radial beat to the left of it. This caliber distance is then transferred 
to the left of the ordinate in 
the venous tracing. The foot 
point of the c wave will 
be one tenth of a second to 
the left of this point, for this 
marks the difference in time 
between the onset of the carotid 
and radial beats. The width 
of the one tenth second is 
readily derived, because the 
time marker marks and spaces 
one fifth seconds. With the c 
wave determined, it becomes a 
simple matter in good curves to determine the a and v waves when the pulse 
beats rhythmically: for the pre-carotid is the a and the post-carotid, the v 
wave. 
The third positive wave (Figs. 35, 37) v, the ventricular wave which fol- 
lows the second depression, is due to ventricular systole; it results almost 
entirely from reflux of the stored auricular blood being forced into the venous 
system during ventricular systole while the auriculo-ventricular valves are 
still closed. Another factor in the production of the v wave is sudden release 
of the base of the ventricle at the commencement of ventricular diastole. 
The slightly variable beginning of the v wave depends upon the varying 
amounts of blood stored up during auricular diastole. Its termination is 
coincident with the opening of the tricuspid valves; hence it, in conjunction 
with the a and c waves, form certain definite landmarks of the time events of 
the contracting chambers. 
The third fall or depression (Fig. 37, 3) is caused by the rapid drop in pres- 
sure which follows the beginning of ventricular diastole and the opening of 
the auriculo-ventricular valves. 
By translating the knowledge gained from the orderly sequence of aur- 
icular and carotid pulsations (the a and c waves) as transcribed graphically, 
into terms of auricular and ventricular systoles, we have the means of study- 
ing rhythmical sequential cardiac cycles—the normal pulse and phlebogram— 
as well as the numerous disturbances of rhythm that may affect auricles and 
ventricles. 
Variations in the Normal Phlebogram.—There are certain variations in 
the normal phlebogram which requires consideration. The a wave is occa- 
Fig. 38.—Normal venous and radial tracing 
showing rhythmical a-c-v waves in the jugular 
tracing, and regular radial beats. The points S-S 
are coincident ordinates derived by sliding the 
pens when the driving mechanism is at rest. The 
method of derivation of the foot point of the c 
wave is also shown. GRAPHIC METHODS 
87 
sionally bifurcated at its apex, i.e., at the height of auricular systole; such 
splits may possibly result from a venous reflux wave produced by a sharp 
flapping action of the valves in the jugular bulb. The c wave is sometimes 
split (Figs. 39, 40, 41). When this occurs, the first part is usually high and 
its fall sharp. It is due to the fling of the lever caused by placing the cup too 
close to the carotid, or to causes similar to those of the dicrotic notch of the 
~1U£J 
Ka^uiO 
Fig. 39. 
Fig. 40. 
Fig. 41. 
Figs. 39, 40 and 41.—These figures show a split c (c-c) wave in the venous tracing. 
radial (q.v.). Another variation of the phlebogram is the occasional blend- 
ing of venous and arterial tracings; the c-v waves then resemble an arterio- 
gram (Fig. 42). The v wave is sometimes divided; this division is probably 
caused by the two factors in its production acting somewhat asynchronously. 
hzacet 
Fig. 42.—Combined venous and 
arterial tracing in the jugular. 
Fig. 43- 
Fig. 44. 
Figs. 43, 44.—Phlebograms showing h waves. 
Another wave, the so-called h wave is sometimes seen in middiastole 
or directly preceding the a peak (Figs. 43,44), especially when the heart beats 
slowly. It is usually regarded as a reflux wave due to the rather sharp 
ballooning of the right ventricular tricuspid valve from the rush of inpouring 
blood during diastole, It has also been regarded by some as related to the 
third heart sound. The h wave, however, may be present even when there is 
no electrocardiographic evidence of a third heart sound (Chapter XIII). 
Limitation of Inferences from the Phlebogram.—With reference to infor- 
mation derived from the normal rhythmic tracing, it must be emphasized 88 
GRAPHIC METHODS 
that, because of the mechanical limitations of the polygraph, because the 
waves measure volumetric (not pressure) changes, and because of the manner 
of application of the venous cup, only very rarely can conclusions regarding 
auricular-or ventricular energy be drawn. I have, for example, taken many 
Fig. 45.—Normal 
phlebogram from a case 
of aortic regurgitation. 
Fig. 46.—R, radial 
tracing. Normal jugu- 
lar tracing from a patient 
with aortic stenosis and 
a double mitral lesion. 
Fig. 47.—Normal jugular 
tracing from a patient with aortic 
stenosis and a double mitral 
lesion. 
venous tracings from patients with compensated and decompensated valvular 
and myocardial lesions, and after comparison with normal tracings, I have 
been unable to discover any distinction between them. Figures 45-52 taken 
Fig. 48.—Normal sized a and other 
peaks from a case of mitral stenosis. 
Fig. 49.—Normal a wave from a 
case of mitral regurgitation. 
from patients with various diseases illustrate this fact. Another important 
consideration which applies particularly to interpretation of arrhythmias 
from the phlebogram is that the waves in the tracing must be clear and 
Fig. 50. 
Fig. 51. 
Fig. 52. 
Figs. 50, 51, and 52— Normal jugular tracings from cases of exophthalmic goiter. 
distinct; otherwise the diagnosis of arrhythmias becomes to a great extent a 
matter of hazard. 
The Radial Pulse. — Because of the method of instrumental application 
—a spring and pelotte pressing upon the radial artery the arterial sphyg- 
mogram (arteriogram) represents only crass differences of arterial pressure. 
The amount of spring tension required to sufficiently occlude the artery for GRAPHIC METHODS 
89 
the purposes of tracing is quite variable, hence the resultant curve is in many 
instances neither an accurate nor an approximate measure of the amount of 
arterial pressure. In addition to these mechanical drawbacks, extraneous 
factors, e.g., the position of the radial, its accessibility, the pliability of its 
walls, etc., are considerations which profoundly modify and mar inferences 
drawn from the pulse tracing; hence doubtless the confusion, the differences 
of opinion and the varied interpretations drawn by clinicians from arterio- 
grams. The special value derived from the radial tracing in the polygram 
Fig. 53. 
PiGS. 53, 54.—Normal radial pulse tracings. 
Fig. 54. 
1—2, Abrupt rise probably due to instrumental fling of the lever (also called primary or 
percussion wave); 1—3, time of ventricular systole, the aortic valves are open; D.N, dicrotic 
notch; D.W, dicrotic wave; S.W, systolic wave (also called tidal and predicrotic wave). 
rests upon knowledge gained regarding cardiac rate and rhythm, and in the 
aid it gives in fixing the time relation of events in the cardiac cycle; for, as 
already noted, the foot point of the radial serves as a standard for determining 
the incidence of the c wave in the venous tracing. 
The first elevation of the radial beat (Figs. 53, 54), usually called the pri- 
mary or percussion wave, is generally steep; its fall, sharp. It is due to the 
sudden instrumental fling given to the pelotte and lever by the sharp impact 
of the onrushing blood. It occurs in, and is part of the wave produced by 
systolic arterial distension, and may be regarded as an initial artificial peak 
superimposed upon the arterial wave during systole. It is immediately 
followed by the systolic wave, sometimes called the secondary tidal or predi- 
crotic wave (Figs. 53, 54, S.W. 2, 3). The degree of the fall of systolic 
pressure—graphically represented in the tracing by the angle of slope and 
suddeness of fall of the wave—depends upon the difference between 
the systolic and diastolic pressures. This difference which can be measured 
by a blood pressure apparatus (Chapter XXV) is called the pulse pressure 
(Chapter XXV). If this be large, the down slope is apt to be steep; if small, it 
becomes a gradual one. The termination of the systolic, and the beginning 
of the dicrotic wave (Figs. 53, 54, D.W.) is marked by the dicrotic notch 
(Fig. 54, D.N.). This notch corresponds to certain events in the cardiac 
cycle: The end of ventricular systole and the foot point of the v wave in the 
venous tracing (Fig. 53). Other small waves are sometimes found in the 
radial tracing; their cause and significance are not known. 
The cause of the dicrotic wave is still in dispute. Mackenzie regards 
it as due to sudden relaxation of the ventricular wall, including that portion 
supporting the aorta. According to him there is thus developed a tendency 90 
GRAPHIC METHODS 
to the production of a negative aortic wave, which is checked by the sudden 
stretching of the membranous aortic valves, thereby causing a second posi- 
tive—the dicrotic wave. It has been experimentally demonstrated in a 
circulatory model in which the arterial system is represented by elastic 
tubing, that sudden check of the inflow produces a suction or negative pres- 
sure behind the column of fluid; as a consequence, there are resultant waves. 
Indeed, “dicrotic” waves have been produced in an “arterial system” in 
which the pumping mechanism was a syringe not comparable to the heart, 
a fact showing that these waves may be entirely the result of pressure effects 
in elastic arteries. With the influx of fluid, the tube expands; with the 
sudden cessation of the flow, the resultant negative pressure in a rigid tube 
would lead only to a reflux of fluid. In elastic tubing, however, represented 
in the human being by the aorta, there is the additional force of elastic 
recoil. Both forces—suction and elastic recoil—produce shrinkage beyond 
the natural caliber of the tube (aorta); the elastic, constricted tube causes 
secondary expansion, and with it, the secondary pulsatile “dicrotic” wave. 
These physical facts applied to the heart, in addition to sudden ventricular 
relaxation following systole, may account for the dicrotic wave in man. 
It has also been held that the dicrotic wave is “reflected” from the peri- 
phery. Under such circumstances, the distance between dicrotic and pri- 
mary crests ought to diminish as the arteries recede in distance from the 
heart, and there should be no dicrotism in the proximal part of the compressed 
artery. These suppositions, however, are not borne out by arterial tracings 
which have been taken under such conditions. In addition, the manifold 
arterial division at the periphery would appear to make one large “reflected” 
wave improbable. 
The height of the dicrotic notch is ordinarily about one half that of the 
systolic wave. In cases with sharp fall of arterial pressure following ventric- 
ular systole, the notch is abnormally, low. This happens frequently in 
Fig. 55.—Low dicrotic 
notch (d) from a case of 
aortic regurgitation with 
decompensation. 
Pig. 56.—Low dicrotic notch (d) from a case 
of aortic aneurism with cardiac failure. 
aortic regurgitation with cardiac failure (Fig. 55), but it is also found in 
other decompensated heart lesions, valvular or myocardial in origin (Fig. 56), 
especially when the pulse pressure is large. 
Types of Pulse.—From what has preceded, it is evident that only excep- 
tionally can definite conclusions regarding the “strength” or “weakness” 
of the circulation be drawn from graphic records. In fact, the terms “weak” 
and “strong” pulse are usually misapplied to what should properly be called 
“soft” and “hard,” respectively. The old terms previously in use had the 
advantage of describing the physical impression given to the examining GRAPHIC METHODS 
91 
Myograms 
Aur. Pressure ■ 
byito)d 
Ventricle Snstole 
Diast Fall 
Election 
Period 
: 1 
End of Isometric period 
/6ustolic Summit 
Relaxation Period 
Aur. Wave 
Primary 
VJqve. 
Incisura^v1 
Diastasis 
Vent. Pressure 
Aur. U/ave 
Vifed 
Aorta Pressure" 
Pre) immar.n 
wave 
Verit. Volume 
Aur. 
Systole 
' Sy stolic 
' v. Ejection 
Elastic 
Diastole 
Primary' 
Vlav e 
Dicrotic 
vJYJave 
Radical Pulse" 
C-ujave 
b>vibclavia>v 
)>r> pact" 
Early diastolic 
Pc or V-ujave 
Presystol ic 
or 0lwave 
Mid-diastolic 
or H-vuave. 
Supraclavicular" 
Venous Pulse 
— lst|Sound 
Isometric 
Iperiod _ 
2nd Sound' 
Llectro / 
Card io^ram 
Heart" Sounds 
Fir at Sound 
Se cond 3o~u~ncL 
Fig. 57.—Simultaneous events in cardiac cycle. (After Wiggerj.) 92 
GRAPHIC METHODS 
finger. When thus descriptively applied, their limitations understood, and 
no deductions regarding the state of circulation drawn from them alone, the 
old terms serve a useful purpose. These terms and their definitions are as 
follows: A sudden fall of the pulse wave produces what is known as the “col- 
lapsing” pulse; if extreme, it becomes the typical “water hammer” or Corri- 
gan pulse. The radial pulse can also be described as large and expansile 
{pulsus magnus), small or compressible {pulsus mollis), or hard and incom- 
pressible {pulsus durus). The rise of the pulse wave may be quick {pulsus 
celer) or slow {pulsus tardus). If dicrotism is sufficiently marked to be felt 
in taking the pulse, it is known as dicrotic; if the dicrotic notch breaks 
low and the dicrotic wave is marked, it is called hyperdicrotic. Occasion- 
ally, the pulse wave feels unduly sustained at the point of its maximal pulsa- 
tion and falls slowly—the anacrotic pulse. This is commonly regarded as 
diagnostic of some form of compression of the aorta; it has, however, also 
been found as a result of peripheral factors alone (Lewis). The bisferiens 
gives the sensation of a double pulsatile impact: It is produced by the rather 
equal split of the systolic plateau by the predicrotic or instrumental wave. 
Important information of the condition of the radial artery itself is 
sometimes gained by careful palpation. Marked nodosity, thickening, and 
tortuosity are immediately apparent. The opposite information—that of a 
normal elastic arterial wall—is not so readily derived. Examination is best 
practiced by emptying the artery and stripping back the blood with the 
finger of one hand and palapting the collapsed radial with the other hand. 
The radial, if normal, will be barely definable as a separate strand; if 
the radial be thickened and its walls stiff, the emptied artery is distinctly 
palpable below the point of compression. 
REFERENCES 
Broadbent: The Pulse, Philadelphia, 1890. 
Foster’s Physiology, Edition 1888, Part I. 
Francois, Franck: Note general sur la disposition d’un sphygmopalpeur. Compt. rend. 
Soc. de biol., 1908, IXV, 226. 
Frank: Der Puls in den Arterien. Zeitschr f. Biol., 1905, XXVIII, 441. 
Frank and Fetter: Ein neuer Sphygmograph. Zeitschr f. Biol., 1907, XXXI, 70. 
Gibson, G. A.: Further Observations on Heart Block; British Medical Journal, 1906, II, 
1113. 
Grantstrom: Zur Frage uber die Richtung der dikrotischen Welle. 
Hirshfelder, A. D.: Diseases of the Heart and Aorta, Edition 1910. 
Herz: Onchyograph. Zentralbl. f. Physiol., 1896, X, 143. 
Jaquet: Zur Technik der Pulsregistrierung, Cor-Bl. f. schweiz. Aerzte. 1910, XL. 
Kreidl: Ein nener Apparat zur Aufnahme von Nagelpuls. Zentralbl. f. Physiol., 1902, XVI, 
257- 
Kronecker: Der Kapillar Spygmograph. Zentralbl. f. Physiol., 1910, XXIV, 828. 
Lewis, F.: Mechanism of the Heart Beat. 
Landois: Dir Lehre von Arterienpuls, Berlin, 1872. 
Mackenzie, T.: Diseases of the Heart, Edition 1913. GRAPHIC METHODS 
93 
Marey, B. J.: La methode graphique. 
Morrow, W. S.: Various Forms of the Negative or Physiological Venous Pulse. British 
Medical Journal, 1906, II, 1807. 
Muller and Weiss: Ueber die Topographie des menschlichen Sphygmogrammes. Deutsch. 
Arch. f. klin. Med., 1912, CV, 105. 
Mosso: Die Diagnostik des Pulses, Leipzig, 1879. 
Ohm: Beitrag zur photographischeor Pulsregistrierung. Muenchen, med. Wochnschr. 
von Frey: Untersuchung des Pulses, Berlin, 1892. 
Wiggers, C. J.: Circulation in Health and Disease, 64. CHAPTER VIII 
THE ELECTROMETER—THE ELECTROCARDIOGRAPH— 
ELECTROCARDIOGRAMS 
Records obtained from the use of the capillary electrometer and of the 
electrocardiographic apparatus are based upon the fundamental physiological 
fact that any muscle in contracting produces a definite although minute 
amount of electricity. 
Capillary Electrometer.—The capillary electrometer consists essentially 
of a capillary tube containing mercury; the tube dips into a weak solution of 
sulphuric acid. If the electrical reaction of a contracting muscle is to be 
tested, one end of the muscle preparation is placed in circuit with the mercury, 
and the other end with the sulphuric acid solution. The muscle is thus 
connected with the capillary electrometer by means of these electrodes. If 
then, as a result of muscular contraction, an electric current passes through 
the electrometer, the mercury in the capillary tube is displaced in the 
Fig. 58.—Electrometer record of changes in the rabbit’s heart with one contact on the 
right auricle and the other on the apex of the right ventricle. A = auricular, V = ven- 
tricular beat. The heart rate is 250 per minute. Upward movement signifies relative 
negativity ( = muscular activity) at or near the auricular contact. (After Gotch.) 
direction of the induced current. The motion of the mercurial column can 
then be photographed by an appropriate lighting and photokymographic 
apparatus. The resultant graphic record (Fig. 58) therefore expresses 
muscular activity in terms of changes in the mercurial column. The electro- 
meter does not possess the accuracy or sensitiveness of the electrocardiograph, 
which, where available, has become the standard modern instrument for 
94 ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
95 
measuring and transcribing the electrical reaction produced by the 
living heart. 
The Electrocardiograph or String Galvanometer.—There seems to be a 
current impression among physicians not especially interested in the field 
of cardiology that the principles of electrocardiography are too intricate to 
grasp; this feeling also applies to electrocardiograms and their interpretation. 
I believe that the fault is at least partly due to the cardiologists themselves, 
for their description of the apparatus and of the resultant graphic curves 
(electrocardiograms) is often highly technical, while the underlying facts, in 
themselves simple and easily grasped, are usually lost or become confused 
in a maze of unnecessary technical detail. I therefore wish to emphasize that 
the practitioner can readily understand the workings of the electrocardiograph 
and the interpretation of electrocardiograms, if he will but grasp the few 
underlying simple electro-physiological facts, some of which have already 
been briefly alluded to. The entire field of electrocardiography with its 
many symbols will then become bereft of much of its complexity. As in 
many other new sciences, there are indeed still many debatable points regard- 
ing the causation and interpretation of various deflections and curves, but for 
clinical purposes much of the disputed ground can be discarded. 
■Earth 
Fig. 59.—Scheme of monophasic action current. (Modified after Kraus and Nicolai.) 
M, Muscle consisting of parallel fibers; S, point of stimulation; Ei, non-polarizable 
electrode; E2, earthed electrode; G, galvanometer; C, resultant monophasic curve. 
It is a well established electro-physiological fact that a minute amount of 
electricity is caused by any muscle during its stage of contraction. The 
electrical current thus produced, if allowed to pass through a sensitive 
galvanometer, causes deflection of the needle. For example, if a muscle 
consisting of parallel fibers (Fig. 59, M) be stimulated at the point S, the 
surface at the area connected by means of a non-polarizable electrode (Ei) 
to a galvanometer (G), and the other electrode (E2) grounded so that it 
remains constant (equipotential),then the muscle at S in contracting becomes 
electrically negative relative to the remainder of the musculature. Hence 
negative electricity and muscular contractibility are equivalent and synono- 
mous. As the current passes, the stimulated ends become electrically qui- 
* escent; hence the electropotential falls to and reaches zero, at the same time 96 
ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
that the needle of the galvanometer has been deflected and comes back to 
rest at zero. If recorded, such deflection would be a monophasic curve (Fig. 
59). If, instead of being grounded, that electrode is connected with the other 
end of the same parallel fibered muscle (Fig. 60, E2) and the latter is then 
stimulated at the point S (Fig. 60), the stimulated area in contracting again 
becomes electronegative, while the other 
areas of the muscle remain electropositive 
because they are not yet in contraction. 
With the beginning of the flow of the electric 
current the needle of the galvanometer starts 
its deflection. When the wave of muscular 
contraction arrives at the center of the muscle, 
the needle does not move because this zone 
now draws negative electricity in equal 
amounts from both sides. With the passage 
of the contraction wave toward E2, the lat- 
ter becomes electronegative, the current 
flows from E2 to + Ei and the needle is 
deflected in the opposite direction. In other 
words, with each change of electrical signs, 
the needle is deflected, and in the assumed 
instance of a parallel-fibered muscle, a 
diphasic curve results. 
In view of later electrocardiographic con- 
siderations, it is important to emphasize, as 
evidenced by the above simple experiment, 
that the resultant curve depends upon the direction of a contraction wave 
in the muscle and upon the point at which the contraction arises. It further 
depends upon the axis of the muscle mass; an oval or an irregularly shaped 
muscle, for example, will not give an equally balanced diphasic curve in 
contracting because the electrical waves themselves would not be equally 
balanced, so to speak. It is also evident that the course of the contraction 
wave, of the galvanometric deflections, and of areas of relative electrical 
negativity are intimately correlated. Finally, it is important to remember 
that, as already stated, a muscle at the moment of contraction is electrically 
negative, so that muscular activity and electrical negativity are practically 
interchangeable terms. These simple considerations regarding the action 
of a contracting muscle upon a galvanometric needle will serve to clarify 
the principles underlying the electrocardiographic apparatus. 
It was chiefly through the work of Einthoven that the electrocardio- 
graphic apparatus (Figs. 63, 64) reached its present stage of perfection as a 
laboratory and clinical instrument. The standard instrument consists 
essentially of a fine conducting fiber scarcely visible to the naked eye, 2 to 
4 microns (0.002 to 0.004 m.m.) in diameter, that lies in a narrow space between 
Fig. 6o.—Scheme of diphasic 
action current. (Modified after 
Kraus and Nikolai.) 
Mu, parallel fibered muscle; 
C, center point; S, point of stim- 
ulation; Ei, E2, nonpolarizable 
electrodes. Minus signs over Mu 
show that that area has become 
electronegative when reached by 
the contraction wave, and that 
both ends are then temporarily 
positive. (See text.) ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
97 
two approximated poles of a powerful electromagnet (Figs. 61, 62, 63). 
The fiber or string, as it is usually called, is deflected by currents induced in 
it. These movements are magnified by a microscope resting in the magnetic 
pole shoes; the magnified movements are photographed by a moving photo- 
Fig. 61.—Schematic view of electrocardiographic apparatus. 
N.S., north and south poles, respectively, of electromagnet; G.S., galvanometric string; 
M, microscope set in the electro-magnet; L, electric bulb light; C, camera containing film 
fed by motor; M.S., magnified image of string. 
BODY 
SHUNT 
VOLTAGE 
o o 
\REGULATOR 
COMPENSATING 
o\o O 
STANDARDIZING 
AMMETER 
COMPARISON 
ONE DRY CELL 
-STRING 
PROTECT 
Fig. 62.—Scheme of rheostats and connection with the galvanometer. 
film apparatus. The films, when developed, constitute the electrocardio- 
grams. The string is usually made of an exceedingly fine quartz fiber coated 
with silver. The silver gives the conducting surface. Some strings are 
doubly coated with both silver and gold: This adds to their toughness and 
durability. The resistance of the string varies from 1500 to 7000 ohms. The 98 
ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
electrocardiographic apparatus which I use—the standard type—is sche- 
matically shown and described in Figs. 61 and 62 respectively. Figures 63 
and 64 show the apparatus set in position. Figure 64 shows how the patient 
is placed in circuit with the apparatus. The electrodes used are described 
in the succeeding paragraph. 
Method of Taking an Electrocardiogram. The Three Leads or Deriva- 
tions.—In the human being, the indirect method of taking electrocardiograms 
must of course be employed. This is accomplished by various types of 
electrodes applied to the body: The current thus drawn off and flowing 
between the electrodes constitutes the “leads” or “derivations.” There are 
Fig. 63.—Photograph of the electrocardiographic Hindle-Williams apparatus in position. 
L, Electric bulb; P.R., rheostat for “leads” to patients; C, coil containing 3 “leads;” 
Mi, microscope; T.M., time marker; F.B., box containing roll of film; N.S., north and south 
poles of electromagnet; S.H., string house containing quartz fiber; Mo, motor for driving 
film; R, rheostat for storage batteries; C.R., crank rheostat. 
various methods of employing non-polarizable electrodes to conduct the 
electric potential produced by cardiac activity to the galvanometer. One 
method consists in wrapping flannel bandages, each about six inches wide 
and g feet long, thoroughly soaked in a strong warm salt solution (6 oz. of 
salt to one pint of water), around each forearm and around the left leg of the 
patient. After these extremities have been covered by a few turns of the 
bandage, German silver electrodes with binding posts are included in its 
folds. These electrodes are 6 inches long and 5 inches wide, and are suffici- 
ently thin and pliable to be bent and snugly applied. When patients can 
sit up, a simpler and more expeditious method consists in having three 
separate vessels containing strong warm salt-water solutions. In each ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
99 
Fig. 64.—Electrocardiographic apparatus with a patient in circuit. The electrodes 
are fastened on right- forearm, left forearm and left leg. 
Fig. 65.—Lead foil electrodes devised by Robert Neubuck. IOO 
ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
vessel is placed a porous cup containing a ioo per cent, zinc sulphate solution 
and a zinc plate with a binding post. Thus electrical connection is estab- 
lished between the patient and the electrocardiographic apparatus. In 
either case, binding posts are connected by wires distinguished by various 
colors, and are placed in circuit with the galvanometer by means of plugs 
and swatches. More convenient, easier, as accurate, and giving no discom- 
fort to the patient, are the lead foil electrodes recently devised (Fig. 65). 
The lead foil is made of an alloy of tin and lead (roentgen-ray protection foil) 
which is cut into strips approximately 9 inches long by 4 inches in width. Each 
is fastened by means of a brass screw and binding post to a rubber strip one 
half inch longer and wider than the foil strip. The forearm and left leg are 
washed and rubbed with a strong warm saline solution; a strip of gauze 
dipped in the same solution is then wound around these extremities, and the 
lead foil electrodes applied. As a convenient method of keeping the elec- 
trodes in place, broad rubber bands or pieces of tape may be used. These 
electrodes are also connected with the electrocardiographic apparatus in the 
usual way. I have also occasionally employed the same type of lead foil 
electrodes but cut into small one inch squares directly over the precordium in 
an effort to get the leads more directly from the corresponding underlying 
parts of the heart surface. In this manner it may be possible to take electro- 
cardiograms in the human being somewhat comparable to the electrocardio- 
grams taken with the leads placed in direct contact with the exposed hearts 
of animals. 
Just as any other contracting muscle, so the heart in contracting, gives 
rise to waves of electric potential which spread from their source over the 
entire body. It is these that are conducted to the galvanometer by means 
of the non-polarizable electrodes wdiich 
are wound around the patient’s three 
extremities. There are three arbitrary 
directions of the current coursing 
through the heart that are employed in 
taking an electrocardiogram and that 
correspond to the three extremities. 
These are the so-called “leads” or 
“derivations.” The current (Fig. 66) 
from the right to left arm (R.A.—L.A.), 
running chiefly across the base of the 
heart, is the first lead or derivation; 
that from the right arm (R.A.) to the 
left leg (L.L.), approximately parallel 
to the long axis of the heart, is the second, sometimes called the “strong” 
lead; that from the left arm (L.A.) to the left leg (L.L.) is the third 
lead and draws off the current coming mainly from the left side of the heart. 
To these I have occasionally added another lead by placing one electrode 
Fig. 66.—Diagram illustrating the 
three leads. R.A., right arm; L.A., left 
arm;L.L., left leg. ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
IOI 
over the anterior surface of the chest and the other over the spine of the left 
scapula. For this purpose I place the “right arm” (R.A.) electrode ante- 
riorly and the “left arm” electrode (L.A.) posteriorly, thus drawing off the 
electrical potential of the heart in an antero-posterior direction. I have not 
yet studied the subject sufficiently to discover whether the information thus 
derived is of added clinical value. 
The photographic reproduction of the magnified deflections of the gal- 
vanometric string during the registration of the various leads constitutes 
the electrocardiogram. While the elec- 
trocardiograms of no two persons are 
exactly alike, and while physiological 
differences vary within wide limits, 
there is a general conformity to a 
normal type. A typical normal elec- 
trocardiogram is schematically shown 
in Fig. 67. It demonstrates the various 
waves or deviations and the approximate 
time required for each when the heart 
is beating rhythmically at the rate of 
72 per minute. Each division parallel 
to the base line (the line of isopotential) 
is equivalent to one millivolt (one 
thousandth of a volt, (io~4 volt) of 
current that is produced by cardiac 
contraction. The electrocardiogram, 
that is, the registration of the difference 
of electric potential, precedes the actual 
cardiac contraction by about .03 second. 
The Normal Electrocardiogram (Fig. 69) will now be considered. The 
nomenclature I adopt is that first introduced by Einthoven and, with few 
exceptions, now in general use. Following the sequence of normal cardiac 
activity, the electrocardiogram is conveniently divided into that produced 
by auricular contraction—the auricular complex—and that by ventricular 
contraction—the ventricular complex. Animal experimentation, and 
observations on the human subject with normal and abnormal rhythms, 
especially those with heart block and auricular fibrillation, have confirmed 
the fact that the auricular complex (known as the P wave) is caused by 
auricular contraction. The P wave is normally directed upward and is 
usually somewhat flattened at its summit. After reaching the base line it 
is succeeded by a short horizontal isoelectric line, an evidence of quiescence 
of electric potential; that is to say, during this period, cardiac contraction 
has ceased and the heart is at rest. The ventricular complex consists of the 
QRST deviations; the chief of these are the R and T deflections. The Q and 
S vary in size; they are usually short, sharp peaks directed downward. 
S3 ' 5ec6N)os - ». e v 
• pci^/wj- 
Fig. 67.—Schematic representation of 
a typical electrocardiogram, second lead. 
Each horizontal space measures one 
millivolt of current. The ordinates 
measure one-fifth second. The form and 
size of the various deviations are seen, as 
well as the time required for their for- 
mation. 102 
ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
Upward deviations imply electrical negativity (i.e., muscular contractility), 
at or near the base of the ventricles; downward deviations, at or near the 
ventricular apex. Hence the downwardly directed Q and S deviations 
imply that the base of the heart is at that moment electrically positive, (not 
contracting) and that the apical region consequently has the opposite 
electric sign, negativity (apex activity). Confusion will be avoided if one 
always bears in mind that “negativity” (the electrical term) and “activity” 
(muscular contraction) are synonymous. The Q and S deviations may be 
exceedingly minute or may be entirely absent. The height of the R wave in 
any one deviation in terms of R waves in the remaining deviations may be 
determined by Einthoven’s formula, namely R I = R II — R III (Chapter 
XXXIII). The numerals after the R correspond to the respective leads. 
The R deviation, the most prominent of all the waves of the normal electro- 
cardiogram, is directed upward a distance varying from io to 15 millivolts. 
As measured at the base line, the time required for its formation varies from 
0.02 to 0.05 second. Because of the quick deflection of the string, the sides 
of the R deviation appear as fine lines, the apex is sharp. The T wave slopes 
gradually; the down stroke is somewhat thinner than the upstroke, the 
summit is broad and flattened. The R and T waves are sometimes called 
the first and second ventricular spikes, respectively. Occasionally a U 
wave is present. It rises only slightly above the isoelectric line; when pres- 
ent, it is found in mid-diastole. All curves are taken 
with a known deflection time of the string (Fig. 68). 
This is determined by rapidly throwing in and 
cutting out a millivolt of current by means of the 
rheostat (Fig. 63, P.R) with the string tension at its 
usual standard (Fig. 68). The limit of accuracy for 
this deflection time is approximately 0.02 second; that 
is, the string should cover a distance of one centi- 
meter with a millivolt of current in 0.02 second or 
less. When slower, the string registers curves 
inaccurately flattened and low. 
Normal Variations from the Standard Electro- 
cardiogram.—The usual variations are absence of 
the U wave; marked differences in the height of the R 
in the several leads; a split R wave with thick sides or summit; abnormally 
large, flat, or diphasic T waves, especially in leads 2 and 3; a partially inverted 
T wave in the first lead; a low, flat, or split P wave or its absence in one of the 
leads; deep Q and S waves, and a so-called QRS complex or as I prefer to 
designate them from their appearance, M and W complexes (Chapter IX). 
While the cause of some of these variations is known, the etiology of others 
is obscure or still in dispute. 
The variations of the T wave will be taken up in detail in the succeeding 
chapter. (Chapter IX.) 
Fig. 68.—Electrocar- 
diogram showing the de- 
flection time of the string. 
The points A and B are 
about 0.02 of a second 
apart. ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
IO3 
The Normal Electrocardiogram and Its Interpretation.—A typical 
standard electrocardiogram—three leads—of an adult with a normal heart is 
shown in Fig. 69. The R deviation is tallest in the second, the “strong” 
derivation (Figs. 66, 69), which leads off the current in a direction parallel 
to the long axis of the heart. It is necessary to describe certain basic facts 
regarding the electrocardiogram in order that the reader may more readily 
comprehend the difference in size and direction of the deviations in the 
various leads in normal and abnormal hearts. As already stated, the electro- 
cardiogram is the graphic representation of the spread of the electrical impulse 
throughout the heart. With normal cardiac rhythm, the peaks or deviations 
Pig. 69.—Normal electrocardiogram. L I, L II, L III are the three leads. The darker 
shaded ordinates measure one fifth second; the horizontal spaces, one millivolt each. The 
S wave is scarcely discernible in L III. The R wave is tallest in L II. (Courtesy of Dr. 
A. E. Cohn.) 
of the electrocardiogram represent at any instant of time the sum of total 
difference of electrical potential in those parts of the heart which are in con- 
traction. The QRS and probably the T deviations are caused by the spread 
to both ventricles of the excitation wave along the auriculo-ventricular 
junctional tissue. An upwardly directed R peak denotes contractility of the 
ventricular base relative to the remainder of the musculature. This may be 
proved experimentally by placing two electrodes, one upon the right ventricle 
in front, the other upon the apex; if the right ventricle be first stimulated, 
the R is deviated upward (base-active); if the apex be first stimulated, then 
the resultant deviation is downward (apex-active). 
How the “Clinical” Electrocardiogram is Taken (Fig. 56).—It is best to 
sit the patient in a room other than that in which the electrocardiograph is 
placed, in order to obviate the possible effect of nervous excitement upon the 
heart. In addition, it is always advisable to assure the patient that he will 
feel no electric shock, and that the entire procedure is absolutely painless. 
After both forearms and the left leg have been exposed they are rubbed vigor- 
ously with a piece of gauze dipped in a strong warm solution of salt water; 
about y2 cup of salt to a pint of water gives a solution of proper strength. 104 
ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
The exposed limbs are rubbed in order to assure proper electrical contact. 
The electrodes, the lead foil surfaces of which have been washed with the 
brine, are then wound and snugly tied about the exposed extremities. The 
wires, marked R.A., L.A., and L.L. are then placed in the binding posts 
respectively of the right arm, left arm and left leg. The patient is told to sit 
or to lay quietly, as the case may be. This finishes the manipulation as far 
as the patient is concerned. 
Attention is now devoted entirely to the electrocardiograph. The room 
is darkened. Depending upon the source of light, the arc or electric bulb 
is turned on and focused so as to give a clear image of the projected magni- 
fied string. Additional focussing is usually required; this is done by manipu- 
lating one or both ends of the microscope (Fig. 63, M) by turning the collar 
to which the microscope is attached, just as one turns an adjustment screw 
of the ordinary microscope. The string is now tested. The time marker 
(Fig. 63 T.M.), which is usually regulated to make and break the light 
every fifth second, is then set in motion. The result in the electrocardiogram 
shows vertical parallel lines (Fig. 69), the distance between which represents 
fifth seconds intervals. There is a small needle galvanometer (potentiom- 
eter), arbitrarily set at a certain figure (usually io°), which is placed in 
circuit by turning a shunt (Fig. 62): this regulates the voltage. The patient 
is then placed in circuit by means of a shunt or key shunt (Fig. 63, P.R.). 
Lead I is the first to be taken. Lead I is marked on the shunt box, that is, 
the wires that come from right arm and left arm are now in circuit. A milli- 
volt of current is then passed through the string by manipulating the appro- 
priate rheostat, (that is, by turning the handle of that which measures 
millivolts, the millivolt rheostat). The amount of excursion of the string 
is then noted either upon a scaled rule measuring centimeters attached to the 
top of the front face of the camera, or upon a centimeter ruled card toward 
the bottom of the camera. The card is better because it can be moved so 
that the image of the string falls upon one of the ruled lines. If it is seen 
that the string moves less than one centimeter, it denotes that the string 
is too tight: It is therefore loosened by turning a micrometer screw of the 
string house (Fig. 63, S.H.) which regulates the tension of the string. Loosen- 
ing is continued until one millivolt of current makes the string jump exactly 
one centimeter. If the string jumps more than 1 cm. for 1 millivolt, the 
micrometer screw is correspondingly tightened. Should the string leave the 
center of the field during the time the electrocardiogram is taken it can be 
brought to the center by turning the millivolt rheostat a sufficient number of 
turns; if that be insufficient, the pext larger rheostat (the centivolt bank) 
can be used. Thus the standard electrocardiogram is taken. During 
this manipulation the string, being activated by the current from the heart, 
is of course casting its magnified shadow on the front of the camera box. 
There are various types of the latter. They all contain a focusing lens with 
a micrometer lined surface, in order to show in millivolts the height of the ELECTROMETER, ELECTROCARDIOGRAPH AND ELECTROCARDIOGRAMS 
105 
shadow cast by the string (Fig. 63, F.B). They all also contain shutters to 
expose the film when all is ready, and a motor to turn the film on its spool 
in the camera box. Plates are sometimes used instead of film. This has 
the disadvantage that only exposure of a certain length can be employed, 
while with a film camera the exposure can be made long or short as required, 
depending upon the type of case. 
After lead I is finished all shunts are turned to zero. Then leads II and 
III are similarly taken; the film is then cut off by a sliding knife and drops in 
the camera box and is later developed. This is the electrocardiogram. The 
patient is then disconnected. All these steps naturally seem intricate to the 
beginner. With practice however, a complete electrocardiogram can be 
taken in a few minutes after the patient is in circuit. 
REFERENCES 
Cohn, A. E.: A New Electrode for Use in Clinical Electrocardiography. Arch, of Internal 
Medicine, 1920, XXVI, 105. 
Cohn, A. E.: Present Status of the Electrocardiographic Method in Medicine; Association 
of American Physicians, May n-13, 1915; American Journal of the Medical Sciences, 
1916, CLI, 529. 
Einthoven, W.: Weiteres ueber das Elektrokardiogram; Pflueger’s Archiv, 1908, CXXII, 
536. 
Einthoven, W., Fahr, G., and de Waart, A.: Ueber die Richtung und Manifest Groesse der 
Potentialschwankungen . . . des Elektrokardiogramms; Archiv fuer die ges, 
Physiologie, 1913, CL, 275. 
Einthoven, W.: Le Telecardiogramme; Archives Internationales de Physiologie, 1906, IV, 
Fasc, II, 132. 
Einthoven, W.: Neuere Ergebnisse auf dem Gebiete der thierischen Elektrizitaet; Gesell- 
schaft deutscher Naturforscher und Aertzte, Verhandlungen, 1911, 3. 
Einthoven, W.: Ueber die Deutung des Electrocardiogrammes; Archives fuer die gesammte 
Physiologie, 1912, CXLIX, 65. 
Fahr, G.: On Simultaneous Records of the Heart Sounds and the Electrocardiogram; 
Heart, 1912, IV, 147. 
Fahr, G., and Weber: Ueber die Ort und Bestimmungen der Erregung . . . mit Hilfe der 
Elektrokardiographie; Deutsches Archiv fuer klinische Medizin, 1914-15, CXVII, 361. 
Fahr, G.: Spread of the Excitation Wave, Archives of Internal Medicine, 1920, XXV, 146. 
Gotch: Electrometer Records, Heart, 1909-10, I, 235. 
Hoffman, A.: Die Elektrocardiographie als Untersuchungsmethode des Herzens und ihre 
Ergebnisse, Ed. 1914. 
Kraus, F., and Nicolai, G.: Das Elektrokardiogramm des gesunden und kranken Menschen, 
1910. 
Lewis: Mechanism and Graphic Representation of the Heart Beat. 
Lewis, T.: Lectures on the Heart, 3. 
Lewis, T. and Gilder, M. D. D.: The Human Electrocardiogram, A Preliminary Investiga- 
tion, etc.; Philosophical Transactions of the Royal Society of London, 1912, Series B, 
CCII, 351. 
Pardee, H. E. B.: Form of the Electrocardiogram; Journal of the American Medical 
Association, 1914, LXII, 1311. 
Tigerstadt: Physiologie des Menschen, I, 15. 
Willius: Initial Ventricular Complex, Archives of Internal Medicine, 1920, XXIII, 515. 
Wedd: Notching of the R Wave. Archives of Internal Medicine, 1919, XXIII, 515. 
Waller, A. D.: The Electrical Action of the Human Heart; Lancet, May 24, 1913, 1435. CHAPTER IX 
VARIATIONS IN THE MUSCULAR MASS OF THE HEART THAT 
INFLUENCE THE RHYTHMIC ELECTROCARDIOGRAM—VEN- 
TRICULAR HYPERTROPHY AND DILATATION—SPLIT WAVES— 
VARIATIONS OF THE T WAVE—SUMMARY OF CLINICAL 
INTERPRETATIONS. 
So much confusion, contradiction and ill-grounded conclusions are found 
in electrocardiographic literature, especially in the attempt to diagnose 
hypertrophy and myocarditis from the electrocardiogram, that the physician 
must continually hark back to fundamental considerations, otherwise electro- 
cardiograms instead of aiding in clarifying clinical interpretation, may have 
just the reverse effect. There is indeed much unequivocal and definite 
information that the electrocardiogram can give regarding hypertrophy and 
myocarditis, particularly in conjunction with clinical data; but I now refer 
in the main to debatable and questionable interpretations. In that which 
follows, some of these will be discussed. 
From what has been said regarding monophasic and diphasic curves and 
their fundamental electrophysiological causes (Chapter VIII), it is evident 
that purely physical considerations affecting a contracting muscle may 
influence the resultant electrocardiogram. For example, let us in Fig. 60 
conceive the muscle to consist of fibers of various lengths running in various 
directions, instead of being parallel and of the same length; we should then 
expect some change in the resultant electrocardiogram and not a simple 
diphasic curve. It has already been pointed out that the muscular archi- 
tecture of the heart is an extremely intricate one, and that there are layers 
which run in various directions from one chamber to the other (Chapter I). 
This phase of pure mass consideration as affecting and influencing the electro- 
cardiogram has been admirably summed up by A. E. Cohn as due to the 
“disposition and volume of the muscular mass of each pair of cavities.” 
Volumetric and mass considerations apply not only to the involved archi- 
tecture of the normal heart, but also to diseased and hypertrophied hearts. 
For example, it seems probable that the hypertrophic process does not always, 
or even regularly, express itself by hypertrophy of one chamber as compared 
with the other, but rather as a process affecting the fundamental complicated 
muscle layers. To such observations should be added the extremely 
important experimental one that in electrocardiograms of dogs with the chest 
wall intact, the direction of the main deviation—the R wave—is often 
changed by turning the animal to one side or the other. This can only 
mean that such manipulations serve to so change the ventricular axis in 
io6 THE ELECTROCARDIOGRAM 
107 
the relative positions of right and left ventricles, that one or the other 
becomes electrically predominant, and hence correspondingly deviates the 
R wave. Such experiments have their analogies in the human electro- 
cardiogram, and as will be pointed out later, should serve to caution us in 
dogmatically diagnosing hypertrophy of a cardiac chamber from the 
electrocardiogram alone. 
Remembering then the purely physical side of the heart as expressed 
by its mass and volume, and the various shapes and forms the heart muscle 
mass as a whole may take, it can be understood how changes in muscular 
volume and mass profoundly influence the size and direction of the electro- 
cardiographic deviations. To use a crass but perhaps expressive comparison, 
excessive hypertrophy of the left ventricle, by distorting the normal muscu- 
lar (and therefore the normal electrical) balance of the heart, would have the 
tendency to “pull down” the excitation wave somewhat as a magnet attracts a 
needle. It is evident, however, that any classification based upon differ- 
ences of shape, mass and volume of the cardiac musculature will meet with 
numerous exceptions, for in the present state of our knowledge of roentgen- 
ology and physical diagnosis, it is impossible to diagnose with any degree of 
exactness, many instances of distorted muscular balance such as are found 
in hypertrophy and dilatation of the various cardiac cavities. Indeed, it 
seems conceivable that right and left chamber distortions may balance each 
other; the resultant effect on the electrocardiogram would therefore be nil. 
Bearing the above limitations in mind, the following tabulation is offered 
in an attempt to clarify many of the causes for variations from the normal 
electrocardiographic standard in the rhythmically beating heart. 
Abnormal Size, Disposition and Volume of the Ventricular Musculature 
as Affecting the Electrocardiogram. 
A. Horizontally disposed (squatty) hearts. 
B. Vertically disposed (drop) hearts. 
C. Cardiac displacements. 
D. Congenital dextrocardia. 
E. Phasic variations with breathing. 
F. Ventricular hypertrophy (left and right). 
G. Ventricular dilatation (left and right). 
H. Abnormal ventricular mobility. 
(vl) Horizontally Disposed (Squatty) Hearts.—If from any cause the 
heart lies abnormally flat on the diaphragm, the ventricles are apt to be 
“disposed” with a preponderant balance to the left, as diagrammatically 
illustrated in Fig. 70, D. In some clinical cases of “squatty heart,” R III1 is 
either dwarfed or negative. Leaving the question of hypertrophy for later 
consideration, examples of squatty hearts are found oftenest in obese, middle- 
aged individuals. Electrocardiograms from several such patients are shown 
(Figs. 71, 72, 73). Cardiac symptoms are rarely present. Fluoroscopic 
examinations (Chapter XII) reveal the ventricular mass lying flat upon the 
1 The numerals placed after the deviations refer to the latter in their respective leads. 108 
THE ELECTROCARDIOGRAM 
NORMAL HfAyfT^ 
Ay ci/wpi-e. 
-E*p i i?ATyoy 
A V OUWDLC 
—N OR^Au * 
j s Pi rs it, 
Fig. 70.—Schematic representations showing the angles made by the direction of the 
leads with varying ventricular axes, and the corresponding electrocardiograms. Although 
the ventricles are schematically of different sizes, it is here assumed that the volumetric 
contents of both chambers are alike. 
A, Normal heart; B, left ventricular dilatation; C, right ventricular dilatation; D, left 
ventricular hyperbalance; E, right ventricular hyperbalance; F, left ventricular hyper- 
trophy; G, right ventricular hypertrophy (electrocardiogram as in C); H, block of right 
bundle branch; I, block of left bundle branch; J, left ventricular extrasystole; K, right 
ventricular extrasystole; L, change of position of the heart with inspiration and expiration. THE ELECTROCARDIOGRAM 
109 
diaphragm; the dome of the latter is less curved and the diaphragmatic 
excursion is reduced in range. These factors are of importance in the eti- 
ology of the abnormal position of the ventricles. Gaseous distention of the 
stomach may have a similar effect upon the position and action of the 
diaphragm, and hence upon the position of the heart. 
Fig. 71. 
Fig. 72. 
Fig. 73. 
Figs. 71, 72, 73.—Electrocardiograms of patients with normal hearts and with negative R 
in L III. In all these cases the ventricle lay flat upon the diaphragm. 
(.B) Vertically Disposed (Drop) Hearts.—Quite opposite, theoretically, 
to the foregoing is the distribution of the ventricular musculature when the 
heart is narrow and lies vertically in the chest. The assumed muscular axis 
is then diagrammatically represented in Fig. 70 E; R I becomes abnormally 
small or negative. Clinically, patients with vertically directed (so-called no 
THE ELECTROCARDIOGRAM 
“drop”) hearts are apt to be young, tall and gaunt individuals with loosely 
hung hearts. With the fluoroscope the entire organ appears narrow and 
Fig. 74.—Electrocardiogram of patient with narrow heart (“drop” heart) illustrating 
right ventricular hyperbalance. 
Fig. 75.—Orthodiascopic tracing of heart of a 
normal child lying on its back A, left B, and right 
side G, respectively. 
graceful, and for the most part hidden behind the sternum. At times, the 
apex scarcely touches the diaphragm. An illustrative electrocardiogram is 
shown in Fig. 74. THE ELECTROCARDIOGRAM 
Ill 
(C) Cardiac Displacements.—The heart can be displaced, as is known, by 
pleural exudates, adhesions, mediastinal tumors, etc. If the heart be dis- 
placed laterally so that there is no disturbance of the muscular balance 
of the heart, the electrocardiogram does not change. The latter is only 
affected when the new position (made, for example, by tilting the heart) has 
brought about change in. the relationship and disposition of the ventricles, 
for then the electrical axis as well as the electrical potential of the ventricles 
is changed. The effect of displacement can be best exemplified in children, 
(Ynj&uJo 
A 
fa 
o 
\ 
Fig. 76.—Orthodiascopic tracing of a normal child 
lying on its back A, left B, and right side C, 
respectively. 
and is illustrated in Fig. 76, A, B, C—the orthodiascopic tracings of a healthy 
boy of ten lying respectively on his back, left and right sides. The tracings 
show marked variations in the disposition and contour of the heart, mainly 
due to ventricular rotation and consequent foreshortening or lengthening of 
the cardiac outline. Another illustration of the mobile heart is Fig. 75 
(positions A, B, C), orthodiascopic tracings of the normal heart of a child of 
seven lying respectively on her back, left and right sides. Corresponding 
electrograms were taken (Fig. 77, A, B, C). In addition to slight changes 
in the Q and S deviations, the heights of the R in the A, B, C positions varied 
as follows: Lead I, R = 6A, $B, 6C (the numbers refer to the number of milli- 
volts of deflection); in Lead II, R = ioA, 15s, i6c; in lead III, R = 6A, 13®, 
ioc. 11 2 
THE ELECTROCARDIOGRAM 
(D) Congenital Dextrocardia.—As a corollary to the observations already 
made regarding the effect of change of the planes of electrical potential upon 
the electrocardiogram, it is apparent that congenital dextrocardia in the 
first (sometimes called the symmetrical) lead will produce electrocardiographic 
deviations exactly opposite in direction to the normal (Fig. 78). All the 
Fig. 77.—Electrocardiogram of a child whose orthodiascopic tracing is Fig. 75. The 
letters A, B and C again refer to the position of the child on its back, left and right side 
respectively. 
Pig. 78.—Congenital dextrocardia. All the deviations are directed downward in L I. 
R III is taller than R II. 
peaks are directed downwards instead of upwards; R III becomes taller than 
RII. Such an electrocardiogram offers indubitable proof of congenital 
dextrocardia and serves to distinguish the latter from acquired rightsided THE ELECTROCARDIOGRAM 
113 
malposition of the heart due to fluid in the chest, pulmonary tumors, pneumo- 
thorax, adhesions, etc. For example, Fig. 79 is the electrocardiogram of a 
patient with an acquired dextrocardia, in whom the heart was drawn into 
the right chest by adhesions following a right-sided pulmonary abscess and 
subsequent pleural fistula from thorocatomy. Fluoroscopically, the heart 
was seen to occupy an area in the right chest practically identical with that of 
congenital dextrocardia. Since the heart had been 
pulled in a lateral direction only, the electrocardiographic 
deviations remained normal in direction. 
(E) Phasic Variations with Breathing.—As the result 
of breathing, some electrocardiograms, usually in the 
second and third leads, present a rhythmic waxing and 
waning, an increase and decrease respectively in the size 
of the R waves. In fluoroscopy, I have often noted a 
marked variation in the position of the heart during 
respiration (Fig. 70, L,) sometimes sufficiently pronounced 
to produce a movement of the apical portion of the 
ventricle through an arc of several centimeters. This 
shift is most evident in younger individuals with thin 
chest walls and large respiratory excursions of the 
diaphragm; it is least noticeable in patients with fat 
abdominal walls and broad hearts. The heart moves 
with its base as a comparatively fixed point. During 
inspiration there is a descent in a clockwise direction of 
the ventricular mass, especially of its apical portion; 
the heart tends to assume an erect posture. The rise 
of the diaphragm during expiration produces a contrary 
effect, the left ventricle then moving anti-clockwise. 
These movements, when marked, necessarily affect the 
muscular relationship of the ventricles and, as a con- 
sequence, alter the electrocardiogram. This is usually 
most noticeable in the third lead, probably because the 
left ventricle is especially influenced by the respiratory phases. R III 
becomes taller during inspiration and smaller during expiration as the 
ventricular mass tends to assume a more vertical or horizontal position, 
respectively (Fig. 70, L). 
Respiratory phasic variations are also found in patients with ventricular 
hypertrophy, but since the cardiac excursion is ordinarily less, the phasic 
electrocardiographic variations become correspondingly limited. Figures 
80 and 81 are examples of a moderate respiratory effect upon the size of the 
deviations. Figure 81 is the electrocardiogram of a stout individual with a 
normal heart lying in a squatty position; Fig. 82, of a patient with left ven- 
tricular hypertrophy. When R III is small, phasic variations may not 
only dwarf it but may cause its final disappearance, as shown in Fig. 82. 
Pig. 79.—Acquired 
dextrocardia with nor- 
mally directed devia- 
tions in all three leads. 114 
THE ELECTROCARDIOGRAM 
(F) Ventricular Hypertrophy—Left and Right (Fig. 70, F.G.).—It has 
sometimes been assumed that negative R I (S I) and positive R III are indica- 
tive of right ventricular hypertrophy, and positive R I and negative R III 
(S III), of left ventricular hypertrophy. This observation has been partly 
substantiated by necropsies. On the other hand, exceptions have been noted 
both at postmortem and as the result of clinical observation. Some 
undoubted cases of left ventricular hypertrophy, for example, do not give the 
deviations assumed for this condition. Besides, it is by no means infre- 
Fig. 8o.—Slight phasic variations with 
breathing. 
Fig. 8i.—L II. Slight phasic 
variation with breathing. 
quent to find perfectly normal hearts in a normal position in the chest, 
which present the deviations supposedly typical of hypertrophy. It will 
thus be seen that there are many drawbacks and exceptions to definite con- 
clusions regarding the existence of hypertrophy based upon the direction 
of the electrocardiographic deviations alone. Again, a case may show 
undoubted clinical evidence of left ventricular hypertrophy, the X-ray may 
show the heart in a normal position as far as the cardiac axis is concerned; and 
yet a deep negative deviation in the third lead (S 3) may be missing. In 
Fig. 82.—Marked phasic variation with breathing. 
such instances one can only assume that there is a right as well as a left ventricu- 
lar hypertrophy, and that therefore the muscular (and with it the electrical) 
balance has not been disturbed sufficiently to distort or “pull down” the 
third deviation and make it negative. In other words, with a heart that 
shows definite clinical evidence of left ventricular hypertrophy, whose axial 
position in the chest is normal, and whose electrocardiogram shows spikes 
normally directed, it is fair to assume that the electrocardiographic prepon- 
derance due to left ventricular hypertrophy has been offset by a right ven- 
tricular one. THE ELECTROCARDIOGRAM 
n5 
It has already been shown that a squatty (transverse) and a vertical 
(elongated) heart may yield abnormally directed deviations in the third and 
first leads respectively, even though these organs are otherwise normal. 
Applying these considerations, for example, to a 
heart that not only lies too transversely but also 
has a hypertrophic left ventricle, it would mean that 
the third lead would be disproportionately negative 
for that amount of hypertrophy; that is to say, there 
would be a summation and re-inforced negative devia- 
tion due both to the abnormally flat position of the 
heart and to the hypertrophy. If, on the other hand, 
a left-chambered hypertrophic heart were too vertical 
in the chest, it would tend to decrease the length of 
the negative deviation in the third lead. Finally, it 
seems probable that the influence of ventricular 
dilatation (see Fig. 70, G) may possibly counter- 
balance or at least vitiate in one direction or another 
electrocardiographic deviations due to hypertrophy 
alone. All these factors necessarily influence electro- 
cardiographic inferences regarding hypertrophy. It 
is evident also that these factors themselves or their 
interdependence cannot always be known; hence 
electrocardiographic formulae which deal with electro- 
cardiograms alone and which give no information 
regarding the direction of the cardiac axis in the 
living, or the relative hypertrophy and dilatation of 
the ventricular chambers at autopsy omit important 
data for proper inference. Even with the data re- 
garding the direction of the cardiac axis in the living 
it seems a difficult mathematical as well as clinica 
problem to determine the correlation and relative importance of the known 
and unknown quantities. Hence electrocardiographic formulae for hyper- 
trophy, unless carefully construed from various aspects, may cause 
misleading information. On the whole it is better to speak of the electro- 
cardiogram as showing ventricular predominance or preponderance than 
ventricular hypertrophy, for, as just indicated, other considerations must 
be weighed before the diagnosis of hypertrophy can be concluded from 
the electrocardiogram alone. As a general rule, however, it will be found 
that when the R I is tall and positive, and R III deep and negative, left 
ventricular hypertrophy exists. This is clinically best exemplified in aortic 
disease with left ventricular hypertrophy. Examples are given in Figs. 
83-85. Occasionally, however, R III is positive, even when left ventricular 
hypertrophy is present (Fig. 86) . 
dila^S'on3of 
with left ventricular 
deviaUoThfLead* m.' 116 
THE ELECTROCARDIOGRAM 
Naturally, as in the left, similar considerations govern electrocardio- 
graphic conclusions regarding right ventricular hypertrophy. The electro- 
cardiographic evidence of right ventricular hypertrophy is best exemplified 
by congenital cardiac disease due to malformation of the pulmonary artery. 
This is illustrated in the case of a boy of 17 with patent ductus arteriosus 
Fig. 84.—Aortic stenosis. Left ventricular hypertrophy. 
Negative R in L III. Ventricular extrasystole (Ex) in 
ead III. 
Fig. 85.—Negative 
ventricular deviation in 
lead III. From a case 
of left ventricular hy- 
pertrophy 1 and aortic 
aneurism. 
Fig. 86.—Electrocardiogram of patient with aortic regurgitation and left ventricular 
hypertrophy; the R deviation is positive in L III. 
(Fig. 87). Both R I and R II are negative. Upon the theory of mass 
imbalance affecting the electrocardiogram, it would seem that a negative 
R II in addition to negative R I is indicative of very marked right ventricu- 
Fig. 87.—Electrocardiogram of a boy of 17 with congenital patent ductus arteriosus 
Note negative R I, R II. evidence of marked right ventricular hypertrophy. 
lar hypertrophy. The same theoretical consideration applies to negative 
R II and R III as indicating extreme left ventricular hypertrophy. This is 
exemplified in Fig. 88 taken from a patient with aortitis, and with clinical 
and fluoroscopic evidence of extreme left ventricular hypertrophy. Infants THE ELECTROCARDIOGRAM 
117 
and young children are also apt to have the electrocardiographic complex of 
right ventricular enlargement, because in them the walls of the right ventri- 
cle are relatively thick. 
Cases of mitral stenosis do not always yield electrocardiograms indicative 
of right ventricular hypertrophy, a condition usually associated with this 
Fig. 88.—Electrocardiogram showing an interpolated extrasystole (L III, Ex). R is 
abnormally wide, especially in L I and L III. The direction of the R deviations in the 
various leads indicates marked left ventricular hypertrophy. T I and T II are negative, 
presumed evidence of myocarditis. (From a patient with left ventricular hypertrophy and 
luetic aneurismal dilatation of the entire thoracic aorta.) 
lesion. Thus, Figs. 89 and 90 are from cases of marked typical stenoses. 
In Fig. 89, the main ventricular deviation is negative; in Fig. 90, it is positive. 
Whether similar electrocardiograms in cases 
in which right ventricular hypertrophy is 
clinically assumed, are due to some of the 
factors already discussed (abnormally dis- 
posed ventricles, ventricular dilatations or 
hypertrophy) or whether they may even be 
due to counterbalancing left ventricular 
hypertrophy, it is at present impossible to 
state. 
(G) Ventricular Dilatation (Fig. 70, 
B.C.).—Although hearts which are organically 
sound may occasionally become temporarily 
dilated as the result of overstrain or of 
tachycardial attacks, the term ventricular 
dilatation is here meant to apply to decom- 
pensated, diseased hearts. To a great extent, 
our clinical knowledge regarding cardiac 
dilatation, especially of one chamber as con- 
trasted with the other, or of dilatations as 
differentiated from moderate hypertrophy, is 
meager (Chapter VI), although autopsy 
findings of dilated cavities are by no means infrequent. There exists, 
however, some definite evidence that cardiac dilatation following acute 
endocarditis is not uncommon in children. This subject has never been 
Fig. 89.—A d v a n c e d mitral 
stenosis. RI is negative. Auricular 
fibrillation is present. 118 
THE ELECTROCARDIOGRAM 
studied from the electrocardiographic aspect, but, as with considerations 
regarding the effect of mass changes, it seems probable that muscular 
redistribution resulting from dilatation can also bring about changes in the 
electrocardiographic deviations. 
I possess some electrocardiographic data which, when combined with 
clinical examination, have a bearing upon my assumption that changes in 
Fig. 90.—Advanced mitral stenosis with auricular fibrillation. All the R deviations are 
positive. 
the volume of ventricular chambers from dilatation and consequent distor- 
tion of ventricular mass relationship, can bring about changes in the direction 
of the ventricular spikes of the electrocardiogram. Thus in a few instances 
of patients with severely decompensated valvular lesions, there was a definite 
change in the direction of the ventricular deviations in at least one lead 
shortly before death. This change was not due to any bundle lesion (Chap- 
ter X), for the electrocardiograms presented no such evidence. Naturally 
sudden hypertrophy as a terminal condition could also be ruled out. Ip 
my opinion, such an electrocardiographic change from positive to negative 
or the reverse could be brought about by but two causes: Some force from 
without (e.gpericarditis with effusion) causing sudden compression of one 
ventricle and thus disturbing the pre-existing interventricular mass relation- 
ship; or changes in the degree of dilatation of the ventricular chambers 
themselves. The latter appears the more plausible since the changes 
occurred in severely decompensated hearts shortly before death. Autopsies 
were not obtained. 
Abnormal Ventricular Mobility (H)—Splitand Slurred R Complexes— 
M and W R S Complexes.—Split, slurred and various types of 
abnormal ventricular waves have been described. About them much con- 
fusion has arisen as to their etiology, and especially as to their clinical signifi- 
cance. I shall attempt to group and separate these abnormal waves into 
somewhat more orderly groups, and as far as possible shall give my interpre- 
tation of them from the clinical and experimental standpoints. In this 
mannef, even if the etiology be still partially or entirely unknown, we shall 
at least be able to state with fair accuracy that some of these bizarre com- 
plexes, while of extreme interest from the electro-physical and electro- 
cardiographic standpoints, do not of themselves indicate cardiac disease 
in man. THE ELECTROCARDIOGRAM 
119 
I shall first take up those split complexes which I have termed M and W 
deviations (Figs. 93, 94, 95) because they so closely resemble these letters. 
During the course of routine fluoroscopic examination of normal and 
abnormal hearts, I have encountered occasional cases in which there was a 
sort of to-and fro tilting, rocking motion of the ventricular mass, with the 
base of the heart acting as the fulcrum. At times the entire ventricular 
mass, at others only its apical portion was seemingly involved in this 
abnormal motion. Before I had the opportunity 
to attempt experimental splitting of the R wave 
in electrocardiograms of narcotized dogs, my con- 
ception had been that this abnormal rocking or 
tilting motion of the ventricular mass interfered 
with the mass relationship of the ventricular 
chambers, and thus brought about a condition in 
which the ventricular excitation wave was really repeated; in other words, 
a split M or W wave really consists of two component R (M) or S (W) 
deviations, respectively. I would emphasize that I refer only to split waves 
whose measurement at the base line shows that they have not taken an 
abnormally long time for their production: That is, the entire width of 
the wave is not longer than 0.07 of a second. Although I believe clinically 
that abnormal rocking or tilting of the heart during ventricular contraction 
has a decided influence in causing these split waves, experimental observa- 
tion1 however has caused me to partially change my views as to their 
etiology. The essence of these experiments has been as follows: If the 
forelimbs and left leg of a narcotized dog be connected with the electro- 
cardiographic apparatus, the chest opened, a hook be introduced in either 
Fig. 93; — Electrocar- 
diogram showing split R 
(M) complex. 
Fig. 94. 
Fig. 95- 
ventricle, and the ventricle be then slowly or violently twisted in any 
direction, it will not cause splitting or even slurring or thickening of the 
main ventricular deviation (R or S wave). There are however two methods 
by which splitting (M or W waves) can be produced. One is by introducing 
a slightly bent, long steel sound through the jugular, superior vena cava 
and tricuspid orifice so that the sound rests against the inner ventricular 
surface of the right ventricle. Tilting of the exposed end of the sound in 
the neck in such manner that its ventricular end is held firmly against the 
Figs. 94, 95.—Electrocardiograms showing split R (W) complexes. 
1 These experiments, as yet unpublished and incomplete were done in conjunction with 
and through the kindness of Dr. Edwards, of the Department of Physiology, Cornell 
University. 120 
THE ELECTROCARDIOGRAM 
ventricular wall will in the majority of instances cause M or W complexes. 
This of course has no analogy in man. It demonstrates however that any 
physical influence which can tilt out even slightly, the right ventricular 
wall (it is experimentally difficult to introduce a sound in the left ventricle) 
may split the main ventricular complex into two component parts. The 
second experimental procedure consisted in pressing two fingers through an 
abdominal incision against the under surface of the diaphragm. The fingers 
were pressed against that part of the heart—right or left ventricle—which 
beat most forcibly. As a result, the R or S waves were also split into M 
or W complexes, respectively. 
While the underlying electro-physiological cause of these experimentally 
split complexes has not as yet been ascertained, what happened to the ven- 
tricles was apparently some physical disturbance of the ventricular balance. 
With the sound introduced into the right ventricle, there was presumably 
slight ballooning of a small ventricular area: With the fingers pressed against 
the under surface of the diaphragm, the heart bobbed or pounded against the 
fingers, thus producing a sort of muscular rebound. Perhaps some similar 
physical ventricular disturbance happens clinically when the healthy or the 
diseased heart overacts or tilts during ventricular contraction. At any rate, 
the experiments show that purely physical facts can account for the M and 
W split waves. Hence alone they cannot be used as evidence of myocardial 
disease. 
In addition to splitting of the R wave from causes just described (vari- 
ations due to change in relative position and volume of the ventricular mus- 
culature), asynchronous activity of the chambers may also possibly act in a 
similar manner. There are conditions in which, for various reasons, there is 
Fig. 91.—Electrocardiogram 
showing somewhat thickened R 
summit. 
Fig. 92.—Electrocardiogram 
(L II) showing slightly notched 
R summit. 
a retardation of the excitation wave in one chamber as compared with its 
fellow. Such retardation may thus also account for many of the “split” and 
“notched” complexes. The normal difference in contraction time between 
the two ventricles may amount to as much as 0.03 second. If there be but 
slight retardation of the excitation waves in the ventricles due to abnormal 
ventricular asynchronism, it may account for the thickening of the R devi- 
ation at its summit (Fig. 91) as well as for various degrees of notching at the 
apex (Fig. 92). 
Similar in etiological significance to the notched R waves from asyn- 
chronous ventricular activity are the notched or split P deviations (Fig. 96); 
these occasionally give rise to the appearance of two distinct undulations. THE ELECTROCARDIOGRAM 
121 
Such complexes are probably due to asynchronous auricular contractions. 
A notched P is found most often in mitral stenosis. 
Intraventricular or Arborization Block.—A QRS complex has been 
described (Oppenheimer and Rothchild) in which the time required for the 
Fig. 96.—Notched P wave from a case of mitral stenosis. (Courtesy of A. E. Cohn.) 
completion of this group was prolonged beyond 0.10 second, the extreme 
normal limit. The other characteristics were an R wave abnormally broad; 
instead of clean and sharp sides, it was slightly or considerably notched and 
Fig. 97.—Electrocardiogram showing intraventricular block. (Courtesy of G. C. Robinson.) 
Note the notched and splintered complexes. 
broken. The waves were usually of low amplitude in all leads. This bizarre 
electrocardiographic complex was found in cases in which there was marked 
arteriosclerotic or cardio-renal disease, usually associated with severe 
myocarditis. In four cases, the clinical picture was corroborated by necropsy 122 
THE ELECTROCARDIOGRAM 
examination; this showed sclerosis especially in the endocardial and 
subendocardial layers; that is, in the neighborhood of the terminal arboriza- 
tions of the conduction system. This abnormal electrocardiogram was 
considered to be the result of intraventricular arborization block, an inter- 
ference with the normal and orderly spread of the electrical excitation wave 
throughout the heart. It should be pointed out, however, that hearts 
presenting the above clinical or pathological picture need not necessarily 
produce the abnormal electrocardiogram described. For example one of my 
Fig. 98.—Electrocardiogram showing ventricular complexes of abnormal width but of 
normal form. R is not abnormally wide in all leads. 
own cases of the above type of cardio-sclerosis that came to autopsy presented 
a normal electrocardiogram during life. Other exceptions have also been 
reported. Until the causes for such negative findings in the electrocardiogram 
have been established, the diagnostic value of this type of electrocardiogram 
must necessarily be limited. Another type of case has been reported (G. S. 
Robinson) whose QRS complexes also required o.io seconds or longer for their 
completion (Fig. 97). These were assumed to be due to derangement of 
intraventricular conduction from hindrance either in the rate or in the path 
followed by the excitation wave. This hindrance was regarded as due to 
functional fatigue. In most of the cases from whom the electrocardiograms 
were taken there was clinical evidence of a profound disturbance in the 
muscular efficiency of the heart. 
The “Wide R” (For Detailed Study, See Chapter XXXII).—Both of the 
above types of intraventricular block are characterized, as has been stated, 
by a broken and notched complex comprising the QRS group. In an 
entirely different category belong those cases that I have studied, in whom 
the R deviations are normal in shape and form, whose sides are unbroken 
and unnotched, and in whom there was no evidence of a bundle branch 
lesion. The characteristic of my cases was the abnormal length of time 
required for the completion of the main ventricular wave. The normal time 
for the completion of the latter varies from 0.02 to 0.05 second. I have adopted 
as a standard, a width of 0.07 or over as being an “abnormally wide R.” 
A few cases with their electrocardiograms are herewith epitomized: Fig. 88, is 
from a patient who had general anasarca from luetic cardiosclerosis. R I = THE ELECTROCARDIOGRAM 
123 
0.13 of a second in width. Figure 98 is from a case of dilatation of the arch 
of the aorta and moderate left ventricular hypertrophy; the clinical diagnosis 
was cardiosclerosis. R I = 0.12, R III = 0.08. Figure 99 is taken from a 
physician of 53 who developed scarletinal nephritis at the age of 15. At the 
Fig. 99. 
Fig. ioo. 
Fig. ioi. 
Figs. 99, ioo, 101.—Electrocardiograms showing ventricular complexes of abnormal width 
but of normal form. R is not abnormally wide in all leads. 
time of examination the urine contained albumin and casts. The patient had 
the physical signs and symptoms of moderate cardio-nephritis. R I and R II 
each equals 0.07. Figure 100 is that of a woman of 68 who, when first seen, 
was suffering from anasarca as the result of cardio-renal disease. R I = 
0.09. Figure 101 was from a male patient of 55 suffering from hypertension 124 
THE ELECTROCARDIOGRAM 
and moderate cardiosclerosis. R I = 0.07. The electrocardiograms of all 
these patients were taken during the stage of compensation. 
In all, I have studied eighteen cases who presented an R width of 0.07 of a 
second or over. All of these showed unmistakable signs of severe cardiac 
disease, and at one time or another were decompensated. Clinically, most 
of the cases had hypertension and left ventricular hypertrophy. Myocardial 
insufficiency alone was not the cause of the abnormally wide complex, for 
most of the electrocardiograms were taken when symptoms of decompensa- 
tion were slight or absent. Ventricular dilatation, another possible assump- 
tion for the abnormally wide R, can probably be disregarded for the same 
reason. Besides, in a series of decompensated valvular cases which I observed 
in whom ventricular dilatation was presumably a marked feature, the R 
complexes were of normal width. 
Although the fundamental cause of the wide R in my cases is not apparent, 
it is probably due either to delay in the development of electrical excitation 
or to delay in its propagation. Since the complexes are normal in form, the 
excitation wave has presumably followed a normal path in the ventricles. 
Delay in propagation seems the more probable factor. As in intraventricular 
block in which severe cardiosclerotic disease is assumed to be the cause of 
the notched and delayed QRS complex, a wide R of normal shape but of 
abnormal width may conceivably be due to patches of myocardial thickening 
scattered throughout the ventricular wall in amounts sufficient to impede 
and abnormally prolong the excitation wave. 
It should be mentioned that I have studied the complexes of other cardio- 
vascular cases who were clinically as ill as the “wide R” patients but who 
presented no abnormally broad complexes. The reason for this I have not 
been able to discover. 
Of the eighteen cases studied, the R complex was rarely abnormally broad 
in all leads. Since the first, second, and third leads “draw off” the cardiac 
current (Chapter VIII), breadthwise, diagonally, and lengthwise, respectively, 
one may possibly assume that the diseased myocardium lay chiefly in one 
cardiac plane, thus producing a wide R in the corresponding lead. In a 
general way, those cases which clinically showed the most myocardial dis- 
ease were the ones in whom the R complex was widest. 
The T Wave.—The T deviation is normally monophasic and directed 
positively (i.e. upward) in the three leads (Figs. 67, 69), its height varying 
between two and three millivolts. It is occasionally quite tall (Fig. 102), 
sometimes exceeding in height the corresponding ventricular spike (Fig. 
103) Not infrequently it is deviated downward in the third lead (Fig. 
104) in individuals with normal hearts. 
As will be described later (Chapter XXXII) a positively deviated T 
denotes that the excitation wave has entered the ventricular base. In a 
number of cases of organic heart disease, especially of the myocardium, T I, 
T II, or both may be small or negative, (Figs. 84, 88). Such T waves when THE ELECTROCARDIOGRAM 
125 
negative, indicate that the excitation wave has terminated toward the apex 
of the ventricles instead of toward the base, the normal termination. Much 
diagnostic clinical significance has been given to these negative T deviations 
in the first and second leads, especially since Einthoven regarded a well- 
Fig. 102.—Electrocardiogram showing 
tall T deviation. 
Fig. 103.—Electrocardiogram show 
[ing a T deviation taller than R. 
marked positive T as a sign of good cardiac contractility, and its absence or 
diminution, the reverse. It is, however, now known that the T wave may be 
absent in normal, and be very well marked and positive in diseased hearts. 
And since the clinical conditions in which the T wave is diphasic or deviated 
downwards in the first and second leads are only imperfectly understood, 
clinical inference drawn therefrom can for the present be only tentative. 
Pig. 104.—Electrocardiogram showing a negative T deviation in leads II and III in an 
individual with a normal heart. 
Experimental investigation has shown that ligation of any large branch 
of the left coronary artery in dogs is followed by a fairly constant change 
in the T wave: In the majority of experiments, the direction of the wave was 
changed from strongly positive to strongly negative in all leads. The nega- 
tive T remained several days and gradually reverted to the normal form. 
Clinical corroboration of these experiments (a few cases of occlusion of a 
branch of the coronary artery) have been reported and confirmed by autopsy 
in which the T deviations were negative in two of the leads. One of these 
negative T waves was especially deep. 
Effect of Digitalis on the T Wave.—It has been demonstrated that digitali- 
zation of a patient with heart disease may convert a positive T to a flattened 
or negative wave. Although this may be partly due to muscular ventricular 
redistribution as the result of relief of decompensation, experimental evidence 
indicates that the chief factor is probably due to alteration in the contractil- 126 
THE ELECTROCARDIOGRAM 
ity of the heart muscle. Pharmacological experiments in frogs and mammals 
have shown that digitalis produces diminished diastolic relaxation of the 
apical region. In the toxic stage there is systolic standstill of the apex, while 
the base relaxes in diastole. It is possible, therefore, that similar influences 
affect the digitalized human heart, producing continued apical activity and 
thus a negatively deviated T wave. The usual effect of digitalis administra- 
tion on the T wave may not become evident until atropin has been injected. 
Atropin apparently unmasks and removes the inhibitory effect of the drug; 
thereafter the full influence of digitalis on the heart can be observed. Further 
observation of the clinical effect of digitalis on the T wave is reserved for the 
study of the dosage and use of that drug (Chapter XX). 
Some years ago, Einthoven made the observation in one case that as the 
result of exercise, a negatively deviated T III in a normal heart became posi- 
tive. In one instance, I made the reverse observation, namely, a normal 
positively directed T III became negative (Fig. 105) when the patient was 
made to breathe sufficiently rapidly to race the heart somewhat. How long 
T III remained negative I do not know. The patient, a boy of 18, had no 
organic disease. He had been suffering from tachycardia and from cold 
Fig. 105.—Electrocardiogram illustrating the production of a negative T in lead III as 
the result of rapid breathing. A. quiet breathing; B, forced breathing. 
and bluish hands for years. The thyroid was normal. The diagnosis was 
functional tachycardia and vaso-motor disturbance, a combination common 
in those with “irritable hearts.” I shall later point out (Chapter XVIII) 
that this symptom complex is probably the result of hyperexcitability of 
the sympathetic nervous system. Perhaps, then, racing a heart already 
under the influence of the cardiac accelerators (the sympathetic nervous 
system) can have a different effect upon the T wave than when such an 
abnormal accelerator influence is absent. 
It has also been recently demonstrated in a few cases that a negative 
T deviation in decompen sated hearts may become positive with restoration THE ELECTROCARDIOGRAM 
127 
of compensation. The change is probably the result of nerve influences 
occurring during exercise. This view is based upon the fact that exercise 
is accompanied by accelerator excitation, and that various experimental obser- 
vations have shown definite correlation between accelerator stimulation 
and the size of the T wave. It therefore seems probable that a positive T 
produced by exercise, or by the restoration of compensation, is due to a 
neurogenic influence acting upon the ventricular base. Whether, under 
these conditions, a positive T is to be regarded as a favorable change is an 
open question and awaits further corroboration; hence clinical inference 
respecting its value should for the present be guarded. 
It is pertinent to inquire why the T wave, the final end of the excitation 
process in the ventricles, terminates in the ventricular base. It is known 
physiologically that in all muscular contractions there exists an end deflection 
of the electrocardiogram following actual muscular contractions, although 
the exact path followed by the excitation process may not be known. Per- 
haps in the human heart the terminal waning of the excitation process may 
be under a nerve influence that shortens or prolongs the excitation process 
in some parts of the heart more than others, and hence in abnormal instances 
it may serve to bring about a change in direction of the final deflection, the 
T wave. (Lewis.) 
Summary of Permissible Clinical Interpretations of Myocarditis and 
Hypertrophy from the Electrocardiogram Showing Normal Rhythm.—I 
shall not here refer to arrhythmias, themselves often used as criteria of organic 
disease, nor to bundle branch lesions; both are described elsewhere (Chapters 
X, XI). 
Having given the reasons and sounded the warnings regarding what I 
deem equivocal and questional interpretations from abnormal and bizarre 
looking electrocardiograms, I shall briefly summarize the positive evidence 
within our present knowledge. 
An abnormally wide, non-notched, non-split R or S in one or more leads, 
that requires more than 0.07 seconds for its completion, is probably indicative 
of primary or secondary myocardial disease. 
A split QRS (M or W complex) that is completed within a normal time 
(0.07 of a second or less) is evidence neither for nor against myocarditis. It 
may be found both in healthy and in diseased hearts. 
A notched, splintered or low QRS complex that requires an abnormal time 
(more than 0.10 of a second) for its completion is evidence either of a special 
type of myocardial disease (arborization block) or of myocardial fatigue; in 
either case myocarditis is present. 
A negative T in two of the leads, especially if one of the waves be very 
deep and sharply pointed, is evidence of myocarditis, probably from occlusion 
of one of the smaller coronaries. Conclusions regarding myocarditis 
drawn from negative T waves are of no value when the patient has been 
digitalized. 128 
THE ELECTROCARDIOGRAM 
The presence alone of any of the above abnormal or bizarre electrocardio- 
graphic complexes is of diagnostic value. Their absence does not preclude 
organic heart disease: Indeed, severe heart disease of all types and degrees 
may be present and yet the electrocardiogram may be practically normal in 
appearance. 
The presence of an abnormal or bizzare electrocardiogram is rarely a 
clinical measure of the degree of myocardial disease or efficiency. The 
reason for this probably depends upon the fact that abnormal complexes 
depend upon the location, rather than upon the amount of myocardial 
damage. 
Mere thickening or slurring (without actual splitting or division) of the 
R or S wave is found both in healthy and diseased hearts. Hence, alone it 
does not indicate organic heart disease. 
The clinical diagnosis of left ventricular hypertrophy (as against electro- 
cardiographic evidence of preponderance) is permissible when R I is tall. 
S II moderately deep and S III very deep; of right ventricular hypertrophy 
(as against electrocardiographic preponderance) when S I is deep, R II 
moderately tall, and R III quite tall. Ventricular hypertrophy may be 
present clinically, yet the deviations be normal in direction. Small 
abnormally directed deviations are of no clinical value in the diagnosis of 
ventricular hypertrophy of either chamber, because so many other causes 
may produce these abnormally directed deviations. 
REFERENCES 
Barringer, T. B., Jr., and Teschner, J.: The Treatment of Cardiac Insufficiency by a 
Method of Exercise with Dumb-bells and Bars; Archives of Internal Medicine, 1915, 
XVI, 795. 
Carter, E. P.: Clinical Observations on Defective Conduction in the Branches of the 
Auriculo-ventricular Bundle; Archives of Internal Medicine, 1914, XIII, 803. 
Carter: The Electrocardiogram and Ventricular Preponderance; Archives of Internal Medi- 
cine, 1919, XXIV, 638. 
Cohn, A. E., Fraser, F. R., and Jamieson, R. A.: The Influence of Digitalis on the T Wave 
of the Human Electrocardiogram; Journal of Experimental Medicine, 1915, XXI, 593. 
Cushny, A. R.: Pharmacology and Therapeutics, Ed. 1913. 
Lewis: Mechanism and Graphic Representation of the Heart Beat. 
Mathewson, G. D.: Lesion of the Branches of the Auriculo-ventricular Bundle; Heart, 
1912-1913, IV, 385. 
Neuhof, S.: Clinical Cardiology. 
Oppenheimer, B. S., and Rothschild, M. A.: Abnormalities in the Q-R-S Group in the 
Electrocardiogram Associated with Myocardial Involvements; Proc. Soc. Experi- 
mental Med. and Biol., 1916, XIV, 57. 
Pardee: Determination of Ventricular Preponderance from the Electrocardiogram; 
Archives of Internal Medicine, 1920, XXV, 683. 
Robinson, G. C.: The Relation in the Changes in the Form of the Ventricular Com- 
plex ... to Functional Changes in the Heart; Arch, of Internal Med., 1916, XVII, 
830. THE ELECTROCARDIOGRAM 
120 
Rothberger, C. J., and Winterberg, H.: Ueber die Beziehungen der Herznerfen zur Form 
des Elektrokardiogramms; Archiv fuer die ges. Physiologie, 1910, CXXXV, 506. 
Smith, F. M.: The Ligation of Coronary Arteries with Electrocardiographic Study; 
Archives of Internal Medicine, 1918, XXII, 8. 
White and Bock: Electrographic Evidence of Abnormal Ventricular Preponderance; 
American Journal of Medical Sciences, 1918, CLVI, 17. CHAPTER X 
THE ARRHYTHMIAS—THEIR POLYGRAPHIC, ELECTROCARDIO- 
GRAPHIC AND CLINICAL RECOGNITION 
In this chapter are grouped pulse and cardiac irregularities illustrated 
either by electrocardiograms or polygrams, or both. The object of this 
apparently promiscuous use of both methods of registration is to accustom 
the reader to think of the curves in terms of auricular and ventricular activity, 
no matter what form of graphic representation is used. Reduced to their 
simplest elements, all types of arrhythmias, even the most complex, depend 
essentially upon abnormal activity of one or both cardiac chambers. It 
therefore seems best to accustom the mind and eye to grasp simultaneously 
the fundamental conception underlying the arrhythmias and thus simplify 
their study. In this manner, also, once the fundamentals of graphic curves 
is understood, and the corresponding abnormal activity of the heart is 
visualized, the student will the more easily apply these lessons at the bedside; 
for as will be shown (Chapter XI) the great majority of arrhythmias can be 
readily diagnosed without the use of either the polygraph or electrocardio- 
graph. This can scarcely be done, however, unless the graphic basis of the 
arrhythmias is first thoroughly grasped. 
The passage of the normal impulse, as exemplified in polygraphic and 
electrocardiographic tracings of the normal rhythmic cardiac mechanism, has 
already been described. We shall now discuss those abnormal mechanisms 
known as cardiac arrhythmias and irregularities. A. E. Cohn has succinctly 
grouped the arrhythmias as coming under variations of a few fundamental 
normal functions. He states that cardiac irregularities arise from the abnor- 
mal passage of the impulse, from abnormal sequence of contraction of the 
pairs of chambers, and from abnormal coordination of the muscle mass. So 
far as possible, these basic considerations have been incorporated into my 
Tabulation of the Arrhythmias. As will be seen, I have grouped all the 
arrhythmias either as arising in the auricle, in the ventricle, or in the special- 
ized tissues, namely, the sino-auricular and the auriculo-ventricular nodes. 
Tabulation of Types of Arrhythmias and Cardiac Irregularities 
from the normal site, 
from an abnormal site (ec- 
topic). 
I. Auricular extrasystoles.* 
II. Paroxysmal tachycardia of auricular origin. 
A. Auricular arrhythmias 
(1) Auricular fibrillation. 
(2) Auricular flutter. 
(3) Incoordination intermediate 
between flutter and fibrillation. 
III. Auricular incoordination. 
* Because of its more common usage the term extrasystoles is here employed instead of 
“premature contractions.” Both terms, however, may be used interchangeably. 
130 THE ARRHYTHMIAS 
A. Nodal extrasystoles. 
I. Ventricular extrasystoles (from right or left ventricle). 
II. Interpolated extrasystoles. 
III. Automatic ventricular activity (ventricular escape). 
IV. Paroxysmal tachycardia of ventricular origin. 
V. Ventricular incoordina- 
tion. 
B. Ventricular arrhythmias. 
(1) Ventricular fibrillation. 
(2) Branch-bundle lesions. 
(1) Sinus arrhythmia or irreg- 
ularity. 
(2) Sino-auricular block (sinus 
block). 
(3) Blocked auricular beat. 
C. True bradycardia. 
f I. Disturbance in the sino- 
l auricular node. 
(1) Prolonged conduction time. 
(2) Shortened conduction time. 
(3) Backward conduction. 
D. Arrhythmias produced by abnor- 
mal sequence of contraction of 
auricles and ventricles. 
II Disturbance in 
atrio-ventricular 
node. 
(4) Auriculo-ven- 
tricular heart 
block. 
(a) Incomplete 
heart block, 
(b) Complete heart 
block (disso- 
ciation). 
It is the aim of graphic methods to exactly transcribe the cardiac mechan- 
isms, normal and abnormal. It has always been the aim of progressive clin- 
ical medicine to accept and adapt the knowledge gained by the use of exact 
instrumental methods for immediate use at the bedside, where instruments 
may not be available. It is thus that, in the light of knowledge gained by a 
careful study of the graphic methods, and with a full appreciation of the 
physiological pathology involved, it is possible to diagnose most types of cardiac 
and pulse irregularities by ordinary methods of examination. For this 
purpose, the stethoscope should be placed over the cardiac apex and the 
fingers kept on the pulse so that cardiac beats that are not propagated as pulse 
waves (so-called missed beats or pulse deficit) may be recognized. The 
neck should at the same time be carefully scrutinized for jugular and carotid 
pulsations (a and c waves). The value of keen observation will be discussed 
in connection with the clinical recognition of the arrhythmias. 
A. I. AURICULAR EXTRASYSTOLES 
Regarding the general nature of extrasystoles—auricular, ventricular 
and nodal—some preliminary observations are required before their various 
types, and instrumental and clinical recognition are discussed. 
Contractions of auricle or ventricle which anticipate the normal rhythmic 
time of their occurrence and disturb the normal rhythm are known as extra- 
systoles or premature contractions. Fundamentally, the normal passage of 
the impulse is disturbed. Extrasystoles were formerly termed “pulsus 
bigeminus.” They are now sometimes popularly termed “dropped beats.” 
As will be later pointed out, this is frequently a misnomer, for the beats 
are not actually “ dropped; ” they simply are at times not sufficiently powerful 
to lift the aortic cusps and produce a propagated pulse wave to the wrist. 
The term “premature contraction” is preferable because it so aptly describes 
the phenomenon. Extrasystole is also in a sense a misnomer, for the contrac- 132 
THE ARRHYTHMIAS 
tion is not “extra” or additional; it is simply anticipatory. However, since 
“extrasystole” is commonly used, it will be here employed. If extrasystoles 
recur at regular intervals after each normal beat, the resultant rhythm is 
known as coupling, coupled rhythm, or coupled beats. There are certain 
characteristics, as Lewis has pointed out, which physiologically differentiate 
the premature from the normal contraction. The normal physiological 
(or homogenetic) beat is one of a series of similar normal rhythmic contrac- 
tions; the contractions are equally spaced; there is an orderly building up of 
impulse formation which requires at least one half second for each beat. 
Fig. 106. 
Fig. 107. 
Fig. 108. 
Fig. 109. 
Fig. iio. 
Fig. hi. 
Figs. 106-111.—Diagrams illustrating the origin of physiological and pathological 
contractions. 
Figs. 106-107.—S.A., Sino-auricular node; A.V., part of the atrioventricular con- 
duction system. 
Fig. 106.—X.X., Origin of homogenetic beat in the sinus region with normal propaga- 
tion in the junctional tissue. 
Fig. 107.—X, Ventricular extrasystole. 
Fig. 108.—X, Auricular extrasystole. 
Fig. 109.—X, Nodal extrasystole. 
Fig. 110.—Disturbance in rhythm from a premature auricular contraction. 
Fig. hi.—Disturbance in rhythm from a premature auricular contraction. 
This power of rhythmic impulse formation resides chiefly, if not entirely, in 
the specialized tissue of the sino-auricular node, of the atrio-ventricular node, 
or in the bundle of His (Fig. 106). Regarding the premature, extrasystolic, 
heterogenetic, or pathological contraction, (terms used here synonymously), THE ARRHYTHMIAS 
133 
whether single or multiple, they are exceedingly rapid and abrupt; indeed 
there may be no time for impulse formation. Ventricular extraystoles, for 
example, may follow each other at intervals as short as 0.25 second or even 
less. Extrasystoles are further differentiated from normal beats by their 
prematurity and by their lack of rhythmic tendency; even when multiple or 
when occurring in showers, the rate of production is usually maximal. Fur- 
ther, there is no relationship between the heightened activity of the physio- 
logical heart rhythm and the prevalence of extrasystoles. Often, influences 
which depress the one favor the occurrence of the other; such an example is 
Fig. 112.—R,1 Rhythmic beat; C.P., compensatory pause; r', extrasystole; R', larger 
post extrasystolic beat. In the jugular tracing, the premature wave c' is synchronous with 
r\ Its foot-point is determined by measuring off with dividers the distance Rr' from the 
preceding rhythmic c (Rr' — Cc'). The auricular beat A is not premature. It falls at its 
rhythmic time; hence, the inter-auricular distance o — A' is equal to the normal beat (R). 
A occurs before the c' wave has completed its fall, hence the abnormal width of the com- 
bined c'A. The A wave is often not indicated as a distinct part of the c'A because it may 
be lost in the more prominent o' wave. 
1 In all the polygraphic tracings the time-marker measures pj second. 
Fig. 113. 
Figs. 113, 114.—Ventricular extrasystoles with typical compensatory pauses. 
Fig. 114. 
chloride of potassium in the experimental animal. Premature contractions 
bear a different relationship to the cardiac nerves than does the normal beat; 
for instance, gradually increased right vagus stimulation retards the normal 
rhythm; it has no effect on, or produces abrupt cessation in, a series of pre- 
mature contractions. Extrasystoles rarely originate from the normal 
rhythmic center, a fact electrocardiographically shown by differences in their 
form. Finally, the nearer the origin of the normal physiological beat to the 
vicinity of the superior vena cava, the faster the rhythm. This law does not 134 
THE ARRHYTHMIAS 
apply to extrasystoles; their rate does not depend upon their origin in auricle 
or ventricle. 
Premature beats (Figs. 107, in, 112), because of their inherent weakness 
and because the blood may not be properly directed against the aortic cusps, 
Fig. 115. 
Figs. 115, 116.—Ventricular extrasystoles with c' in the jugular but no representation 
in the radial tracing. X marks the point where the extrasystole should have produced a 
pulse wave. 
Fig. 116. 
are occasionally “frustrane” or “abortive;” that is, they either do not open 
the aortic cusps at all or do so insufficiently; hence in either instance, they fail 
to produce a propagated radial wave. These frustrane contractions are 
Fig. 117. 
Fig. ii8. 
Figs. 117, 118. — Auricular extrasystoles. The auricular beat a' is premature and is 
followed by the c' wave. The v wave of the rhythmic beat has fallen with a\ 
sometimes popularly termed “missed” or “dropped” beats, an evident misno- 
mer, because ventricular contractions do actually occur, but the blood is not 
propagated as a pulse wave for the simple mechanical reasons above described. 
Yet I have found much confusion among students and practitioners regarding 
this simple fact in physics. It is therefore worth repeating that the only THE ARRHYTHMIAS 
i35 
Figs. 119-120.—Auricular extrasystoles with shortened conduction time (a'c'). There is lengthened conduction time (a-c 
interval) in some of the rhythmic beats. + 
Figs. 122-123.—Multiple auricular extrasystoles. The radical tracing resembles coupled rhythm, but the frustrane con- 
tractions are well seen in the jugular tracing (a"c", a'"c'"). 
Fig. 121.—Auricular extrasystole (a'c'). Lengthened conduction (a) of the rhythmic beat. 
+ 
Fig. 123. 
Fig. 120. 
Fig. 121. 
Fig. 122. 136 
THE ARRHYTHMIAS 
reasons an extrasystole may be heard or felt at 
the heart and not always felt at the wrist are 
two—The premature contraction is too weak 
to open the aortic cusps sufficiently to push 
the blood along the systemic circulation; or the 
blood is not directed towards the aortic cusps 
and hence blood is not ejected into the systemic 
circulation. Not only may abortive contrac- 
tions escape palpation, they may be even too 
minute to be seen in radial tracings. In such 
instances the phlebogram shows the usual 
evidence of premature contractions (Figs. 115 
c, 116 c). The method of seeking the point of 
incidence of the rhythmic auricular beat has 
already been shown (a wave, Figs. 112, 113, 
114). Abnormal contractions, single or multiple, 
that originate outside of the sinus region are 
sometimes technically called “ectopic” contrac- 
tions (Lewis). Auricular extrasystoles are 
usually “ectopic” in this sense, but this fact 
can only be demonstrated electrocardio- 
graphically by the difference in the form of the 
abnormal auricular complex (P waves, Fig. 128) 
from the normal; that is to say, in any tracing 
the normal electrocardiographic P wave derived 
from the normal pace-maker site (the sino- 
auricular node) has a different form from that 
coming from any abnormal auricular point of 
origin. Auricular extrasystoles are not neces- 
sarily premature in their occurrence and hence 
may not disturb the normal rhythm. This 
statement also applies to any type of extrasys- 
toles, for, while usually premature, they occa- 
sionally occur at the time of, or even shortly 
after the time the normal beat should occur. 
When auricular extrasystoles are present, 
the ventricle usually responds to the premature 
auricular contraction after normal conduction 
time; this means that there is no delay or 
shortening of the interval required for the 
impulse to travel from the auricular extrasystolic 
contraction to the ventricle. 
As may be seen in the polygram, auricular 
extrasystoles produce radial waves of varied 
Fig. 124.—Auricular extrasystoles. THE ARRHYTHMIAS 
137 
size and strength (r, Figs. 117, 118); frustrane contractions (that is, those 
that produce no pulse waves) are comparatively rare. The auricular 
Pig. 125.—Auricular extrasystoles. The conduction time (P'R') is slightly prolonged. 
extrasystole in the jugular tracing is usually marked by normal con- 
duction time between it and the answering ventricular beat (a, c, Figs. 
Fig. 126.—Auricular extrasystoles superimposed upon the T wave (TR'). The pre- 
mature auricular contraction P2 is followed by an ectopic ventricular beat (V.Ex); i.e., the 
latter has followed a course in the ventricle different from the rhythmic beats (ventricular 
extrasystole). 
117, 118); the conduction time however, is occasionally diminished (a, Figs. 
119, 120) or increased (Fig. 121). Extrasystoles are sometimes multiple 
(Figs. 122, 123). If they are registered in the radial 
curve, the latter resembes coupled rhythm; the jugular 
tracing will then reveal the frustrane extrasystoles 
(Figs. 122, a, c, 123, a', c', a", c",) which have pro- 
duced jugular but no radial waves. 
When auricular extrasystoles originate in the 
pacemaking area, i.e., at the normal site, the electro- 
cardiograms are identical in shape with those of the 
normal; the only distinguishing feature is their pre- 
maturity. The ventricle usually responds after a 
normal P-R interval, (the measure of the conduction 
time in electrocardiograms), and its complex is the 
same as the other rhythmic beats because it follows 
the normal path in the conduction system (Figs. 124, 
Pig. 127.—Auricular 
extrasystole showing the 
superposition of P and 
T waves (P'T'). 138 
THE ARRHYTHMIAS 
125, i26). The premature auricular contraction often falls at such time 
that its complex is superimposed upon the T wave (Fig. 127), so that upon 
superficial examination the P wave (auricular beat) appears absent. 
Careful scrutiny, however, indicates that 
the composite P-T wave is somewhat 
taller and thicker than the P wave alone 
(Fig. 126). As has been stated, “ ectopic” 
auricular contractions which originate in 
an abnormal site outside the pacemaker 
show their origin by change of complex. 
This is exemplified in Fig. 128, which 
demonstrates beats starting from different 
ectopic foci (A, Ex. 1; A, Ex. 2); these 
abnormal complexes are deviated upwards 
and resemble the normal. This probably 
indicates an origin close to the pacemaker. 
It is to be noted that in this instance the 
ectopic beats are neither premature nor 
are they followed by compensatory pauses; 
the only feature differentiating them from 
the normal is their slight difference in form 
from that of the rhythmic P wave. 
Clinical Recognition of Extrasystoles 
(Premature Contractions) .—It should be 
emphasized that arrhythmias, especially 
extrasystoles and paroxysmal tachycardia, 
are often transient; hence they may not 
be present at the time patients present 
themselves for examination. As will be 
pointed out, however, the patient’s de- 
scription of his sensations is usually so 
clear and vivid, that the physician can 
often venture not only the diagnosis of a 
cardiac irregularity, but even its type. 
On the other hand it should be remem- 
bered that irregularities do not always 
cause subjective sensations. Here natur- 
ally the diagnosis must be made by the 
physician’s objective examination. 
Only occasionally can a clinical dif- 
ferentiation between auricular and ven- 
tricular extrasystoles be made without 
graphic tracings. Hence, in what follows, the recognition of either type 
is meant except when otherwise stated. 
Fig. 128.—Auricular extrasystole coming from two ectopic foci, A.E X. 1, A.E X. 2. These beats are neither premature 
nor followed by compensatory pauses. Their ectopic origin is denoted by the difference in form from the normal rhythmic 
complex (P wave). THE ARRHYTHMIAS 
139 
Isolated extrasystoles, occurring once in several normal beats, and fol- 
lowed by long (compensatory) pauses are readily diagnosed. When inter- 
polated (q. v.) or when occurring in showers (multiple extrasystoles), their 
recognition is more difficult. If the premature contraction is frustrane, that 
is, if its course in the ventricle is improperly directed or the beat itself is not 
sufficiently powerful to open the aortic valves, there is no corresponding 
pulse beat at the wrist; otherwise, the extrasystole causes a stronger or weaker 
pulse beat. Depending entirely upon the mechanics of intraventricular 
pressure affecting the aortic cusps, one or two cardiac sounds of varying 
intensity accompany the premature contraction. If the extrasystoles open 
the aortic valves, and the latter subsequently close, a premature first and a 
premature second sound accompany the extrasystole, just as with a normal 
beat. These sounds are however fainter than those of the normal beat. 
If the ventricular pressure remains lower than the aortic, a premature first 
sound alone is heard. Only rarely is this sound too faint to be audible. 
While graphic methods of registration are required to determine the exact 
length of the compensatory pause (Fig. 112), distinct shortening of the latter 
is readily determined by palpation at the wrist. Marked differences in the 
duration of the compensatory pauses characterize auricular, rather than 
ventricular, extrasystoles. The likelihood of a premature contraction being 
auricular is increased if it produces a fairly strong pulse beat; the weaker or 
absent pulse beat is more characteristic of a ventricular premature contrac- 
tion. It is occasionally possible to distinguish auricular from ventricular 
extrasystoles by observation of the jugular pulsations, for in the ventricular 
type a large summation wave (corresponding to the polygraphic a and c 
waves, Fig. 112) may occasionally be seen. 
Coupled Rhythm.—Its diagnosis rests upon the clinical recognition of 
regularly recurring extrasystoles, that is, an extrasystole occurs after every 
rhythmic beat. Sometimes a type of coupling occurs in auricular fibrillation, 
especially as the result of digitalis medication. The distinction from the 
coupling just described can only be made from observation of the clinical 
characteristics of auricular fibrillation (q. v.). 
Extrasystoles occurring at irregular times and with varying force in a 
rapidly beating heart are most apt to be confused with auricular fibrillation, 
for, like the latter the heart and pulse are apt to be confusedly irregular. 
The clinical differential guide is observation of the jugular and of carotid 
beats to find out whether one can distinguish normal auricular and carotid 
waves in the neck; even then, differentiation is often impossible because of the 
rapidity of the pulsatile waves which makes it extremely difficult for the eye 
to decipher them. 
A. H. PAROXYSMAL TACHYCARDIA OF AURICULAR ORIGIN 
The term simple tachycardia should be applied to the common accelera- 
tion of the normal sinus rhythm, that is, to the usual types of rapid heart 140 
THE ARRHYTHMIAS 
action. The usual ventricular rate is then between no and 130 per minute. 
Paroxysmal tachycardia of auricular origin (paroxysmal auricular tachy- 
cardia) as shown by the electrocardiogram usually consists of auricular 
extrasystoles coming in attacks. In typical instances, there is extreme, 
abrupt acceleration of the normal rhythm, with an abrupt termination and 
return to the normal. The attack may last minutes, hours, or, more rarely, 
Figs. 129, 130.—Varying ventricular rates from a case of exophthalmic goiter recorded 
on different days. When the rate is 150 per minute (Fig. 129) the a-c interval is normal. 
When the rate is 225 (Fig. 130), the a-c interval is slightly diminished; the diastole is 
entirely abolished, the a wave falls with the v of the preceding beat. 
Fig. 129. 
Fig. 130. 
days. Like the single auricular extrasystole, it is basically due to the fact 
that the excitation wave and impulse follow an abnormal passage through 
the heart. Graphically studied, the attack is seen to begin with a definite 
“onset” and to end with a definite “offset.” Typical attacks are initiated 
Fig. 131.—-Paroxysmal tachycardia, 
rate, 130 per minute. Onset and offset 
not recorded. The a wave falls with 
the preceding v. 
Fig. 132.—Exophthalmic goiter. Ventricu- 
lar very much shortened conduction time (a-c 
interval) despite only moderate acceleration 
(simple tachycardia). 
and terminated by extrasystoles. The ventricular rate usually varies from 
170 to 200 per minute. The rapid heart action of simple and paroxysmal 
tachycardia is usually at the expense of diastole (Figs. 129-131). The con- 
duction time as well is occasionally diminished (Figs. 13 2-13 5). In some 
cases of exophthalmic goiter, I found diminished auriculo-ventricular con- 
duction time despite the fact that ventricular acceleration was not extreme 
(Figs. 132-135). 
Studied electrocardiographically, it is found that the paroxysms com- 
monly originate from an abnormal (“ectopic”) auricular focus. When the 
change in the auricular complex is not marked, an origin close to the normal 
pacemaker is assumed. When the auricular complex (the P wave) is 
deviated negatively, it indicates an origin in the lower part of the auricular 
musculature. THE ARRHYTHMIAS 
141 
Clinical Recognition of Simple Tachycardia and of Paroxysmal Tachy- 
cardia of Auricular Origin.—The former refers to rhythmic pulse and ventricu- 
lar action at the rate of about 120 or more per minute. Its recognition is 
simple in the vast majority of cases. It may be confused with the rapid 
heart action of auricular fibrillation, but the pulse of the latter will be found 
arrhythmic upon longer or shorter observation. Paroxysmal (auricular) 
tachycardia is also readily recognized by the rapid, regular heart action vary- 
Fig. 133. 
Fig. 134. 
Fig. 133, 134.—Exophthalmic goiter. Ventricular rate 120 per minute; simple tachy- 
cardia; shortened a-c interval. 
ing from 170 to 200 per minute, accompanied by a feeble and rapid pulse; 
by the regular rapid jugular pulsations in the neck, and by the characteristic 
onset and offset of the paroxysm, for an extrasystole with its compensatory 
pulse often initiates and completes the typical attack. During the attack 
rapid, regular heart action is so constant that the rate rarely varies more than 
two or three beats from minute to minute. Hence if the heart rate is counted 
carefully for an entire minute and then 
again for an entire minute a few minutes 
thereafter, the cardiac rate for both obser- 
vations will be found to be almost the 
same. This is another simple method of 
diagnosing paroxysmal tachycardia of 
auricular origin when the patient can be 
observed during the attack. Data or ob- 
servation, however, often can not be 
obtained by direct clinical observation 
because the attacks are apt to be transient, and one may entirely miss the 
attack, or miss its beginning or termination. In most instances, therefore, 
we shall have to depend upon the history of sudden beginning and termi- 
nation of the attack or upon the description of a sudden fluttering in the 
chest that begins or ends suddenly. In addition, we may obtain a fairly 
Fig. 135. — Exopthalmic goiter. 
Ventricular rate 130 per minute; 
simple tachycardia; a-c considerably 
decreased. 142 
THE ARRHYTHMIAS 
accurate description of the occurrence of an extrasystole by such accounts 
as: “The heart stops for a moment,” or: “There is a momentary faint feel- 
ing in the chest before or after the palpitation,” or: “ My heart knocks or 
kicks before it beats fast.” Intelligent and observing patients may give 
a sufficiently accurate account of the cardiac rate during the attack by asking 
them to tap with their fingers approximately as rapidly as they thought 
their heart was “palpitating.” 
The differentiation of paroxysmal tachycardia from auricular flutter 
(q. v.) and from the tachycardial attacks accompanying auricular fibrillation 
(q. v.) will be discussed under those arrhythmias. 
A. III. AURICULAR INCOORDINATION 
It will be noted that the three types of arrhythmia to be described— 
fibrillation, flutter and the intermediate form—result primarily from auricu- 
lar incoordination, hence this caption. An extreme degree of inchoate 
auricular activity results in auricular fibrillation. When incoordinate 
activity is less marked, it results in auricular flutter (also called auricular 
tachysystole). 
A. III. (1) AURICULAR FIBRILLATION 
A correlation of various statistics shows that auricular fibrillation com- 
prises approximately 40 per cent, of arrythmias from all causes. We know 
now that the great majority of cases which Mackenzie called nodal rhythm 
belong to this category. When auricular fibrillation is typical, ventricular 
activity is completely irregular in rhythm and force so that no two successive 
beats are alike. When induced experimentally in animals, the auricles show 
irregular tremulous fibrillating activity; sometimes and in some parts of the 
auricles the fibrillation is fine, and at other times and other places it is coarse. 
There is no uniformity in auricular contractility, although occasionally waves 
of fibrillation proceed with a fair degree of regularity over the entire muscula- 
ture. The auriculo-ventricular conduction system is bombarded, as it were, 
by numerous irregular impulses, only some of which can pass through 
the junctional tissue and excite the ventricle to irregular and discordant 
response. 
The polygram corresponds to the pathological physiology just described. 
In typical instances the radial tracing shows gross and complete irregularity 
in the force and rhythm of the radial beats; in other words, a grossly irregu- 
lar pulse. In the jugular, the representative of orderly rhythmic auricular 
contraction, the a wave, is absent (Figs. 136-150). It is said that fibrilla- 
tion is sometimes sufficiently coarse to produce small fibrillary reflux waves 
in the superior vena cava and jugular bulb; these are then indicated in the 
tracing as irregular wave-like lines. When found in mitral stenosis with a 
marked diastolic thrill, it seems to me that such fibrillary waves may be due, THE ARRHYTHMIAS 
143 
Figs. 136-149.—Different types of polygrams of auricular fibrillation. The radial 
tracings show varying degrees of irregularity of rhythm and force of the pulse beats; some 
are grossly irregular (for example Figs. 137, 143, and 146); others more nearly approach 
the normal pulse rhythm (Figs. 142, 147, 149). The jugular tracings are of the most 
varied types. Their pathognomonic characteristic is the absence of the rhythmic a wave 
regularly preceding the c. Small waves preceding the c are sometimes o.bserved (Figs. 136, 
137 and 139), but their incidence and size are irregular. The t wave may be split (Figs. 
144, 148) or may form a combined wave with the v (Figs. 147 and 149), especially when 
ventricular action is slow. 
Fig. 136. 
Fig. 137- 
Fig. 138. 
Fig. 139. 
Fig. 140. 144 
THE ARRHYTHMIAS 
Fig. 141. 
Fig. 142. 
Fig. 143- 
Fig. 144. 
Fig. 145- 
Fig. 146. THE ARRHYTHMIAS 
i45 
Fig. 147. 
Fig. 148. 
F*g. 149. 146 
THE ARRHYTHMIAS 
not to auricular fibrillation per se, but to turbulent diastolic ventricular 
eddies propagated as small waves from vibrations of the stiffened mitral 
valves, and transmitted directly through the heart muscle to the superior 
vena cava and jugular veins. Figure 151 shows fibrillary waves from a case 
Fig. 150.—Auricular fibrillation, anacrotic radial pulse. 
Fig. 151.—Auricular fibrillation with mitral stenosis showing presystolic (sc) and fibrillary 
if) waves. 
of mitral stenosis with a loud, exceedingly rough, diastolic murmur and 
thrill. There was in addition, a short, sharp, regularly recurring presystolic 
wave (Fig. 151, X) whose etiology is not clear. Electrocardiograms taken 
at that time preclude the possibility of its being an auricular wave. 
Fig. 152. 
Fig. 152 and 153.—Auricular fibrillation; sharp fall of pressure following the ventricular fill- 
ing wave. In Fig. 153, the radial pulse is quite rhythmical. Digitalis had been given. 
Fig. 153- 
In some jugular tracings of auricular fibrillation, a sharp rise and subse- 
quent fall of pressure succeeding the v wave is found (Figs. 152, 153). As 
already indicated, a completely irregular pulse accompanies auricular fibrilla- THE ARRHYTHMIAS 
147 
Figs. 154-158.—Auricular fibrillation illustrating the usual types of accompanying pulse irregularit: 
Fig. 154- 
Fig. 155. 
Fig. 156. 
Fig. 158. 
Fig. 157- 148 
THE ARRHYTHMIAS 
Fig. i6i.—Fairly regular fibrillation waves which at times resemble 
auricular flutter (q. v.). (Impure flutter). 
Fig. 159.—Small, fairly regular fibrillary (/) waves in parts of leads I and III. 
Fig. 160.—Fibrillation waves 
scarcely visible. THE ARRHYTHMIAS 
149 
tion in a great majority of cases (Figs. 154-158). Very rarely the pulse 
becomes absolutely regular as the result of digitalis medication, although 
fibrillation still continues (Fig. 153). 
Corresponding to the state of incoordinate hap-hazard auricular activity 
characteristic of auricular fibrillation, there is in the electrocardiogram 
an absence of regularly recurring auricular deviations; that is, P waves are 
Fig. 162.—Fine fibrillation waves. Note the absence of P waves. 
Fig. 163.—Various types of fibrillation waves, coarse and fine, in the same lead, 
Fig. 164.—Fairly regular fibrillation waves in parts of L II and L III. 
missing. In their place, there are undulations representing fibrillation, at 
rates between 350 and 900 per minute. These fibrillatory waves vary con- 
siderably in type. In short runs they may resemble the regular and rapid 
auricular activity of flutter (impure flutter); at other times the waves are 
coarse and arrhythmic, or are so small as to be scarcely distinguishable as 
separate deviations. Examples of these various types are shown in Figs. i5° 
THE ARRHYTHMIAS 
159—167. At present there is no clinical distinction based upon these differ- 
ences, except possibly in their reaction to quinidin (Chapter XX). 
In older people with cardio-sclerosis, or as a result of digitalis medica- 
tion, the pulse and heart action may be fairly regular in force and rhythm, 
Fig. 165.—Auricular fibrillation showing tachycardia in L I. Note the varying rates of 
ventricular rapidity in leads II and III. 
Fig. 166.—Auricular fibrillation with ectopic beats (extrasystoles, Ec.) 
Fig. 167.—Auricular fibrillation with coarse fibrillation. (Courtesy of A. E. Cohn.) 
so that graphic tracings are required in order to establish the diagnosis of 
fibrillation. In another clinical type of fibrillation, the pulse rate varies 
between 180 and 225 per minute, is small in volume and is easily compressible. THE ARRHYTHMIAS 
151 
Upon palpation, the individual beats appear equal in force. Clinically, 
this resembles paroxysmal tachycardia. Electrocardiographically, it is 
distinguished from the latter by the absence of P waves and by the absence 
of an “onset” and “offset” (Fig. 165). 
Abnormal “ectopic” beats are sometimes present in auricular fibrillation 
(Fig. 166, Ec.). They are erroneously called extrasystoles; the latter term 
is properly applicable only to premature beats which disturb an otherwise 
regular rhythm, and not to beats occurring in the complete irregularity of 
auricular fibrillation. 
Transient Auricular Fibrillation.—Only exceptionally is it possible to 
note sudden transitions from normal rhythm to auricular fibrillation. Such 
attacks may be the result of digitalis therapy. They are also found in exoph- 
thalmic goiter or in the crises of severe infections (for example, in pneumonia). 
They are by no means infrequent in older patients with cardiosclerosis in 
whom hypertension is a marked clinical feature (q. v. Carcio-Vascular 
Clinics). Attacks of auricular fibrillation, in addition, may occur in the 
decompensatory stages of all types of valvular disease, especially mitral 
stenosis. Its occurrence with auricular flutter has already been pointed out. 
Its presence in a patient with no temperature and with no sign of organic 
cardiovascular disease is very rare. Figure 168 is an example. It was taken 
from a child of eight, not neurotic, who had had several attacks of tonsillitis. 
Tonsillectomy had been performed two years previously. Shortly before 
she came under my observation, she suddenly felt her heart “jump:” this 
“jumping” has since been occasionally repeated. There were no gastric 
symptoms. The child was somewhat anemic and undersized. There were 
no signs of decompensation. The urine contained no abnormal elements. 
There was a very soft faint systolic murmur of functional nature at the apex; 
the murmur was not transmitted. The electrocardiogram (Fig. 168, L III) 
shows the above-mentioned short run of auricular fibrillation (A.F. . . . 
A.F.) following the ventricular extrasystole (V.Ex.). In addition, there is 
fairly marked sinus arrhythmia. There are several ventricular extra- 
systoles, (V.Ex.) in some of which the auricular beat is seen as a separate 
deviation (P). There is also an auricular extrasystole of sinus origin with an 
abnormal ventricular complex (L I, A.Ex.); which is not followed by a 
compensatory pause. 
Clinical Recognition of Auricular Fibrillation.—The pulse and ventricular 
irregularity of typical auricular fibrillation is sufficiently obvious to be readily 
manifest. At the apex there is marked irregularity in force and rhythm of the 
heart’s action. Sometimes scarcely two beats are alike. Indeed, the old 
term of a generation ago—delirium cordis—aptly describes the clinical 
impression. Sometimes there is fairly regular heart action lasting several 
seconds or longer. At the wrist, if all the cardiac beats are propagated and 
come through as pulse waves, the pulse, completely irregular, takes on a 
helter-skelter characteristic. In the neck, the carotids are correspondingly 152 
THE ARRHYTHMIAS 
Fig. 168.—Various parts of a continuous electrocardiogram. The leads are indicated by the numbers. 
Several ventricular extrasystoles (Ex), some showing distinct auricular beats (P'). are seen. An auricular 
extrasystole of sinus origin and followed by an abnormal ventricular complex is shown in L I (A.Ex.). In 
L III a short run of auricular fibrillation (AF-AF) followed by a ventricular extrasystole (V.Ex.) is shown. THE ARRHYTHMIAS 
153 
irregular; the jugular pulsations are usually too rapid to be individually 
identified. If there are many frustrane ventricular contractions (so-called 
pulse deficit), the radial seems fairly regular in force and rhythm, for it is 
mainly the small and weaker beats which produce the picture of complete 
irregularity: Ausculation at the cardiac apex will readily reveal these small, 
numerous, discordant beats. Indeed, in thin persons, mere inspection of the 
apical region shows the characteristic arrhythmic ventricular action of 
auricular fibrillation. 
The “ectopic” beats (erroneously called “extrasystoles”), occasionally 
present in auricular fibrillation, can sometimes be recognized even when 
ventricular action is rapid and irregular, because they are commonly followed 
by momentary (not compensatory) pauses, and by beats much louder and 
stronger than themselves. In the tachycardial attacks occurring with auric- 
ular fibrillation, there is usually no sudden beginning or termination; there 
is no onset or offset, the beats are sufficiently irregular in force and rhythm 
to be palpable and are apt to be interrupted with the typical gross irregu- 
larity of auricular fibrillation; after the attack, a completely irregular pulse 
is again present. These are data which serve in the differentiation between 
this type and the paroxysmal (auricular) tachycardia already discussed. 
In auricular fibrillation with coupled rhythm, and fairly slow and regular 
ventricular activity and pulse, or in those rare instances of a perfectly regular 
pulse following digitalis medication, differentiation from normal rhythm 
or from extrasystolic arrhythmia can only be made by direct observation of 
the jugular pulsations. If distinct auricular waves can be recognized, their 
presence serves to exclude fibrillation. 
A. m. (2) AURICULAR FLUTTER—AURICULAR TACHYSYSTOLE 
In this type the auricles beat regularly and rapidly from 225 to 350 times 
per minute. Since the ventricle cannot respond at a like rate, heart block 
(q.v.), incomplete or complete, results. If the block be incomplete at a 
2:1, 3:1, or 4:1 ratio, it is evident that the pulse remains regular, the rate 
depending upon the ratio. If incomplete heart block be present with con- 
stantly varying auriculo-ventricular ratios, the pulse becomes irregular. 
The polygraphic recognition of auricular flutter may be difficult, for the 
auricular waves in the polygram are often small and distorted by respiration. 
Lewis contends that when the pulse is irregular in auricular flutter, the arrhy- 
thmic groups of radial beats form exact multiples, so that auricular flutter 
may be diagnosed from the radial curve alone. I have not found this to 
apply to some cases of flutter that I measured and attempted to diagnose in 
this manner. When auricular waves are well marked (Figs. 169, A and B, 
Fig. 170), flutter is readily recognized. In the interpretation of the degree of 
block, it must be remembered that, when incomplete, the a-c interval may 
be abnormally prolonged; this may then give the appearance of shortened 154 
THE ARRHYTHMIAS 
Fig. 169.—Tracing of auricular flutter. A and B were obtained on different days. 
a, b, c are continuous. In A, the auricular rate is 210; in B, 245 per minute. The numbers 
on the radial beats denote their respective lengths in multiples of Jo seconds. The block 
is complete in A (a and b) and changes from incomplete to complete in c. The block is 
incomplete in B (a and part of b) and then later becomes complete. 
Fig. 170.—Auricular flutter. The numbers on the radial beats denote their respective 
lengths in multiples of seconds. The auricular impulse and its corresponding ventricular 
response are shown by arrows. THE ARRHYTHMIAS 
i55 
conduction time, for the ventricle has probably responded, not to the 
immediately preceding auricular beat, but to the one previous (indicated by 
arrows, Figs. 170, 171; the conduction time is approximately 0.4 second). 
Partial heart block with a 3 :1 rhythm is shown in Fig. 173. 
The pulse is almost regular throughout, although there are 
shorter and longer beats indicative of change in auriculo- 
ventricular ratio. In other instances of flutter there may 
be found a change from partial to complete block, or the 
reverse (Fig. 169). 
An electrocardiographic example of auricular flutter with 
incomplete and complete block in the same electrocar- 
diogram is shown in Fig. 172. Rapid, regular auricular 
activity is best seen in L II and III. The ventricular rate is 
75; the auricular, 300 per minute; that is, incomplete block 
at a 4: 1 ratio was present. The P and T waves are oc- 
casionally superimposed. The P waves are contiguous and 
distinct in L II and III. They are scarcely discernible in L 
I; this is characteristic of auricular flutter. At a later date, 
while the auricular speed remained the same (300 per minute), 
the ventricular rate varied from 60 to 100 per minute. 
There is no group-proportion discoverable in the varying 
ventricular rates; complete heart block is present. After 10 
drachms of tincture of digitalis, given over a period of 10 
days, there was no diminution of auricular speed; the ventric- 
ular activity was arrhythmic. There was also a difference 
in the heights of the R deviations. This difference was not 
of respiratory origin; it may have been due to differing 
degrees of ventricular excitability from digitalis medication. 
The electrocardiogram (Fig. 172) was derived from a case of 
acute endopericarditis without decompensation; flutter 
developed during the course of acute rheumatic joint 
manifestations. In this instance, digitalis did not have the 
effect sometimes found in flutter with cardiac decompen- 
sation, namely, first, auricular fibrillation; later, the resump- 
tion of normal rhythm with cessation of medication (Chapter 
XX). As stated, there was no decompensation in this case. 
The rhythm became normal only when the joint symptoms 
subsided, the temperature had reached the normal, and the 
endocardial lesion had become quiescent. From the clinical 
course, I conclude that the cause of the flutter was the acute 
endocarditis. In what manner the latter produced the arrhy- 
thmia it is impossible to state. One year after the onset of 
the disease, the rhythm was still normal and the signs of the endocardial 
lesion (mitral regurgitation) were the same. 
Fig. 171.—Auricular flutter—partial heart block. The occasional difference in the lengths of the radial are due to 
changes in the ratio of auriculo-ventricular rhythm or possibly to differences in conduction time. 
Contains 15 Auricular 
Beats; 3:1 Rhythm 156 
THE ARRHYTHMIAS 
Clinical Recognition of Auricular Flutter.—In the exceptional instances of 
this arrhythmia in which the veins of the neck are tremendously distended 
by each auricular systole, the diagnosis becomes at once evident on inspection 
and estimation of the rapidity of the jugular pulsations. The later, however, 
are more often minute and scarcely distinguishable as separate beats. 
Fig. 172.—Auricular flutter, incomplete heart block, the ratio is 4:1. The auricular 
rate is 300 per minute; the ventricular, 75. Note that the P waves in L I are almost indis- 
tinguishable; they are prominent and contiguous in L II and L III. 
Although not thus definable as individual waves, the jugular pulsations are 
usually sufficiently distinct for one to note that their number greatly exceeds 
that of the ventricular contractions. In this manner the diagnosis of flutter 
may occasionally be ventured; but most diagnostic reliance must finally be 
placed upon recognition of heart block with the varying auriculo-ventricular 
ratios typical of flutter. If, for example, incomplete heart block at a con- 
stant 2 :i ratio is present, the pulse and heart action are regular; the rate, 
usually between 90 and 120. If the auriculo-ventricular ratios are incon- THE ARRHYTHMIAS 
IS7 
stant and constitute changing multiples, as from 2:1 to 4 :1 or the reverse, 
the diagnosis of flutter can be made from the fact that the ventricular pauses 
also constitute similar multiples. If the auriculo-ventricular ratio constantly 
varies, however, or if complete heart block is present, then ventricular action 
and pulse become arrhythmic and clinically resemble the irregular action of 
frequent extrasystoles or of auricular fibrillation. Clinical differentiation 
Fig. 173.—Paroxysmal auricular tachycardia. F....F (L III) shows change of 
paroxysmal tachycardia to auricular fibrillation (absence of regularly recurring auricular 
complexes). (Courtesy of A. E. Cohn.) 
of auricular flutter may then be possible from auricular fibrillation by the 
absence of its characteristic jugular pulse; and from extrasystoles by the 
absence of compensatory pauses. 
A. III. (3) INCOORDINATION INTERMEDIATE BETWEEN FLUTTER AND 
FIBRILLATION 
In a few instances, I have observed a state of irregular auricular activity 
which may be regarded, I believe, as an intermediate stage of incoordination 
between flutter and fibrillation. The auricular rate was usually between 
no and 150; the beats, as shown by the differences in the auricular com- 
plexes, came from many scattered ectopic foci; the auricular rhythm was 
irregular. The ventricular rhythm was also irregular; the rate usually 
between 100 and 120. Many of the ventricular electrocardiographic com- 
plexes varied in the length of their deviations; very few ventricular extrasys- 
toles were present; the picture betokened impulses following many vicarious 
paths in the ventricle. Although the electrocardiographic picture of the 158 
THE ARRHYTHMIAS 
ventricular arrhythmia was not as distinct as was the case with the irregular 
(ectopic) auricular activity, it seemed probable that ventricular arrhythmia 
was likewise due to incoordinate activity, but of a degree considerably less 
than in ventricular fibrillation (q. v.). 
The patients who presented this rare and interesting arrhythmia were in 
the terminal stages of pneumonia or of cardionephritis. It seemed possible, 
from the clinical pictures presented, that several factors deserved etiological 
consideration: e.g., in pneumonia, the toxins; in cardionephritis, retained 
exerementitious products. In all, there were probably changes in the 
intracardiac circulation which profoundly affected the nutrition of the general 
musculature, as well as of the auriculo-ventricular conduction system. 
Although, as indicated, irregular auricular activity may be due to two 
fundamentally different causes (abnormal passage of impulses and auricular 
incoordination), it is interesting to note the gradations and transitions in 
auricular irregularity. First are the isolated auricular extrasystoles. These, 
if numerous and originating outside the sinus area, give rise to auricular 
tachycardia. The rate is then between 150 and 225. If auricular speed be 
increased from 225 to 350 per minute, flutter results. This appears to be 
the limit of regular auricular activity in man. Any further increase in rate 
results in irregular activity—auricular fibrillation. The fibrillatory waves 
may be as numerous as 900 per minute. In some instances it is possible 
to observe a transition from auricular flutter to fibrillation. Between flutter 
and fibrillation is the intermediate type of inchoate auricular activity 
just described. There is in addition another transition stage called impure 
flutter (Fig. 161) that can be diagnosed only from the electrocardiogram. 
The fibrillary waves show a transient tendency to become as regular as those 
in flutter, to again break into the irregular waves of auricular fibrillation. 
Cause of Auricular Fibrillation.—In this connection it is of interest to 
point out the newest physiological conception of the fundamental cause 
of auricular fibrillation. Some years ago, the latter was thought to be due to 
pathological changes (usually sclerotic in nature) in the pacemaker. But 
some cases that fibrillated during life did not show such changes at autopsy. 
It was also assumed that auricular fibrillation was caused by frequent abnor- 
mal excitation originating in or outside the sinus area. The actual explana- 
tion for auricular fibrillation seems to lie in the fundamental observations 
of Garrey and Mines. Working independently, they showed that if the 
auricles are made to fibrillate by faradization, and if then a portion of the 
auricular tissue (e.g., the auricular appendix) is clamped off, fibrillation will 
continue in the remainder of the auricular musculature. With removal 
of the clamp, the entire auricle again fibrillates. They also found that if 
the auricle is incised trouser-fashion so that sufficiently broad auricular strips 
remain connected by sufficiently broad auricular bridges, and then the auricle 
be faradized anywhere, contraction of the auricular strips will continue long 
after faradization has ceased. Garrey calls such contractions “circus con- THE ARRHYTHMIAS 
159 
tractions” for he assumes that such an excitation wave travels in a continuous 
circuit, and that the impulse spreads from fiber to fiber. In the experimentally 
slit auricle, the excitation impulses are irregularly and sinuously blocked 
because of the difference in refractory periods of the incised fiber groups and 
because impulse conduction is interfered with. Thus while the excitation 
continues its “circus” path, the auricular strips are actually contracting at 
various times and with varying energies. The result is the incoordinate, 
auricular tremor which we denote clinically as auricular fibrillation. Lewis 
and his coworkers have recently corroborated Garrey’s observations in a 
series of experimental and clinical papers. Lewis has likewise shown that 
auricular flutter is due to the breaking up of the excitation wave in a series of 
sinuous movements. He regards flutter (especially impure flutter), as a 
gradation of auricular fibrillation. 
Concisely stated, therefore, auricular fibrillation is essentially due to any 
influence—toxic, nutritional, reflex etc.—which breaks up the simple, normal, 
single, “circus” wave starting from the pacemaker by interfering with and 
blocking the propagation of the wave. 
Fig. 174.—Nodal extrasystoles showing coincidence of P and R waves. (Courtesy of 
A. E. Cohn.) 
Premature contractions having their origin in the auriculo-ventricular 
node are called nodal extrasystoles. The auricular and ventricular impulses 
start simultaneously, or almost so from their nodal origin. Hence, in the 
jugular tracings, the a and c waves, and, in the electrocardiogram, the P 
and R waves fall coincidentally (Fig. 174). In the phlebrogram, a large 
summation a-c wave is produced (Figs. 175, 176); in the electrocardiogram, 
A. NODAL EXTRASYSTOLES i6o 
THE ARRHYTHMIAS 
the small P is often lost in the larger R complex. This type of extrasystole 
cannot be diagnosed without the use of graphic methods. 
B. VENTRICULAR ARRHYTHMIAS 
1. Ventricular Extrasystoles.—As with the auricular type, ventricular 
extrasystoles depend upon the abnormal passage of the impulse through the 
ventricle. 
Fig. 175.—Nodal extrasystole, graphically 
illustrated by the synchronous occurrence of 
the foot points of A'c'. 
Fig. 176.—Nodal extrasystole 
which has not produced a pulse 
wave. (Frustrane contraction.) 
Among other distinctions between such aberrant (heterogenetic) ven- 
tricular beats (ventricular extrasystoles) and those arising in the auriculo- 
ventricular node'—true idioventricular rhythm—is the one of rate. The 
node originates rhythmical contractions at a speed of from 25 to 40 per minute 
(heart block). The rate of extrasystolic ventricular rhythm is between 130 
and 200 per minute. 
In ventricular extrasystoles (Fig. 112) the auricle follows its normal 
rhythm and contracts when the ventricle is in a refractory state; and, as a 
Fig. 177. 
Fig. 178. 
Figs. 177, 178.—The ventricular extrasystole plus the compensatory pause is slightly 
greater than two rhythmic beats. (Increased compensatory pause, C.P.). 
result, there is no ventricular response until the next succeeding ventricular 
contraction. Thus the time of ventricular prematurity, added to the 
compensatory pause, equals two rhythmic beats. This fact is of value in the 
recognition of ventricular extrasystoles from radial tracings alone, or in poly- 
graphic tracings in which the jugular is not sufficiently clear to be of value. THE ARRHYTHMIAS 
161 
In auricular extrasystoles, both chambers contract prematurely, and the 
succeeding pause may or may not be compensatory (Fig. 120). Ventricular 
extrasystoles, however, are sometimes followed by pauses which are not 
exactly compensatory in length (Figs. 177-180). Occasionally extrasystoles 
Fig. 179.—Ventricular extrasystole plus compensatory pause is less than two rhythmic 
beats (diminished compensatory pause (C.P.). 
Fig. 180.—Ventricular extrasystole without compensatory pause (G.P.). 
Fig. 181.—Extrasystole which is not “premature.” r' is greater than P (the pause 
following the extrasystole). 
occur so late that they lose their characteristic “prematurity” (Fig. 181). 
The amplitude of the radial beat following the extrasystolic pause in any type 
of premature contraction is usually larger than that of the normal beat, and 
expresses graphically its greater strength (Figs. 112, 114, 181). This is some- 
times regarded as indicative of favorable cardiac recuperative power. 
B. II. INTERPOLATED VENTRICULAR EXTRASYSTOLES 
When the cardiac rate is slow, ventricular extrasystoles do not always 
interfere with the time of the next normal ventricular contraction; these are 
known as “interpolated” extrasystoles. This type of premature contraction 
occurs in the course of normal rhythm, and is not followed by a compensatory 
pause. Such extrasystoles are found in mid-diastole and in groups, rarely as 
isolated phenomena. Figure 88 is therefore of interest because it shows a 
single interpolated extrasystole (L II Ex.). The electrocardiogram was 
derived from a male patient 54 years old who was extremely decompensated. 
He had had syphilis 30 years previously. The Wassermann blood reaction 162 
THE ARRHYTHMIAS 
was positive. He had severe myocarditis and marked left ventricular hyper- 
trophy. Fluoroscopy and radiography demonstrated aneurismal dilatation 
of the entire thoracic aorta. Under vigorous antiluetic, and the usual treat- 
R \/ 
L V 
GASE- 
APEX 
We> 
Fig. 182.—Schematic view of types of ventricular extrasystoles arising from various 
ectopic foci, showing the direction of the corresponding R deviations. R.V., right 
ventricle. L.V., left ventricle. 
ment for decompensation, the patient improved to such an extent that at 
the last examination he considered himself well. The electrocardiogram 
is of further interest because it gives some corroboration of the clinical find- 
ings: Negative T in L I and an abnomrally wide R deviation inL I and III, 
Fig. 183.—Ventricular extrasystole (V.Ex.) 
from right ventricle near the base. (Courtesy 
of A. E. Cohn.) 
Fig. 184.—Ventricular extrasystolfe 
(V.Ex.) from left ventricle near the 
base. (Courtesy of A. E. Cohn.) 
presumed evidences of myocarditis (Chapters IX, XXXII); the positive R I 
and negative R II and R III also confirm the clinical and orthodiascopic 
findings of a markedly hypertrophic left ventricle. THE ARRHYTHMIAS 
163 
Electrocardiograms of ventricular extrasystoles vary considerably from 
normal complexes because their course in the heart (Fig. 70, J. K.) is quite 
different from that followed by the normal excitation wave. The extrasys- 
toles may originate in either ventricle. There is experimental evidence that 
extrasystoles arising from the various areas of the ventricular musculature— 
so-called ectopic foci (Lewis)—conform 
to definite electrocardiographic types. 
By analogy, it is possible to determine 
in the human being the abnormally 
excited areas in the ventricles from 
variations in the form of the atypical 
electrocardiograms (Fig. 182). How- 
ever, one must remember that the 
abnormal path followed by extrasystoles 
need not necessarily indicate a corre- 
sponding abnormal ventricular focus as 
its starting point. 
Although studies of the various 
forms of ventricular extrasystoles are of 
considerable interest and importance, 
there is at present no correlation, except in isolated cases, between these 
different types and the clinical condition. It is to be noted that the P 
deviation is usually not visible because it is lost in the larger ventricular 
complex; occasionally, however, it appears at such time that it distinctly 
notches the R wave. 
A schematic view of the usual aberrant foci and their corresponding 
electrocardiographic types is given in Fig. 182; it shows the direction of the R 
and T deviations in the L I and II. These types are also illustrated by exam- 
ples of ventricular extrasystoles derived from human beings (Figs. 183, 184, 
185). That there are intermediate types coming from various intermediate 
aberrant foci one may assume from certain rare cases of ventricular extrasys- 
toles with heart block showing gradual and regularly varying abnormal 
complexes (Fig. 186). It is as if the abnormal excitation had affected, 
ladderwise and in progression, various successive areas of the ventricular 
musculature. 
Instances of regularly recurring extrasystoles (coupled rhythm) are given 
in Figs. 187, 188-A, 188-B. Occasionally several originate in the same 
ectopic focus (Fig. 189), producing short runs of paroxysmal tachycardia of 
ventricular origin. 
Fig. 185.—Ventricular extrasystole 
(V.Ex.) from the left ventricle near the 
apex. (Courtesy of A. E. Cohn.) 
B. III. AUTOMATIC VENTRICULAR ACTIVITY—VENTRICULAR ESCAPE 
This rare type consists in the sudden “escape” of the ventricle from auricu- 
lar control, and results in ventricular automatism or independent activity. 
In a few reported cases, there was marked retardation of the auricular, and, 164 
THE ARRHYTHMIAS 
in most instances, of the ventricular rate. In the case that I observed there 
was never any marked pulse retardation (Fig. 190); the lowest rate was 55 per 
minute, and the auricular speed was not abnormally slow. Its etiology will 
be discussed in a later chapter (Chapter XI). 
When auricles and ventricles beat at such rates 
that their waves and deflections in the tracings are 
regularly superimposed, their origin in or near the 
auriculo-ventricular node is assumed; these are called 
nodal extrasystoles (q. v.). Such simultaneous 
action is seen in parts of the electrocardiogram of 
the case of “ventricular escape” (Fig. 191 S); however 
it is apparently due to temporarily identical auricular 
and ventricular speeds, for as these vary, varying a-c 
and c-a (Fig. 190) or P-R and R-P intervals (Fig. 191) 
soon occur. Besides, nodal beats are usually either 
regularly interpolated in the normal rhythm, or when 
premature, are followed after longer or shorter com- 
pensatory pauses by the normal dominant beat. 
The assumption of nodal extrasystoles is therefore 
not warranted, I believe, by the electrocardiogram of 
the case of ventricular escape here shown (Fig. 191), 
all of whose complexes are alike. Backward conduc- 
tion (q. v.) from ventricle to auricle, a rare reversal 
of the cardiac mechanism, also requires consideration 
as a possible explanation. In a case of backward con- 
duction reported, that rhythm, when established, 
showed a definite ventriculo-auricular conduction 
time similar to the normal, and was accompanied by 
marked ventricular slowing. This conception if 
applied to my case would necessarily assume that the 
“reversed mechanism” suddenly and irregularly 
ceased from time to time in those parts of the tracing 
which do not show a “retrograde conduction time” 
(c-a or R-P intervals) of less than one fifth second, 
and that frequently, isolated beats were retrograde. 
This hypothesis is highly improbable and is not sup- 
ported by the electrocardiogram. Rihl describes a 
case of occasional automatic ventricular action pro- 
duced by vagal pressure. Lewis reports a case of 
rheumatic mitral stenosis with decompensation; 
digitalis had been given with resulting ventricular automaticity (“ventricular 
escape,” Lewis). Gallavardin, Dufourt, and Petzetakia describe three 
cases with slow pulses (in one case the rate was 36 per minute) in which 
there was no clinical evidence of organic cardiovascular disease. In two, 
Fig. i 86.—Extrasystoles arising from various ventricular foci, as shown by the differences in R complexes. Com- 
plete heart block present. (Courtesy of A. E. Cohn.) THE ARRHYTHMIAS 
165 
numerous polygraphic and electrocardiographic tracings showed the 
occurrence of ventricular automatism; in all three, it was readily evoked by 
ocular and vagus pressure, and by atropin injection. The writers suggest 
two causes for the phenomena: Relative retardation of the auricular as com- 
Fig. 187.—Regulary recurring ventricular extrasystoles (V.Ex.); coupled rhythm (pulsus 
bigeminus). (Courtesy of A. E. Cohn.) 
Fig. i88^4. 
Fig. i 885. 
Figs. 188A and 188B.—Frustrane ventricular extrasystoles; coupled rhythm. 
pared with the idio-ventricular rate, that is, the ventricular rate is increased 
when the ventricle beats independently of auricular control; or acceleration 
of the ventricles beyond the auricular rate. Two of their cases had very 
slow auricular rates occurring either spontaneously or induced by the methods i66 
THE ARRHYTHMIAS 
Fig. 190.—Ventricular escape. Part of a long series of tracings showing at times normal rhythm; at others, ventricular automatic 
activity (ventricular escape). Retrograde conduction from ventricle to auricle (backward conduction) could be excluded because of the 
irregular c-a intervals. 
Fig. 189.—Short runs of paroxysmal tachycardia of ventricular origin (V.Ex. 1, 2, 3, 4, 5, etc.). The normal beats are marked P-R-T. 
Fig. i89A. THE ARRHYTHMIAS 
167 
described; the third showed no auricular retardation on vagus or ocular pres- 
sure, or after atropin injection. The arrhythmia in the first cases was appar- 
ently due to relatively increased idioventricular (auriculo-ventricular nodal) 
rapidity beyond that of the sinus node. Except for a very slight change in 
the complexes of the automatic ventricular beats in two of the cases—the 
absence of a very small S wave—all of the complexes were identical. In digi- 
Fig. 191.—Ventricular escape. Sections of a continuous tracing. At X the ventricle 
“escapes” from auricular control and beats independently at such rate that auricle and 
ventricle occasionally contract synchronously (superposition of P and R waves). The 
rhythm is normal in the other parts of the tracing. 
talis poisoning, Cohn and Fraser have occasionally found either identical 
auricular and ventricular speeds, or ventricles beating more rapidly than 
auricles, with ventricular escape. In the case I here report there was at no 
time any marked pulse retardation—the lowest rate was 55—nor was there 
any evidence of auricular slowing, although there was, at the periods of ven- 
tricular automatism, some slight difference between auricular and ventricular 
rapidity. Except for occasional somewhat slower beats, the idioventricular 
and normal ventricular rates were approximately the same. Slight sinus 
arrhythmia was sometimes present, but was not more marked than is fre- 
quently found as a physiological phenomenon. 
B. IV. PAROXYSMAL TACHYCARDIA OF VENTRICULAR ORIGIN 
As with the auricular, paroxysmal tachycardia of ventricular origin is 
marked by a rapid succession of ventricular extrasystoles (Fig. 189). It i68 
THE ARRHYTHMIAS 
differs from auricular paroxysmal tachycardia 
(auricular tachystole) in that the latter originates 
a new rhythm by starting in an auricular focus 
outside of the normal pacemaker, while paroxysmal 
ventricular tachycardia consists of a sudden run 
or shower of ventricular extrasystoles. The 
diagnosis can naturally be made at once from the 
electrocardiogram (Fig. 189) by the difference in 
form of the extrasystolic beats. A paroxysm 
usually comprises from 8 to 10 premature con- 
tractions; very exceptionally, there may be as 
many as 25 or 30. Sometimes there are several 
runs of rapidly recurring paroxysms that make up 
an entire attack, so that to the patient, it may seem 
one long-continued paroxysm. 
Clinically, paroxysmal ventricular tachycardia 
can be distinguished from the auricular variety by 
its shorter course; by the pulse deficit, for many of 
the extrasystoles do not produce pulse waves; by 
the strong “thumps” heard at the apex indicating 
the extrasystoles; by the absence of regular rapidly 
recurring auricular (a) waves in the neck; and 
finally by the fact that ventricular tachycardia is 
not controlled by pressure of the vagus in the neck. 
Fig. 192.—Ventricular fibrillation. (After Robinson and Bredeck.) 
B. V. VENTRICULAR INCOORDINATION 
i. Ventricular Fibrillation, similar to the 
incoordination of auricular fibrillation, is due to 
incoordinate ventricular activity. It has only 
been very rarely studied electrocardiographically 
in the human being (Fig. 192). When it occurs, 
it is usually followed by death within a very few 
minutes. The reason for this is that the inchoate 
ventricular contractions have no propulsive effect 
upon the blood in the ventricular chambers, and 
hence blood is improperly or not at all supplied to 
the systemic circulation. However one case has 
been reported in which the patient lived 30 hours 
after an attack of ventricular fibrillation lasting 15 
minutes. It is assumed that ventricular fibrilla- 
tion is sometimes the cause of sudden death in 
some cases of cardiac decompensation, in which at 
autopsy no other cause can be found. THE ARRHYTHMIAS 
169 
2. Bundle-branch Lesions.—The simplest type of ventricular incoordina- 
tion consists of asynchronous ventricular contraction from lesions of the main 
branches of the auriculo-ventricular bundle. Such lesions may be permanent 
or temporary. In bundle-branch lesions, the impulses originate in the A-V 
Fig. 193.—Lesion of the right branch of the conduction system. Conduction takes 
place along the left branch. The initial deflections are tall and positive in L I, and tall 
and negative in L III. (Courtesy of A. E. Cohn.) 
Fig. 194.—Lesion of the left branch of the conduction system. Conduction takes 
place along the right branch of the bundle. The initial deflections are tall and positive in 
L III, and tall and negative in L I. (After E. P. Carter.) 
bundle (junctional tissue) before its bifurcation, and follow the unblocked 
branch in the ventricle (Fig. 70, H.I.). Experimental and clinical obser- 
vations have shown that bundle-branch lesions produce characteristic 170 
THE ARRHYTHMIAS 
electrocardiograms. Microscopic sections of post-mortem specimens have 
corroborated and confirmed the electrocardiographic evidence in a few 
instances. 
Since the excitation wave travels along the healthy branch and excites 
the corresponding ventricle to contraction, the electrocardiogram in the 
various leads shows the characteristics of contraction of one ventricle alone, 
without the counterbalanced contraction of the other. Hence for example, 
in lesions of the right branch, by far the more common, the initial deflections 
show left-sided conduction. The deviations are tall and positive in L I, and 
deep and negative in L III (Fig. 193). The opposite is the case in the left- 
sided lesions (right-sided conduction) (Fig. 194). A further characteristic 
of bundle lesions is the abnormal length of time required for the completion 
of the excitation wave, the width of the R usually being about 0.10 second. 
In addition, the deviations are frequently notched, the ventricular complex 
usually diphasic. The T wave is commonly deviated in a direction opposite 
to that of its accompanying R peak. 
The electrocardiograms of cardiac hypertrophy are somewhat similar to 
those of branch lesions. They are differentiated by a narrower R, the lesser 
amplitude of their deflections, the direction of the T which is the same as 
that of the R, and by the tri- or quadriphasic character of the ventricular 
complexes. 
The cardiac rate is normal in bundle branch lesions. The diagnosis can 
occasionally be made by hearing a definite split first sound at apex, probably 
due to the asynchronous ventricular activity present in such cases. 
C. TRUE BRADYCARDIA 
This term should be applied only to types of slow, regular heart action 
in which there is normal conduction time from auricle to ventricle and in 
which each beat represents a sequential auriculo-ventricular contraction. 
Thus defined, it has its proper place in a classification of arrhythmias. 
Otherwise, when loosely used in a sense of slow pulse rate (so-called spurious 
bradycardia), it takes no cognizance of auricular rhythm or of auriculo- 
ventricular conduction, and may therefore haphazardly include such diver- 
gent cardiac irregularities as auricular fibrillation, extrasystoles, and heart 
block (q. v.). It is difficult to fix a definite rate as typical of true bradycardia. 
Cardiac and pulse rates ranging from 60 to 65 per minute are by no means rare 
in normal healthy adults, especially in those with rather marked vasomotor 
instability, flushed hands and face, sudden irregular pallor, and cold and 
moist extremities. Examples of regular, slow heart action due to extra- 
cardial causes are given in Figs. 195-199. An instance due to salicylate of 
soda is shown in Fig. 198. 
In the electrocardiogram of true bradycardia, all the ventricular com- 
plexes are alike; there is slow, regular heart action. Thus, Fig. 199 taken THE ARRHYTHMIAS 
171 
from a young epileptic with a normal cardiovascular apparatus shows regular 
sequential heart beats at the rate of 50 per minute. 
Clinical Recognition of True Bradycardia.—The rate is rarely below 40 
per minute; the cardiovascular apparatus is often organically normal. 
Fig. 195. 
Fig. 196. 
ftAcuAi- rate- so pen M. 
Fig. 197. 
Figs. 195-197.—True bradycardia from patients with gastric symptoms and normal hearts. 
- W-8 PB« M. 
Fig. 198.—True bradycardia caused by salicylate of soda. 
Fig. 199.—L I, True bradycardia. The auricles and ventricles beat sequentially. The 
rate is 50 per minute. 
Since in true bradycardia the auricles and ventricles beat sequentially, 
the jugular waves (a waves) are seen to precede the carotid pulsations 
(c waves). True bradycardia must be differentiated from the slow heart 
action found in heart block. In the former, the jugular pulsations occur with 
the same frequency as the carotid, the ventricular, and the pulse beats; in 172 
THE ARRHYTHMIAS 
heart block, jugular pulsations occur more frequently than the carotid. 
Jugular pulsations may be rendered more prominent by having the patient 
lay flat and then inspecting the right side of the neck. By holding a white 
card in the space between the jugular and the carotid, it is sometimes possible 
to reflect the jugular pulsations on the card by placing the patient in a proper 
light. 
D. ARRHYTHMIAS PRODUCED BY ABNORMAL SEQUENCE OF CONTRACTION 
OF AURICLES AND VENTRICLES 
This sequence may be disturbed either at the pacemaking area (the 
sinoauricular node) or at the junctional tissues (the atrio-ventricular 
node). 
D I (i) Sinus Arrhythmia.—This pulse irregularity is produced both by 
physiological and abnormal influences which affect the sinus region, the 
pacemaker of the heart. Sinus arrhythmia of the physiological respiratory 
type consists of alternate moderate acceleration and retardation, a waxing 
and waning of the pulse rate, corresponding to expiration and inspiration 
respectively. The arrhythmia is of vagal origin and is ascribed to difference 
in the vagal inhibitory tone from phasic changes in respiration. It is a 
physiological phenomenon in children (Figs. 200, 201) and young adults 
(Fig. 202) (“the youthful irregularity” of Mackenzie), although it is by no 
means uncommon as a normal variation in the middle-aged, especially upon 
forced deep respiration. Sinus arrhythmia due to other causes is also 
illustrated (Figs. 203-206). 
In the electrocardiogram, sinus arrhythmia is recognized by varying 
lengths of the pauses between the beats (Fig. 207); there is no difference in 
any of the complexes unless phasic respiratory variations (Chapter IX) are 
present. In such cases there is a gradation in the height of the ventricular 
complex due to changes in the position of the heart from movement of the 
diaphragm during respiration. 
Clinical Recognition of Sinus Arrhythmia.—The physiological type with 
normal pulse rate is readily diagnosed because it wanes and waxes with inspira- 
tion and expiration, respectively. The pathological types of sinus arrhyth- 
mia do not usually show this correlation. Their clinical diagnosis is then 
made by the comparatively slow pulse rate with irregularly long diastolic 
pauses. The interventricular interval may be sufficiently long to block out 
an entire auriculo-ventricular contraction, thus producing sino-auricular 
block (q. v.). The distinction between sinus arrhythmia of the non-respira- 
tory type and auricular fibrillation with slow and fairly regular ventricular 
activity depends upon the observation of the jugular pulsations. In the 
former, there are regularly recurring jugular waves (a waves) which precede 
the carotid pulsations; in the latter this relationship naturally does not exist 
since auricular contractions are absent. THE ARRHYTHMIAS 
T73 
Fig. 202.—Retardation (sinus slowing) from holding the breath at the end of inspiration. The arrow indicates the point 
at which normal breathing ceased (from a young healthy adult). 
Fig. 201.—Moderate sinus arrhythmia (from a 
normal child). 
Fig. 203.—Slight sinus arrhythmia at the time of crisis in recovery from pneumonia. I, Inspiration; E, expiration. 
BREATH HEt-O at EldD OP )NSP|<\AT/0tf. 
CA (TOTID 
Pig. 200.—Carotid pulse of a normal child, the breath 
ing curve with the inspiratory (I) and expiratory (E) 
phases, and corresponding difference in pulse rate are shown. 
C AHOT-ID 
Pu L JATI6IV/ i74 
THE ARRHYTHMIAS 
Fig. 206.—Sinus arrhythmia, non-respiratory type, from an adult suffering from severe intestinal hemorrhage. 
Fig. 204.—Sinus arrhythmia during critical defervescence in a child recovering from tonsillitis. 
Fig. 205.—Respiratory sinus arrhythmia in a boy of 15 with an aortic lesion. THE ARRHYTHMIAS 
175 
D. I. (2) SINO-AURICULAR BLOCK 
Occasionally abnormal influences affect the vagus or its endings in the 
sino-auricular node so that an entire beat is blocked out. This arrhythmia 
is rare. There is stoppage of the entire heart (Figs. 208, 209). The pause is 
Fig. 207.—Electrocardiogram showing sinus arrhythmia of respiratory origin. Note the 
varying lengths of the diastolic pauses. (After T. Stuart Hart.) 
Fig. 208.—Electrocardiogram showing sino-auricular block (S.A.), due to smoking. 
usually somewhat less than that required for two normal contractions; when 
extreme, the pause may represent the time required for three, or even four 
normal beats. I have seen two cases due to tabagism, one of whom had an 
organically normal heart; the other patient had myocarditis with mild 
decompensatory symptoms. Figure 208 is taken from one of these patients. 176 
THE ARRHYTHMIAS 
In addition to the sino-auricular block there is moderate tachycardia. This 
double effect of nicotine—moderate tachycardia and sino-auricular block— 
was probably due to the varying action of the poison upon the ganglionic 
terminations of the vagus and sympathetic nervous system (Fig. 210). In 
Fig. 209.—Electrocardiogram showing sino-auricular block (S.A.) due to smoking. 
the other case, a smoker with myocarditis and decompensation, ventricular 
extrasystoles (Fig. 209) were also present; sino-auricular block disappeared 
two days after smoking was stopped; the extrasystoles ceased some days 
later when compensation was restored 
by the use of digitalis and theobromin 
sodium salicylate. 
D. I. (3) BLOCKED AURICULAR BEAT 
This is a very rare arrhythmia. It 
is usually due to digitalis medication. 
Ventricular action does not follow the 
blocked auricular impulse, consequently 
there is a quiescent period equivalent 
to two beats (Fig. 211). It is dis- 
tinguished from extrasystoles by the 
absence of the characteristic small pulse 
wave and of the extrasystolic heart 
sounds; from sino-auricular block, only 
by recognition of an auricular jugular wave in the former and its absence 
in the latter. 
Fig. 210.—Diagram showing the 
effect of nicotine upon the ganglionic 
terminations of the vagus and accel- 
erators. (Modified from Cushny) V, 
vagus; A.C., accelerator fibers; Ven, 
ventricle; A, auricle; M.S., cardiac 
musculature; G.V., ganglia at vagus 
termination; G.S., ganglia at termina- 
tion of sympathetic nerve; SP.C., 
spinal cord. THE ARRHYTHMIAS 
177 
D. n. (1) PROLONGED CONDUCTION TIME 
This represents the simplest type of heart block. Various factors cause 
moderate prolongation of the impulse from auricle to ventricle, that is, of the 
P-R time. These are chiefly digitalis medication, myocarditis and acute 
endocarditis. I have also observed lengthened conduction in several 
Fig. 21 i.—Blocked auricular beat showing absence of ventricular response, as well as 
prolonged conduction time. (Courtesy of A.E. Cohn). 
patients with auricular extrasystoles of functional origin. Cases of extreme 
prolongation of the P-R time up to or even more than 0.50 of a second some- 
times occur. For example, Fig. 212 is the electrocardiogram of a male 
patient, aged 62, who had myocarditis and nephritis; at the time that the 
Fig. 212.—Electrocardiogram showing very slow ventricular rate (37 per minute) 
with a P-R time of 0.8 second. (From a patient with severe myocarditis.) 
Fig. 213.—Prolonged conduction time. P-R, 0.3 second (from a patient with acute 
rheumatic endocarditis). 
electrocardiogram was taken he was suffering from a third attack of severe 
decompensation: dyspnoea, oedema of the legs and ascites. He died later 
with uremic symptoms. The electrocardiogram shows a ventricular rate of 
37 per minute with a conduction time of 0.8 second. A less marked instance 
is shown in Fig. 213. Prolonged conduction time can only rarely be recog- 
nized clinically by observing the prolonged interval between the a and c 
waves in the neck. 178 
THE ARRHYTHMIAS 
D. II. (2) SHORTENED CONDUCTION TIME 
The normal P-R interval is from 0.16 to 0.20 second. This interval— 
the conduction time from auricle to ventricle—is occasionally shortened in 
both paroxysmal and simple tachycardia; however, as already stated, rapid 
cardiac activity in these arrhythmias occurs mainly at the expense of diastole. 
D. II. (3) BACKWARD CONDUCTION FROM VENTRICLE TO AURICLE 
This exceedingly rare anomaly is exemplified in Fig. 214, a case reported 
by Williams and James. It shows the auricular (P), regularly following the 
ventricular beat. Backward conduction was also corroborated in that case 
by fluoroscopic examination. The patient, a laborer of 51, suffering from 
diarrhea for one year, had attacks of Stokes-Adams syndrome. The cardio- 
vascular system was apparently normal organically. The arrhythmia per- 
sisted for many months and was not affected by atropin injections. Finally, 
the rhythm again became normal. The writers suggest as possible etiolog- 
ical factors abnormal vagus control or a toxic cause. 
D. H. (4) (a) INCOMPLETE HEART BLOCK 
In its simplest type, this consists in the absence of ventricular response to 
auricular impulses. There is a geometric ratio between auricular and ven- 
tricular beats; for example, the ventricle responds to every second, third or 
fourth auricular impulse. Such cases are termed incomplete heart block at 
a 2:1, 3:1, etc. ratio respectively (Figs. 215, 216). The ventricle and pulse 
beat rhythmically unless disturbed by occasional premature ventricular 
contractions (Fig. 216, c). In other types of incomplete block the ventricular 
response varies irregularly from one ratio to another; the ventricle, for 
example, answers haphazardly every second or third or fourth auricular 
impulse. Thus the pulse becomes correspondingly irregular. In both incom- 
plete and complete block, the auricles beat rhythmically at approximately 
normal speeds, 60 to 80 times per minute. In incomplete heart block, the 
ventricular rate is considerably diminished; as stated, its regularity depends 
upon the auriculo-ventricular ratio. The clinical recognition of a 2:1 heart 
block lies in noting that the jugular (a) pulsations are twice as numerous as 
the c waves. In addition the auricular beats may be occasionally heard aS 
fainter heart sounds interspersed between the ventricular beats. 
D. II. (4) (b) COMPLETE HEART BLOCK 
This is said to exist when there is no relationship between auricular and 
ventricular speeds. The ventricle follows its own inherent independent 
rhythm (Figs. 217-226). This is called the idioventricular rate, the rate 
initiated by the atrioventricular node, and is usually between 25 and 40 THE ARRHYTHMIAS 
179 
Fig. 214.—Electrocardiogram showing backward conduction from ventricle to auricle. (After William and James.) 
Figs. 215, 216.-—Incomplete block with a 2:1 ratio. In Fig. 216 there is a premature ventricular contraction (c'). 
The preceding auricular beat is not premature. The pause following r' is not compensatory but is equal to an entire 
rhythmic beat. 
RATE ko PER M 
Fig. 215. 
wptcre otocic z.:l i8o 
THE ARRHYTHMIAS 
Figs. 219, 220.—Complete heart block showing occasional superposition of a and c waves. 
Figs. 217, 218.—Complete heart block. 
Fig. 217. 
Fig. 218. 
Fig. 219. 
Fig. 220. THE ARRHYTHMIAS 
i8i 
Fig. 221.—A.B., Complete block. In A the block is only apparently incomplete because the auricular speed is exactly 
twice that of the ventricle. In B, continuous with A, there is a slight variation in auricular and ventricular rates; the a-c 
interval becomes progressively smaller until a and c are superimposed, showing that the exact doubling of speeds and the 
apparently normal a-c interval in A were purely accidental. 
Fig. 222.—Complete block; ventricular rate 25 per minute; auricular rate 105 per minute. This tracing was corroborated 
by an electrocardiogram. 
j Fig. 223.—Complete heart block with irregular ventricular action. The shorter radial beats are underlined. 182 
THE ARRHYTHMIAS 
Fig. 224.—Complete heart block with a ventricular extrasystole (r'). The ventricular rate is 27; the auricular rate is 81 
per minute. The pause following the extrasystole is not compensatory; it equals a rhythmic beat. 
Fig. 225.—AandB. Parts of continuous tracing. Heart block with auricular fibrillation. Some of the weaker heart beats 
are shown as small pulse beats at r' and r". Others are frustrane. Note the absence of a waves in the phlebogram. 
Fig. 225A. 
Fig. 225B. THE ARRHYTHMIAS 
i«3 
Fig. 226.—A and B. Taken from the same patient on different days. (1) and (2) are continuous. There are two ventricular 
rates: 66 and 47 per minute. The auricular speed is constant at 66 per minute. The conduction time (a-c, interval) of the faster beats 
(within brackets) is extremely prolonged (from 0.5 to 0.55 second). The slower beats apparently occur when the conduction time 
is so prolonged that the ventricle no longer answers the auricular impulse. The ventricle and auricle then beat at the same speed, 
the auricle following the ventricular contraction. Another possible interpretation is that the ventricle acts temporarily as pace-maker, 
and the auricle answers impulses generated in the atrio-ventricular node. (See Backward Conduction.) 
Fig. 226A. (1) 
Fig. 226A. (2) 
Fig. 226B. 184 
THE ARRHYTHMIAS 
per minute. Complete heart block represents the purest type of regular 
heart action. Polygraphically, the carotid (c) waves are identified in the 
usual manner. Since the auricular 
speed varies but slightly if at all, 
the auricular (a) waves are recognized 
by their occurrence at regularly 
spaced intervals (Figs. 217, 218). 
Because of their varying rates, the 
a and c waves occasionally fall simul- 
taneously with, and are superimposed 
into, taller or broader peaks (Figs. 
220-223). Figure 221 resembles in- 
complete block, because auricular 
and ventricular rates temporarily 
correspond. Examinations of longer 
sections, however, show that this 
ratio is accidental, for, with slightly 
varying auricular and ventricular 
speeds, there is at first closer ap- 
proximation and finally superposition 
of the a and c waves (Fig. 221 B). 
In complete heart block, auricular 
activity occasionally is abnormally 
rapid, so that its ratio to ventricular 
beats is as four or five to one. While 
regular rhythmic activity is the rule 
in complete heart block, there are ex- 
ceptions; as, for instance, slight vari- 
ations in the ventricular rhythm 
(Fig. 223). The regularity may also 
be disturbed by ventricular extra- 
systoles. These are usually single 
(Fig. 224, r'). The pause following 
them is not compensatory, but is 
equal in length to a rhythmic beat. 
Very rarely such extrasystoles are 
multiple (Figs. 225, A and B, r' r"). 
The case illustrated by Fig. 225 
was originally one of complete heart 
block with a rhythmic ventricular 
rate of 35, and an auricular speed of 
72 per minute, as demonstrated by poly graphic and electrocardiographic 
tracings. The auricular beats could be plainly heard in the interventricular 
Fig. 227.—Complete heart block. The ventricular rate is 43, the auricular, 75 per minute. THE ARRHYTHMIAS 
i85 
Fig. 228.—A and B are parts of the same electrocardiogram. A shows incomplete block with a 2:1 rhythm. B shows 
complete block. i86 
THE ARRHYTHMIAS 
pauses. Through inadvertence on the part of the nurse, digitalis was 
administered for several weeks after having been ordered discontinued. The 
pulse then became arrhythmic. The auricular beats were no longer heard. 
“Extrasystoles” (i.e., ectopic aberrant beats), most of which were frustrane, 
were heard at the apex. The tracing showed some of them registered in both 
the radial and jugular curves (Fig. 225, A, B, /, c', a", c"); others, in the 
jugular only (Fig. 225, A, B, c"); regularly recurring auricular waves could 
not be identified. Digitalis was discontinued. After two weeks, electro- 
Fig. 229.—Complete heart block. The ventricular rate is 30; the auricular, 75 per 
minute. (Courtesy of A. E. Cohn.) 
cardiographic tracings showed that the original type of heart block was pres- 
ent, and the auricular beats were again heard. From the ausculatory evi- 
dence, from the absence of auricular waves in the jugular, and from the fact 
that digitalis poisoning sometimes induces auricular fibrillation and “extra- 
systoles,” it seems probable that the polygraphic tracing represents heart 
block, auricular fibrillation, and aberrant beats—a unique instance of digitalis 
poisoning in a patient with complete heart block. 
Another rare example of peculiar disturbance of ventricular rhythm is 
that represented in Fig. 226 A and B, taken from a patient on successive 
days. Digitalis had not been given. The radial tracing showed ventricular 
arrhythmia due to abrupt and reciprocal changes from faster to slower rates. 
The faster rate was 66; the slower, 47 per minute. The auricular speed 
remained constant at 55. A study of the polygraphic tracing corresponding 
to the faster beats (included in the brackets) showed an extremely long 
conduction time, the a-c interval varying from 0.50 to 0.55 of a second. Occa- 
sionally the ventricle did not respond but contracted at the idioventricular 
rate (complete heart block). This condition existed for one week. There- 
after electrocardiograms taken frequently for a period of one year always 
showed complete block (Fig. 209), the auricular speed being 100 to no, 
the ventricular 45 to 50 per minute. The block was uninfluenced by atropin 
injections. THE ARRHYTHMIAS 
1:87 
Comparatively rapid ventricular rates are occasionally encountered in 
heart block. For example, in one of my cases, the ventricular speed was at 
one time as high as 77 per minute and the rhythm slightly irregular. The 
Fig. 230.—Complete heart block with extrasystoles (Ex.). The latter occur after every ventricular beat: The auricular 
rhythm (P waves) remains undisturbed. 
following curves are examples of heart block with varying auricular and ven- 
tricular rates. Figure 227 is that of a man of 60 with myocarditis and 
aortitis, and shows complete heart block. Figure 228 is given in two parts: 188 
THE ARRHYTHMIAS 
A, illustrates incomplete block with a 2 : i rhythm; B, taken a few moments 
later, shows complete block. In section A the block only appears incomplete 
because of slightly varying auricular and ventricular speeds. This tracing 
was taken from a young man who had peritoneal tuberculosis with irregular 
fever and who, except for the arrhythmia, presented no sign of cardiac disease. 
The lungs were normal. The patient had been in the habit of feeling his 
pulse before his illness and had always found it of normal rapidity, that is, 
about 70 per minute. The peritoneal tuberculosis became quiescent following 
laparotomy. The heart block continued. Atropin was injected several 
times without influencing the block. Its only effect was a slight transient 
increase of the ventricular rate. The patient died two years later as the 
result of an accident. A necropsy was performed. In the abdomen, omental 
tuberculosis was found. The lungs were normal; there were no enlarged 
glands at the pulmonary hilus. On careful macroscopic examination, the 
cardiac valves and musculature were found normal. Although the atrio- 
ventricular conduction system has not been microscopically examined, there 
was no evidence of any gross lesion at the site of the bundle. In other words, 
there was no apparent pathological change in the heart itself to account for 
the block. This case will be etiologically discussed in another connection 
(Chapter XI). 
Another case of complete heartblock is shown in Fig. 229. A case of 
heartblock with extrasystoles is shown in Fig. 230. 
Clinical Recognition of Heart Block.—The ventricular rate in complete 
heart block is usually between 25 and 40, although rates as low as 8 per 
minute have been reported. The auricular beats are often heard in the 
apical region or at the third left interspace as soft, faint, distant sounds 
interspaced between the ventricular contractions. Synchronous with the 
sounds of the auricular contractions, jugular pulsations unaccompanied by 
carotid beats may be seen in the neck. There are no compensatory pauses in 
the regular ventricular action of heart block, thus distinguishing this arrhy- 
thmia from extrasystoles. Incomplete heart block with changing ventricular 
ratios, for example from 2:1 to 3: 1, requires differentiation from sino-auricular 
block; this distinction is based chiefly upon the auricular contractions which 
are present and sometimes audible in the first type of arrhythmia, and upon 
the absence of auricular beats, visible or audible, in sino-auricular block 
It is sometimes possible to diagnose complete heart block merely from obser- 
vation of the pulsation of the neck. Prominent pulsations indicative of the 
simultaneous contraction of auricle and ventricle (a-c wave), or of the auricu- 
lar and the ventricular filling wave (a-v) can then be observed. Similar 
large jugular waves, sometimes seen with extrasystoles (cV, a'c' or c'a waves), 
are differentiated from those in heart block by the slow ventricular rate of 
the latter. 
Pulse Alteration—Pulsus Alternans.—This is a disturbance, not of 
rhythm but of strength of the ventricular contractions, and therefore of the THE ARRHYTHMIAS 
189 
Fig. 231.—Normal rhythm; slight alternation. 
Figs. 232, 233.—Alternation following extrasystoles. 
Fig. 232. 190 
THE ARRHYTHMIAS 
pulse beats; strong beats regularly alternate with weaker ones. Alternation 
of the pulse is often not sufficiently marked to be detected by palpation (Figs. 
231, 232), hence the importance of radial tracings for its diagnosis. It may 
be occasionally diagnosed by observing alternating difference in the systolic 
blood pressure readings when making blood pressure observations. It occurs 
in tachycardia, especially when paroxysmal, and results then directly from 
the ventricular acceleration. Alternation is also fairly common after 
extrasystoles (Figs. 232, 233). 
Alternation is usually found in patients with dangerously weakened 
myocardium and is commonly regarded as of grave prognostic import. 
Indeed, most patients with heart disease and decompensation who have an 
alternating pulse die within one year. However, alternation is occasionally 
found in patients with normal hearts, or as a result of digitalis medication. 
The mechanism of alternation is still the subject of many conflicting opinions 
and theories. The condition has been ascribed to disturbance of the function 
of contractility; to the fact that not all the ventricular fibers contract with 
the smaller beat; or because the systoles of the stronger are of longer duration 
than those of the weaker beats, thus encroaching upon the rest period of the 
latter. Electrocardiographic tracings of patients with alternation have 
partly upset some of these hypothesis. For example, there is no evidence 
that varying amounts of ventricular musculature are involved or that the 
path followed by the weaker differs from that of the stronger contractions; 
nor is there any difference in duration of their contraction times. Einthoven 
suggested an explanation similar to that involved in the irregular pulse 
excursions of auricular fibrillation, namely, that the increased blood pressure 
of the stronger contractions acting upon the weakened myocardium prevents 
the heart from emptying itself at the next systole, and consequently produces 
a smaller pulse. This theory puts the explanation a step nearer, but scarcely 
explains the rhythmic alternating regularity in pulse pressure. 
Pulsus Paradoxus.—This irregularity is indicated by a gradual waning 
and waxing in the strength of the pulse beat with respiration, but without 
any change of rhythm. It has been regarded as characteristic of pericarditis 
with effusion. I have found it especially frequent in cases of severe myo- 
cardial insufficiency. Occasionally the pulse becomes so weak and small 
as to be scarcely perceptible on palpation. 
Hemisystole is mentioned for the sake of completion of the subject of 
arrhythmias. It refers to inaction of one ventricle at the same time that the 
other is in systole. One can scarcely conceive how, in any pumping mechan- 
ism like the heart with its well-balanced pulmonary and systemic circulation, 
the circulation can be carried on by one ventricle without its fellow for any 
appreciable length of time. Up to the present, there has not been reported 
any undoubted clinical case of hemisystole. THE ARRHYTHMIAS 
191 
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Medical Congress, 1913, Section 6, Part 2, 258. 
Cushny, A. R.: Pharmacology and Therapeutics; Edition 1913. 
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Einthoven, W., and Korteweg, A. J.: On the Variability of the Size of the Pulse in Cases of 
Auricular Fibrillation; Heart, 1913-1916, VI, 107. 
Fulton, F. T.: Auricular Flutter; Archives of Internal Medicine, 1913, XII, 475. 
Gallavardin, L., Dufourt, P., et Petzetakis: Automatisme Ventriculaire Intermittente; 
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Gaskell, W. H.: On Innervation of the Heart, with Special Reference to the Innervation 
of the Heart of the Tortoise; Journal of Physiology, 1883, IV, 43. 
Griffith, T. W., and Cohn, A. E.: Remarks on the Study of a Case Showing Greatly 
Lengthened A-C Intervals, etc.; Quarterly Journal of Medicine, 1910, III, 126. 
Halsey, R.: A Case of Ventricular Fibrillation; Heart, 1915, VI, 67. 
Hart, T. S.: Abnormalities of Myocardial Function; Archives of Diagnosis, 1915, 26. 
Hart, T. S.: Paroxysmal Tachycardia; Heart, 1912-1913, IV, 128. 
Hertz, A. F., and Goodhart, G. W.: The Speed Limit of the Human Heart; Quarterly 
Journal of Medicine, 1908-1909, II, 213. 
Hering, H. E.: Die nomotope und heterope Automatic des Herzens; Kongress fur Innere 
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Hirschfelder, A. D.: Simple Methods in Cardiac Diagnosis; The Virginia Medical Semi- 
Monthly, 1913, XVIII, 573. 
Jolly, W. A., and Ritchie, W. T.: Auricular Flutter and Fibrillation; Heart, 1910-1911, II, 
177. 
Levine, S. A.: Observations on Sino-Auricular Heart Block; Archives of Internal Medicine 
1916, XVII, 153. 
Levy, A. G.: The Genesis of Ventricular Extrasystoles under Chloroform; Heart, 1913- 
1914, V, 299. 
Lewis, T.: Clinical Electrocardiography; Edition 1913. 
Lewis, T.: Auricular Flutter; Heart, 1912-1913, IV, 171. 
Lewis, T.: Pathology of the Heart Function; Lancet, October 10, 1914, 883. 
Lewis, T.: Irregular Action of the Heart in Mitral Stenosis; Quarterly Journal of Medicine, 
1908-1909, II, 336. 
Lewis, T.: Graphic Registration of the Heart Beat. 
Lewis and others: Observations on Flutter and Fibrillation; Heart, VII, 127; 1919-1920; 
Heart, VIII, 83; 311, 1921. 
Mackenzie, J.: Diseases of the Heart; 3d Edition, 238. 
Mines: On Dynamic Equilibrium in the Heart; Journal of Physiology, XLVI, 349, 1913. 
Neuhof, S.: Transient Auricular Flutter Accompanying Acute Endo-pericarditis; New 
York Medical Record, December n, 1913. 
Neuhof, S.: Auricular Flutter occurring during Rheumatic Endocarditis; New York 
Medical Record, 1914, LXXXVI, 63. 
Neuhof, S.: Independent Ventricular Activity occurring during Acute Articular Rheuma- 
tism; Archives of Internal Medicine, 1915, XV, 169. 
Neuhof, S.: Sino-auricular Block Due to Tobacco Poisoning; Archives of Internal Medi- 
cine, 19x6, XVII, 659. 
Neuhof, S.: Independent Ventricular Activity; Archives of Internal Medicine, 1915, XV, 
169. 192 
THE ARRHYTHMIAS 
Neuhof, S.: Complete Heart Block with Rapid Irregular Ventricular Activity; American 
Journal of Medical Sciences, 1913, CXLV, 513. 
Parkinson, J., and Mathias, H. H.: Tachycardia of Auricular Origin and Flutter with 
Phasic Variations in Auricular Rate and in Conduction; Heart, 1915, VI, 27. 
Rihl, J.: Klinische Beobachtungen ueber atrioventrikulaere Automatic mit Bradykardie; 
Zeitschrift fuer Expt. Pathologie und Therapie, 1911, IX, 496. 
Ritchie, W. T.: Further Observations of Auricular Flutter; Quarterly Journal of Medicine, 
1913-1914,VII, 1. 
Ritchie, W. T.: Auricular Flutter. 
Robinson and Bredeck: Ventricular Fibrillation in Man with Cardiac Recovery; Archives 
of Internal Medicine, 1917, XX, 725. 
Rothberger, C. J., und Winterberg, H.: Studien ueber die Bestimmung des Ausgang- 
punktes ventrikulaerer Extrasystolen mit Hilfe des Elektrokardiogramms; Archiv 
fuer die ges. Physiologie, 1913, CLIV, 571. 
Rothberger, C. J., und Winterberg, H.: Ueber die Entstehung und die Ursache des Herz- 
flimmerns; Zentralblatt fuer Herz und Gefaesskrankheiten; 1914, VI, 453. 
Sutherland, G. A.: Auricular Flutter with Acute Rheumatic Carditis; British Journal of 
Diseases of Children, 1914, XI, 337. 
Thayer, W. S.: Adams-Stokes Syndrome; Persistent Bradycardia . . . Remarkable- 
Prolongation of the As-Vs Interval; Archives of Internal Medicine, 1916, XVII, 13. 
Thayer, W. S., and Peabody, F. W.: A Study of Two Cases of Adams-Stokes Syndrome 
with Heart Block; Archives of Internal Medicine, 1911, VII, 289. 
Williams, H. B., and James, H.: Reversal of the Cardiac Mechanism; Heart, 1913-1914, V, 
109. 
White, P. D.: Alternation of the pulse; a common clinical condition; American Journal of 
Medicine, 1915, CL, 82. CHAPTER XI 
THE ARRHYTHMIAS—THEIR CLINICAL ETIOLOGY AND THERAPY 
At the outset it is important to emphasize that, although certain types 
of arrhythmias may be associated with various pathological entities, almost 
any irregularity may be the result of non-organic, neurogenic, so-called 
“functional” causes. From the standpoint of etiology, therefore, the 
primary essential is to discover, if possible, whether the arrhythmia is of 
functional or of organic origin. Therapy will be only briefly indicated here; full 
details will be found in the chapter on Circulatory Remedies (Chapter XX). 
Sinus Arrhythmia.—As a physiological phenomenon, sinus arrhythmia is 
quite common not only in children and young adults but also in the middle- 
aged. It is, however, also present in organic heart disease. I have found 
it for example in young individuals suffering from aortic and mitral disease. 
The hearts of these patients were compensated; they had not received digita- 
lis. Possibly this arrhythmia in patients with heart disease can be regarded 
as a favorable sign, since it is an evidence of physiological vagal control. 
Sinus arrhythmia is also frequent as a phenomenon after febrile respiratory 
catarrah terminating by critical defervescence. The arrhythmia is then 
regarded by many observers as the result of toxic or infectious myocarditis. 
Its innocent nature, however, is proven by its disappearance within a few 
days, and by the absence of all signs of cardiac disease. Sinus slowing is 
sometimes a purely pathological occurrence; it then bears no relation to 
breathing. For example, it occurs in severe secondary anemia following 
sharp hemorrhage. I have observed two such cases. In both, the sensorium 
was clear and the arrhythmia gradually disappeared with improvement in the 
anemia. In such instances, I believe sinus arrhythmia is due to nutritional 
changes in the sino-auricular node, or to increased vagus inhibition on the 
part of the cardio-inhibitory center. In another case, an adult whose heart 
at necropsy showed marked cardiosclerosis involving the endocardium, 
mitral valves, aorta and the coronaries—the pulse ranged between 50 and 60 
per minute during the last year of life. Polygraphic tracings showed sinus- 
arrhythmia. Microscopic examination of the sino-auricular node was not 
made; sclerotic changes in that region may have been the etiological factor. 
Pathological sinus arrhythmia, or sinus arrhythmia encountered in febrile 
crisis, requires no medication. When due to the other serious etiological 
factors above mentioned, treatment should be directed to them rather than 
to the arrhythmia itself. 
Sino-auricular Block.-—This is usually the result of digitalis poisoning. 
It has also been produced by pressure over the vagus in the neck, by pressure 
upon the eyeballs (oculo-cardiac reflex) in human beings, and by various 
193 194 
THE ARRHYTHMIAS 
experimental procedures in animals. It is occasionally the result of tobacco 
poisoning (Figs. 208, 209). Otherwise it is exceedingly rare as a clinical 
phenomenon. The condition itself requires no medication unless accompa- 
nied by dizziness; atropin sulphate is then sometimes of value. At the be- 
ginning the dose should be small, gr. 3d250 three times daily before meals. 
The amount should then be increased up to the individual’s physiological 
tolerance. 
Extrasystoles.—Although there are many exceptions, auricular extra- 
systoles are usually of functional origin, while the ventricular are often of 
organic nature. When accompanying organic disease, auricular or ventricu- 
lar extrasystoles may mark the beginning of decompensation and then re- 
main as permanent arrhythmias. In acute heart failure, they are sometimes 
the forerunners of a fatal termination. The onset of exacerbations of acute 
endo- or pericarditis may be accompanied by extrasystoles. We do not 
know the exact manner in which organic cardiac lesions increase ventricular 
excitability and thus produce premature contractions; it seems probable, 
however, that impaired cardiac nutrition plays an important role when severe 
cardiac disease is present. 
When extrasystoles are found in cardiac failure, treatment of the latter 
(Chapter XIV) is the prime consideration. With the establishment of 
cardiac compensation, the extrasystoles usually disappear; when caused by 
endo- or pericarditis, the therapy consists mainly of salicylates, preferably 
sodium salicylate in large doses. My usual procedure is to give 10 grs. 
hourly for six doses unless tinnitus occurs. Thereafter, the same dose is 
given three times daily. Occasionally the addition of bromides is of value. 
Functional Extrasystoles of Extracardiac Origin.—Cerebellar and 
cerebral conditions which exert pressure directly or indirectly upon the 
cardio-inhibitory center can cause premature contractions. Such pressure 
factors apparently act by direct excitation of the vagus center. Thus a 
patient with cerebellar tumor and normal circulatory apparatus had occa- 
sional extrasystoles during the last few months of life. That they were due 
to pressure was demonstrated at operation for the removal of the tumor. 
The latter was deeply seated, each attempt at its removal being accompa- 
nied by premature contractions. Acute gastric diseases with vago-excitive 
characteristics (belching, pyloro- and cardiospasm), less often intestinal 
disease, is occasionally accompanied by extrasystoles, usually auricular in 
type. Their etiology has been variously explained. The usual theory is 
that, after a meal, the distended stomach presses the diaphragm against the 
heart, thus embarrassing circulation. Another reason given is the action of 
absorbed toxic products upon the neurogenic cardiac control. In the ma- 
jority of cases that came under my observation, the extrasystoles occurred 
most frequently when the stomach was empty. Several of these patients, 
fluoroscoped after a barium meal, showed no gastric distention or other evi- 
dence of abnormal pressure against the diaphragm; in fact, their stomachs THE ARRHYTHMIAS 
195 
were contracted, and hypermotility was present. These observations 
nullify, I believe, the commonly advanced theories. The intimate physio- 
logical relationship between the nerves of the stomach and those of the heart 
lead me to believe that extrasystoles accompanying gastric disturbances 
are probably caused by reflex excitation of the cardiac nerves but the path 
followed by the reflex arc is not clear. 
Acute inflammation of the gall-bladder and bile ducts, with or with- 
out gastric symptoms, may also be accompanied by premature contrac- 
tions. Although the theory is based upon insufficient data, toxemia has been 
assumed as the etiological factor for such extrasystoles. The arrhythmia 
is often present very early in the disease, when extensive toxic absorption 
appears improbable. Similar to the views expressed with reference to extra- 
systoles in gastric disturbances, I believe that most cases occurring in gall- 
bladder disease are caused by reflex excitation of the neurogenic control of the 
heart, although at present the centripetal nerve-path involved is unknown. 
Peritonitis is another disease in which premature contractions may occur. 
One case of appendicitis, followed by general peritonitis and death in an 
elderly individual with cardiosclerosis, had ventricular extrasystoles at 
the onset of the attack; during the last few days of life, auricular fibrillation 
was present. It was impossible to decipher the varying roles played by 
toxemia and reflex nerve excitation in the production of these arrhythmias; 
in this case I believe both were factors. 
The onset and crisis of acute catarrhal febrile affections are frequently 
marked by premature contractions. The latter are generally regarded as 
evidence of toxic myocarditis. This relationship seems doubtful for several 
reasons. Most of the cases I have observed were not toxic: For example, the 
extrasystoles occurred with mild grippe and tonsillar affections in patients 
who scarcely felt ill. The arrhythmia was found at the crisis or immediately 
thereafter, that is, when the severe symptoms had disappeared. There were 
no circulatory symptoms. On clinical grounds, therefore, it seems probable 
that such extrasystoles are due to abnormal products (toxins?) flowing in the 
general circulation and affecting the cardio-inhibitory center, but not the 
myocardium. 
Regarding extrasystoles in pneumonia, it should at the outset be stated 
that this disease can insidiously cause severe cardiosclerosis (Chapter V); 
but this does not apply to premature contractions occurring in the acute 
stage of pneumonia. Unless circulatory symptoms are already present, 
pneumonic patients with critical or post-critical extrasystoles do not suffer 
from cardiac failure as a result of the arrhythmia. The latter usually dis- 
appears within a few days without any treatment. If myocarditis or other 
severe pathological damage to the heart caused these extrasystoles, symptoms 
of circulatory failure, instead of being absent, would be prominent. The 
present theory regarding crisis in pneumonia is that the system is at such times 
suddenly flooded with toxins elaborated in the pneumonia area. That the 196 
THE ARRHYTHMIAS 
cerebral centers become involved is shown by critical sweats and vasomotor 
symptoms. Correlating these observations, it seems most likely that such 
extrasystoles are the result of pneumonic toxins acting on thecardio-inhibitory 
center. 
Among drugs, the digitalis bodies, less frequently the salicylates, produce 
extrasystoles. When the former are given the arrhythmia is usually coinci- 
dent with the full therapeutic effect of the digitalis. Premature contractions 
are common in hypertensive diseases (Chapter XVII). Fright, nervousness 
and epileptic seizures, overindulgence in coffee, tea and tobacco, are addi- 
tional causes of premature contractions. Extrasystoles also occur in conjunc- 
tion with the vaso-motor symptoms of the climacterium. 
There still remains a group of patients in whom no cause for extrasystoles 
can be discovered. It is interesting in this connection to note that functional 
extrasystoles, even though they later disappear, are apt to recur after any 
slight disturbance (for example, overexertion, acute indigestion) which 
reflexly affects the normal inhibitory control. 
Finally, it should be emphasized that extrasystoles can occur in perfectly 
healthy individuals, young and old, in whom there is no evidence of cardio- 
vascular disease. Frequently these individuals are not cognisant of any pulse 
irregularity. The fact that individuals with healthy hearts can have pre- 
mature contractions had long been disputed, but its occurrence in them is by 
no means infrequent, and examination of such cases years later shows no 
evidence of cardio-vascular disease. 
General Therapy for Extra systoles.—Such underlying diseases as gastric 
disturbances, appendicitis, etc., naturally require their appropriate remedies, 
and the presence of extrasystoles in no wise affects the usual therapeutic indi- 
cation and procedures. Unless extrasystoles of reflex or neurogenic origin 
cause such subjective sensations as “fluttering in the chest,” transient faint- 
ness, etc., or are in themselves causes of circulatory failure (an exceedingly 
rare occurrence), they require no therapy. When medication is indicated, 
the bromides are of value, the dose is 15 to 30 grains, preferably given once 
daily. Another excellent drug for quieting the nervous system is luminal. 
The usual dose is 1V2 grains given once every morning. Atropine sulphate 
in small doses (gr. jdmo to Moo three times daily) is of use when the extrasys- 
toles are due to reflex gastro-intestinal disturbances. 1 have found the solid 
extract of suprarenal gland given in tablet form in one or two grain doses 
of special use when the extrasystoles are accompanied by vaso-motor dis- 
turbances. Digitalis has occasionally been advised because of its effect in 
increasing vagus inhibition. 
True Bradycardia.—The term has already been defined (Chapter X). 
It may appear as a rare congenital anomaly in patients with normal hearts 
and circulation. A sequential rhythm and pulse rate between 45 and 60 per 
minute is sometimes encountered in senile cardiosclerosis. Most cases of 
true bradycardia are of extracardiac origin. Patients with lead colic, and THE ARRHYTHMIAS 
197 
gastrointestinal disorders accompanied by abdominal pain, belching or diar- 
rhoea, are apt to have a slow pulse rate. This is probably due to reflex vagus 
inhibition from excitation of gastric and intestinal nerves. 
Catarrhal jaundice is not infrequently accompanied by true bradycardia, 
and is then usually ascribed to toxic myocarditis. In the patients whom I 
have observed, there was no evidence of the latter disease. The bradycardia 
in these cases may be ascribed to two causes: In those with cholemic symptoms 
it is probably of central inhibitory origin while in non-toxic cases with painful 
local symptoms, it is due, I believe, to reflex vagus inhibition from abnormal 
excitation of the nerve filaments surrounding the gall bladder. 
Appendicitis.—Slight bradycardia with pulse rates between 60 and 65 
per minute is occasionally encountered in this disease. Myocardial involve- 
ment or quiescence of the appendical lesion has usually been assumed as the 
cause. Unless general peritonitis and severe toxemia are present the first 
factor—myocarditis—seems improbable. Regarding the second, it appears 
more likely that a slow pulse with temperature is an indication of continued 
and active excitation at the inflammatory focus rather than an evidence 
of the latter’s quiescence. 
Among drugs, the digitalis bodies and salicylates can cause a slow pulse 
by increasing vagus inhibition. 
Epileptics occasionally have an abnormally slow pulse. This is also 
true of those types with so-called vago-vasal attacks (Gowers) in which there 
are no convulsions, but vaso-motor symptoms, vomiting, syncope and pains 
along the distribution of the intercostal nerves are present. 
A slow pulse is also fairly common at the crisis of pulmonary affections, 
or during the course of the disease. When present at the crisis, I believe it is 
due to the neurotropic effect of toxins liberated during critical defervescence. 
Therapy for bradycardia is only indicated when the slow pulse rate is 
accompanied by subjective symptoms. Atropine is then of most value, given 
first in small, later in increasing doses, until the full physiological effect has 
been obtained. 
Clinical and Experimental Causes of Auriculo-ventricular Heart Block 
(a) Destruction of the A-V bundle or auriculo-nodal junction by tumors 
(benign or malignant), calcareous deposits, fatty and inflammatory 
infiltration, fatty degeneration, coronary infarct, hemorrhage in the 
node, fibrosis. 
(b) Severe myocardial degeneration. Destruction of the branches or terminal 
arborizations of the conduction system, 
I. Cardiac causes. 
II. Drugs (digitalis—morphine—nicotine(?). 
III. (a) Asphyxia. 
(6) Chemical 
poisons 
Producing acidosis, toxins, anaphylatoxins. 
II. Extra-cardiac fac- 
tors. 
IV. Interference with cerebral circulation. 
V. Abnormal pressure on the cardio-inhibitory center. 
VI. Abnormal pressure on the vagus. 
VII. Increased vagal inhibition. 
(a) Digital pressure on the vagus. 
(b) Peripheral excitation. 
VIII. Endocrine disturbances. 198 
THE ARRHYTHMIAS 
Heart block is here used to denote auriculo-ventricular dissociation, 
complete or incomplete; it does not refer to lengthened conduction time, 
blocked auricular beats, or to sino-auricular block. In order to establish 
a certain coherence between the diverse etiological factors concerned in heart 
block, I have made and adopted the etiological classification given above, 
which probably includes the great majority of known factors. Experi- 
mental causes are also mentioned because they may furnish an insight into 
some clinical cases which have experimental analogies. 
I. (a) Any lesion which completely severs or destroys the main branch 
of the conduction system produces complete heart block. If the destruction 
is incomplete, there may be enough healthy strands left to carry impulses 
from auricle to ventricle. A suddenly deficient coronary supply, the result 
of thrombosis, infarct or disease of the nutrient artery of the bundle of His, 
can so profoundly disturb the nutrition of the conduction system as to 
produce transient or permanent heart block. 
(b) Just as fibrotic and calcareous degeneration in the conduction system 
is almost invariably accompanied by gross pathological changes in the 
ventricular musculature, so in extensive cardiosclerosis there are often 
fibrotic and other degenerative changes in the connecting bundle. Even if 
the bundle remains sufficiently normal to convey auricular impulses to the 
ventricle, cardiosclerosis in itself can probably produce heart block by de- 
struction of the branches or terminal arborizations of the conduction system 
in the ventricular musculature (Chapter I) so that impulses passing through 
the bundle are prevented from reaching their final destination in the ven- 
tricles. And even if these final conduction strands (terminal aborizations) 
are sufficiently normal to carry impulses to their final ventricular distribu- 
tion, one may still conceive a pathological condition in which the ventricular 
musculature may be so diseased as not to be capable of normal response. 
Any or all of these causes (Group I (b)) may operate in those cases of heart 
block in which the main conduction system is found quite or fairly normal 
upon pathological examination. The causes would then lie either in the 
subsidiary branches of the conduction system or in widespread myocarditis. 
Therapy.—When syphilis is the etiological factor, vigorous antiluetic 
treatment—salvarsan, bichloride injections, and iodide of potash is indicated 
(Chapter XVI). Before intravenous medication with neosalvarsan, arsphen- 
amin or salvarsan is begun, it is advisable to start with a few injections of 
mercury. One should also start cautiously with intravenous medication, 
beginning with about one quarter of a full dose and then gradually increasing 
every week until the full dose is reached. The advisability of using digitalis 
and atropin in cardiac disease with heart block is discussed subsequently. 
A few cases of heart block have been reported in which the administration 
of thyroid extract was followed by beneficial results. 
II. Digitalis can produce complete or incomplete block. This arrhy- 
thmia has not only been observed in those with heart disease who had received THE ARRHYTHMIAS 
199 
digitalis but it has also been induced by digitalizing healthy hearts. 
Complete heart block has also been induced by the injection of mor- 
phine in dogs, and was regarded as an effect upon the cardio-inhibitory 
center. Morphine poisoning in man is sometimes accompanied by very 
slow pulse rates. These have never been graphically recorded; they may be 
due to the same cause found in the animal experiments; namely, heart block. 
Tobacco poisoning is also occasionally accompanied by a very slow pulse. 
To determine its precise nature, graphic tracings are necessary. In this 
manner it may in the future be demonstrated that some of these tobacco 
arrhythmias are likewise due to heart block. 
III. (a) In animals, the experimental production of asphyxia is accom- 
panied by varying degrees of heart block; the essential cause is assumed to be 
nutritional disturbance from lack of oxygen in the junctional tissue. With 
our present imperfect knowledge of the chemistry of the blood, it is impos- 
sible to state whether other chemical factors (Group III (b)) can act similarly 
in the production of heart block by profoundly interfering with cardiac 
nutrition. Such factors are abnormal constituents in the blood causing les- 
sened blood alkalinity (acidosis); chemical poisons elaborated in infectious 
diseases (toxins); and anaphylotoxins. Regarding acidosis, I have several 
times observed a peculiar form of heart block in the terminal stages of patients 
suffering from cardiosclerosis and nephritis, in whom electrocardiograms 
showed very rapid and irregular auricular and ventricular activity (Terminal 
Arrhythmias, Chapter X). Cyanosis was not a constant factor. Blood 
examinations for non-protein nitrogen and other products were not made, but 
from the clinical syndrome, it seemed that retained chemical poisons con- 
stituted the essential cause of the arrhythmia. With reference to toxins, it 
has been shown experimentally that transfused pneumonic blood profoundly 
impairs cardiac contractibility. I have had occasion to study two cases 
which have a bearing upon these experimental observations. Both developed 
heart block during the course of pneumonia. In one an autopsy was per- 
formed. Upon macroscopic examination the heart was found normal. 
Careful microscopical examination of the conduction system also showed 
that it was normal. Such clinical and experimental observations indicate 
that in pneumonia, at any rate, toxins have an action not only upon the 
cerebral centers, but also locally upon the heart. Block may then result 
from interference with nutrition of the A-V conduction system alone or in 
conjunction with the remainder of the cardiac musculature. 
Complete heart block has been produced in animals by experimental 
anaphylaxis; the cause is assumed to be due to an effect upon the heart itself. 
IV. Interference with Cerebral Circulation.—This factor probably 
operates by interference with nutrition of the cardio-inhibitory center. 
Sclerotic change in the arteries at the base of the brain is the pathological 
condition most frequently observed. In one reported case of heart block, 
few changes were found in the conduction system or cardiac musculature, 200 
THE ARRHYTHMIAS 
the cerebral arteries constituting the circle of Willis were markedly diseased. 
The brain itself was normal. Tumors and other pathological conditions 
which impede cerebral circulation may have a similar effect in producing 
heart block. 
V, VI. Abnormal Pressure on the Cardio-inhibitory Center and Vagus. 
Tumors and adhesions affecting the vagus or even the cardio-inhibitory cen- 
ter are the most likely pathological entities which can produce heart block. 
One case of heart block from pressure on the vagus has been reported; a 
large tumor involving the nerve in the anterior mediastinum was found. 
VII. Increased Vagal Inhibition.—It has been shown that in children 
with heart disease, digital pressure on the vagus in the carotid sheath may be 
followed by temporary heart block. This manoeuver probably acts by caus- 
ing increased vagal inhibition. A case has also been reported in which swal- 
lowing induced heart block in a patient with delayed conduction time. These 
are examples of induction of this arrhythmia from direct excitation of the 
vagus in susceptible individuals. 
(b) Reflex Peripheral Excitation of the Vagus.—I have observed cardiac 
inhibition with the production of complete heart block, apparently reflexly 
evoked by peripheral stimulation of the pneumogastric branches supplying 
the stomach. The clinical history of the patient showed that the pulse had 
been normal before the onset of tuberculous peritonitis from which the patient 
suffered when he first came under observation. For several weeks high tem- 
perature and abdominal pain had been present. The abdomen was opened, 
and fluid evacuated. Some weeks after operation, the symptoms of tubercu- 
lous peritonitis entirely subsided. Two years later the patient was killed 
in an accident. Complete heart block, as shown by numerous polygraphic 
and electrocardiographic curves, was present before and after the operation, 
and up to the time of the patient’s death. The presence of the arrhythmia 
caused no symptoms. A necropsy was performed; the lungs were found 
normal; a mass of enlarged suppurating tuberculous glands adherent to 
stomach and intestines was found. Careful macroscopic examination showed 
the heart to be absolutely normal. Microscopic examination of the conduc- 
tion system was not done but careful scrutiny showed the absence of any gross 
lesion. Toxemia as the cause of the heart block could be excluded, for the 
patient was clinically well, had had no temperature, and was at work for 
months prior to his death. Weighing the pathological and clinical data it 
seems probable to me that the heart block was due to abnormally increased 
vagal inhibition reflexly excited by involvement of peripheral nerve filaments 
in the abdominal tuberculosis. 
VIII. Endocrine Disturbances.—I have seen complete heart block in an 
individual who presented the typical syndrome of a mixed endocrine dis- 
turbance (so-called pluriglandular syndrome); there was no evidence of a 
cerebral new growth. Aside from the arrhythmia, the cardio-vascular 
examination presented nothing abnormal. Our knowledge of endocrinology THE ARRHYTHMIAS 
201 
is at present too limited to discuss the possible etiological factors concerned 
in heart block of this type. 
General Therapeusis of Heart Block.—Therapeutically, atropine sulphate 
should be tried in all cases of heart block; it should be given hypodermatically 
until the full physiological effect is reached. As much as or even of a 
grain may be given in the effort to remove the block. Should block be thus 
removed, atropine is to be continued three times daily in doses from gr. 
3a 50 to Moo- Recently the extract of. thyroid gland (thealpha iodin fraction 
of Kendall) has been advised in order to increase the ventricular rate in heart 
block. The drug is to be pushed until the full physiological effect is reached. 
I have had no personal experience with the drug; if given cautiously and 
begun with small doses, I see no harm in its trial. When possible, appropriate 
treatment should be directed toward the individual etiological factors and 
toward the clinical symptoms. This applies particularly to the usual decom- 
pensation so frequently present in heart block, and should be treated in the 
usual fashion with digitalis, caffein, etc. (Chapter XX). In some cases of 
incomplete heart block, however, special caution in the use of digitalis should 
be observed (Chapter XI). 
Prolonged Conduction Time.—Among drugs, digitalis occasionally pro- 
duces increased conduction time from auricle to ventricle. The chief 
cardiac cause of this arrhythmia is myocardial degeneration; indeed, a pro- 
longed a-c interval in the polygram or a prolonged P-R interval in the electro- 
cardiogram (Chapter X) may be the only evidence of this disease. Prolonged 
conduction time is encountered fairly frequently during the course of, or 
immediately after, attacks of rheumatic endocarditis. It is then assumed to 
be due to myocardial involvement. It is also met with in acute or sub-acute 
nephritis in which there are none of the usual clinical manifestations of myo- 
carditis. In addition, prolonged conduction time is occasionally of neuro- 
genic origin. Therapy is indicated for the symptoms of myocarditis or 
for other etiological factors, but not for the prolonged conduction time: The 
latter itself causes no symptoms and requires no medication. 
Shortened Conduction Time.—I have found a shortened conduction 
period from auricle to ventricle especially frequent in exophthalmic goiter 
(Chapter X). The fact that experimental excitation of the right accelerator 
nerve is accompanied by a slightly, and excitation of the left accelerator by a 
considerably, shortened conduction time (Chapter I) is doubtless of etiologi- 
cal significance in exophthalmic goiter, in which the ch.ef symptoms are due 
to hyperexcitation of the sympathetic system. Tachycardia is usually 
present with a shortened auriculo-ventricular conduction time. Tachycardia 
with its other clinical manifestations may then require medication, the 
shortened conduction time as such does not. 
Auricular Fibrillation.—This is the usual arrhythmia accompanying 
decompensation in rheumatic mitral stenosis in the young and middle-aged. 
It is rare in valvular disease affecting the aorta. It is especially frequent in 202 
THE ARRHYTHMIAS 
the advanced cardio-sclerotic changes present in the old. It is also sometimes 
found in children; I have seen isolated instances in patients between io and 
12 years of age with advanced valvular disease. 
While auricular fibrillation is often a permanent arrhythmia; (indeed, it 
was formerly regarded as always permanent, hence the old term, perpetually 
irregular pulse) it is occasionally transient or it may even occur only in attacks. 
(See Cardio-vascular Clinics.) I have observed such attacks lasting several 
days in two cases of aortic aneurism. In one, it occurred with the gradual 
onset of severe decompensation; in the other, there was no discoverable cause 
for the attack. Another instance of transient auricular fibrillation was that 
of a woman of 60, a sufferer from mild myocardial insufficiency, who had been 
operated upon for empyemia of the gall bladder. Following the operation, 
there were several distinct attacks of broncho-pneumonia; the onset of each 
was marked by a moderate rise of temperature and by auricular fibrillation 
lasting one day. In mitral stenosis, pari-passu with fresh exacerbations of 
endocarditis, auricular fibrillation may occur. Thus, in a man of 45 with a 
double mitral lesion, from whose blood a non-hemolytic streptococcus was 
isolated, each sharp febrile invasion was accompanied by an attack of auricular 
fibrillation; these attacks lasted several hours or days. Patients with mitral 
disease who suffer from acute febrile disturbances of non-rheumatic origin are 
also prone to attacks of this arrhythmia; these may last throughout the fever. 
I have seen two such instances: One, a patient with mitral regurgitation, the 
other with mitral stenosis; both developed fibrillation during erysipelas. 
Auricular fibrillation may also be an initial symptom of coronary embolism 
or thrombosis (Chapter XXIII). 
From these observations it is evident that in diseased hearts any addi- 
tional insult to the endocardium, myocardium, or coronary arteries may be 
accompanied by auricular fibrillation. The permanence of the arrhythmia 
may depend upon the severity or permanence of the pathological damage. 
The sovereign remedy for this irregularity when found in decompensated 
cardiac disease is digitalis. In some types, quinidin sulphate may also be 
employed. In many cases both digitalis and quinidin may be administered 
at the same time. The details of the administration of these drugs is else- 
where described (Chapter XX). I have occasionally added large doses of 
bromides or luminal (Chapter XX), or have initiated digitalis medication with 
one or two large doses of morphine when patients were very dyspnoeic or restless. 
Auricular fibrillation also occurs, though very rarely, in individuals with 
normal hearts. For example, I have observed several cases of temporary 
auricular fibrillation coming on at the critical defervescence of lobar pneu- 
monia; there was no evidence of heart disease or heart failure during the 
entire course of the disease or during convalescence. Some of these patients 
were examined months after the pneumonia; their hearts were found perfectly 
normal. Temporary or permanent auricular fibrillation is also fairly common 
in exophthalmic goiter. Apparently influences affecting neurogenic cardiac THE ARRHYTHMIAS 
203 
control are essential factors. I have likewise seen auricular fibrillation in a 
heavy smoker whose heart was normal. A case due to hydrogen sulphid 
poisoning in a man with a normal heart has also been reported. 
In those cases of fibrillation which are apparently of toxic or of neuro- 
genic origin, I have found very little value in digitalis; the pulse or ventricu- 
lar rate was not appreciably affected; dyspnoea, if present, continued. 
Such cases may perhaps be especially benefited by quinidine (Chapter XX). 
Our experience with this new drug has not yet been sufficiently large to state 
dogmatically in what type of case quinidin is apt to be of especial value. 
Large doses of bromide or luminal alone or combined with small doses of 
codeine seem occasionally of value. 
Simple Tachycardia—Ordinary Pulse Acceleration.—Rapid, regular 
pulse rates usually range between no and 160 per minute, and are the result 
of excitation of the accelerator nerves. The causes are manifold. Excite- 
ment, fright, overexertion, fever are some of the commoner. In exophthalmic 
goiter, tachycardia is one of the cardinal symptoms. Gastro-intestinal 
disturbances of functional or organic nature are frequently accompanied by 
rapid heart action. Persistent tachycardia may be the only clinical evidence 
of a fresh exacerbation of an old endocarditis. Cardiac decompensation 
from any source is often accompanied by moderate tachycardia, and is 
sometimes the forerunner of other arrhythmias. Among other causes of 
rapid heart action are pulmonary tuberculosis, dyspnoea from pulmonary 
disease, tabagism, overindulgence in tea and coffee, and atropine. 
Pulse acceleration requires medication only when the pulse rate is high 
or when subjective sensations are present. Even then, drugs are not of much 
value unless the primary disturbance in the stomach, lungs, etc., can be con- 
trolled. When tachycardia is due to fever, digitalis has no effect in reducing 
the pulse rate. The bromides or codeine are occasionally efficacious in slow- 
ing the heart in such cases. Digitalis may decrease the pulse rate wrhen the 
tachycardia is due to cardiac decompensation. 
Paroxysmal Tachycardia.—This cardiac irregularity is more often of 
functional than of organic origin. Its most frequent extracardiac cause is 
acute indigestion; the paroxysm is apparently brought on by excitation of the 
accelerators. For example, I have seen several patients in whom every 
attack of indigestion was accompanied by this arrhythmia. Another instance 
is a woman of 50 with abdominal cancer, gastric symptoms and severe secon- 
dary anaemia; with her, any slight fright or nervous excitement would 
frequently initiate an attack. At necropsy, the cardiac musculature was 
somewhat pale, otherwise the heart was normal. In another patient, a 
woman of 45 with a luetic history and positive blood Wassermann, sudden 
gastric attacks also initiated paroxysmal tachycardia. It is interesting to 
note that during these attacks there was marked dilatation of the left pupil, 
presumably an evidence of sympathetic nerve excitation. Other cases are 
described in Cardio-vascular Clinics. 204 
THE ARRHYTHMIAS 
Before medicinal treatment is begun with gastric sedatives, etc., the first 
therapeutic procedure should be firm pressure over the vagus in its course 
in the carotid sheath in the neck. Pressure on the right side should be first 
tried; if this does not succeed, pressure should be exerted over the left vagus. 
There are very few if any procedures in medicine more dramatic than the 
immediate cessation of an attack of paroxysmal tachycardia by vagus 
pressure. The antecedent discomfort, the sensation of fluttering in the chest, 
the dyspnoea, stop at once; the rhythm returns to normal, the attack ceases. 
The attack rarely recurs at once even if the underlying cause (fright, indiges- 
tion, etc.) be not entirely under control. There are a few important little 
points which must be remembered in the use of vagus pressure. The 
patient should be reassured and be told that the finger will be pressed into 
the neck for a moment or two; that the pressure will be somewhat painful 
but that it will not have any tendency to choke him or increase his shortness 
of breath. The patient is then asked to lay as flat and as comfortable as 
possible. The index finger is then placed lightly over the carotid at about 
its middle point in its course in the neck so that the carotid pulsations can 
be distinctly felt. Then, sudden, sharp pressure on the carotid (and vagus) 
is made directly backward, and the pressure continued for a minute or 
two. The finger pressure is then slowly relaxed. I believe that the effect 
of vagus pressure is somewhat enhanced if at the moment that vagus pressure 
is begun the patient is able to take a deep breath and will hold it as long as he 
comfortably can. 
In one instance of paroxysmal tachycardia, I tried simultaneous pressure 
over both vagi in the neck when the paroxysm was not controlled by alternate 
right and left vagus pressure, respectively. The case is of sufficient interest 
to warrant a brief report of the history as well as the unique therapeutic 
procedure. M. T., age 45, female, unmarried, regular menses, has had 
attacks of paroxysmal tachycardia for many years. Between the attacks 
she has no cardiac symptoms of any kind. The paroxysm lasts from several 
minutes to several hours. She had scarlet fever when eight years old. The 
first attack is supposed to have started at about the age of ten. Since ado- 
lescence the paroxysms seem more frequent at the time of the menses. She is 
a rapid eater and has a tendency to bolt her food. Seasoned and heavy food 
causes gastric distension which is generally relieved by belching. Physical 
exertion itself has never initiated a paroxysm: For example, the previous 
summer she enjoyed ocean bathing without cardiac discomfort. The attack 
in which I first saw her was the worst she had ever had. It began in typical 
fashion. She suddenly felt a throb in her throat (very probably an extra- 
systole), immediately succeeded by tachycardia. The tachycardia was 
constantly present for three days with the ventricular rate regular and 
varying from 180 to 200 per minute. The bromides, chloral, morphine and 
digitalis were tried by her physician without any effect. Upon examination I 
found the systolic blood pressure 80, the diastolic, 70. Except for somewhat THE ARRHYTHMIAS 
205 
distant heart sounds at the apex and rapid regular action, the heart showed no 
abnormality. There was passive congestion at the base of the left lung; 
the temperature was ioi°, probably the result of the pulmonary stasis. The 
patient was dyspnoic and somewhat cyanotic; there was slight edema of the 
legs. I first tried sharp pressure over the right vagus; this was followed 
by a normal cardiac rate for several beats. The tachycardia then continued 
as before, and thereafter was not influenced by several other attempts at 
pressure over the right or left vagus. Because of the desperate condition of 
the patient, I ventured sharp simultaneous pressure over both vagi, encir- 
cling the neck with the thumb and index finger of one hand. The pressure 
was instantly followed by a sudden momentary convulsive seizure of the 
muscles of the face; the patient seemed dazed for about a minute; at the same 
time normal heart rate was resumed. There was no return of the tachy- 
cardia. Convalescence was uninterrupted, cyanosis and dyspnoea slowly dis- 
appeared. About two weeks later, I took an electrocardiogram and 
fluoroscoped the patient’s chest. Nothing abnormal was found. The heart 
rhythm and sounds were normal. The cardiac response to exercise was nor- 
mal. One month later I again saw the patient in another typical paroxysmal 
seizure which had lasted one hour. Again pressure over the right and left 
vagus alternately had no effect. I therefore again tried simultaneous pressure 
over both vagi, but this time instead of pressing sharply and suddenly, I 
slowly brought digital pressure to bear. The attack was again immediately 
controlled, but without any alarming symptoms; there were no convulsive 
seizures or a dazed sensorium. Simultaneous double vagus pressure has its 
risks, but I think its trial is justified in desperate cases especially if the 
digital pressure be gently graded instead of being sudden and sharp, which is 
the proper procedure in single vagus pressure. 
As an alternative to unsuccessful vagus pressure, pressure on the right 
or left, or both eye-balls may be tried in attempting to control the tachy- 
cardia by inducing the oculo-cardiac reflex, a nerve arc which also induces 
vagus inhibition. The procedure however, is more painful than vagus 
pressure and is not as apt to be followed by success. Inducing emesis may 
also effect the vagus control, hence this may be of value in stopping the 
attack. Hot water, mustard, turpeth mineral are safe emetics that can be 
employed. Strophanthin may occasionally be employed hyperdermically 
or intravenously because of its quick, powerful effect in increasing vagus 
inhibition. As an addition to any drug or proceedure, morphine hyper- 
dermically, bromides or luminal are excellent adjuvatants, where indicated, 
in order to quiet the patient’s nervous system. 
Atropine in small doses three times daily before meals, and an ant-acid 
powder after meals, with limitation of the diet to bland food eaten slowly, 
are often of value in avoiding future attacks of paroxysmal tachycardia of 
gastric or intestinal origin. The powder which I use contains equal parts of 
magnesium usta, bicarbonate of soda and oleosaccharated peppermint 206 
THE ARRHYTHMIAS 
powder in equal parts; of this the patient is given about teaspoonful 
three times daily after meals. 
Auricular Flutter (Chapter X).—This arrhythmia is most frequent in 
older people with cardiosclerosis during the period of decompensation. It 
may also occur during the course of acute endocarditis without decompensa- 
tion. Occasionally auricular flutter is of functional origin. When flutter 
accompanies acute endocarditis, digitalis does not control the arrhythmia. 
Since the drug has not been employed in flutter of functional nature, nothing 
is known of its effect in such cases. In auricular flutter with decompensation 
and cardiosclerosis, digitalis is of very great value. It should be adminis- 
tered in large doses (Chapter XX) so as to obtain the maximum effects as 
soon as possible. Digitalis then usually changes the flutter to fibrillation. 
If then the drug be discontinued, the rhythm often returns to the normal and, 
coincidentally, compensation is restored. In some patients, several courses 
of digitalis have been given when flutter recurred, and each time normal 
rhythm was resumed after the flutter first changed to fibrillation under the 
influence of the drug. 
Ventricular Escape—Independent Ventricular Activity.—In order to 
emphasize the etiological factors involved in this arrhythmia a brief report 
of a case of this interesting cardiac irregularity with comment on the 
clinical aspects is given. 
S. P., male, aged 20, was first observed on February 4, 1913. He had 
measles when 3 years old and typhoid when 10; otherwise there was no 
history of previous illness. He was not addicted to tea, coffee, tobacco or 
alcohol. Five days prior to hospital admission, he developed a typical attack 
of acute articular rheumatism involving the ankles, wrists, knees and elbows. 
The attack was accompanied by fever; there were no chills or gastric 
disturbances. 
Except for swelling and redness of the inflamed joints, the general and 
neurological examination revealed nothing abnormal. There was no urethral 
discharge. The complement-fixation test for gonorrhea was negative. The 
cardiac outline was normal to percussion, the beat was in the fifth interspace, 
8.5 c.m. from the midsternal line; the heart sounds were normal; the pulse was 
rhythmical. The systolic and diastolic blood pressures were within normal 
limits. The temperature ranged between ioi° and 103°. There was no 
dyspnoea. The patient did not appear very ill. Sodium salicylate in 
moderate doses was given for two days. 
Two days after hospital admission, a transient pulse irregularity 
appeared. Six days thereafter, it recurred and clinically resembled extra- 
systoles; no tracings were made at that time. February 12, the irregularity 
occurred with every third or fourth beat. From that day frequent poly- 
graphic and later, electrocardiographic tracings were taken. February 14, 
a rough blowing systolic murmur was heard at the apex for the first time. 
Occasionally there were runs of from three to twelve stronger thumping beats THE ARRHYTHMIAS 
207 
unaccompanied by the murmur; studies of the tracings showed that these 
were due to simultaneous action of auricle and ventricle, and that the ventri- 
cle was beating automatically and independently (ventricular escape, 
Chapter X). Four days later the arrhythmia appeared only infrequently 
and the systolic murmur had almost entirely disappeared. The patient left 
the hospital feeling well. 
As possible causes for the production of automatic ventricular action, 
neurogenic, toxic and organic factors require consideration. A neurogenic 
factor in the sense of a so-called neurosis due to extracardial conditions 
(for example, gastric disorders) causing abnormal excitation in the afferent 
(centipetal) arm of a reflex arc, can be dismissed in our case because of the 
type of the disease, its course, and the definite completion of the arrhythmia 
with the end of the rheumatic attack. Concerning toxins in general, their 
action seems to depend upon their complicated chemical composition and 
upon intricate chemical reactions taking place in the body. By analogy, it 
seems possible that a rheumatic toxin may also produce an arrhythmia by 
directly poisoning the heart, although there is no evidence for such assump- 
tion in this case. Concerning an organic cause for the arrhythmia, it is to be 
recalled that the patient developed a loud systolic murmur at the apex one 
week after the appearance of the arrhythmia; the murmur remained for two 
days, then gradually disappeared. It also disappeared during those arrhyth- 
mic beats when auricle and ventricle contracted simultaneously, an apparent 
corroboration that it was due to mitral insufficiency, organic or relative in 
nature. It is not my intention to discuss cardiac murmurs at any length in 
this connection (q.v. Chapter XIII). Briefly, systolic apical murmurs which 
occur during the course of any febrile disease, and then disappear without 
evidence of an organic cardiac lesion, are by no means infrequent. On the 
other hand, organic murmurs usually increase in intensity and do not disap- 
pear. In the case under discussion, the occurrence of the murmur in con- 
junction with acute articular rheumatism makes its presence suspicious of 
some transient valvular or myocardial involvement. Rheumatic infections 
cause myocardial inflammation in the form of submiliary myocardial 
(Aschoff) bodies (Chapter IV). Thus, healed or healing isolated Aschoff 
bodies have been found on the interventricular septum in hearts which were 
the subjects of rheumatic reinfection. During their inflammatory state, if 
situated close to, or even partly involving the bundle of His before its division, 
they can conceivably cause local irritation and excitation sufficient to pro- 
duce occasional ventricular automatism, with beats of supraventricular ori- 
gin. The bundle, however, need not be sufficiently compromised to prevent 
the excitation impulse from following its normal course in the conduction 
system—a fact which probably accounts for the identical electrocardiographic 
complexes here present in all the beats, both rhythmic and arrhythmic. 
Right and left vagus pressure had no effect on auriculo-ventricular 
sequence. One of the atropine experiments was followed by a number of 208 
THE ARRHYTHMIAS 
independent ventricular contractions, with no marked difference between 
ventricular and auricular rates. This observation does not necessarily 
exclude the possibility of an organic cause for the ventricular “escape,” 
for an irritative lesion which does not entirely and permanently affect the 
bundle may nonetheless upset normal nerve control and mechanism, and 
make the latter susceptible to atropine poisoning. It would thus seem that 
the automatic ventricular mechanism was not sufficiently sensitive to respond 
to vagus pressure, but that atropine poisoning prevented inhibitory vagus 
control and permitted ventricular escape. 
Summarized, a case of independent ventricular activity is described: 
The lowest ventricular rate is 50 per minute, the usual rate is 60 and remains 
so whether independent ventricular activity is present or not. The electro- 
cardiographic complexes of all beats are identical. At one time atropine 
administration was followed by ventricular escape. The occurrence of 
automatic ventricular activity during the course of acute articular rheuma- 
tism and its disappearance later, combined with.a study of the physical 
signs make it probable that a small transient myocardial inflammatory 
focus (Aschoff body) at or near the auriculo-ventricular bundle is the irri- 
table cause of the abnormal mechanism. Therefore it may be stated that 
transient independent ventricular activity (ventricular “escape”) may occur 
with no change in the usual path followed by the excitation impulse, with no 
difference of rate between normal and abnormal beats, and with no marked 
retardation of the auricular rate. 
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TELEROENTGENOGRAPHY, ORTHODIASCOPY AND 
FLUOROSCOPY 
Orthodiascopy is essentially a method of outlining a viscus by 'means of 
parallel roentgenographic rays; in this manner the exact size of the organ is 
reproduced. With the tube stationary and near the patient, the rays from 
the focus of the tube diverge; hence the object to be examined becomes 
artificially enlarged to a variable extent. If the organ itself is large, this 
distortion is magnified, for the impinging rays become still more divergent; 
an hypertrophied heart, for example, produces a disproportionately enlarged 
shadow. This was well exemplified in a case in which the roentgenogram 
taken two days before death showed the shadow of a tremendously enlarged 
heart. At necropsy the heart was found only moderately enlarged; peri- 
carditis causing a tightly adherent pericardium prevented terminal cardiac 
dilatation which might have been assumed as the cause for the enlarged 
roentgenographic shadow. 
Two methods of avoiding distorted images have been devised, (i) 
Teleroentgenography and (2) orthodiascopy. 
1. Teleroentgenography.—In following this procedure, the X-ray tube 
is placed about six and one half feet (2.3 meters) from the patient, so that the 
rays reach the organ approximately parallel. The X-ray plate should be 
held parallel to the anterior surface of the midsternum, and the X-ray tube 
so placed that its central rays are at right angles to the center of the plate 
at about the level of the infrasternal notch. Properly applied, teleroentgenog- 
raphy has given excellent results. Its great advantage is its rapid technic 
under modern conditions. There is also no danger of an X-ray burn to the 
operator. Compared with orthodiascopy, its disadvantages are the amount 
of X-ray plates required and especially the fact that the action of the heart 
cannot be actually studied and observed, for a photograph can naturally 
give only the picture of the heart at and during the time the plate is exposed. 
Another advantage of orthodiascopy over X-ray plates is that questionable 
shadows may be at once interpreted without the necessity of having the 
patient return for another plate. As will be shown later, very many 
important facts can be gleaned by observing the heart in action. 
2. Orthodiascopy.—With this method, the focus of the X-ray tube and 
the center of the fluorescent screen are adjusted so that they are in a straight 
line, and the X-ray tube and the fluoroscopic screen move together. As the 
outline of a viscus (in this case, the heart) is seen, the screen is moved and 
210 TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
211 
Fig. 234.—Groedel orthodiascope, front view. The patient sits with his feet resting 
comfortably on the adjustable step (ST); the side plates (SP) can be lowered or raised and 
pushed in or out; they are placed so that they fit snugly in the axillae and against the chest 
of the patient. The fluoroscopic screen (FS) is grasped by the finger of the right hand in a 
small ring (R). The bar B' carrying the screen is connected by the hollow bar (CB) with 
the bar B"; the latter carries the X-ray tube so that any motion imparted to the fluoroscopic 
screen by the observer moves the X-ray tube as well. By loosening the nut (N) the bar 
(B') may be slid along the crossbar, thus the screen may be placed at any convenient dis- 
tance from the patients chest. RB, rubber bulb used for marking purposes; SC, sliding 
counterweights so that the screen and X-ray bars may be properly counterpoised; C, cranks 
used to place the table in the horizontal position if necessary; LS, levelling screws; FSW, the 
electrical foot switch. 212 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 235.—Details of marking mechanism: XR, X-ray tube which may be raised or lowered in its frame (F). It 
is partially protected by its rubber shield (RS). The marker (M) is in line with the center of the screen (see Fig. 234) 
and the focus of the X-ray tube. The rubber tubing (RT) is connected with the rubber bulb (Fig. 234) through the 
hollow cross bar. When the bulb is squeezed and the marker inked, the pencil is pushed forward and dots the paper 
(P) fastened upon the board (B). W, are the wires connecting the X-ray tube with the coil. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
213 
brought in alignment, so that, with the simultaneous movement of the tube 
and screen, parallel and not divergent rays impinge upon the organ and reach 
the observer. The application of this principal is exemplified in the Groedel 
apparatus (Figs. 234, 235). It is the one I have found suitable for ortho- 
diascopy of the heart. Examinations can be made in the sitting, standing, 
or lying postures. For general convenience as well as for the comfort of the 
patient I prefer the sitting position. After the patient is properly seated 
(see legend, Fig. 234) the room darkened, and the electric foot switch pressed 
upon, a rapid survey is first taken of the entire heart by moving the fluoro- 
scopic screen over the cardiac area. The cardiac outline is thereafter 
systematically mapped out. The central spot of the screen (F. S. Fig. 234) 
is brought over the edge of the area to be delimited; this point is then marked 
by pressing the rubber bulb with the left hand. My practice is to start the 
tracing on the left side by dotting out the left outer limit of the aortic arch, 
then continuing downward and marking the other curves of the heart 
(Fig. 236) until the entire left side is outlined. To expose the lowest part 
of the apex, the patient is asked to hold his breath for a moment at the end 
of a deep inspiration. The upper right border of the aorta, then the 
remainder of the right border of the heart, are mapped out down to the diaph- 
ragm. Finally, the diaphragm is outlined on each side. The cardiac 
contour is best dotted out during the time of systolic contraction. There is 
very little danger of X-ray burns since the amount of current used is small 
(about 5 amperes). The entire orthodiascopic procedure requires generally 
about two minutes. During the examination and for a minute or two there- 
after, the observer can carefully study the heart action, and thus not only 
gain important data regarding the various types of contractility, especially 
of the left ventricle and aorta, but also fluoroscopically study shadows, the 
interpretation of which may be uncertain in a roentgenogram. 
The details of the marking mechanism are shown in Fig. 235. 
Orthodiascopic Tracing of the Normal Heart.—It is important to have a 
definite visualized image of what the heart actually resembles when seen in 
the chest, for it will aid tremendously in checking up some of the percussion 
findings at the bedside where naturally an X-ray is not at hand. The com- 
bined contour of the normal heart and aorta is an irregular oblique ovoid; 
its larger end is directed downward and to the left (Fig. 236). The outline 
is made up of several curves formed by different portions of the heart. On 
the right side above, we find the ascending aorta, which forms a curve with 
a slight outward convexity (A1, Fig. 236). Above it, the great vessels are 
sometimes seen as indefinite shadows. Very rarely, the superior vena cava 
is visible as an attenuated shadow stretching across the aorta. Below the 
ascending aorta is the curve formed by the right auricle (R. A. Fig. 236). 
It is usually a well-defined arc and forms an acute angle with the arch of 
the diaphragm. In cases of extreme right ventricular enlargement, or in 
pericarditis with effusion, this angle may be obliterated. The left-sided 214 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 236A. 
Figs. 236A and B.—-Orthodiascopic tracing of the normal heart.1 
AI, Ascending aorta; R.A., right auricle; A2, aortic arch; P.A., pulmonary artery; 
L.A., left auricular appendix; L.V., left ventricle; M.R., greatest distance from median line 
to the right; M.L., greatest distance from median line to the left; L.O., longest oblique 
diameter of the cardiac ovoid; B1-B2, greatest width of the orthodiascopic tracing. 
1 In order to show clearly the areas occupied by the cardiac silhouette, the orthodias- 
copic tracings have been blocked in figures of the chest. 
Fig. 236B TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
215 
silhouette is composed of four more or less distinct curves. From above 
downwards, these are the aortic arch (A2, Fig. 236), the pulmonary artery 
(P. A.), the left auricular appendix and auricle (L. A.), and the left ventricle 
(L. V.). The arch of the aorta protrudes slightly beyond the left sternal 
border, describing a convex arc; when the aorta curves sharply downward 
and backward to reach the spine, this arc assumes a knoblike prominence. 
The normal pulsatile excursions are slight (about 0.5 centimeter) and require 
careful scrutiny in order to identify them. The average length of the arch, 
visible as a separate shadow, is from 3 to 5 centimeters. The left margin of 
the descending aorta can sometimes be traced downward for several centi- 
meters as a lighter shadow; in exceptional instances, it is dimly seen as a 
pulsating silhouette behind the body of the left ventricle. Beneath the aor- 
tic arch and distinguished from it as a much smaller and less convex silhouette 
is the pulmonary artery; its average visible length is from 2 to 3 centimeters. 
The contour of the pulmonary artery is distinguished from that of the under- 
lying left auricle by the difference in pulsation time. The left auricular 
curve is obtusely oblique and variable in size; it consists mainly of the left 
auricular appendix, but sometimes also includes part of the left auricle. 
The left ventricular curve constitutes the greater portion of the left ventricle, 
and forms its ovoid end. The extent to which the left ventricle is visible 
depends upon the shape of the heart and the mobility of the diaphragm. 
In stout individuals with thick abdominal walls, diaphragmatic excursion is 
usually limited, and the apex of the heart may not be visible; in thin individu- 
als with good diaphragmatic mobility the entire left ventricular surface 
including the apex is plainly seen at the end of inspiration. 
In addition to giving definite information about the exact size of the 
heart, orthodiascopy has several advantages over teleroentgenographic 
plates. For example, as not infrequently happens, there may be a dubious 
shadow which in a plate may be variously interpreted as a mediastinal tumor 
or an aortic aneurism. Orthodiascopy can at once clear up this distinction 
by seeing the actual pulsatile excursion of the aorta in suspected aneurism, 
and by turning the patient in various lateral directions in order to discover 
whether a suspected mediastinal tumor fills out the posterior mediastinal 
space (Chapter XVI). Besides, orthodiascopy gives unique and important 
information regarding the type of contraction of aorta and pulmonary artery, 
and of right auricle and left ventricle. It is direct observation of the contrac- 
tion of the left ventricle which is of great help in diagnosing questionable 
hypertrophy, as well as in segregating individuals who complain of “weak 
heart” (Chapter XVIII) but who none-the-less show vigorous ventricular 
contractions. The manner and amount of aortic pulsatile excursions some- 
times helps in the diagnosis of aortic regurgitation where that diagnosis may 
be otherwise uncertain (Chapter XV). Orthodiascopy can also demonstrate 
extrasystoles and the irregular ventricular action typical of auricular fibrilla- 2l6 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
tion, as well as other data of interest found in various types of cardiac 
irregularities. 
Orthodiascopic Standards.—In order to determine accurately the stand- 
ard size of the heart, numerous statistical studies and measurements of 
orthodiascopic tracings have been made. For this purpose, oblique and 
other diameters of the cardiac ovoid (Fig. 236) have been devised and 
measured; from these, attempts have been made to establish normal cardiac 
areas. The diameter representing the greatest width of the heart ( B 1 B 2, 
Fig. 236) depends for its accuracy upon the left auricular curve; this is a 
variable quantity even in normal individuals and hence unreliable as a 
standard for measurement. Some observers have, therefore, chosen the 
largest oblique diameter (L.O., Fig. 236) and the distance of the cardiac borders 
from the median line (M.R., M.L.) as being more exact. These axes have 
been studied principally by GrOedel, Dietlin, and Veith in individuals of both 
sexes, of various ages, weights, and size, with varying types of thorax, and 
following different vocations. The chief objection to the use of the long axis 
(L.O.) as a standard is the fact that it is by no means always possible to see 
and delimit the tip of the apex, partly because some patients do not breathe 
properly, partly because in some individuals diaphragmatic excursions is 
limited, and often, (especially in those with heart disease) dyspnoea interferes 
with accurate X-ray exposure of this area. All these considerations may 
considerably influence the value of the long axis as an accurate standard of 
measurement. Since the transverse diameter is not so affected, the most 
recent observations are based upon this as the best available basis of measure- 
ment. Morever it has been found as accurate as any of the other measure- 
ments, including estimation of the cardiac area. Groedel has found the 
following average figures in the vertical orthodiagram: 
M.R. 
(see Fig. 236A 
and B), c.m. 
M.L., c.m. 
L.O., c.m. 
Adult males 
4.6 
8.4 
14.0 
Youths 
4 •1 
7.8 
Adult females 
Young females 
3 • 7 
7 •2 
12.1 
Tables of measurements of other observers are given at the end of this 
chapter. One of these is based upon the teleroentgenographic examination 
of soldiers (A. E. Cohn). Since, however, the size of soldiers hearts, even 
after several months of active service, has not been found to vary appreciably 
from that of the civilian adult of the same weight and physique, these 
tables may also be used as a standard of size of the adult male heart. In 
this connection it is interesting to note that another observer (Bertrand TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
217 
Fig. 237.—Orthodiascopic tracing of long and slender heart. 
Fig. 238.—Copy of orthodiascopic tracing of a broad heart. 2l8 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Smith) making similar teleroentgengraphic studies of the “irritable heart 
of soldiers” (Chapter XVIII), has found that these likewise do not vary from 
similar corresponding adult hearts in the civilian. 
In all these tabulated measurements, a certain correlation has been found 
to exist between the cardiac area, and size and weight of the individual. The 
ratio of the heart to body weight in the adult male is approximately i :2oo. 
There are important considerations, however, which tend to lessen the value 
of measurements as standards. Size, weight, type of thorax, and occupation 
are factors which have already been mentioned. In these alone there is a 
wide range of maximal and minimal measurements which may amount to 
more than 3 c.m. Another factor capable of producing wide variations from 
the standard and still be within the normal is that of different types of cardiac 
contour which do not correspond with the muscular make-up of the individual. 
The extremes are those with long, slender, graceful hearts scarcely resting 
upon the diaphragm, and those whose hearts are broad, lying flat almost 
along their entire lengths. For example: In a youth of 19, tall and slender 
(Fig. 237) M.R. = 3 c.m.; M.L. = 6 c.m.; the other is the orthodiagram of a 
robust male of 35 (Fig. 238). Both are healthy and have normal hearts; 
marked differences in all diameters are immediately apparent by reference to 
the diagrams. An added consideration, already alluded to, tending to lessen 
the value of measurements as comparative standards is the difference 
produced by movements of the diaphragm. When excursion of the latter is 
limited, less of the heart is uncovered, its ovoid contour appears flattened, 
and the transverse measurement is correspondingly enlarged. With a mobile 
diaphragm the reverse is usually true. From all these facts it is apparently 
impossible to establish normal mathematical orthodiascopic standards of 
measurement. This statement, however, does not preclude such general 
conclusions as that “normal” hearts may be unusually large or small, or that 
pathologically enlarged hearts often overstep the somewhat ill-defined normal 
limits. There is naturally no doubt of the value of orthodiascopy in the 
determination of marked variations in the size of the heart. 
The Narrow and Broad Heart.—Returning to the discussion of the two 
types of cardiac silhouette (Figs. 237, 238)—the abnormally narrow and 
the abnormally broad—there is not only a difference in size but also a marked 
difference in form. The left ventricle of the broad heart is flat, it hugs the 
diaphragm, and forms a flattened ovoid. The other type is ellipsoid, 
and rests lightly upon the diaphragm; Figs. 239, 240 are additional examples. 
One silhouette is that of a man of 25 suffering from bronchial asthma (Fig. 239); 
the other that of a woman of 26 suffering from marked vasomotor symptoms 
(Fig. 240). This type, sometimes called the “drop heart,” has assumed 
considerable clinical importance, for it has been found in patients with 
visceroptosis; it is regarded as one of the characteristics of habitus asthenicus, 
and is apparently the type of cardiac hypoplasia described in stasus thymo- 
lymphatious. The symptoms I have found in these individuals are those TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
2ig 
Fig. 239. 
Fig. 240. 
Fig. 239, 240.—Orthodiascopic tracings of abnormally slender hearts resting lightly upon 
the diaphragm (“drop” hearts). 2 20 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 241.—Orthodiascopic tracing of a woman of 30 with a compensated mitral regurgitant 
lesion showing normal cardiac contour and size. 
Fig. 242.—Orthodiagram of a girl of 17 with a compensated double mitral lesion. The 
tracing is normal in size and contour. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
221 
Fig. 243. 
Fig. 244. 222 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Figs. 243, 244, 245.—Examples of globular hearts of varying degrees of rotundity and 
size. From three cases of decompensated double mitral lesions with auricular fibrillation. 
In Fig. 243 the aortic curve is normal. 
Fig. 245. 
Pig. 246.—Globular heart of extreme size. Copy of an orthodiascopic tracing of a boy of 
11 suffering from a double mitral lesion and auricular fibrillation. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
223 
connected with vasomotor instability—hushed, pale and cold extremities, 
dizziness, etc. These are often erroneously interpreted as due to a “weak 
heart” (Chapter XVIII). It should be emphasized however that individuals 
with habitus asthenicus as well as those with vasomotor symptoms often 
have hearts of perfectly normal size and shape. 
Orthodiascopy in Mitral Disease.—Orthodiascopy has been used as a 
method of establishing the diagnosis of valvular lesions upon the assumption 
that these produce typical changes in cardiac contour. With reference to 
mitral disease, it is true that many advanced decompensated patients con- 
form in a general way to an orthodiascopic type, but those with quiescent and 
compensated lesions may possess hearts of normal size and contour. This 
indeed might be suspected from postmortem findings of mitral disease where 
the process has caused little change from the normal in the size, form and 
weight of the organ. Two illustrations are given in Figs. 241 and 242 of 
mitral disease with a normal sized heart. The former is of a woman of 30 
with a mitral regurgitant lesion of ten years duration; the latter is from a girl, 
aged 17, with a double mitral lesion of four years duration. In both there 
were typical physical signs of the respective valvular lesions; both were 
compensated, the patient with double mitral disease was still suffering from 
rheumatic manifestations at the time that the orthodiagram was taken. 
Another instance is the tracing of a tall, well-built lad of 18, (Fig. 251), who 
recently recovered from the acute manifestations of mild rheumatic mitral 
regurgitation. 
Decompensated double mitral lesions with auricular fibrillation are those 
w’hich usually conform to a general orthodiascopic type. The aorta may 
retain its normal outline or be dilated to a varying degree, even in the absence 
of physical signs of an aortic lesion. The remainder of the cardiac contour 
forms one large fused outline—the globular heart—consisting of the dilated 
pulmonary artery, left ventricular and auricular curves on the left side, and a 
ballooning out of the right auricular curve on the other. Figures 243, 244, 
245 are examples showing varying degrees of size and rotundity of outline 
from three cases of decompensated double mitral lesions with auricular 
fibrillation. All the patients were adults. In one (Fig. 243), the aortic 
curve is normal; in the others, it is dilated. Another interesting example 
of the globular heart (Fig. 246) is the orthodiagram of a boy of 11 with 
a decompensated double mitral lesion and auricular fibrillation. Occasion- 
ally, the orthodiascopic tracings of patients with these lesions show neither 
extreme enlargements nor definite rounded outline. Thus Fig. 244 is the 
tracing of a man of 50 who only recently developed auricular fibrillation; 
Fig. 248 is that of a woman of 46 who has had the valvular lesion and arrhyth- 
mia for many years. Other variations from the typical globular form are 
sometimes found in chronic cases of double mitral disease with fibrillation 
in which there is disproportionate right- and left-sided enlargement. For 
example, the tracing in Fig. 250 is from a patient of 55 with an old double 224 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 247. 
Fig. 247, 248.—Orthodiascopic tracings showing a somewhat globular heart with moderate 
enlargement. From cases with double mitral lesions and auricular fibrillation. 
Fig. 248. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
225 
Fig. 249.—Extreme rounded right-sided enlargement. The left contour is enlarged 
downward. From a case of double mitral lesion, auricular fibrillation and cardiac failure. 
Fig. 250.—Copy of orthodiascopic tracing of a woman of 35 with a double mitral lesion of 
20 years’ duration. There is only very slight left-sided enlargement. 2 26 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 251.—Normal orthodiascopic tracing of a tall boy of 18 suffering from a recent mitral 
regurgitant lesion. 
Fig. 252.—Orthodiagram of a woman of 35 with a mitral regurgitant lesion showing a 
somewhat ovoid contour with moderate dilatation to the left. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
227 
mitral lesion, frequently decompensated, and with auricular fibrillation. 
There is a sharply rounded right-sided enlargement, the left side is enlarged 
downwards and outwards; the resultant silhouette is an irregular ovoid. 
Of great interest from the orthodiascopic standpoint are those patients 
with chronic double lesions without auricular fibrillation in whom there 
has never been any severe break of compensation. The tracings are some- 
times normal in configuration and size, as in the cases already described 
(Figs. 241, 242), or the enlargement is too slight to be of diagnostic significance. 
Thus, a woman of 45 had a double mitral lesion over twenty years. Recently 
she developed occasional extrasystoles accompanied by a subjective feeling of 
“weakness” in the chest. Otherwise she has never had any cardiac com- 
plaint. The orthodiascopic tracing (Fig. 251) shows only very slight left- 
sided enlargement. 
In chronic mitral regurgitation with decompensation, the orthodiascopic 
tracing is usually ovoid or somewhat circular in shape. The longest axis 
lies diagonally, the larger end corresponding to the left ventricle. The 
elements constituting the abnormal form are moderate enlargement of the left 
auricular, the left ventricular-, and the right auricular curves. An instance 
of this is seen in Fig. 252, a female aged 35, with a rheumatic mitral regurgi- 
tant lesion; the orthodiagram shows an ovoid heart with moderate dilatation 
of the left border. If decompensation in patients with chronic mitral regur- 
gitant lesions is extreme, the entire contour becomes circular. 
Orthodiascopy in Rheumatic Aortic Disease.—With reference to rheu- 
matic lesions of the aorta, one of the chief fluoroscopic characteristics is the 
degree of the aortic excursion—the aortic fling. This is often observed in 
patients with double aortic lesions whether compensated or not. As a 
rule, the aorta itself is not permanently enlarged, although the erroneous 
impression is gained from its occasional violent systolic expansion. There 
appears to be some relation between the clinical severity of the disease as 
gauged by the dyspnoea and cardiac reserve power, and the degree of the 
aortic fling. In patients severely ill, the entire aorta—the ascending arch 
and the descending portions—pulsates so violently as to resemble an aneu- 
rism; those less ill usually show excursion limited to individual sections of 
the aorta. Another fluoroscopic characteristic of aortic lesions is the sharp, 
vigorous left ventricular contraction, with a distinct lifting motion of the 
apical region. When left ventricular hypertrophy is extreme, the contrac- 
tion of the apical region is so marked as to appear separate from the remain- 
der of the left ventricle, the whole giving the impression of a see-saw motion. 
In general, it may be stated that the ventricular excursion during systole is 
greater in aortic valvular lesions than in the other types of cardiac disease; 
this is sometimes of diagnostic significance in suspected aortic disease with 
indistinct and atypical physical and clinical signs. 
The change in cardiac contour found in aortic valvular lesions is more 
constant than in mitral disease. The apical region is enlarged and obtuse, 2 28 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 253.—Orthodiagram of old double aortic lesion showing left ventricular hypertrophy 
(so-called “duck-shaped” heart). 
Pig. 254.—Orthodiagram of a patient with aortic regurgitation. From a boy of 19, 
showing left ventricular hypertrophy and moderate enlargement of the aortic arch. The 
pulmonary and left auricular curves are small. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
229 
and the apex itself is often found near the axillary line. The body of the 
left ventricle is egg-shaped. The right auricular curve is moderately 
increased in convexity, the entire auriculo-ventricular outline presents an 
abnormally broadened, flat, somewhat egg-shaped oval, with the wide end at 
the apex. In conjunction with curves formed by the aorta and pulmonary 
artery, the entire cardiac outline sometimes roughly resembles the “duck- 
shaped heart” described by Groedel. 
Several typical illustrations of double aortic lesions follow: Fig. 253 is the 
orthodiagram of a woman of 55 with an old rheumatic history. There was 
dilatation of the arch and first part of the aorta. The entire left ventricle 
was greatly hypertrophied, its outline enlarged, the pulmonary curve flat- 
tened, the left auricular curve very small. Fluoroscopically, there was very 
marked aortic fling of the entire visible aorta. 
Figure 254 is the tracing of a boy of 19 with a rheumatic aortic lesion of 
twelve years’ duration. There was marked left ventricular hypertrophy, 
the pulmonary and left auricular curves were small. There was moderate 
dilatation of the aortic arch; fairly marked aortic fling was present. Whether 
the right-sided enlargement was due to the right auricle itself, or whether an 
enlarged left ventricle pushed the right auricle abnormally to the right, was 
not clear. 
While the entire foregoing description applies especially to double 
aortic lesions, with some difference it also applies to the comparatively 
rare cases of aortic stenosis alone. In the latter the size and shape are 
similar to the former, but enlargement of the various curves is not extreme, 
and the aortic fling is not as marked. 
Orthodiascopy in Combined Aortic and Mitral Disease.—When both the 
aortic and mitral valves are affected, the orthodiascopic tracing usually 
follows the type of the lesion clinically predominant. Thus, Figs. 255 and 
256 are taken from two cases with mitral regurgitation and double aortic 
lesions. The first is that of a girl of 12 in whom endocarditis developed at 
the age of 5; the second, that of a girl of 19 the duration of whose endocarditis 
could not be determined. The first is not characteristic of either lesion; the 
second shows the characteristics of aortic lesions from which this patient 
clinically suffered. 
Orthodiascopy in Aortitis.—Aortitis (Chapter XVII) with secondary 
involvement of the aortic cusps belongs in a different category from the 
rheumatic valvular lesions. Although calcification and thickening of the 
aorta do not necessarily imply enlargement and dilatation, nevertheless 
the latter is the rule in aortitis. The lesion may be confined to the first part, 
(the ascending aorta), to the arch, or to the descending thoracic aorta; or it 
may involve the entire thoracic and even part of the abdominal aorta. 
Hence, it is important to distinguish aneurismal dilatations and enlargements 
of various parts of this vessel. 230 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 255. 
Figs. 255, 256.—Orthodiagrams of two cases of double mitral and aortic lesions. The 
outlines are characteristic of the latter in Fig. 256. Fig. 255 is not characteristic of either 
lesion. 
Fig. 256. ■TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
231 
Fig. 257.—Dilatation of the aortic arch and left ventricular hypertrophy. From a patient 
with chronic nephritis and moderate hypertension. 
Fig. 258.—Aortitis with enlargement of the first portion and arch of the aorta, and left 
ventricular dilatation. From a patient of 65 with symptoms of general arteriosclerosis 
appearing one year after a severe grippe infection. 232 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 259.—Dilatation of the aortic arch and left ventricular hypertrophy. From a patient 
of 60 with arteriosclerosis. 
Fig. 260.—Aortitis of the first portion and arch of the aorta, and extreme left ventricular 
hypertrophy. From a man of 50 with cardiosclerosis and decompensation. The first 
clinical symptoms occurred six months after a very severe streptococcus pneumonia. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
233 
Fig. 261.—Luetic aortitis affecting the arch. Left ventricular hypertrophy. From a 
patient of 60 with a luetic history and a positive Wassermann reaction. 
Fig. 262.—Enlargement and low implantation of the first portion of the aorta; moderate 
enlargement of the left ventricle. From a male patient 58 with chronic nephritis and 
myocarditis. 234 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Fig. 263.—Luetic aortitis affecting the arch; left ventricular hypertrophy. 
Fig. 264.—Diffuse aneurismal dilatation of the descending thoracic aorta. From a 
patient of 69 with a history of a luetic infection 40 years ago, and a positive Wasser- 
mann reaction of the blood. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
235 
Moderate dilatation and enlargement of the first or ascending part of the 
aorta are characterized by an abnormally broad shadow which originates 
below the normal level. The left border of the arch is found beyond its 
usual limits and, in addition, may be sharply curved. The entire aortic 
G. 265.—Photograph from X-ray plate, showing aneurismal dilatation of the descending 
thoracic aorta. 
shadow thus becomes abnormally broad. This type of enlargement accom- 
panies aortitis from any cause-—senile arteriosclerosis, chronic nephritis with 
hypertension, luetic aortitis. It is rarely found in rheumatic aortic valvular 
disease. 
As with standards of measurements for the cardiac orthodiagram, simi- 
larly there are several objections to a standard measurement for the normal 236 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
aorta. Some of these objections are the indefinite point of origin of the 
aorta, the difficulty at times of deliminating its borders, the high or low 
position of the arch, the normal variation in size and shape of the heart of 
each individual. In aortic dilatation of moderate degree, the diagnosis may 
Fig. 266.—Photograph of Roentgenogram of aneurismal dilatation of the descending 
thoracic aorta; left ventricular hypertrophy. From a woman of 50 with a positive Wasser- 
mann reaction of the blood. 
therefore depend upon abnormal contour rather than upon abnormal size 
of the vessel. In moderate dilatation of the ascending aorta there is a slight 
outward ballooning of the right aortic outline; in moderate dilatation of the 
arch, the curve is broadened, while in that of the descending part of the arch, 
there is distinct widening of the entire aorta. Finally, there are dilatations TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
237 
confined to the descending thoracic aorta (Chapter XVI); the latter then 
assumes a spindle-like or diffuse enlargement, which lies mainly behind the 
ventricles. The various types of aortic enlargement are best seen and recog- 
nized by turning the patient in different directions in order to obtain lateral 
and diagonal views of the aorta. This is of particular value in differenti- 
Fig. 267.—Aneurismal dilatation of the arch and descending thoracic aorta. 
ating aortic shadows from other structures, for example, from tumors, which 
in a sagittal direction may resemble and be mistaken for the aorta in area 
and position. 
Orthodiagrams of various types and degrees of aortitis with accompany- 
ing cardiac hypertrophy, and of aneurismal dilatations are shown in Figs. 
257-267, with a brief summary of their etiology and clinical diagnosis. 
The X-ray and orthodiascopic examination of aneurisms is described in 
Chapter XVI. 
REFERENCES 
Bardeen: Determination of the Size of the Heart by Means of X-ray; American Journal of 
Anatomy, 1918, XXIII, 423. 
Cohn, A. E.: An Investigation of the Size of the Heart in Soldiers by the Teleroentgen 
Method; Archives of Internal Medicine, 1920, XXV, 499. 
Dietlin, H.: Ueber Groesse und Lage des normalen Herzens und ihre Abhaengigkeit von 
physiologischen Bedingungen; 2^len Kongress fuer Innere Medizin, 1906, 267. 
Emerson, H.: Status Lymphaticus in Adults, Its Clinical Diagnosis and Importance; 
Archives of Internal Medicine, 1914, XIII, 169. 
Groedel, F. M.: Die Roentgendiagnostik der Herz-und Gefaesskrankheiten. 
Meakins and Gunson: Orthodiagraphic Observations on the Size ... of Irritable 
Heart; Heart, 1918, VII, 1. 238 
TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
Moffatt, R. D. and Neuhof, S.: Congenital Dextrocardia with Patent Interventricular 
Septum; American Journal of Diseases of Children, 1915, X, 1. 
Norris, C.: On Status Lymphaticus; Johnson’s Surgical Diagnosis, III, 705. 
Smith, Bertrand: Teleroentgen Measurements of the Hearts of Normal Soldiers, Archives 
of Internal Medicine, 1920, XXV, 522. 
Veith, A.: Ueber orthodiagraphische Herzuntersuchungen bei Kindern, etc., Jahrbuch 
fuer Kinderheilkunde, 1908, LXVIII, 268. 
Table of Averages1 
No. of cases 
Weight, 
kg.2 
Height, 
c.m. 
Age, 
yrs. 
Trans- 
verse 
diam- 
eter, 
c.m. 
Long 
diam- 
eter, 
c.m. 
Area, 
sq. c.m. 
Angle,3 
deg. 
2 
53 
154 
25 
13.0 
13-5 
98 
37 
2 
54 
163 
3° 
11.9 
13.2 
97 
43 
I 
55 
158 
29 
12.8 
14-5 
122 
42 
4 
56 
167 
24 
12.8 
14.2 
106 
44 
4 
57 
166 
23 
11.9 
14.2 
107 
50 
3 
58 
167 
24 
11.8 
13-3 
100 
46 
4 
59 
169 
22 
12.0 
13-7 
hi 
46 
9 
60 
171 
24 
12.3 
138 
103 
4i 
S 
61 
168 
26 
11.9 
13.2 
IOI 
4i 
6 
62 
169 
27 
12.S 
14.1 
no 
44 
IX 
63 
169 
28 
12.6 
13-8 
I OS 
43 
IO 
64 
170 
26 
12.7 
13-9 
106 
40 
9 
65 
171 
23 
12.6 
13-9 
112 
43 
6 
66 
170 
23 
12.4 
14.4 
in 
45 
IO 
67 
170 
25 
13-7 
14.4 
no 
35 
IO 
68 
173 
25 
13.2 
14-5 
122 
4i 
12 
69 
175 
28 
T3 -3 
14-5 
117 
4i 
IO 
70 
175 
27 
i3-i 
14.2 
108 
4i 
8 
7i 
172 
27 
13-4 
14.8 
112 
38 
9 
72 
173 
23 
13.2 
14-5 
118 
43 
2 
73 
175 
23 
14-3 
14.8 
114 
36 
7 
74 
174 
24 
13-4 
14.4 
no 
38 
8 
75 
172 
25 
13.2 
14.7 
107 
39 
i 
76 
176 
25 
14-5 
15-3 
121 
33 
2 
77 
180 
29 
12.S 
15-4 
126 
48 
2 
78 
171 
26 
14.2 
i4-5 
108 
3i 
3 
83 
180 
24 
13-5 
15-7 
123 
43 
i 
86 
180 
26 
13-8 
14.7 
no 
36 
1 From A. E. Cohn, Archives of Internal Medicine, 1920, XXV, 504. Table of averages 
derived from the data and measurements of the normal hearts of 161 soldiers. 
2 x kg. = 2.2 lbs. 
3 Angle degrees = Angle formed by long axis (L.O.) with transverse axis (M.L.). 
See Fig. 236A and B. TELEROENTGENOGRAPHY, ORTHODIASCOPY AND FLUOROSCOPY 
239 
Table Showing the Average Transverse Diameter Corresponding to a Given 
Body Weight as Reported by Various Observers Compared to the Standard 
Given in Tables A and B1 
Average transverse diameter 
Veith 
Claytor and 
Bardeen, 
Merrill, vertical 
sitting 
Weight 
Stand- 
Supine 
Sitting 
Dietlen 
Otten, 
ard 
supine 
supine 
Male 
Male 
Female 
Male 
Female 
Male 
Female 
I 
2 
Kilos 
c.m. 
c.m. 
c.m. 
c.m. 
c.m. 
c.m. 
c.m. 
c.m. 
c.m. 
c.m. 
c.m. 
15-19 
8.3* 
8.9 
8.9 
8.75 
8.1 
8.7 
8.1 
20-24 
9.0 
10.2 
8.6 
9.42 
9.1 
9-3 
8.6 
25-29 
9.6 
9.4 
10.0 
9.2 
94 
9-4 
30-34 
10.2 
10.8 
10.5 
10.3 
9-5 
9-8 
35-39 
10.7 
10.2 
10.4 
10.57 
9.8 
10.6 
9.8 
40-44 
II . I 
10.7 
11.3 
11.1 
10.2 
45-49 
IX.5 
10.8 
11.3 
11.4 
11.4 
10.2 
50-54 
11.9 
12.0 
11.7 
12.4 
11.6 
10.7 
55-59 
12.3 
12.4 
12.2 
12.9 
12.3 
10.9 
11.0 
60-64 
12.6 
12.7 
12.2 
13.i 
12.7 
11.8 
11.2 
65-69 
13.0 
13.0 
14.2 
13.2 
12.7 
11.8 
11.1 
70-74 
13-3 
12.9 
12.8 
13.4 
130 
12.3 
11.6 
75-79 
13.6 
13.5 
143 
13-2 
12.4 
11.9 
8O—84 
139 
13.7 
14.4 
12.9 
1 From C. R. Bardeen, American Journal of Anatomy 1918, XXIII, 448. 
Tables A and B contain Bardeen’s standard measurements derived from many individuals with 
normal hearts. CHAPTER XIII 
HISTORY RECORD—NORMAL HEART SOUNDS—PHYSICAL 
EXAMINATION OF THE HEART—ABNORMAL SOUNDS 
AND MURMURS 
History Record.—I know of no more important preliminary in the 
physical examination of the heart than a painstaking history, carefully 
obtained, of the patient’s illness and complaints. This phase of cardio- 
vascular examination is often neglected, yet it is here that the clinician of 
broad general experience holds a well-merited position, for by his experience 
he is enabled to evaluate perhaps a prolix story, separating the important 
from the non-important. Where indicated he may concentrate his attention 
upon apparently trivial symptoms. He may, for example, be more interested 
in the gastric symptomatology of a patient with precordial pains and stomach 
complaints than in the cardiac complaints per se, especially if the examiner 
gain the impression that the cause of the pains lies outside of the heart. 
The questions then must bring out such complaints and symptoms as eructa- 
tions, pyrosis, discomfort after meals, local tenderness, etc., particularly if the 
patient has given no definite history of a rheumatic, tonsillar or scarlatinal 
infection, the usual forerunners of cardiac disease. Often the history must be 
pieced together or again gone over after the physical examination has been 
completed. For instance the latter may demonstrate entire absence of 
organic cardiovascular disease and yet extrasystoles may be present. More 
searching questioning may then reveal sudden fright, for example—perhaps 
long since forgotten by the patient—as the underlying cause of the cardiac 
irregularity. As has been previously pointed out (Chapter XI), the clinician 
must possess full knowledge of all the peculiar and varied subjective sensa- 
tions that extrasystoles produce in some individuals, for these cardiac irregu- 
larities may never show themselves even during prolonged or repeated 
examinations and yet the patient’s sensations are so characteristic that, if 
properly interpreted by the clinician, the presence of the arrhythmia can be 
correctly diagnosed in the majority of instances. In this connection, I 
may state that it is very important to know the patient’s temperament, 
especially whether phlegmatic or excitable. One is sometimes deceived into 
thinking that an apparently phlegmatic manner reflects the individual’s 
temperament. But by further questioning he may elicit the fact that the 
patient is often aroused and “fussed up ” over apparent trifles; or that business 
worries cause restless nights; or that he is too busy to eat calmly and hence 
bolts his food; or in the case of women, that apparently trivial household 
240 HISTORY RECORD—PHYSICAL EXAMINATION 
241 
derangements cause nerve tension and even extreme excitability. I could 
exemplify these statements by many examples; but common sense, experience 
and the tact of the examiner alone must guide his questions along the proper 
channels. I simply wish to emphasize the importance of personal knowledge 
of each individual’s temperament. Temperament is often an extremely im- 
portant factor not only in the initiation of symptoms but also in their con- 
tinuance, and especially in their reaction to therapy. This statement applies 
to organic as well as to functional cardiac disease. 
I have not been able to follow any invariable method of procedure in 
procuring a history record. As an opening question, the usual and most 
natural one is to discover why the patient seeks medical advice. Since in 
cardiac cases, the chief complaints are dyspnoea and abnormal chest sensations, 
one inquires searchingly regarding these: Their duration, mode of onset, 
peculiarities, what aggravates them, etc. One should especially inquire into 
the effect of exercise upon dyspnoea and precordial sensations. It must of 
course be remembered that there are various grades of dyspnoea (Chapter 
XIV)—slight breathlessness, actual dyspnoea, polypnoea—and that a certain 
amount of breathlessness accompanies any severe exertion. It is for the clini- 
cian to judge how far these sensations are abnormal by observing the patient 
during rest, both sitting and lying down, as well as the patient’s reaction 
to such exercise as the physician sees fit to employ in order to test the patient’s 
functional capacity (Chapter XIV). One inquires how far the patient can 
walk comfortably. Do the pains, if present, radiate? Does he get short of 
breath with their onset? What are the characteristics of the pains: Tearing, 
agonizing, burning, tingling, etc. (Chapters XXIII, XXIV). Does excitement 
produce them? Does his heart “thump” or “palpitate” when exer- 
cising? Does he avoid stair climbing? These are examples of some sugges- 
tive preliminary questions. The clinician of course does not neglect careful 
inquiry into a history of actual rheumatism, tonsillitis, scarlet fever, syphilis 
and of alcoholism. I emphasize actual rheumatism, especially inflammatory 
rheumatism, for there is scarcely any individual who at one time or another, 
has not had muscular pains. Regarding syphilis, tact is often required, at 
least in private practice, in order to elicit this etiological factor. With 
married men, unless the information is volunteered, I inquire regarding 
venereal disease prior to marriage. With married women, we must usually 
approach this subject by inquiring about miscarriages, eruptions, sore throats, 
etc., the usual manifestations of syphilis. 
After the history has been obtained, my usual routine is to have the 
patient rest comfortably in a chair with the chest entirely bared. First I 
examine the teeth and tonsils. Then I search for enlarged glands about the 
jaw and palpate the thyroid. The next procedure is the taking of the blood 
pressure. If hypertension be present and if I believe from the history or 
from actual observation that the reading has been abnormally heightened 
because of a nervous element," I either take another reading at the end of the 242 
HISTORY RECORD—PHYSICAL EXAMINATION 
examination or better still, I allow the cuff to remain on the arm for a few 
minutes in order to nullify or decrease an abnormally heightened vasomotor 
tone (Chapter XXV). Next follows the routine physical examination of the 
heart itself, described later. The lungs are then examined while the patient is 
still seated. Unless the patient is obviously severely decompensated, the 
heart is again examined after such exercises as rapid walking, bending, hop- 
ping, etc. The type of exercise is guided by the special observation the ex- 
aminer wishes to make, as for example, the effect upon rate and cardiac 
activity, upon blood pressure, upon the first appearance of dyspnoea, 
etc. 
The next procedure is to examine the heart with the patient lying com- 
fortably upon the examining table. A routine abdominal examination 
follows. Points of tenderness, an enlarged liver, gastric distention, viscerop- 
tosis are looked for. The physical examination of the abdomen should be 
particularly searching when gastric symptoms and functional arrhythmias are 
present. The knee and pupillary reflexes are examined while the patient is 
still in the recumbent position. Then follows orthodiascopy of the heart, 
entire chest, lungs and mediastinum. The taking of an electrocardiogram 
is the next step. While the left leg electrode is still in place the leg is 
examined for edema. The purpose of pressing upon the tibia should not 
be made too obvious to the patient. In order to distract attention 
from the real purpose, I usually inquire whether the pressure is painful. 
Urinary examination—preferably of a 24 hr. specimen—completes the routine 
examination. When indicated, but often as a routine, a Wassermann blood 
examination, and a red and white blood cell examination are made. A chemi- 
cal examination of the blood, a phthalin test (Chapter XXI) and an examina- 
tion of the eye grounds may be required in individual instances. 
Normal Heart Sounds.—The time relationship of the heart sounds in the 
cardiac cycle has been definitely fixed by the aid of phonocardiograms 
(Chapter XXXI). The cause of the normal heart sounds is still a matter of 
dispute, the main question at issue being whether the normal heart in con- 
tracting can produce a sound. Weighing physiological, dynamic and phono- 
cardiographic considerations, the most probable cause of the normal first 
sound is as follows: With beginning ventricular contraction, there is simul- 
taneous contraction of the papillary muscles. At the same time, with 
beginning rise of intraventricular pressure, the mitral and tricuspid valves 
close synchronously and noiselessly. This closure is immediately followed 
by that very brief interval known as the isometric period (Chapter VI) during 
which all valves are closed. The increasing intraventricular pressure before 
actual systole (the ejection period), the vibrating valves, the ventricular 
muscular contraction, are all factors that produce the first part of the first 
sound; this part of the first sound is transmitted throughout the heart and 
great vessels. With ejection of the blood (immediately after the isometric 
period) during ventricular systole, a large fluid' column is thrown against the HISTORY RECORD—PHYSICAL EXAMINATION 
243 
walls of the pulmonary artery and aorta; this ends and produces the second 
part of the first sound, at the same time that it changes its acoustic character 
(Wiggers). 
The second sound is usually regarded as being entirely valvular in 
character, and as due to closure of the semilunar valves. According to Wig- 
gers, these valves close noiselessly and the second sound is produced by after- 
vibrations of the closed valves caused by the arterial columns in the aorta 
and pulmonary artery. Some clinical observations, however, do not entirely 
conform to this theory of the origin of the second sound, at least as far as 
pathological hearts are concerned. For example, in some cases of mitral 
disease one may not only hear but actually feel the snappy click of a sharply 
closed pulmonic valve synchronous with the second sound. 
Third Heart Sound.—In some young normal adults, a faint third heart 
sound at the apex in mid-diastole may be heard by placing the patient in the 
left lateral position. It is soft and low-pitched. Phonocardiograms (Chap- 
ter XXXI) of the sound have been obtained. The explanation given for the 
third heart sound is that it is due to the sudden floating up and tension of the 
auriculoventricular valves from the first onrush of blood from auricle to 
ventricle. Other observers (Lewis, Einthoven) have questioned this eti- 
ology, so that, for the present, the cause of the third heart sound cannot be 
considered as definitely established. 
The character of the first heart sound in individuals with normal hearts 
is often regarded as of considerable importance, since upon it wide-reaching 
conclusions regarding the circulation are based. Thus it is often spoken 
of as being of “poor muscular quality,” or as being “weak.” Such con- 
clusions, however are often erroneous, for there are many extraneous physi- 
cal factors, such as thickness of the thorax, distance of the heart from the 
chest wall, an intervening pad of lung tissue, configuration of the chest wall, 
which can “weaken” an otherwise normal and strong first sound. In 
addition, some so-called “weak” hearts are often surprisingly strong in their 
contractions (Chapters XII, XVIII). On the other hand if a heart that is 
obviously hypertrophied causes weak heart sounds, especially in the pres- 
ence of hypertension, I consider it suggestive of weakened cardiac contrac- 
tility, for such a heart, when compensating, ordinarily produces a vigorous 
first sound at the apex. 
The normal pulmonic second sound is ordinarily less loud than the 
second aortic (P2<A2). When the reverse is true (P2>A2) it is usually 
regarded as an evidence of an overforceful right ventricle due to disturbance 
in the pulmonary circuit. This is sometimes true, especially in mitral 
disease. But, as with the first sound, many physical extra-cardiac condi- 
tions may invalidate conclusions based upon an accentuated second pul- 
monic sound alone, if other important clinical and circulatory factors are 
not considered. These will be discussed more in detail in conjunction with 
the various valvular diseases. 244 
HISTORY RECORD PHYSICAL EXAMINATION 
Physical Examination of the Heart.—Each of the usual methods of 
clinical examination—inspection, palpation, percussion and auscultation— 
yields valuable information in appropriate cases. Ordinarily, most emphasis 
is placed upon auscultation and percussion,—less upon inspection and palpa- 
tion. In my opinion the two latter, although frequently neglected as routine 
methods of examination, are often of diagnostic and prognostic importance. 
Least valuable and most deceptive of all methods is information gained by 
percussion. 
I reserve for later consideration, (Chapter XV) the special abnormal 
physical signs found in various types of heart disease. Here I shall describe 
the general information to be gained by following routine procedures appli- 
cable to all kinds of cardio-vascular disease. 
Inspection.—Inspection of the chest and neck frequently reveals impor- 
tant data concerning the cardiovascular system. 
Jugular Pulsation.—The manner of filling and the degree of distention 
of the jugular veins is best observed by placing the patient in the supine 
position. Even pulsation of the thyroid veins may thus become visible. 
In patients with long-continued decompensation it is common to find the 
jugular veins tortuous, thickened, engorged and greatly distended; the 
situation of the venous valves is then well outlined and may be recognized 
as small knob-like prominences. These evidences of chronic venous stasis 
are especially marked in old stenotic lesions with auricular fibrillation, 
or in old patients with decompensated cardiosclerosis. Tricuspid regurgi- 
tation from relative insufficiency or valvular disease is sometimes accom- 
panied by engorged or hyperactive pulsatile jugulars, although, as previously 
mentioned, (Chapter VII), the interposition of the right auricle probably 
prevents such jugular hyperaction in many instances. In cases of auricular 
extrasystoles, the premature jugular pulsation (a' wave) may occasionally 
be visible. More often the coincidence of auricular and carotid waves 
(composite a'-\-c' waves, Chapter X) found in ventricular extrasystoles, is 
recognized in the jugulars as abnormally large and premature pulsations. 
A similar jugular wave, not premature in the time of its occurrence, is present 
in complete heart block when auricles and ventricles beat synchronously 
(a+c waves; Chapter X). This observation is of use in the differentiation, 
by inspection, between complete and incorfiplete heart block, for in the latter 
there are no such superimposed waves. In auricular flutter the jugular 
pulsations are usually too faint and indistinct to be counted. However in 
one case which I observed the jugular veins literally throbbed, and were so 
engorged that the number of pulsations could be clearly discerned at a dis- 
tance of several feet. In auricular fibrillation, in addition to the distention 
already referred to, the jugulars beat irregularly in consonance with the 
arrhythmic c—v waves. 
The Carotid Pulse.—The inspection of the carotid pulse is of great 
importance. By its overaction, pulsatile distention and vigor, it is often HISTORY RECORD—PHYSICAL EXAMINATION 
245 
indicative of aortic disease or hypertension; if, in addition, the carotids 
visibly and markedly collapse with diastole, they indicate an aortic regurgi- 
tant lesion. Vigorously throbbing carotids also accompany rapid and 
violent heart action from any cause, (for example, exopthalmic goiter). 
But marked carotid hyperaction with a normal pulse rate in the middle-aged 
or in the old is usually evidence of aortitis or of hypertension; its absence, 
however, does not necessarily exclude these conditions. This type of carotid 
action is also seen, although rarely, in young individuals with normal hearts; 
in them, it often corresponds to strong systolic ventricular contractions which 
can be very readily observed by fluoroscopic examination. Extrasystoles 
corresponding to so-called “missed beats” at the radial are sometimes visi- 
ble as momentary breaks in the otherwise rhythmical carotid pulsations. 
Occasionally the extrasystolic beat itself is seen as a fainter beat. Grossly 
irregular carotid pulsations are often seen in auricular fibrillation; these 
naturally correspond to the usual tumultuous irregular cardiac activity 
typical of this arrythmia. 
Aortic Pulsation.—Allied to carotid overaction in clinical significance is 
aortic pulsation, recognized by the pulsatile rise of the tissues in the jugulum. 
This indicates more advanced aortic change than does carotid overaction 
alone. Aortic expansion is most noticeable in aortic regurgitation with left 
ventricular hypertrophy, and in aneurism and aneurismal dilatation of vari- 
ous parts of the aorta (Chapter XVI), especially during the stage of decom- 
pensation. On the chest wall, capillary pulsation characteristic of aortic 
regurgitation may occasionally be seen. A band of dilated venules and 
capillaries over the lower anterior part of the chest sometimes accompanies 
aortic lesions, particularly aneurisms or aneurismal dilatations. Unless 
well marked, however, they are not characteristic of aortic disease, for they 
are sometimes found in obese individuals (especially in men) without aortic 
disease. Large aneurisms that touch, adhere to, or erode the chest wall 
naturally give rise to visible pulsatile expansion; their usual site is the 
second and third interspaces and the interclavicular notch, more rarely the 
left upper interspaces. Aneurismal dilatations of the aorta very infrequently 
cause erosion, and are rarely adherent. If they touch or approach the chest 
wall, pulsatile expansion, not noticeable otherwise, may be seen by placing 
the eye on a level with the chest. By this method, not only dilatations of the 
first part and arch, but even aneurismal dilatation of the descending thoracic 
aorta (Chapter XVI) may be discerned as distinct systolic heaves above 
and partly behind the rise of the left ventricle. 
Inspection of the Apical and Precordial Region.—Regarding the apical 
and precordial region, important information can be gleaned by inspection 
alone. In thin-chested individuals with decompensated mitral stenosis, it is 
often possible to discern an overacting pulmonary artery which, upon auscul- 
tation, produces an accentuated, clicking second sound. Many varieties of 
abnormal ventricular action are also readily recognized by inspection. Thus 246 
HISTORY RECORD PHYSICAL EXAMINATION 
ventricular activity is visible over almost the entire precordium in massive 
left ventricular hypertrophy, in the violent action of tachycardia, in the 
ventricular dilatation of the acute stages of valvular endocarditis, or in 
some congenital lesions. An overactive ventricular impulse may be confined 
to a small area at the apex in mitral lesions, especially in young individuals. 
One often finds heaving, broad ventricular impulses in old, decompensated 
mitral lesions. Obviously the thickness of the chest wall, the posture of the 
patient and the illumination are considerations which considerably mask 
or influence these physical signs. In thin-chested individuals or in women 
with the left breast well raised, it is sometimes possible to distinguish a double 
systolic impact corresponding to the reduplicated first sound (q. v.) heard on 
auscultation. Some types of arrhythmias are also recognized by inspecting 
the apex. The regular, slow ventricular activity of heart block, the irregular 
ventricular action of auricular fibrillation, the apparent intermission of cardiac 
activity denoting premature contraction—all these are often distinguishable 
upon inspection of the apical region. The extrasystolic contraction itself 
is rarely seen because it is usually too weak to cause a visible ventricular 
impact. The movement of the apical region during the respiratory phases 
may likewise be observed in those thin or moderately thick-chested indivi- 
duals who possess a fair amount of diaphragmatic excursion. 
Inspection of the Right Lower Interspaces.—Over the right lower chest, 
aside from aneurisms and aneurismal dilatations already mentioned, very 
little information can be gleaned by inspection. Right auricular and 
ventricular enlargement rarely give rise to visible pulsation. I have met 
with isolated exceptions, however. One case was that of a boy of 17 with 
a double mitral lesion and a somewhat enlarged liver. At the time of hos- 
pital admission he was suffering from an acute rheumatic exacerbation of 
his endocarditis. To the right of the sternum, in the third and fourth 
interspaces, there was a visible pulsatile area approximately the size of a 
pigeon’s egg. Over this, there was heard a very loud harsh murmur; a rough 
palpable thrill was also present; both were systolic in time. Fluoroscopic 
examination showed that the pulsation was due to a greatly enlarged right 
auricle. The patient died a few weeks later. At necropsy, a double mitral 
lesion, hypertrophied right and left ventricles, and a hugely dilated, engorged 
and thickened right auricle were found. In situ in the chest cavity, the 
longest measurement of the auricle was 17 c.m., its broadest, 8 c.m., (Fig. 268). 
In another instance of decompensated double mitral lesion in a woman of 26, 
intensely dyspnoeic, cyanotic, and with a pulsating liver there was a similar 
but less marked visable auricular pulsation in the third and fourth inter- 
spaces; a thrill was also heard over the same area. 
Visible epigastric pulsation in patients with dilated and hypertrophied 
hearts is fairly common. It is usually attributed to hypertrophic enlarge- 
ment of the right ventricle, but necropsy reports have not always substan- 
tiated this supposition. HISTORY RECORD—PHYSICAL EXAMINATION 
247 
Liver pulsation as the result of engorgement of the portal circulation is 
not infrequent in decompensated mitral lesions, or in relative (functional) 
tricuspid regurgitation. It is less common in aortic lesions. The pulsations 
may be sufficiently gross to be seen at a distance; at other times close exam- 
ination, with the observer’s eye placed on the level with the patient’s abdomen, 
is necessary to discern the pulsating liver. Auricular fibrillation may occa- 
sionally be diagnosed by inspection of the liver, if its pulsations are mani- 
Fig. 268.—Heart with hugely dilated right auricle (see text). A, dilated right auricle; 
B, midline of body; C, enlarged right ventricle. 
festly and grossly arrhythmic. In one instance of heart block, I was able to 
see the venous auricular pulsations as distinct, small rhythmic pulsatiLe rises. 
That they were actually auricular pulsations was proven by taking polygra- 
phic tracings with a large “venous” cup over the liver (a liver cup), and by 
electrocardiograms showing heart block. 
Palpation.—Palpation in the neck often substantiates the information 
gained by inspection. Extrasystoles may be felt in the carotids when they 
are missed at the wrist. Overacting hearts (for example, in exopthalmic 
goiter) often produce palpable carotid thrills; these may be due to whorls and 
eddies from the violence with which the blood is thrown into the arterial 
circulation. Such short, sharp thrills must be distinguished from the steadier, 
longer continued ones accompanying rheumatic aortic stenosis, and from 
arteriosclerotic roughening and thickening of the aortic valves and walls. 
The typical quick filling and collapsing pulse of aortic regurgitation can also 
be readily diagnosed by palpation of the carotids alone. A point insufficiently 248 
HISTORY RECORD—PHYSICAL EXAMINATION 
emphasized is the knowledge regarding arteriosclerosis which may be gained 
by carotid palpation; the condition of the external carotids whether tortuous, 
thick, hard, and non-elastic, or the reverse, is thus often determined. Simi- 
lar information is occasionally derived by palpation of the common carotid. 
Aortic Pulsations.—With a normal cardio-vascular system and an aortic 
arch situated moderately high in the chest, the finger tip placed in the inter- 
clavicular notch and insinuated behind the manubrium recognizes aortic 
pulsation as a soft quiet impact. In marked hypertension a sense of sharp 
fling is often given to the examining finger. In luetic aortitis with aneurismal 
dilatation, there is a feeling of a broad, strong aortic impact, especially 
when decompensation is present; this is sometimes combined writh a palpable 
thrill. The rough thrill accompanying aortic stenosis, and the sharp rise 
and subsequent collapse of the aortic walls in aortic regurgitation, can also 
be diagnosed by palpation in the jugulum. 
Palpation over the right base of the heart may be of great diagnostic 
importance. In extreme cases of rheumatic aortic stenosis, a rough rasping 
systolic thrill is readily felt in the second and third right interspaces. The 
overacting aorta in aneurism and aneurismal dilatation of the first part of the 
aorta (Chapter XVI), and the sharp aortic pulsatile distension in hyperten- 
sion, are sometimes palpable over the same area. If present in the former, 
it probably denotes an extremely roughened, thickened aortic wall, or extreme 
dilatation. Bulging of the right anterior chest, found in adherent or erosive 
aneurisms, is usually palpable. Pulsations of aneurisms or aneurismal dilata- 
tions of the descending part of the arch, or even of the descending thoracic 
aorta, may occasionally be felt by placing the fingers snugly against the chest 
over the base of the heart on the left side, or in the third and fourth left 
interspaces. In the latter position, the location of the impact area near the 
sternum, and the time of its appearance, serve to distinguish it from the 
impact due to ventricular systole (Chapter XVI). 
In congenital pulmonary stenosis and in patent ductus arteriosus, thrills, 
usually systolic in time, are often palpable over the left base. In congenital 
patent interventricular septum, there is a rough, harsh thrill, systolic in time, 
palpable over the entire precordium, but especially over the lower sternum. 
In patients with dilated and overacting pulmonary arteries, the sharp click- 
like closure of the valves can occasionally be felt by palpation over their site. 
This condition, combined with a murmur over the same area, is common in 
mitral valvulitis in children, in whom it is sometimes incorrectly diagnosed as a 
congenital pulmonary lesion. Similar hyperaction is occasionally present as 
a temporary phenomenon in normal individual. 
Palpation in Mitral Lesions.—In typical mitral stenosis, with the heart 
beating rhythmically, there is a short presystolic thrill or occasionally 
a long diastolic one palpable in the apical region. When the auricles fibrillate 
and the ventricles beat irregularly and tumultuously, an intense rough thrill, 
most prominent at the apex and occupying a varying part of the diastole, HISTORY RECORD—PHYSICAL EXAMINATION 
249 
may be felt; if the irregular ventricular activity be controlled by digitalis, 
the thrill becomes less marked or it may entirely disappear. A palpable 
systolic thrill over the lower precordium not infrequently accompanies 
rheumatic regurgitant lesions, and may indeed be present when the murmur 
itself is faint or absent. This condition was found, for example, in a young 
girl without any previous rheumatic history; she had had frequent attacks of 
dyspoena, and edema of the face and extremities. At the apex a scarcely 
perceptible murmur was heard; it was not transmitted. Over the lower 
precordium there was a very pronounced palpable thrill. Systolic precordial 
thrills may also be felt when the mitral cusps are thickened or covered with 
lime deposits as the result of a cardiosclerotic non-rheumatic process (Chapter 
XVII). 
Further information regarding the character of ventricular contraction 
and of the apex beat may be gained by applying the flattened palm snugly 
over the lower precordial area. The booming broad ventricular shock and 
diffuse apical impact of hypertrophy may thus be readily diagnosed, par- 
ticularly if the heart action be normal in rapidity or be abnormally slow. 
Rapid action, even of a normal sized heart, usually gives the impression of 
enlargement, probably because of the rather violent impact against the 
chest wall. I have often corroborated the normal size of such hearts by 
fluoroscopic examinations. A somewhat thrill-like sensation is imparted 
to the examining hand during systole by the violent overaction which usually 
accompanies tachycardia from any cause. Here the thrill may be due to 
sharp vibratory action of the auriculo-ventricular valves transmitted through 
a thin chest wall or one of moderate thickness. It is sometimes possible to 
recognize the weakened impulse of an enlarged, dilated heart by palpation. 
A double systolic apical impact, corresponding to the reduplicated first 
sound (so-called gallop rhythm, q. v.), when due to left ventricular hyper- 
trophy, hypertension or to aortic valvular lesions, may also be distinguished 
by palpation over the apex. The etiology of these reduplications will be 
discussed in connection with auscultation. Pulsus paradoxus (Chapter 
XI) may be diagnosed by palpation, for there is a gradation in the strength 
of ventricular contractions corresponding to the rhythmic waning and waxing 
of the pulse volume with inspiration and expiration, respectively. This is 
commonly attributed to pericarditis with effusion or to intrathoracic tumors. 
I have observed it in occasional cases of myocarditis with severe decompensa- 
tion, or in the late stage of cardiac failure. 
Finally a double valvular click, occasionally present and due to asynchro- 
nous closure of the individual leaflets of the aortic or pulmonary valves, may 
sometimes be diagnosed by palpation over the respective sites of these valves. 
This sign is present oftener over the pulmonary than over the aorta. 
Percussion.—To the ordinary and older methods of finger and pleximeter 
hammer percussion have been added the auscultatory, and more recently the 
flexed finger (Goldscheider’s orthopercussion) methods. The auscultatory 250 
HISTORY RECORD—PHYSICAL EXAMINATION 
method consists in placing the bell of the stethoscope over the center of the 
sternum and noting when scratch marks or light tappings made by the finger 
nail or finger tips first become audible. Orthopercussion consists in light 
perpendicular tapping over a sharply flexed finger held perpendicular to the 
chest wall, the finger acting as the pleximeter. These two methods have 
been advanced as refinements by which the exact cardiac border could be 
more delicately and accurately outlined. 
Inaccuracy of Percussion Methods (Figs. 269-271).—Careful and con- 
tinued use and observation of the above special as well as the usual methods of 
percussion, checked by comparison with the unequivocal standards fur- 
nished by orthodiascopy and fluoroscopy, have convinced me that all methods 
of percussion are inaccurate and unreliable even for clinical purposes. Besides 
varying among themselves considerably in accuracy, there is no means of judg- 
ing in advance which method will prove sufficiently exact in any individual 
case. In many instances, I have requested experienced and excellent clini- 
cians to map out the cardiac border according to their own favorite method 
of percussion, and I have demonstrated to them by fluoroscopy that the 
results of their examination were rarely of sufficient exactness even for 
general bedside purposes. These statements apply to percussion for super- 
ficial dullness as well as for flatness. For example, very marked aortic 
dilatations were at times entirely overlooked; definite extension of the cardiac 
border to the right was not even approximately delimited. My own gross 
errors by the various methods of percussion have included practically all 
miscalculations: The delimination of the size and of the upper border of the 
aorta, the right border of the heart, and the upper ventricular border. 
Figures 269-271 demonstrate some of these errors in patients with normal 
hearts, in whom mistakes of outline varying from several centimeters to 
almost grotesque proportions have been committed. From the viewpoints 
of physics and acoustics, there seem to be good reasons for diagnostic errors 
in the use of percussion. From the physical standpoint, the heart may be 
succinctly regarded as a blood-containing, more or less soft bag situated at 
various depths from a chest wall of varying thickness. Between the chest 
wall and the heart lies a lung pad of varying dimensions. The great vessels 
—the aorta and the pulmonary artery—are of such heterogenous densities 
that the sound evoked by percussion of the chest wall can but rarely give 
reliable data regarding the size and shape of the heart; tissues of different 
densities do not conduct sound evenly, hence it is impossible to state which 
of the many acoustic variants actually cause the differential dullness. Un- 
less greatly enlarged and near the surface, the aorta, situated normally, 
mainly behind the sternum, is scarcely sufficiently thick-walled or, with 
its contained blood, of sufficient density to cause differential dullness or flat- 
ness on percussion. Similar reasons make difficult the delimination by per- 
cussion of the right cardiac border, consisting of the right auricle below and 
the great vessels above (Chapter XII). Percussion of the left ventricular HISTORY RECORD—PHYSICAL EXAMINATION 
251 
Fig. 269. 
Fig. 270. 252 
HISTORY RECORD—PHYSICAL EXAMINATION 
area is surrounded by less difficulties, for the ventricular mass is denser and 
more uniform; but its approximate size and contour—whether squatty, 
broad, erect or flat, subjects already discussed in connection with orthodi- 
ascopy (Chapter XII)—are considerations which I believe are beyond the 
physical limits of percussion. Frequent comparisons between percussion 
and radiographic findings have also convinced me that the left border of 
the heart may actually be several centimeters beyond the percussed outline, 
and that the lowest point of the heart—the apex as viewed fluoroscopically 
Fig. 271. 
Figs. 269, 270 and 271.—Inaccuracy of percussion methods. The dotted outlines show 
the heart delimited by percussion. The solid lines show the actual cardiac contour obtained 
by orthodiascopy. 
at the end of inspiration—is usually from 2 to 4 c.m. below its position as 
located by percussion or palpation. This difference between the “palpable” 
and “fluoroscopic” apex is especially noticeable in tall, lean individuals with 
flat chests, narrow elongated hearts, and mobile diaphragms. 
A Rational Method for the Determination of the Cardiac Outline.—In 
view of the limitations and of the inaccuracy of percussion methods, I have 
attempted to apply the more exact knowledge gained by roentgenography 
to bedside study of the cardiac outline. The routine I use for this purpose is 
as follows: First, inspection, and second palpation of the precordium. Then 
auscultation to determine the presence and type of a possible cardiac lesion. 
Finally the mapping out of the cardiac outline. 
I begin mapping out either above or at the apex. Assuming that we are 
starting with the latter, I determine the point of the maximal apical impulse. HISTORY RECORD—PHYSICAL EXAMINATION 
253 
In the normal adult heart, if it cannot be readily seen or palpated, it can be 
fixed by auscultation as the point at which the heart sounds at the apex are 
loudest. In children, the maximal apical impulse is readily determined by 
palpation. As determined by fluoroscopy, the apex, regarded as the lowest 
point of the heart, is situated from 2 to 4 centimeters below the site of maxi- 
mal impulse. This variable distance depends on the amount of diaphrag- 
matic excursion and on the type of cardiac contour. The former can be 
roughly estimated by the structure of the chest and the amount of chest 
expansion. The cardiac contour is apt to correspond to the general physique 
of the individual. In the thickest, with short extremities and pudgy hands, 
the ventricular outline is apt to be broad and flat, and to lie with a large part 
of its lower ventricular surface on the diaphragm; diaphragmatic mobility is 
usually limited, therefore the lowermost point of the heart and the maximal 
apical impulse roughly correspond. In the slender and agile with elongated 
cardiac contours, diaphragmatic mobility is usually marked, the lowermost 
part of the heart being much below the area of the maximal impulse. If the 
latter type of individual does not possess an elongated heart, that fact is 
often disclosed by strong and forceful cardiac action, and the cardiac contour 
is determined accordingly. 
Thus, by gauging the two variants—diaphragmatic mobility and the 
type of cardiac contour—the position of the actual apex may be determined 
with a fair degree of accuracy. When thus determined, that point is marked 
upon the chest wall. 
The next fixed line to be marked is the highest part of the aorta corre- 
sponding to the upper level of the aortic arch. The tip of the finger is intro- 
duced as deeply as possible behind the sternum. If aortic pulsation is plainly 
palpable the aorta is regarded as “high” and the upper line of the arch is 
situated within a centimeter below the tip of the palpating finger. If aortic 
pulsation is not plainly palpable, there is low implantation of that vessel. 
The point at which aortic sounds are heard most prominently is then sought 
as a landmark; the upper limit of the aorta is usually about two centi- 
meters above this area. After the upper aortic limit is determined by either 
of these methods, it is marked across the sternum. When viewed fluoroscop- 
ically, it may be roughly estimated that the upper two fifths of the right 
cardiac contour consists of the right aortic curve, and the lower three fifths 
of the right auricular curve (Fig. 236). Normally the ascending aorta, seen 
fluoroscopically, extends about two centimeters from the right sternal border 
and is visable a distance of about 4 to 6 centimeters—that is, this measures 
the distance from the upper aortic limit to the point at which it touches 
the upper border of the right auricle. In thin individuals with long and 
slender hearts, frequently also in those with broader hearts, the right auricle 
extends but a slight distance—a centimeter or two—beyond the right border 
of the sternum and forms a gently convex curve. In short chested, pudgy 
individuals, the right auricle commonly forms a sharper, more convex curve, 254 
HISTORY RECORD—PHYSICAL EXAMINATION 
extending as much as 4 or 5 centimeters from the right sternal border. From 
these considerations, the right cardiac border is marked upon the chest wall. 
The arch of the aorta does not usually extend as low on the left as does the 
aortic curve on the right. In fact, a similar leftsided distance usually includes 
the curve of the pulmonary, contiguous to the lowermost point of the arch, 
(Fig. 236). Depending on its contour, the aorta may make a smooth, some- 
what long curve, which stretches but a centimeter or two beyond the left 
sternal margin; or it may be a sharp, knoblike structure, extending 4 or 5 
centimeters to the left of the sternum. I have as yet found no method of 
determining at the bedside the probable contour of this part of the aortic 
curve. 
After the right side of the heart and the aortic arch have been drawn upon 
the chest wall, the left auricular, and especially the left ventricular curves 
are blocked in. The former is very variable in extent, fluoroscopically, and 
in this bedside clinical method, cannot be separated from the left ventricular 
curve. The latter curve will depend for its contour on the physique of the 
individual. Here, ordinary percussion may be an added aid in delimiting 
this part of the left ventricular outline. People who are short and muscular 
usually have broad hearts, and the ventricular curve is correspondingly flat; 
those with graceful thoraces and limbs have narrow, more erect hearts and 
narrower aortae, hence the left ventricular curve is more elongated. 
I have thus far dealt with the contour of the normal heart. I shall only 
briefly touch upon this method as applied to diseased hearts. In old quies- 
cent mitral regurgitant lesions that have never decompensated, and that 
present no evidence of hypertrophy, with no booming first sound or heaving 
impulse, the contour and size of the heart is approximately that of a corre- 
spondingly normal heart in a person with the same physique (Figs. 241, 242) 
for I have frequently found that such mildly diseased hearts are identical 
with the normal in contour and size. In old decompensated mitral regurgita- 
tion, the left ventricular curve is more rounded, the right auricular curve 
larger, thus the entire heart is broader and more rotund (Figs. 247, 248). In 
old decompensated double mitral lesions, especially with auricular fibrillation, 
the left cardiac border is enlarged to the left; less, in a downward direction; 
the right auricle makes a sharper, rounded curve, so that the entire cardiac 
outline, including its vessels, assumes an extremely rounded form (Figs. 
243-245). This knowledge is important, for the enlarged right auricle can 
rarely be percussed properly. The general knowledge derived from ortho- 
diascopy regarding the type of contour and size of these hearts, if remem- 
bered, will help us considerably in blocking in the cardiac outline after the 
position of the actual apex and the upper aortic margin are determined in the 
manner already described. 
The typical left ventricular hypertrophies which accompany rheumatic 
aortic lesions (especially double aortic lesions) usually give us definite visible 
and palpatory evidence of the enlargement. Booming and reduplicated HISTORY RECORD—PHYSICAL EXAMINATION 
255 
Fig. 272.—Solid outline—actual orthodiascopic contour; dotted line—contour mapped 
out by author’s method; functional tachycardia in a man of 40. 
Fig. 273.—Solid outline—actual orthodiascopic contour; dotted outline—contour mapped 
out by author’s method; normal heart of a man of 35. 256 
HISTORY RECORD—PHYSICAL EXAMINATION 
sounds at the apex occasionally give the impression of extreme enlargement, 
while the fluoroscope will show an aorta only slightly enlarged, but with 
tremendous systolic excursions. This should be recalled in clinically mapping 
out the aorta in such cases, and it should also be borne in mind that the pal- 
pating finger in the jugulum registers and feels this fling, and hence does not 
localize the line of the actual upper aortic limit. In other words, such abnor- 
mal aortic excursion must be taken into consideration, in determing the actual 
upper line of the aorta. 
Another important fact is that rapidly beating hearts, or those overacting, 
almost invariably give the impression of enlargement. I believe they 
Fig. 274.—Solid outline—actual orthodiascopic contour; dotted line—contour mapped 
out by author’s method; normal heart of a m n of 42. 
too, can be mapped out according to the rational scheme already referred to. 
Otherwise, the impression gained by auscultation alone will almost inevitably 
lead to erroneous deductions as to the actual size of the heart. 
Since following what appears to me this logical and rational method of 
mapping out the heart, I have been saved from many of the pitfalls and errors 
into which I had previously fallen. The method follows no rule-of-thumb. 
It presupposes some knowledge of heart size actually seen fluoroscopically and 
orthodiascopically, gained from a study of these subjects. The chief objection 
is that it is not mathematically exact. I should rather call it a scientific 
gauging and weighing of varients, some of which can, after all, be quickly 
and fairly accurately determined at the bedside. On the whole I have found 
the conclusions derived from this method to be much less erroneous, and HISTORY RECORD—PHYSICAL EXAMINATION 
257 
therefore much more satisfactory than those derived by practicing various 
percussion methods. Figs. 272-274 are examples of actual orthodiascopic 
cardiac contours compared with the outline derived by the method I have 
just described. 
AUSCULTATION 
Despite drawbacks and opportunities for error, auscultation is the most 
accurate of the four methods for the detection of the type of valvular or 
myocardial disease. Indeed, the diagnostic aid given by murmurs is often 
overlooked or minimized, because many individuals with valvular disease 
and murmurs are compensated and carry on as well as those with organically 
sound hearts. The presence of cardiac murmurs (by which are meant 
adventitious sounds, not merely modifications of the normal), their time 
relationship to events in the cardiac cycle, their intensity, quality, pitch 
and timbre, and the direction of their propagation anteriorly, laterally and 
posteriorly as well as through the larger arteries, the presence of audible 
thrills and rumbles, all require auscultation for their recognition. It is 
important to remember that murmurs may change in character with change 
in the patient’s position as well as with the state of compensation. They 
are usually more intense when the patient is lying down; this may be because 
in other positions (standing or sitting) the apical impulse masks the murmur. 
Rapid heart action commonly intensifies the murmur of a mitral stenotic 
lesion, although its duration is considerably diminished. For purposes of 
careful auscultation, one may attempt to slow the cardiac rate by having 
the patient breathe deeply and slowly; and to accelerate the heart action, 
by asking the patient to take a few rapid breaths or to exercise. Another 
consideration which occasionally modifies both normal sounds and murmurs 
is the amount of pressure used when applying the stethoscope to the chest 
wall; hence care must be exercised in applying the bell of the instrument to 
the chest wall. 
Valvular Murmurs in Rheumatic Endocarditis.—Organic valvular defects 
do not always produce murmurs. It is sometimes difficult from auscultation 
alone to determine which valve is affected, or to distinguish valvular from 
non-valvular affections. Differential criteria applicable in such instances 
will be discussed later. As further complicating factors in auscultation the 
intensity and propagation of the murmurs are considerably modified by the 
state of cardiac compensation, the amount of dilatation and hypertrophy, 
the rapidity of heart action, the thickness of the chest wall and the position 
of the patient. 
Organic valvular murmurs are best grouped into those due to narrowing 
of the caliber of the valvular orifice (stenotic lesions) and those allowing 
leakage (regurgitant lesions or valvular incompetency). 
Murmurs of Mitral Regurgitation (Mitral Incompetence).—A mitral 
regurgitant lesion produces a murmur systolic in time; the second pulmonic 258 
HISTORY RECORD—PHYSICAL EXAMINATION 
sound is often accentuated. The murmur may be soft and blowing in 
character, occupying only a part of the systole, and accompanying, not 
replacing, the first sound. When typical and well marked, the murmur is 
rough, low or rather high pitched, occupies the entire systole, replaces the 
first sound, is heard loudest in the apical region and is transmitted laterally 
to the axilla. More rarely it is heard over the entire precordium. It is 
sometimes heard posteriorly between the angle of the left scapula and the 
spinal column; this is especially true in children. The murmur may be 
accompanied by a palpable thrill over the mitral area. In decompensation 
with cyanosis, a diastolic murmur transmitted downward (the Graham- 
Steele) is occasionally heard at the second right interspace; it is probably due 
to dilatation of the pulmonary orifice with consequent relative insufficiency 
of the pulmonary valve. 
Murmurs of Mitral Stenosis.—In this lesion the second pulmonic is 
frequently accentuated as compared with the second aortic sound. The 
murmur itself is caused by auricular contraction forcing blood through a 
more or less narrowed mitral orifice; the name, auriculo-systolic, given to this 
murmur many years ago by Gairdner, aptly describes its mechanism. It is 
characteristically a rough, rasping, vibrant murmur. The first sound at the 
apex is often accentuated to a varying degree. Frequently there is a redupli- 
cated second sound at the apex. The murmur gives the impression of being 
crescendo in character, but electrocardiographic sound records (Chapter 
XXXI) tend to show that this “crescendo” quality is only produced by its 
proximity to the loud first sound. 
Some confusion has been brought about by various descriptions of the 
time relationship of the murmur of mitral stenosis as presystolic, middiastolic, 
late diastolic and diastolic. In a sense all these are presystolic since they 
occur at some time before systole. The term presystolic should be applied 
only to murmurs immediately preceding systole, a characterization which 
clarifies the time relationship of this and the other murmurs. In typical 
instances, the murmur is heard immediately preceding systole (presystolic) 
or in late diastole. It is occasionally mid-diastolic, with a distinct gap 
between its completion and the following systole. This has been demon- 
strated by electrocardiographic sound records from patients in whom there 
was prolonged auriculo-ventricular conduction time (usually caused by 
digitalis); the murmur then occurred at the time of auricular systole, which 
in such instances bears varying time relations to the diastole. A similar 
instance came under my observation—a young woman with mitral stenosis 
and gastric symptoms. Electrocardiographic tracings showed progressively 
prolonged P-R intervals (Chapter X), so that at times there were independent 
auricular contractions; the rough, rasping murmur was always synchronous 
with auricular systoles, and, depending upon the conduction time, was heard 
in varying places in diastole. Such observations clinch the cause of the 
mitral stenotic murmur as due to auricular contraction. A mitral stenotic HISTORY RECORD—PHYSICAL EXAMINATION 
259 
murmur often varies in intensity and duration. These variations probably 
depend upon the difference in pressure existing in the auricular and ventricu- 
lar chambers. In the normal heart, at the beginning of ventricular diastole 
(and therefore of ventricular filling), the auricular pressure is high, the rate 
of flow more rapid (Chapter VI). With the filling of the ventricle, the differ- 
ence between ventricular and auricular pressures becomes less and less 
until the advent of auricular systole which of course precedes ventricular 
systole. At the same time there is a sharp rise of auricular pressure and an 
increased rate of flow into the ventricle. Applying these facts to the slow 
rhythmically beating heart with moderate mitral stenosis, the differential 
auriculo-ventricular pressure is manifest only at the moment of auricular 
contraction, consequently the murmur here is presystolic alone. With more 
marked stenosis or with more rapid heart action (shortened diastole), the 
differential pressure favors the auricle at the immediate completion of 
ventricular systole; hence the murmur occurs not only in presystole but 
also in early diastole, or it may occupy the entire diastolic period. In 
addition a Graham-Steel murmur (Chapter XXXI) is present in a certain 
proportion of advanced mitral stenotic cases. 
It should be emphasized that the murmur of mitral stenosis can vary 
considerably; it may even be entirely absent on some days and present on 
others. Various expedients may then be resorted to in order to bring out 
or intensify the murmur when mitral stenosis is suspected. A simple 
procedure is to lay the patient on his left side; this sometimes intensifies the 
murmur. If the condition of the patient allows it, various types of sharp 
exercise (e.g., hopping, bending, walking stairs) may be resorted to in order 
to race the heart and increase its activity for a few minutes. Another expedi- 
ent that is sometimes tried is to have the .patient inhale a pearl of nitrite of 
amyl. It seems to me, however, that any of the other simpler methods will 
accomplish the same purpose without the possible disagreeable after-effects 
of amyl nitrite. 
It is especially in auricular fibrillation that the murmurs of mitral stenosis 
undergo marked changes, for the absence of rhythmic auricular contractions 
in this type of irregularity precludes the usual presystolic element found in 
the rhythmically beating heart. With comparatively slow and fairly 
regular ventricular action, there is a distinct pause between the diastolic 
murmur and the following systole. Or the murmur may occupy early 
diastole alone and gradually wane and tail away with the filling of the ventri- 
cles, for then intraventricular pressure increases as compared with intra- 
auricular pressure. A rough, rasping diastolic murmur and a palpable 
thrill may lose these characteristics under the influence of digitalis, to- 
become much softer and scarcely audible. The reason for this change seems 
due to steadier ventricular contraction produced by the drug, with consequent 
lessened differences in auriculo-ventricular pressure. When the ventricle 
beats very irregularly and rapidly, the murmur is short, sharp and seemingly 260 
HISTORY RECORD—PHYSICAL EXAMINATION 
occupies the entire shortened diastolic period. With extremely rapid and 
tumultuous cardiac activity the murmur may become barely audible or 
distinguishable, although in the occasional longer diastolic pauses its usual 
characteristics are evident. 
Murmurs of Aortic Stenosis.—It must be remembered that systolic 
murmurs over the right base can be due to causes other than actual aortic 
stenosis. Thus, as already pointed out, functional murmurs in this area not 
uncommonly accompany anemia or cardiac overaction without valvular 
disease. The murmur is also present in aortitis accompanying cardio- 
sclerosis (Chapter XVII) and in aortic aneurisms or dilatations, for here the 
valvular surfaces are roughened and thickened. Typical auscultatory signs 
over the right base are therefore necessary in order to diagnosticate rheumatic 
aortic stenosis, especially since this lesion is rare as an isolated rheumatic 
valvular defect. A radial tracing may show an anacrotic notch (Chapter 
VII). The impulse at the apex is forcible and gives the palpating hand the 
impression of gradually reaching its climax. 
Murmurs of Aortic Regurgitation—Aortic Incompetency.—This murmur 
varies considerably in intensity and in its area of propagation. When 
typical, it is diastolic in time, occupies the entire diastole, and replaces the 
second sound. Occasionally it occupies only part of the diastole. In addi- 
tion there is sometimes a booming apical impulse. To judge from experi- 
ments on animals, the intensity and duration of the murmur seem to be 
roughly parallel to the degree of regurgitation. The murmur is most often 
blowing in character; it may be very soft or, occasionally, quite loud and 
rough. The usual area of greatest intensity is at the right base; however, 
it is often heard loudest at the second and third interspaces near the sternum. 
Not infrequently an aortic regurgitant murmur has exactly the characteristics 
of a mitral stenotic one; that is, it produces a presystolic sharp rumble at 
the apex (Austin Flint murmur). Under such circumstances, the regurgitant 
murmur at the base may be faint or entirely absent. Many theories have been 
advanced for the etiology of the so-called Austin Flint murmur, but as yet 
no satisfactory explanation has been given. The consensus of opinion is that 
it is due to narrowing of the mitral orifice from the regurgitant stream of blood 
in the ventricle. In addition to the diastolic murmur at the base there is 
often a systolic murmur at the apex in advanced cases of aortic regurgitation. 
This murmur is probably caused by relative incompetence of the mitral ring 
and consequent regurgitation during ventricular systole. 
Tricuspid valvular lesions are very infrequently encountered. The 
etiology is rarely rheumatic; more often it is of streptococcic, gonococcic 
or leutic origin. Although both tricuspid regurgitation and stenosis are 
very rare, the former is the more frequent. The regurgitant lesion is charac- 
terized by a blowing systolic murmur, heard best to the left of the lower 
sternum and transmitted to the right; it is not transmitted posteriorly. It 
is often accompanied by a pulsating liver and marked jugular pulsation. HISTORY RECORD—PHYSICAL EXAMINATION 
261 
I observed one case in which a distinct palpable thrill was also present. 
Tricuspid stenosis is exceedingly rare and has never been found as an isolated 
lesion; it has been very infrequently diagnosed during life. The characteris- 
tic murmur is described as a presystolic rumble most prominent in mid- 
sternum or over the xiphoid. The lesion may be suspected in the presence of 
extreme cyanosis, right auricular hypertrophy and marked pulsation of the 
liver and of the veins of the neck. 
Pulmonary valvular insufficiency is exceedingly rare; it has never been 
observed as an isolated lesion and has been correctly diagnosed in but a very 
few instances. The murmur is described as blowing in character, diastolic in 
rhythm, heard best over the left sound and third interspaces, and trans- 
mitted downward. It is usually accompanied by other endocardial murmurs. 
Pulmonary Stenosis commonly occurs as a congenital lesion (Chapter 
XIX). Its differentiation from aortic stenosis, which sometimes presents 
similar auscultatory signs, may be made from the fact that the murmur of the 
latter is propagated along the carotids, while the pulmonary stenotic murmur 
is transmitted to the left. 
A combination of lesions of the various valves, especially of the aortic 
and mitral, is very common. The lesions in themselves tend to cause 
inorganic or so-called functional murmurs (q. v.) from the various degrees of 
ventricular dilatation they produce. In addition the valvular murmurs may 
not be typical; therefore it is sometimes difficult or even impossible to 
determine the exact valvular lesions which are present. The problem is 
further complicated by the frequent coexistence of pericarditis with its 
adventitious sounds. An extremely valuable guide in the differentiation 
of such complicated murmurs is careful comparative auscultation of the 
differing quality, pitch, and propagation of the murmurs. In this manner, 
the characteristic murmur of one of the valvular defects may be followed 
through an apparent maze produced by the presence of other valvular mur- 
murs. Furthermore much information is gained by precordial palpation 
which, with auscultation, may act as guides in the determination of enlarge- 
ments typical of the various valvular lesions. Blood pressure observations 
(Chapter XXV) are also of value in the differentiation. This is especially 
true of aortic regurgitation in which the difference between the systolic and 
diastolic pressure of the femoral artery is often much beyond the normal. 
Murmurs in Cardiosclerosis.—Besides rheumatic valvular affections, 
atheromatous changes in the mural endocardium, in the nrtral valves, and in 
the aortic valves and walls frequently give rise to murmurs whose presence 
and significance have not been sufficiently emphasized. Intraventricular 
murmurs, non-rheumatic in origin, are often present in cardiosclerosis. 
The cardiosclerotic process prevents coaptation of the mitral cusps and thus 
produces mitral regurgitation. This murmur is systolic in time and is heard 
best over the lower precordium; it is usually less loud than the rheumatic 
mitral regurgitant murmur and is transmitted over a smaller area. Thicken- 262 
HISTORY RECORD—PHYSICAL EXAMINATION 
ing and dilatation of the aortic walls, common in aortitis, give rise to a loud 
rough systolic murmur over the right base. As distinguished from aortic 
stenosis the murmur is less rough and vibrant, and is infrequently propagated 
along the carotids. If aortic dilatation is marked, the systolic may be followed 
by a short diastolic murmur, due to regurgitation in the enlarged aortic 
cavity or to valvular insufficiency. 
In some individuals with advanced sclerotic change in the aortic and 
mitral valves there may be heard a loud systolic murmur over the aortic 
and mitral areas. Its significance and characteristics with case illustrations 
are described in Cardio-vascular Clinics. 
Right-sided Murmurs from Auricular Enlargement.—This murmur has 
received only occasional mention in the literature. In a few cases of decom- 
pensated rheumatic mitral disease which I observed there was a loud rough 
systolic murmur over the third and fourth right interspaces; in addition a 
diastolic murmur over the same area was sometimes heard. In all the cases 
with loud right-sided murmurs which I fluoroscoped, there was enlargement 
of the right auricular curve, and no enlargement of the aorta. A few illus- 
trative cases are herewith epitomized. 
Case I.—Male, age 17, with a definite rheumatic history, had upon hospi- 
tal admission, the typical physical signs of a double mitral lesion. There 
was also a visible pulsatile area to the right of the sternum the size of a pigeon’s 
egg, over which was heard a loud rough systolic murmur; a rough palpable 
thrill was also felt. The patient died after one week. At necropsy, a few 
pericardial adhesions were found between the cardiac apex and dia- 
phragm. There was 20 cc. of clear fluid in the pericardial sac, the heart 
weighed 520 gms. The right auricle was hugely dilated (Fig. 268). With the 
heart in situ the right border was 8 c.m. from the midsternal line, the left 
border, 10 c.m. from the same line. The greatest thickness of the right 
ventricle measured 1.2 c.m., theleft, 1.8c. m. The right auricle was irregularly 
circular in outline and was tremendously distended, well shown by distension 
of the veins of the auricle, a few of which were the size of ordinary lead 
pencils. The wall of the right auricle was twice as thick as the normal. The 
right auricular appendix was also enlarged and distended. The tricuspid 
orifice readily admitted three fingers. There was slight thickening of the 
tricuspid valve. There was a typical button hole stenosis of the mitral valve. 
Case II.—Male, age 38, had chorea as a child and heart trouble for years. 
Despite this, he was always athletic and active until two years prior to my first 
examination. He then had his first attack of dyspnoea. A year and one 
half later he suffered from a pulmonary infarct, hemoptysis and long con- 
tinued fever. Since then he has been constantly decompensated: The chief 
symptoms were cough and dyspnoea. Examination: The systolic blood pres- 
sure is 85, the diastolic 79. There is marked venous pulsation in the neck. 
The heart is tremendously enlarged. There is a palpable systolic thrill and 
a heaving impulse over the lower half of the left chest. Over the right base HISTORY RECORD—PHYSICAL EXAMINATION 
263 
there is a somewhat rough systolic murmur transmitted to the aorta in the 
jugulum. At the apex, a double mitral murmur is heard. The presystolic 
is heard only at the apex while the systolic is transmitted to the axilla, and 
to the left sternal border. To the right of the sternum, in the third and 
fourth interspaces, a loud systolic and a loud diastolic murmur are heard; 
both are propagated toward the right axilla and the epigastrium. The 
fluoroscope showed an enlarged right auricle, a normal sized aorta and left 
ventricular hypertrophy. 
Case III.—Female, married, aged 26, had had several attacks of hemop- 
tyses for three years. There has been dyspnoea and edema of the legs for 
over one year. On examination, the patient is quite cyanotic. The typical 
signs of a double mitral lesion are heard at the apex. To the right of the 
lower half of the sternum, there is a rough systolic murmur which is trans- 
mitted somewhat to the left. 
It is apparent that the auscultatory signs of assumed right auricular 
enlargement are not always alike. Whatever its time relationship, however, 
the murmur is always rough and loud. It may be systolic alone or systolic 
and diastolic. Sometimes a systolic palpable thrill is also present. The 
systolic murmur is heard best in the third and fourth interspaces, immediately 
to the right of the sternum and is transmitted to the mid-sternum and to the 
right nipple region. I conceive the systolic murmur as due to tricuspid 
regurgitation through an extremely dilated ring into an enlarged auricular 
chamber, hence the transference of the tricuspid murmur from its usual site. 
It is significant that liver pulsations were absent in my cases, perhaps because 
the regurgitation spent itself in an upward (auricular) direction rather than 
toward the liver. The mechanism of the right sided diastolic murmur which 
was occasionally heard in these individuals seemed similar to that of aortic 
aneurism, that is, the dilated auricle acted like a dilated aorta, and after 
ventricular systole ceased, the regurgitated blood in the auricle passed back 
through the tricuspid valve during diastole. It may be necessary to differ- 
entiate the physical signs of right auricular enlargement from those of aortic 
aneurism, especially when a double murmur is present. This is readily done 
by the fluoroscope, for in right auricular enlargement, aortic pulsation is 
practically normal. Besides, the usual physical signs are present at the 
right base (first and second right interspaces) in cases of aortic aneurism. 
Intracardiac Murmurs of Non-organic Origin.—Murmurs arising in the 
heart and not due to organic disease have received many names and have 
been ascribed to various causes. They have been termed accidental murmurs, 
hemic murmurs, adventitious sounds and functional murmurs. They have 
been ascribed to anemia, to relative valvular insufficiency (incompetency) 
allowing leakage and regurgitation of blood; and to return of the blood in the 
large venous trunks. It is apparent that much confusion exists regarding 
both the terminology and the etiology of these intracardiac murmurs. In the 
description to be given, I shall apply the term “functional murmur” to those 264 
HISTORY RECORD—PHYSICAL EXAMINATION 
adventitious sounds in which no organic cardiac lesion is assumed to be 
present. 
Functional cardiac murmurs are very common. The fact that they can 
occur without cardiac disease and without producing symptoms, requires 
emphasis. They are often merely accidental discoveries in the routine physi- 
cal examination. The presence of these murmurs in healthy people as well 
as in such conditions as fever and anemia, suggests a varying etiology. The 
usual chief characteristics of non-organic murmurs are their softness and limita- 
tion to small areas. There are numerous exceptions, however. The murmur 
may be rather loud, somewhat rough, and when found in the lower precor- 
dium, may be slightly transmitted above or to the left. These exceptions are 
especially frequent in children and young adults. The most common site 
of the functional murmur is at the apex. It is systolic in time and accom- 
panies the first sound, usually as a soft whiff. In addition to their presence in 
normal individuals, such functional murmurs are found in patients with 
rapid heart action, in those with flabby general musculature, and in those 
with anemia. In anemic individuals, the changed character of the blood is 
usually assumed as the etiological factor. This hypothesis, however, is not 
based upon any experimental data. In those with flabby musculature, the 
cause seems to be dilatation of the musculature supporting the mitral ring, 
with consequent leakage and regurgitation; this is commonly termed relative 
insufficiency or incompetency of the mitral valves. Perhaps many of the 
murmurs in anemia (so-called hemic murmurs) heard in this location have 
the same etiology, for grave anemia conduces to lack of proper muscular tone. 
In tachycardia, improper and faulty closure of the mitral cusps, alone or in 
addition to relative mitral insufficiency, may be the cause of this functional 
murmur at the apex. 
A source of diagnostic confusion sometimes exists in differentiating the 
non-organic intracardiac murmur heard over the apex from the organic 
murmur of mitral insufficiency. The distinction between typical non- 
organic and typical mitral organic regurgitant murmurs is not difficult; the 
latter are rougher, louder and are heard and transmitted over larger areas than 
the former. The second pulmonic sound is apt to be accentuated as compared 
with the second aortic. When the characteristics of the two overlap, as, for 
example, in rheumatic fever in which the fever itself or the endocarditis may 
cause the murmur, the distinction between the organic and functional becomes 
exceedingly difficult. In doubtful cases with fever, examination must be made 
after the fever has run its course in order to arrive at definite conclusions. 
In anemia, the association with other “hemic” murmurs, especially systolic 
murmurs at the right base, aids in the differentiation. The correlation of other 
data—lack of symptoms of heart disease, general type of muscular develop- 
ment, occupation (sedentary or otherwise), the type of heart as seen fluoro- 
scopically—all these are elements which require consideration in the differential 
diagnosis between functional and organic murmurs. Non-organic murmurs HISTORY RECORD—PHYSICAL EXAMINATION 
265 
are commonly found in patients of sedentary habits, with flabby musculature 
and ptosed abdominal organs. The distinction in the middle-aged and 
elderly between a mitral inorganic (functional) murmur and that found 
associated with myocarditis and cardio-sclerosis is of extreme importance. 
The differentiation must be based upon the usual characteristics of the non- 
organic murmur. If this be soft and blowing, and be not transmitted, one 
may infer that the mitral ring is dilated and that the murmur is of functional 
origin. The diagnosis of myocarditis must then be predicated upon the 
usual evidence of myocardial insufficiency, and upon the presence of an intra- 
ventricular murmur (q. v.) characteristic of cardiosclerosis (Chapter XVII). 
Aberrant fibers coursing through the ventricle, formerly termed aber- 
rant tendons, can presumably give rise to loud systolic murmurs over the 
precordium. There seems to be no method of distinguishing these from other 
non-organic or organic murmurs. How often such murmurs occur is not 
known; they would seem to be extremely rare however. The tricuspid 
murmur of relative insufficiency may occur with decompensation from any 
cause that produces venous congestion—emphysema, myocarditis, endocar- 
ditis, etc. Indeed the murmur may itself be regarded as an evidence of an 
inefficient circulation, since it is due to interference with venous return flow 
in the pulmonary circuit to the right heart. This tricuspid murmur is of 
varying intensity, is heard over the lower sternum and is usually transmitted 
to the right; an enlarged pulsating liver is occasionally present. Sometimes 
the liver pulsates in the absence of a tricuspid murmur. Since this could 
scarcely occur without regurgitation, it is clear that the latter may be present 
without producing a murmur. The frequency of relative tricuspid insuf- 
ficiency without valvular disease is added evidence that mitral regurgitation 
with its murmurs may also be due to relative valvular insufficiency and to 
abnormal dilatation of the mitral ring. 
A non-organic, soft, blowing systolic murmur is frequently heard over the 
aorta, particularly in anemia. It is also heard occasionally in the overacting 
hearts of young individuals. It has none of the characteristics of aortic 
stenosis, however (q. v,). A similar murmur over the aorta is found in 
decompensated mitral lesions. I have occasionally heard a short diastolic 
aortic murmur in mitral lesions in the young; it has none of the clinical 
characteristics of aortic regurgitation. It is usually temporary and dis- 
appears within a few days. Perhaps mechanical torsion or tension on the 
aortic ring with consequent regurgitation is a factor in its production. 
Extracardiac Non-organic Murmurs.—Pericarditis is not here included. 
We have just described functional murmurs due to intracardiac disturbances. 
We shall now discuss non-organic murmurs of extracardiac origin. The most 
common of these is the so-called cardio-respiratory or cardio-pulmonary 
murmur. It is usually soft and blowing in character, systolic in time, and 
best heard over the left base. Occasionally these characteristics change. 
Thus the murmur may be rough and loud, and be transmitted along the left 266 
HISTORY RECORD—PHYSICAL EXAMINATION 
sternal border and lower precordium as a somewhat superficial, squeaky sound, 
resembling a friction sound. The cardio-respiratory murmur is ascribed 
to compression of lung tissue between the heart and chest wall. During 
inspiration, the lung covers a large part of the root of the pulmonary artery 
and the upper precordial surface, facts which can be corroborated by fluoro- 
scopic examination. This also explains why the murmur is usually heard 
best when the lung becomes inflated at the end of inspiration. However, it 
is sometimes loudest at the end of expiration, possibly because in some 
patients the pad of lung between the chest wall and the heart is abnormally 
large, thus diminishing the transmission of the murmur. The murmur is 
found frequently in children. It is not uncommon in frail women with thin 
chest walls. The fact that the intensity of the murmur depends upon respira- 
tory phases and that it is never accompanied by a palpable thrill aids in dis- 
tinguishing it from other types of organic cardiac murmurs heard in this area. 
Reduplicated Sounds and Reduplicated Apical Impulses.—These 
reduplications represent again a distinct type of adventitious sounds. They 
have received various names such as split sounds, gallop, canter, and triple 
rhythm, and “bruit de rappel. ” The term “reduplication” seems preferable 
because though many of its etiological factors are still obscure and problem- 
atical, it conveys some concrete idea of the underlying phenomenom, namely 
a doubling of a sound. 
Reduplicated second sounds are of valvular origin and can usually be 
clearly defined by ausculation. In the order of their frequency, reduplicated 
second sounds are heard at the apex alone; both at the apex and right base, 
and lastly over the pulmonary artery alone. The time of their occurrence 
in the cardiac cycle and the study of electrocardiographic sound records 
demonstrate that they are due to closure of the semilunar valves. Their 
presence in various positions and combinations suggest differing etiology. In 
many instances conclusions regarding the cause can for the present be only 
tentative. One known cause of reduplicated second sounds however is asyn- 
chronous closure of the pulmonic and aortic valves. In this type the elements 
constituting the reduplication are heard very close to each other. Redu- 
plicated second sounds may also be due to asynchronous closure of the indi- 
vidual leaflets in either artery. I saw an excellent example of this in a case 
of a bulging aneurism of the arch of the aorta in which one could feel as well 
as hear the distinct and seperate closure of the semilunar valves. In other 
types, the sound elements may be separated by a distinct hiatus. In these, the 
first part is undoubtedly due to closure of the semilunar valves, since it occurs 
in the cardiac cycle in early diastole soon after the A-V valves open. The 
second part of the reduplication has been ascribed to a process somewhat 
similar to the causation of the third heart sound, that is, to quick ventricular 
filling with resultant vibration of the floating cusps. This explanation, how- 
ever, seems untenable, for the reduplicating elements Seem identical on auscul- 
tation and have been so proven by graphic sound records. As a more plausible HISTORY RECORD—PHYSICAL EXAMINATION 
267 
explanation, it appears to me that a sharp systolic wave can produce a secon- 
dary reflux one, which, impingeing upon the already closed and tense semilunar 
valves, sets these in vibration and thus causes the second element of the redu- 
plication. This would account for its frequent presence in tachycardia, in 
mitral stenosis, and over the great vessels at the base of the heart. 
Reduplicated first sounds are usually classified under “presystolic gallop 
rhythm.” The term—presystolic—is inexact, however, for the first element 
alone of the reduplication is presystolic. Under reduplicated first sounds— 
a preferable name—I wish to include only those that are not accompanied by 
reduplicated apical impulses, from which, as I shall point out, they are 
etiologically distinct. Thus limited, reduplicated first sounds (i.e., without 
reduplicated apical impulses) are heard only in the apical region. It can be 
demonstrated by simultaneous electrocardiographic sound records and 
electrocardiograms that the first element of this type of reduplicated first 
apical sound actually lies in presystole, and hence must be due to some 
presystolic event in the cardiac cycle. Most probably this is auricular 
contraction. The occurrence of such reduplication may depend upon a 
hypertrophied or overacting auricle. 
Reduplicated Apical Impulse.—This type, always accompanied by a 
reduplicated first sound but of different origin from the above, is found 
especially in conjunction with hypertrophied left ventricles and in aortic 
disease. It is occasionally found in the overacting normal heart. Upon 
auscultation, besides the double first sound, there is a distinct sense of a 
double shock or impulse, often evident upon palpation alone. Since the 
reduplicated apical impulse has been found in lesions of the main branch of 
the auriculo-ventricular bundle, ventricular asynchronism is evidently one 
of its causes. The clinical diagnosis is here aided by the fact that bundle 
lesions are usually accompanied by signs of myocarditis and by regular slow 
pulse rates between 50 and 60 per minute. 
In addition to patients with bundle lesions, I have observed identical 
double apical impulses in those without electrocardiographic or other indica- 
tion of bundle lesions. In several such instances there was definite fluoro- 
scopic evidence that the double impact was due to a secondary ventricular 
movement following the primary systole. The exact cause of this double 
impact I could not definitely determine. In an effort to seek its explanation, 
the following must be recalled. It is known that the normal first sound is 
composed of three elements, first: Tension of the auriculo-ventricular valves; 
secondly, the muscular element, ventricular contraction; and thirdly, 
ventricular impact against the chest wall. The first element of the redupli- 
cated sound under discussion is probably due to these usual three normal 
factors just enumerated. Regarding the second part of this reduplication 
it is difficult to state to what extent and proportion these three factors 
are concerned. To return to the fluoroscopic examination of patients with 
the reduplication, one may observe not only the ventricular systole but, 268 
HISTORY RECORD—PHYSICAL EXAMINATION 
what may be termed “ventricular fling,” seemingly comprising different 
areas. Sometimes this involves the apex alone, at others, the entire left 
ventricle seems to take part in the second movement. It is impossible to 
determine how far such ventricular fling resembles normal physiological 
systolic contraction. It may, for example, represent an attempt to regain 
ventricular tone, an effort interfered with by ventricular distension from 
varying amounts of residual blood following systole. In general, it seems in 
harmony with clinical observations to seek mechanical intraventricular 
causes for the reduplicated apical impulse. A weakened myocardium may 
fail to properly empty the overdistended ventricle, a condition favorable to 
the production of a double impulse and reduplicated first sound. A similar 
condition can occur in patients with long continued fever, as in typhoid when 
myocardial weakness may be only temporary and functional. Again, it can 
occur in those suffering from myocarditis and resultant myocardial insuffi- 
ciency. This was well illustrated in an instance of alcoholic myocarditis in 
which at necropsy the ventricles were found hypertrophied and riddled with 
scar tissue. A reduplicated apical impulse was present during the stage of 
decompensation alone; the electrocardiogram showed a deep M complex 
(Chapter IX). When decompensation was temporarily restored, the double 
apical impulse and M complex disappeared, the ventricular complex assumed 
a normal outline. 
Reduplicated apical impulses are frequently present in aortic regurgita- 
tion. In these cases they may be directly due to the blood which regurgitates 
into the ventricle; this then produces a ventricular shock which becomes 
audible as well as palpable at the apex. A double apical impulse is also 
found in left ventricular hypertrophy with hypertension. The violence of 
ventricular action and the impact of residual blood may here account for the 
second element of the reduplication. 
Physical Signs of Ventricular Hypertrophy.—The possibility of correctly 
diagnosing cardiac hypertrophy by the usual physical signs depends chiefly 
upon the extent of the hypertrophy and the thickness of the chest wall. 
For example, the tremendous impact to the thoracic wall in the far advanced 
and extreme ventricular hypertrophy of typical aortic insufficiency can 
scarcely be mistaken, for it produces a visible and palpable shock to the entire 
left half of the chest. It is however the minor degrees of cardiac hypertrophy 
which require diagnostic consideration. Hypertrophic and enlarged hearts 
in which myocarditis is an important pathological factor, are often not 
diagnosed as enlargements because the impaired condition of the circulation 
is such that the usual vigorous, unhampered action indicative of hypertrophy 
is absent. Indeed, as has already been pointed out, if the diagnosis can be 
made by other means (electrocardiograms and the X-ray) a weakened 
impulse is often a sign of weakened myocardium. The diagnosis of hyper- 
trophy must then depend upon the data already indicated in the description 
of the physical signs of myocarditis (Chapter XVII). HISTORY RECORD PHYSICAL EXAMINATION 
269 
Left ventricular hypertrophy, when typical, produces a booming, loud 
first sound over the entire cardiac area, and a broad, heaving systolic impact 
distinctly palpable well outside the normal cardiac limits. It must be 
remembered, however, that these characteristics may be simulated in thin- 
chested individuals in whom the heart is well applied to the chest wall, or by 
hearts in which the systolic action is violent (for example, in exophthalmic 
goiter). Such instances demonstrate the necessity for reserve in the diagnosis 
of ventricular hypertrophy, particularly in view of the fact, already pointed 
out, that it is extremely difficult to delimit by percussion even the approxi- 
mate size of the cardiac area. In other words, the physical evidence of 
cardiac enlargement must be definite and unmistakable before its diagnosis is 
ventured. An accentuated second sound at the apex or at the second right 
interspace is sometimes accepted as an indication of left ventricular hyper- 
trophy. It is true that these abnormally accentuated sounds are often 
found in hypertrophy; however, they must be regarded not as evidence of 
hypertrophy, but rather of hypertension in which left ventricular hyper- 
trophy is often, but not invariably, present. A reduplicated apical impulse 
(gallop rhythm) is sometimes present in the hypertensive cases, especially 
when hypertrophy exists. 
Right Ventricular Hypertrophy.—Its diagnosis is even more difficult and 
problematical than that of the left. A second pulmonic sound, relatively 
or actually accentuated when compared with the second aortic, is regarded 
as evidence of overstrain of the right heart, and hence indicative of probable 
right sided hypertrophy. However, I have observed moderate accentuation 
of the pulmonic second sound very frequently in children and adults with 
normal hearts in whom tachycardia existed. I believe an accentuated 
second pulmonic sound is of value as indicative of probable impairment 
of the right ventricle only if the accentuation is pronounced and if tachy- 
cardia is absent. Even then the question of hypertrophy must rest upon the 
length of time during which the accentuation has been observed, upon the 
type of lesion, and upon other associated data. In marked right ventricular 
hypertrophy the apex may be pushed to the left so that the anterior surface 
of the heart consists chiefly or entirely of the right ventricle. Furthermore, 
the cardiac area of dullness may not be increased to the right because the 
right ventricle normally lies upon the diaphragm. Marked visible and 
palpable epigastric pulsation and systolic retraction of the apical impulse are 
the physical signs upon which most stress is laid in the diagnosis of right 
ventricular hypertrophy. In a series of cases in which the ventricles were 
weighed at necropsy, Lewis did not find either visible or palpable epigastric 
pulsation or thrust in a sufficient percentage of cases to make these signs of 
diagnostic value. These are examples of the difficulties with which the 
diagnosis of right ventricular hypertrophy is surrounded. 
It is thus evident that, except when massive, the clinical diagnosis of left 
or right ventricular hypertrophy from physical signs alone is often problem- 270 
HISTORY RECORD—PHYSICAL EXAMINATION 
atical, and that in many instances its presence can only be correctly 
inferred in conjuction with the known pathological lesion—valvular, 
myocardial or nephritic. 
REFERENCES 
Bard, L.: Du Bruit de Galop, etc.; Semaine Medicale, 1906, XXVI, 229. 
Bard, L.: De la Multiplication anormale des Bruits de Coeur; Semaine Medicale, 1908, 
XXVIII, 3. 
Flint’s Physical Diagnosis (Emerson). 
Gairdner, W. T.: A Short Account of Cardiac Murmurs; Edinburgh Medical Journal, 
1861-2, VII, 438. 
Lewis, T.: Lectures on the Heart. 
Lewis, T.: Observations upon Ventricular Hypertrophy, etc.; Heart, 1913-1914, V, 367 
Mackenzie, J.: Diseases of the Heart. 
Nothnagel’s Encyclopedia, Diseases of the Heart; American Edition. 
Pawinski, J.: Die Entstehung und klinishe Bedeutung des Gallopprhythmus; Zeitshrift f. 
klinische Medizin, 1907, LXIV, 70. 
Robinson, G. C.: Gallop Rhythm; American Journal of Medical Sciences, 1908, CXXXV, 
607. 
Shattuck, G. C.: Relation of Dullness to Cardiac Outline; Boston Medical and Surgical 
Journal, 1916, CLXXIV, 30. 
Thayer, W. S.: Further Observations on the Third Heart Sound; Archives of Internal 
Medicine, 1909, IV, 297. 
Wiggers: Circulation in Health and Disease. CHAPTER XIV 
GENERAL SIGNS AND SYMPTOMS OF CARDIAC DECOMPENSA- 
TION IN ORGANIC CARDIAC DISEASE—THE NEUROTIC 
ELEMENT IN ORGANIC CARDIOVASCULAR DISEASE—CAR- 
DIAC STRAIN—FUNCTIONAL EFFICIENCY TESTS 
Before proceeding to the special symptomatology affecting the cardiac 
musculature and the various valves (Chapters XV-XVII), it is essential to 
have a broad aspect of the symptomatology of heart disease in general, but 
particularly of its most prominent symptom—heart failure. Various other 
terms are used at times instead of “heart failure” such as decompensation, 
myocardial insufficiency, incompetency or inefficiency. They actually rep- 
resent indefinable differences in degree rather than in kind; hence I shall 
not attempt to distinguish between them but shall use them interchangeably. 
The terminology that includes the muscle element has this decided advan- 
tage that it stresses and emphasizes the prime factor in every case of heart 
failure, namely—the heart muscle—for it is essentially improper perform- 
ance of, and interference with the heart muscle function or functions, no 
matter how brought about, that cause myocardial insufficiency. 
When describing physiological considerations (Chapter III), the fact 
was emphasized that cardiac reserve depends fundamentally upon the ability 
of the heart muscle to properly contract and expand, that is to say, upon the 
adequate shortening and lengthening of the cardiac fibers. Like other organs 
of the body the normal heart has a large margin of safety, a large functional 
reserve. Depending upon the severity and nature of the cardiac disease, this 
margin of safety is diminished to a varying degree; indeed, a point may be 
reached at which the heart carries on the circulation without any reserve 
in store. This means that cardiac activity even though inadequate and 
inefficient, proceeds at maximal capacity for that individual. As one 
corollary, it is important for the observer not to be entirely engrossed in 
minute physical signs and symptoms, but to study the heart from the broad 
aspect of function and dysfunction; for it is apparent that a heart crippled in 
function and carrying on the circulation always with a maximal effort will 
react differently to effort, to recrudesence of disease and to cardiac “insults” 
than one which, although diseased, carries on the circulation adequately and 
with sufficient reserve. 
Symptoms of Cardiac Failure.—Breathlessness and dyspnoea constitute 
the first indications of decompensation in the vast majority of cases of 
cardiac disease. Naturally careful and detailed inquiry must be made 
271 272 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
(Chapter XIII) as to the type and degree of exercise that first bring on these 
symptoms. The usual complaint is that climbing stairs or walking against 
the wind is most apt to cause breathlessness or dyspnoea. It is difficult to 
divide the latter into stages corresponding to definite entities in cardio- 
vascular pathology, for dyspnoea may change or vary with such fleeting 
influences as fever, nervous excitement, acute inflammatory disturbances 
within the heart, etc. It is important to remember that breathlessness may 
be the result of other conditions, especially pulmonary and renal disease, 
severe anemia, recovery from a severe acute illness or operation, and that it is 
also frequently present in cardiac neurosis (Chapter XVII). Painful 
extra-cardiac conditions (e.g., pericarditis, intercostal myalgia) may also 
cause rapid breathing. Hence, alone, dyspnoea is not diagnostic or charac- 
teristic of cardiac disease; other corrobative evidence is required before the 
diagnosis of heart disease can be made. 
The fundamental causes of various types of dyspnoea first require dis- 
cussion. Simple breathlessness is not accompanied by any marked chemical 
changes in the blood. 
Dyspnoea is basically due to improper gas exchange in the tissues. 
This causes a change in metabolism, an alteration which can sometimes be 
discovered and measured by chemical examination of the blood. It is 
chiefly through the latter that our knowledge of dyspnoea has been advanced. 
Abnormal products, or abnormal amounts of normal products in the blood 
that cause diminished blood alkalinity (so-called acidosis), have been found. 
Experiments show that alkalies injected into the blood stream cause apnoea 
(lessened breathing) and that very small quantities of acids and of acid salts, 
similarly injected, produce hyperpnoea (accelerated and deepened breathing). 
Carbon dioxide, the chief product of metabolism, acts chemically in this 
respect like a mineral or organic acid; it causes an increase in hydrogen ions 
in the blood; these ions represent the chemical factor which measures “acido- 
sis.” The respiratory center is quite sensitive to changes in blood reaction, 
hence the various types and degrees of abnormal breathing—breathlessness, 
dyspnoea, etc. The mechanism of regulation of the respiratory center seems 
somewhat as follows: “Acidosis” (diminished blood alkalinity) stimulates 
the respiratory center to increased activity. With increased activity, 
there is increased pulmonary ventilation, and consequent reduction in carbon 
dioxide. This again tends to keep the hydrogen ion concentration of the 
blood at a normal level. Thus there is a nice mechanism between blood 
“acidosis,” excitation of the respiratory center and increased breathing, a 
mechanism which tends to diminish the degree of “acidosis” by ridding the 
body primarily of its increased carbon dioxide. Lack of oxygen (anoxemia), 
a factor insufficiently known or studied, may possibly exert an as yet un- 
known influence in the production of dyspnoea. There are several methods 
of estimating the carbon dioxide content of the blood. It may be measured 
directly by examining the blood withdrawn from a vein (Van Slyke method); DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
273 
or it may be estimated indirectly by various apparatuses for determining the 
carbon dioxide content and tension of the alveolar air. It will be shown 
that conclusions drawn from such examinations bear an important relation 
to cardiac dyspnoea. 
Another method of studying dyspnoea is the simpler clinical one of direct 
observation of the rate and depth of breathing; this naturally gives the 
measure of pulmonary ventilation. As an instrumental method (a calibrated 
recording spirometer) Peabody has recorded not only the rate and depth of 
breathing, but also measured the minute-volume of respiration. Instead of 
using exercise to produce dyspnoea, he had the patients breathe air contain- 
ing increasing amounts of carbon dioxide, the chief factor in the production 
of dyspnoea. It was found that the severely decompensated cardiac cases 
could stand but little increase in the amount of carbon dioxide as compared 
with the normal control. The abnormal rate of respiration was about the 
same as the normals, but the depth of respiration was only about half the latter. 
Clinically, this means that the cardiac patients could not ventilate their 
blood sufficiently to overcome the increasing amounts of carbon dioxide by 
deeper breathing; hence, their blood remained saturated with carbon dioxide 
and the respiratory center remained abnormally stimulated. Stated in 
another fashion, the pulmonary reserve of decompensated cardiac cases is 
considerably below the normal, a result to be expected, and comparable to 
their diminished cardiac reserve. Peabody also studied the vital capacity, 
the maximum amount of expired air following a maximum inspiration of 
normal individuals and those with cardiac disease. He found that in a gen- 
eral way lessened vital capacity ran parallel with the tendency toward or the 
actual presence of cardiac failure. Observations of vital capacity may there- 
fore be a ready objective method for noting degrees of heart failure. 
It should be remarked that dyspnoea occurring with heart failure may be 
composed of several associated factors, such as cyanosis, emphysema, pul- 
monary stasis, congestion and hydrothorax, all perhaps previously due to the 
heart affection, yet any one of which may in individual instances, overshadow 
the heart itself as the cause of dyspnoea. Indeed, mechanical blocking of 
pulmonary ventilation by emphysema etc., may of itself cause lessened vital 
capacity. As with all instrumental methods, so here it is in addition always 
necessary to examine the patient carefully in order to gauge results properly. 
A factor in dyspnoea perhaps insufficiently recognized is the result of 
functional disturbance of the respiratory centers. This sometimes produces 
rapid and shallow breathing—tachypnea, a condition found especially in 
those with cardiac neurosis (Chapter XVIII). 
Cheyne-Stokes Breathing—Periodic Respiration.—Periods of gradual 
increasing dyspnoea followed by periods of apnoea are sometimes found in the 
late stages of cardiac failure. Its periodicity may perhaps resemble etiologic- 
ally a peculiar type of breathing (the so-called Biot type) which is occasionally 
found in patients with advanced arterio-sclerosis and extreme hypertension. 274 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
There are sudden attacks of air hunger with deep respiration (hyperpnoea) 
followed by a phase of absence of breathing (apncea). Its etiology probably 
depends upon extreme, sudden differences in the amount of oxygen and 
carbon dioxide in the blood of the cerebral vessels, combined with localized 
cerebral endarteritis. The apnoeic period would then be due to cerebral 
anemia and lack of oxygen (anoxemia); the hyperpnoea, to massive accumula- 
tion of carbon dioxide in the respiratory center. During apnoea, carbon 
dioxide saturates the blood. This excites the center to increased activity: 
Hyperpnoea and increased pulmonary ventilation results, with consequent 
riddance of the excess carbon dioxide. Again, with a lowered carbon dioxide, 
overstimulation of the respiratory center ceases and the apnoeic period begins. 
Attacks of sudden, almost paroxysmal dyspnoea, often nocturnal in 
character, are not uncommon in heart disease. When unattended by the 
physical signs of pulmonary stasis or edema, or when there is no evidence of 
sudden, added cardiac damage, such paroxysms of dyspnoea are difficult to 
explain. They may perhaps depend upon varying degrees of dilatation in an 
already crippled heart, thus interfering with proper propulsion of the blood 
in the systemic and pulmonary circuits. Such assumed attacks of cardiac 
dilatation, however are not diagnosable by our present methods of examina- 
tion (Chapter VI). Hence, this assumption can be based only upon negative 
findings at the time of examination and upon the probability that cardiac 
dilatation can and does produce dyspnoea. 
Orthopnoea may be defined as an extreme continued state of breath- 
lessness in which the individual must constantly sit up and bring into play 
all the accessory muscles of respiration. When due to the heart alone and 
not paroxysmal in nature, orthopnoea is a sign of extreme decompensation. 
All types of dyspnoea are naturally increased by exercise, for then a greater 
demand is made upon the circulation than when at rest. That vaso-motor 
influences can have a perturbing effect upon dyspnoea especially in those 
with hypertension and cardio-sclerosis is evidenced by the fact that dyspnoea 
is sometimes considerably increased when patients walk or even drive in the 
open air, yet these individuals are perhaps fairly comfortable when walking 
indoors. I believe this is only explicable upon the supposition that the 
colder open air causes contraction of the skin arterioles with consequent 
sudden filling of the venous reservoirs and capillaries. 
Having described the various fundamental patho-physiological causes 
of dyspnoea, it should again be emphasized that dyspnoea—abnormal short- 
ness of breath—is the most common clinical and obvious sign of beginning 
heart failure and that in a general way its degree is roughly parallel to the 
degree of heart failure. 
Cough is another common symptom of cardiac failure, and, like dyspnoea, 
may be due to various causes, hence it too requires careful observation and 
study. Cough may be purely reflex in character. This is the true so-called 
“ cardiac cough,” and is extremely difficult to differentiate from a purely DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
275 
neurotic cough. Such differentiation can only be made upon the basis of a 
careful physical examination not only of the heart but also of the lungs, in 
order to exclude bronchitis and evidence of visceral congestion (q. v.). 
“ Cardiac cough” is dry and hacking in character and is usually accompanied 
by slight dyspnoea. Its origin seems due to reflex irritation of the nerve 
supply of the bronchial tree, the impulse probably passing by way of the 
ganglia surrounding the root of the aorta and the bifurcation of the trachea 
(Chapter III). 
There are other types of cough in heart failure which are due to actual 
physical changes in the bronchial tubes, lung parenchyma or pleura, or there 
may be a combination of several of these pathological conditions. A pul- 
monary infarct, when typical, gives rise to hemoptysis, fever, and more or less 
extensive pulmonic consolidation, with its attendant physical signs. Some- 
times the site of the infarcted area may not be localizable if a central portion 
of the lung be involved, if pulmonary congestion instead of consolidation be 
present, or if there be no accompanying dry pleurisy with its typical rales 
over the infarcted lung. 
When cough is due to bronchial congestion, the physical signs are the usual 
ones of bronchitis. In addition, rather marked sibilant breathing may 
be present, thus resembling bronchial asthma. The wheezing inspiration, 
however, is probably caused by the bronchial congestion and mucus in the 
bronchial tree and not from any anaphylactic reaction. Another type of 
spasmodic bronchial cough is that found occasionally in luetic aortitis 
(Chapter XVI). 
“Cardiac asthma” is a term difficult to define, for different writers place 
it in entirely different etiological categories, such as dyspnoea, pulmonary 
edema, bronchitis, etc. In its strictest sense it applies to the type of nocturnal 
paroxysmal dyspnoea already described (q.v.). Hence, the term “cardiac 
asthma” unless properly characterized and defined is too generic to be of 
clinical use. 
Sudden pulmonary edema, always a threatening complication, gives 
rise to soft, bubbling, mucous rales usually over the entire chest. Extrasys- 
toles or complete irregularity of the pulse (auricular fibrillation) is apt to 
accompany the attack. Limiting ourselves to cardiac causes and not to 
such extracardiac factors as toxemia, drugs, poisons, etc., the etiology of 
acute pulmonary edema is by no means always clear. When due, for example, 
to a resolving pneumonia following an infarct, the cause is sufficiently mani- 
fest. This however does not explain the usual attacks of sudden acute 
pulmonary edema. Although our knowledge of pulmonary edema is still 
inadequate, the prime factor seems due to some influence which markedly 
and suddenly diminishes the ventricular output of one chamber as compared 
with its fellow. Perhaps cardiac dilatation, especially when unequal in the 
two chambers, may represent such a condition. As already pointed out, 
for the present the diagnosis of cardiac dilatation can be based only upon 276 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
surmise and questionable clinical criteria, for such dilatations do not give 
rise to unequivocal physical signs. What seems to me a much more prob- 
able cause of acute pulmonary edema is sudden occlusion of the smaller or 
larger coronary branches (Chapter XXIII) by thrombosis or embolism, the 
pulmonary edema immediately overshadowing the dyspnoea, precordial 
pains and usual prodromata of coronary occlusion. Such etiology of pul- 
monary oedema is further borne out by the clinical fact that it is especially 
frequent in cardiosclerosis with hypertension, a complex in which coronary 
disease is very common. Pulmonary edema is rarely the first sign of cardiac 
failure unless it has followed severe cardiac overstrains or some sudden neuro- 
genic “insult” such as fright or shock. 
Cyanosis.—It is a common clinical observation that cyanosis, often a 
prominent and obvious sign of advanced or long standing valvular disease, is 
not necessarily accompanied by marked dyspnoea. On the other hand, 
patients of the cardio-sclerotic type (Chapter XVII), especially those with 
renal complications, are very apt to be dyspnoeic but not cyanotic; indeed, 
they may be decidedly pale. Nephritic dyspnoea is often nocturnal; it 
may then appear suddenly or in paroxysms. It is thus evident that dys- 
pnoea is present in two different groups of cardiac patients: In those who 
are pale and those with cyanosis. In the cyanotic group, chemical examina- 
tion of the blood shows no abnormal increase of non-volatile acids; the carbon 
dioxide tension of the alveolar air is usually normal; there is no or but slight 
decrease of blood alkalinity (that is, there is no acidosis). In the anemic 
group, renal complications are frequent, the blood pressure often high, and 
venous congestion is, as a rule, absent; the carbon dioxide tension of the 
blood and of the alveolar air is decreased; the acid products, increased 
(acidosis); both changes may be extremely marked. Such patients often 
have uremic manifestations. At present, the belief is that these abnormal 
products in the blood are due, not to overproduction, but to retention from 
renal insufficiency. 
According to recent studies, the cause of cyanosis seems to be deficient 
oxygen saturation of the blood (anoxemia). In heart disease several factors 
may play a role in causing the anoxemia—disturbance of the arterial circu- 
lation; venous insaturation from congestion; or disturbance of the capillary 
circulation. 
With marked or only slight dyspnoea, cyanosis is most strikingly seen in 
chronic uncomplicated valvular disease. Unless renal complications are 
present, the tension of the alveolar air and the blood alkalinity are within 
normal limits. The dyspnoea, when present, is due chiefly to venous engorg- 
ment, the result of myocardial insufficiency. This venous stasis affecting 
the pulmonary circulation produces deficient oxygenation, which finally 
results in cyanosis. Cyanosis without dyspnoea is most frequent in chronic 
decompensated mitral lesions. When the patients are resting quietly, 
dyspnoea is scarcely evident. It should be pointed out that cyanosis shows DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
277 
itself at first in turgescence of the mucous membranes of the lips, cheeks, 
and conjunctivae; later of the extremities. 
Visceral congestion varies considerably in the different valvular lesions. 
Congestion of the bronchial tree is shown at first by symptoms and physical 
signs of bronchitis; in the more advanced cases, by pulmonary congestion 
and hypostatic pneumonia. Mitral stenosis is especially apt to be accom- 
panied by hemoptysis, usually small in amount. Slight febrile changes may 
accompany the bleeding. Pleural transudates, especially right sided hydro- 
thorax, may be present; this preference for the right side has as yet not been 
satisfactorily explained. The presumption is that it is caused by the pres- 
sure of the right heart on the azygos veins. The liver may be slightly or 
tremendously enlarged and may even reach the pelvic brim. The enlarge- 
ment may be permanent or its size may return to the normal when compensa- 
tion is restored. The shape of the engorged liver is globular; its surface, 
smooth. If hepatic congestion is a gradual process, there is little or no 
tenderness on pressure; with sudden decompensation and consequent rapid 
engorgement of the organ, liver tenderness is marked. The usual sites of 
tenderness are the epigastrium and the gall-bladder region. Hepatic con- 
gestion may be an isolated phenomenon, other organs being spared. It 
would seem that in such cases the liver tissue acts almost like a sponge, 
swelling with the venous engorgement. The clinical syndromes in which this, 
condition is apt to occur are mitral disease with the sudden onset of auricular 
fibrillation, and occlusion of one main coronary, usually the right. Jaundice 
sometimes accompanies marked hepatic enlargement and is occasionally 
extreme. In one instance which came to my knowledge, marked destruc- 
tion of the liver parenchyma was found at autopsy. 
The spleen is often found enlarged and congested at autopsy in chronic 
valvular disease. This enlargement often escapes diagnosis during life, 
for the edge of the organ is rarely palpable, and evidence derived from per- 
cussion alone is untrustworthy. Splenic infarcts may be found in those 
suffering from bacterial endocarditis (Chapter XV): During life the infarct 
may be diagnosed by tenderness and pain over the spleen and by a palpable 
enlargement. 
Edema.—It is pertinent to inquire into some of the etiological factors 
concerned in the edema of heart failure because of the complex and intricate 
nature which modern conception assumes in its causation. In the discussion 
of dyspnoea it has already been shown how heart failure causes “acidosis.” 
Cardiac failure also causes disturbance of venous and capillary pressure; as a 
corollary it also disturbs pressure relations in the lymphatics. 
Chemically, the edematous fluid resembles a transudate. It is clear, 
watery, of low specific gravity (around 1005) and contains organic and inor- 
ganic salts. It is the abnormal accumulation of this fluid in the intercellular 
spaces (or serous cavities) which constitutes edema. The formation of 
edema is closely bound up with the flow of lymph. Normally, there is a. 278 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
nice balance maintained between arterial, venous, capillary and lymph flow 
so that there is never any leakage or seepage of lymph during health. With 
the occurrence of heart failure, this balance is disturbed by certain hydro- 
static and physico-chemical factors. Briefly, these physico-chemical factors 
are diffusion, a movement of molecules from areas of greater to those of 
less concentration; transpiration, a movement of molecules through mem- 
branes, (here applied to the cellular walls of lymphatics and capillaries); 
osmosis, a movement of molecules through membranes permeable to them 
but not to the dissolved substances. Colloidal imbibition of water (prob- 
ably a minor factor), and the influence of chlorides and of the amount of 
fluid are other factors. In order that any or all of these physico-chemical 
factors be brought into play, greater hydrostatic forces must be considered, 
just as in the flow of water. These are first, the “pump” (the heart), the 
source of energy which determines the rate and volume of blood (and lymph) 
flow; and second, the “head” of the flow, that is, the difference in potential 
between the various ar«as involved. Thus it may be seen how, in heart 
failure, all these factors may cause complicated interaction; that individual 
factors may assume varying proportions in different types of heart failure; 
for example, where kidney congestion plays a role, chemical factors may pre- 
dominate because the renal filtering function is interfered with; and finally, 
since we possess only incomplete knowledge, and the actual changes are 
hidden from view, often broad clinical knowledge and correlation alone can 
help in the solution of the etiology of the edema. 
Edema itself is easily recognized by the well known pitting on pressure: 
The depressed skin can be readily seen and felt. In pure cardiac failure, 
the feet and ankles first become edematous; in more advanced cases, there 
is also edema of the legs, thighs, scrotum and of the abdominal walls; finally, 
all the subcutaneous tissues and serous cavities become edematous (general 
anasarca). In the edema of pure nephritis, the eyelids and face first show 
the edema, later the ankles; in advanced parenchymatous nephritis, gen- 
eral anasarca may also result. 
Renal involvement in valvular heart failure ranges from moderate passive 
congestion to sclerotic changes in the glomeruli. The former is common; 
the latter, rare. Embolic renal infarcts are rare in chronic rheumatic endo- 
carditis; fairly common in streptococcus viridans infections. Renal conges- 
tion is shown by decrease in the amount of urine, by the presence of albumin 
and casts, and, in severe cases, by lessened excretion of phenolsulphonephtha- 
lein (Chapter XXI). 
Cardiac pain, or as I prefer to call it, precordial pain is discussed separately 
in subsequent chapters (Chapters XVIII, XXIV). I shall here limit myself 
to the precordial pains in chronic valvular disease. The severity of the pain 
apparently depends chiefly upon the degree and suddenness of decompensa- 
tion. Its distribution and character vary from a slight sensation of precordial 
heaviness to agonizing attacks radiating from the chest to the left shoulder, DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
279 
left scapula, neck, abdomen, and rarely, to the legs. Sudden dyspnoea and 
pain may also occur as the result of a profound change in intracardiac cir- 
culation from embolus or infarct of the coronary or its branches. 
Cerebral Manifestations.—Excluding cerebral thromboses and hem- 
orrhage (apoplexy), the majority of the serious cerebral manifestations of heart 
failure are the result of disturbed cerebral circulation. Where there are 
such complicating factors as associated kidney lesions with “acidosis,” or 
pulmonary stasis with or without hydrothorax, the tendency toward insuffi- 
cient cerebral blood supply is present; hence, comparatively slight increase in 
cardiac decompensation will precipitate cerebral manifestations. Drowsiness, 
sleepiness, mental languor and torpidity are the beginning stages of the 
latter. Stupor represents a later stage. In aortic lesions, especially that 
associated with arteriosclerosis and cardio-sclerosis, there are at times periods 
sometimes lasting several days in which the patient is in semi-stupor or even 
coma; the condition seems due to actual slowing of the entire cerebral circu- 
lation, partly from weakened cardiac power, partly from narrowed and 
diseased cerebral vessels. In cardiac failure associated with parenchymatous 
changes in the kidneys and general edema, various stages of cerebral depres- 
sion ranging from mild stupor to deep coma are found. Such manifestations 
seem primarily due to cerebral edema. In some types of cerebral endarteritis 
with accompaning heart failure, epileptic seizures are the rule. Dizziness and 
syncope are common cerebral manifestations due to transient cerebral anemia. 
The Neurotic Element in Organic Cardio-vascular Diseases.—Thus far 
we have been dealing with, and confining our attention to objective signs of 
cardiac disease. There is a marked modern tendency to depend too much 
if not entirely upon such objective phenomena. This tendency has been 
considerably enhanced by the frequent use of instrumental and laboratory 
aids, such as the electrocardiograph, polygraph, X-ray, blood pressure 
instruments, blood chemistry, etc. Practitioners as well as students are only 
too apt to rely implicitly upon data thus furnished, and to pay insufficient, 
or perhaps no attention at all to the mental and psychical make-up of the 
individual, with his reactions and social relationships. The author has 
frequently stressed the outstanding importance of learning how to apply in 
the sick room the lessons learned from instruments; in other words, their 
clinical and practical application. But in addition it is important to under- 
stand the patient as an individual. It is just in this phase of clinical medicine 
that the old master clinicians stood out preeminently. Their vast bedside 
experience taught them almost intuitively to pick out the neurotic, the hyper- 
excitable, the phlegmatic; and with a kind word here, a humane expression 
there, an interest in the commoner complaints, they gained not only a tre- 
mendous insight into the mental fabric of their patients but with it a control 
over their psychic reactions. 
Our intensive rush of work and our intensive resort to instrumental and 
other objective aids, has doubtless hastened, if indeed it has not caused the 280 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
popular interest in the various medical cults and fads of our time. We do not 
sufficiently appreciate the mental anguish, the suffering of the patient, whether 
he has organic disease or not. The patient feels himself a “ sufferer; ” this is the 
phase with which his mind is almost exclusively occupied; while we are wrapped 
up in diagnosis and think little of therapy, especially in chronic or functional 
conditions; offer little or no psychological encouragement, and forget that a 
patient even with a functional complaint actually “suffers.” We are too apt 
to dismiss a functional case as hysterical or neurotic because we discover no 
objective findings. It is perhaps our own disappointment and our own ina- 
decipher and translate into terms of actual pathology apparently 
unfounded complaints that produce in us a certain amount of impatience. 
This impatience is often reflected in a curt demeanour toward the patient. 
Indeed the patient’s point of view is rarely considered; he is simply regarded 
as an impersonal “case” of functional disturbance or as being “nervous.” 
The patient, on the other hand, is seldom interested in the diagnosis as such. 
He is chiefly interested in the length of time he is going to be ill, and in the 
therapy. Is he very sick? Will he get well? How long will it take him to 
get well? Will he be able to continue his work? Will he have to stop work 
entirely? Will he have to go away, and if so, for how long? Such questions 
are even more important to wage earners who must return to their work at 
the earliest possible moment. In chronic or incurable cases particularly, the 
physician sees just the hopeless aspect, forgetting the importance of buoying 
up the patients morale, so to speak, by either minimizing the incurability of 
the condition, or by instilling hope that the illness will improve in the course 
of time. There are after all, but few of us who are brave enough to be told 
frankly that our case is hopeless or incurable, or that the disease will soon kill 
us. Thus, the physicians’ own neglect has nurtured the hope and faith in 
cults and fads, for they at least give exalted hope and promise relief from 
the patient’s “suffering.” In all this, there is of course this definite warning. 
Not that instrumental and other methods of diagnosis are to be discarded; on 
the contrary, they are needed all the more in order that we be as sure as 
possible in the present state of our knowledge that no actual organic lesion 
escapes diagnosis. But when a final diagnosis of a functional disorder is 
made, our task is not ended. We must search for social factors—an unhappy 
married life, fear, fright, business reverses, etc.—as possible etiological factors 
for a disturbed psyche, and with it, a cause for the various functional dis- 
orders. Such factors if found naturally require their proper social adjust- 
ments. We should also instill and fortify these patients with a hope of cure. 
Drugs, even of questionable value; therapy, such as violet ray to the chest 
for pain—-are not only admissible but are of unquestioned value when, in 
addition, the patient is mentally stimulated by hope, and can be assured there 
is no serious pathological background for his complaints. To fortify them- 
selves, it may perhaps be a wise thing for physicians to study, not the cults 
themselves, but the psychic essentials in them which undoubtedly often lead DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
281 
to cures or at least relief, especially when “legitimate” scientific medicine 
fails. Faith, belief, hope, humaneness and sympathy, are the keystones of 
medical cults and fads. These can undoubtedly be used to our own advan- 
tage and to that of our patients, if we have sufficient regard for their impor- 
tance; for important they are, both in organic and functional disease of the 
human economy The entire subject merits this special mention because it 
is an almost neglected field of practical, clinical medicine. 
Chapter XVIII discusses the pure neuroses, many of which are illustrated 
in the Cardio-vascular Clinics. Here I shall confine myself to the Neurotic 
Element in Organic Cardio-vascular disease. 
I do not believe that the role of neurotic and psychic disturbances as 
initiators of symptoms in those with organic cardio-vascular disease has been 
as sufficiently emphasized as in those with purely functional neuroses. The 
soldier’s heart, hyperthyroidism are examples of the latter (Chapter XVIII). 
It not infrequently happens that individuals with heart disease get along 
fairly comfortably until some untoward psychical disturbance such as fright, 
initiates symptoms from which it may take patients months to recover, indeed 
they may never regain their old cardiac stability. We are so apt to be 
engrossed with physical signs during an examination that we may not lend 
sufficient attention and importance to minutae in the history, apparently 
minor factors which often have an important etiological bearing. I have 
found that especially in mitral stenotic lesions, mental disturbances can 
have a markedly deleterious influence. It can not only bring on tachycardia 
but overforceful cardiac action as well; this indeed can occur with lesions 
which from the inflammatory and clinical standpoints had long been quies- 
cent and stable. When studying such hearts prior to the period of abnormal 
excitation, one observes no differences either in their fluoroscopic size, the 
presystolic murmur, or other physical or clinical characteristics which would 
single them out as being especially susceptible to nervous influences. It is 
somewhat surprising to note that even from the psycho-neurotic standpoint 
these individuals present nothing abnormal or characteristic. They have no 
psychopathic stigmata, they impress one as having had stable nervous 
systems prior to the onset of their neurotic cardiac symptoms, and they do 
not show any characteristic in general physique which would align them with 
so-called psycho-neurotic types. It is important to observe that in those 
with mitral stenosis and auricular fibrillation, the effect of a neurotic ‘‘insult” 
is much more marked than in those with rhythmic pulses: Cardiac activity 
becomes more violent, rapid and irregular, and there are more abortive beats. 
Indeed, I believe that such individuals may die suddenly as the result of a 
nerve shock. 
I shall give a few illustrative cases showing the effect of the psychic ele- 
ment in mitral stenosis. 
R. A. E., female, aged 22, of slight physique, has had “heart trouble” 
since childhood. She had however, always been able to play normally with 282 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
other children, with no limitation of her activities. One year ago her mother 
died unexpectedly. That same day she had “palpitation” and irregular 
heart action which has since continued. Physical examination shows a 
typical mitral stenotic lesion with auricular fibrillation. The cardiac rate 
varied from ioo to 130 per minute. During her stay of several weeks in the 
hospital neither rest in bed, digitalis nor bromides had any appreciable influ- 
ence upon the irregularity. She was not dyspnoeic; slow walking did not 
increase the heart rate nor the subjective feeling of palpitation. The main 
complaints were palpitation and some limitation of physical activity. 
L. K. female, aged 19, had a mild attack of grippe trachitis during which 
she had a “choking spell;” this frightened her considerably. From the 
patient’s description the spell was apparently due to spasmodic pharyngeal 
cough. The spell was immediately followed by rapid heart action, later by 
dyspnoea. Upon hospital admission a typical mitral stenotic lesion was 
found, there were no signs of decompensation, the heart action was regular, 
the rate, 90 per minute. There was slight tenderness upon pressure over the 
precordium. Although the patient complained of dyspnoea, she could breathe 
comfortably when lying flat. She was given a few doses of bromides and was 
assured that her heart was not damaged. After two days the patient felt 
relieved and was allowed out of bed. 
This was an instance in which the tachycardia was temporary but the 
subjective dyspnoea and palpitation continued. Reassurance doubtless 
played an important part in the “cure.” 
Mrs. C. W., aged 35, had rheumatism 5 years previously. She had been 
curetted for an abortion several weeks prior to consulting me. The operation 
was followed by fever, and articular pains and swellings. When brought to 
my office she presented all the classical symptoms of severe decompensation; 
anasarca, dyspnoea, hydrothorax. Physical examination showed a typical 
mitral stenotic lesion, auricular fibrillation and an enlarged heart. The 
patient was apparently much pertrubed and frightened during the prelimi- 
nary examination, in spite of the frequent assurance that there was no cause 
for worry and that no part of the examination was painful. The next step 
was fluoroscopy. She was slowly assisted to the apparatus by the nurse and 
myself, apparently reassured and calm. No sooner did she sit down in the 
apparatus than she gave one cry, and died within two minutes. Most 
probably fright was the underlying cause of the sudden death: One can only 
theorize as to how this factor operated, possibly by the induction of ven- 
tricular fibrillation and death. 
I shall now cite two other instances, one of which also ended fatally, in 
order to demonstrate definite correlation between psychic “insults” and grave 
cardiac symptoms. 
I. S., dentist, aged 32, married, had scarlet fever complicated by an 
attack of articular rheumatism lasting one week, eighteen years ago. The 
only other infections were mild attacks of influenza, one and two years ago, DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
283 
respectively. Six years ago he was told by a physician that he had “ valvular 
heart disease.” Despite this knowledge he was always physically active and 
athletic and never had any distinct cardiac symptoms until the onset of his 
present complaint several months ago. He then had a good deal of family 
aggravation and disputes which worried him considerably and which resulted 
in attacks of tachycardia and dyspnoea. He finally developed hemoptyses, 
usually accompanied by severe left sided precordial pains. Fever was never 
present. Tubercle bacilli were never found. On examination the systolic 
blood pressure was 150, the diastole, 50. The mouth, thyroid, and throat 
were normal. There was slight throbbing of the carotids. There was a 
well defined diastolic murmur heard best over the left base. There was 
overaction of the cardiac apex, accompanied by a palpable thrill. A soft 
systolic murmur was also heard at the apex. The fluoroscopic examination 
revealed definite overaction of the aorta and moderate enlargement of the 
heart in a downward direction. The knee reflexes were much exag- 
gerated. The urine was normal. There was nothing of moment in the 
electrocardiogram. 
The case was one of rheumatic aortic regurgitation which had long since 
reached a quiescent stage. Family nagging however had directly caused 
tachycardia, as the result of which attacks of pulmonary edema and hemopty- 
sis had occurred, or possibly emboli were thrown into the circulation by the 
violent cardiac action. At any rate, there was no evidence of any rheumatic 
endocarditic recurrence. 
The further course of the case was interesting. The patient was placed on 
luminal tablets in doses of grains. He was sent to the country for the 
summer and was told to do very little walking and to rest out of doors a good 
part of the day. At the end of several weeks the slight tachycardia and 
continued consciousness of his heart action present at the first examination 
disappeared, he was able to walk at a natural pace without any cardiac 
symptoms. Recently he has again taken up his dental work and feels as 
comfortable as he ever did. He is gradually taking up his old routine of life. 
A. S., male, aged 68, gives a history of an old gonorrhea, otherwise he has 
had no other infections. He has had sugar in his urine as high a,s 1 per cent, 
for many years: There was no albumin. There has been increasing dyspnoea 
for three years. There were no precordial pains. Examination: The 
systolic blood pressure is 125, the diastole 10. The carotids throb. There is 
a broad heaving apical impulse. There is no pain on pressure over the heart. 
The heart is considerably enlarged. On auscultation at the base, there is a 
slightly accentuated second sound; at the apex the first sound is reduplicated 
and is accompanied by a systolic murmur. The margin of the liver is at the 
umbilicus. There is slight edema of the legs. The urine and reflexes are 
normal. Orthodiascopic examination shows left ventricular hypertrophy 
and aneurismal enlargement of the first portion of the aorta. The electro- 
cardiogram shows left ventricular preponderance. The YVasserman blood 284 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
examination is negative. The diagnosis was cardiosclerosis and left ventric- 
ular hypertrophy with moderate decompensation. The patient improved 
after having been digitalized. 
The patient had a very small rectal fissure which caused much pain and 
which was sensitive even to the slightest touch. He was finally sent to 
another physician for further rectal examination with the distinct admonition 
to the physician that undue pain be carefully avoided and that nothing be 
done or said that would upset, pain or frighten the patient. This warning 
was heeded, yet the patient was so frightened that he nearly fainted on the 
examining table. Thereafter, there was immediate aggravation of the car- 
diac symptoms: Dyspnoea became at first distressing, later constant. The 
patient died after a few weeks. 
The patient represented a case of severe cardiac disease in whom the 
fatal termination was undoubtedly hastened by the patient’s fright at the 
very trivial and carefully executed rectal examination. 
I could multiply instances in which the psychic factor initiated symptoms 
in otherwise stabilized cardio-vascular disease, but I believe these few cases 
are sufficiently illustrative. They likewise illustrate why such symptoms 
as tachycardia and auricular fibrillation are not controlled by our usual 
remedies in these individuals, and why our prognostic viewpoint regarding 
them cannot conform to the usual type in which such neurotic factor is 
absent. In addition to the customary drug remedies, reassurance and other 
psycho-therapeutic measures play an important part in the treatment. 
Nervous upsets in otherwise stabilized cardio-vascular disease seem to act 
deleteriously in two general directions: First, by way of the vasomotor 
system; and secondly, by way of the accelerator arc of the sympathetic 
nervous system. The first effect may, for example, upset the balance in the 
venous reservoirs of the splanchnic system or of the systemic venous capil- 
laries, thus storing up blood in unusual quantities somewhat similar to what 
is found in some types of shock (Chapter XXVI). The second effect, that 
on the accelerators—races the heart unnaturally, and in an already diseased 
organ, intensifies a tendency to disturbed circulation. Often these two 
effects are undoubtedly combined. One cannot of course study the effects 
of deleterious nerve influences objectively or quantitatively, but can only 
draw inferences from physiology and physiological experiments. The group 
of clinical cases above described seems best explicable upon such bases. 
Cardiac Overstrain.—This subject is taken up here in connection with 
cardiac failure, not because cardiac overstrain is especially frequent in those 
with organic heart disease—indeed it is infrequent in them—but because the 
symptoms at least superficially resemble those of heart failure and are often 
mistaken for the latter. If through undue physical exertion the heart of 
the patient who already has slight or beginning heart failure be overtaxed, 
the result is increase and persistence of such symptoms as cough, dyspnoea 
and tachycardia. In those with quiescent endocardial lesions, some of DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
285 
whom perhaps have no knowledge of their heart disease, the result of cardiac 
overstrain is comparable to that found in normal hearts (see below), but the 
symptoms are longer continued and they react less readily to therapeutic 
procedures. 
It is however in those with normal hearts that the question of cardiac 
overstrain is of most importance, for in them it occurs most frequently. It 
is often assumed that cardiac dilatation (Chapter VI) is the basic underlying 
factor produced by the strain. Unless one wishes to assume that the type 
of cardiac dilatation accompanying cardiac overstrain in healthy hearts is 
different, symptomatically and otherwise, from that ordinarily found in car- 
diac disease, one does not observe in healthy overstrained hearts, such alarm- 
ing symptoms as pulmonary edema and heart failure. The symptoms and 
signs most often found are tachycardia, precordial pains, extrasystoles and 
dyspnoea (q. v. Cardio-vascular Clinics). They are also present in heart 
failure, hence the frequent confusion with the latter. The importance of 
the proper diagnosis of cardiac overstrain lies not only in the immediate 
discomforting symptoms but also in the fact that the patient often suffers 
for months and even longer with the symptoms common to irritable hearts 
and cardiac neurosis (Chapter XVIII). Based partly on the future progress 
of these individuals, and partly on the absence of evidence of actual decom- 
pensation, it appears most probable to me that the primary injury in cardiac 
overstrain in the healthy heart is a neurogenic one, possibly in the form of 
exhaustion of the normal tone of the controlling nerves of the heart. 
Functional Efficiency Tests.—These are described in this connection 
because they have a certain bearing upon the cardiac reserve, and therefore 
upon heart failure. For years various tests have been in vogue in order to 
graphically or mathematically estimate the cardiac reserve power, the mus- 
cular efficiency, the work force of the heart. The methods employed have 
been of the most diverse kinds; a few will be briefly mentioned. A 
fluoroscopic examination is one means which has been employed (Moritz 
and Dietlen). If orthodiascopic observation reveals increase in the size of 
the cardiac outline after exercise (i.e., if the heart dilates instead of contracting), 
it is regarded as a sign of an insufficient heart: If contraction follows exercise, 
the heart is regarded as efficient. These conclusions have been disputed by 
others. Differences in systolic blood pressure following exercise, and dif- 
ferences in pulse pressure in the standing and sitting positions, are also 
employed as guides of cardiac efficiency. An attempt has likewise been 
made to estimate the muscular efficiency and cardiac load by a standard 
quotient obtained by dividing the pulse pressure by the systolic pressure. 
Another formula (Stone), consists in estimating the heart load as the resul- 
tant of the division of the pulse pressure by the diastolic ;this should normally 
approximate 50 per cent. Still another test for functional efficiency, a modi- 
fication of the older Graupner method, consists in the observation of the time 
required for the blood pressure to return to its level after exercise (Barr- 286 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
inger). It has been found that, in normal individuals, the systolic blood pres- 
sure is raised very soon after a moderate amount of work; with more severe 
exercise, the maximum systolic blood pressure is not reached until one or more 
minutes after exercise has ceased. This is the so-called “delayed rise.” 
This observation has been recently applied in the study of the functional 
capacity of diseased hearts; instead of an ergometer, the foot pounds of 
exercise or work are computed by the use of dumbbells and bars of various 
weights; these are lowered and raised a certain number of times to known 
heights. A criticism of this procedure (Rapport) shows that if blood pres- 
sure readings be taken immediately after exercise, there is at first a preliminary 
fall of pressure. Since however such a preliminary fall is almost constant, 
it may not invalidate clinical conclusions if observations be made according 
to the Barringer method. Another more applicable method is to have the 
patient climb a certain number of steps and then observe what effect the pro- 
cedure has had upon the blood pressure (Wilson). The blood-pressure 
methods of studying functional capacity seem especially applicable to those 
with cardiac neurosis in whom breathlessness, dyspnoea and tachynpncea are 
prominent symptoms, yet whose functional cardiac capacity may be found 
normal according to these blood-pressure tests. Thus, one may perhaps be 
assured of the muscular efficiency of such a heart, despite somewhat alarm- 
ing symptoms. 
It has already been shown that cardiac dyspnoea depends upon the 
vital capacity of the lung and upon the “pulmonary reserve.” These fac- 
tors may perhaps be readily employed as indicators of cardiac efficiency. 
In those with healthy or compensated hearts, the pulmonary reserve is 
ample; in those with decompensation from various causes, it is considerably 
decreased. The instrument employed is a specially calibrated spirometer 
with a recording kymograph attachment. The patient breathes through a 
rubber mouth-piece connected with the spirometer. It seems possible that 
minute-volume estimations may give quick and reliable information of a 
tendency toward dyspnoea and thus the instrument may be used as a clinical 
indicator of the functional capacity of the heart. 
Among other functional tests are the following. The Katzenstein test: 
Here, the heart work is increased by compressing the femoral arteries from 
two to five minutes. The normal reaction found in healthy and compen- 
sated hearts consists in a rise of the brachial blood pressure, of from 5 to 15 
m.m., the pulse rate falls. In cardiac failure, the blood pressure falls and 
the cardiac rate increases. 
The Mendelsohn-Graupner method measures the length of time required 
for the heart rate to return to normal after exercise. The pulse is first taken 
when at rest. Various types of exercise (e.g., raising dumbbells, stair climb- 
ing, ergostat, stationary bicycle) are then performed. Normally, the pulse 
rate should return to normal after a fair amount of work individualized 
according to the muscular make-up and physique of the person tested. The DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
287 
assumption is that the longer the time required for the pulse rate to reach 
the normal, the less is the functional capacity of the heart. 
The Herz Muscle-contracting Test.—If an individual slowly contracts 
a set of muscles (e.g., those of the forearm) so that both extensor and flexor 
groups are employed, the author claims that the pulse rate remains the 
same or is slightly increased in healthy hearts, whereas in decompensated 
hearts, the rate is slowed. 
Graupner Method.—With a measured amount of work, a normal heart 
reacts by an increase of blood pressure after mild exercise; a functionally 
weakened heart, by a fall of blood pressure. 
Plesch’s method depends upon a complicated compilation and deduction 
of the systolic output of the heart by the varying amounts of oxygen found 
in the arterial and venous systems. 
Several methods attempt to study the cardiac function by taking the 
pulse rate in the sitting, standing, and recumbent positions, and observing 
the length of time required for the pulse to return to the normal. 
General Objections to Functional Efficiency Tests.—It appears to me 
that there are several objections to the various methods of using blood 
pressure readings for tests of cardiac efficiency. Blood pressure depends 
upon important factors other than systolic output (Chapter XXV); the cardiac 
rate in circulatory failure often increases disproportionately to pulse pressure; 
increased cardiac work does not necessarily imply increased systolic output 
or increased blood pressure; the state of venous distention in the splanchnic 
area—an unknown factor because it cannot be measured—may considerably 
influence and vitiate the calculation. It is very difficult to eliminate or 
estimate the psychic factor. Finally, the various estimations can give but 
temporary information at the time the tests are made. Far simpler, more 
readily applicable, and clinically as accurate as the above tests, is the usual 
method of observing the patient during various forms of exercise—standing, 
walking, bending, etc.—and of estimating the cardiac reserve by noting the 
rapidity of pulse and respiration, dyspnoea and such subjective sensations 
as discomfort and exhaustion. Information derived from the patient’s sub- 
jective sensations is of special importance, and cannot of course be calculated 
by any instrumental method. The above routine can be further amplified 
in appropriate cases by allowing the patient to follow his ordinary occupa- 
tion, if not too laborious, for part of or the entire day, and then noting the 
effect upon his circulation and cardiac reserve. Such data, in addition to a 
very careful clinical examination, are, I believe, preferable to mathematical 
“efficiency tests” in the great majority of cases. 
REFERENCES 
Barringer, T. B., Jr.: Studies of the Heart’s Functional Capacity, Arch. Int. Med., 1917, 
XX, 829. 
Barringer, T. B., Jr., and Teschner, J.: The Treatment of Cardiac Insufficiency, etc., with 
Dumb-bells and B; Archives of Int. Medicine, 1915, XVI, 795. 288 
DECOMPENSATION—THE NEUROTIC ELEMENT—EFFICIENCY TESTS 
Graupner: Die funktionelle Bestimmung, etc., des Herzmuskels; Deutsche Med. Wochen- 
schrift, 1906, 1028. 
Herz: Eine Funktionspruefung des Kranken Herzens, Deut. Med. Wochensch, 1905, 
XXXI, 215. 
Kiehl, L.: Die Erkrankungen des Herzmuskels, 1913. 
Lewis, T.: Observations upon ventricular hypertrophy, etc.; Heart, 1913-1914, V, 367. 
Mackenzie: Diseases of the Heart, p. 74. 
Mendelsohn: Die Erholung als Maas der Herzfunction, Verh: d. XIX, Kong. f. Innerre 
Medezin, Wiesbaden, 1901, LXIX, 200. 
Moritz: Eine Methode, etc., Orthodiagraphie; Muenchener Med. Wochenschrift, 1900, 
XLVII, 992. 
Peabody: Cardiac Dyspnoea, Harvey Lectures, 1916-1917. 
Plesch: Haemodynamische Studien; Zeitsch. Expt. Path, und Ther., 1909, VI, 380. 
Rapport: The Systolic Blood Pressure Following Exercise, with Remarks on Cardiac 
Capacity. Archives of Internal Medicine, 1917, XIX, 981. 
Romberg: Krankheiten des Herzens u. der Blutgefaesse, 2d Ed. 82. 
Stengel: Paroxysmal Pulmonary Edema, American Journal of Medical Sciences, 1911, 
CXLI, 1. 
Stone, W. J.: The Differentiation of Cerebral and Cardiac Types of Hyperarterial Ten- 
sion, etc.; Archives of Internal Medicine, 1915, XVI, 775. 
Welch: Arch. f. Path. Anatomie u. Physiologie, 1878, LXXII, 375. CHAPTER XV 
RHEUMATIC AND BACTERIAL ENDOCARDITIS—PREVALENCE, 
CLINICAL PHENOMENA, SYMPTOMATOLOGY, PROGNOSIS, 
THERAPY—DYNAMIC CONSIDERATIONS 
Prevalence of Heart Disease.—There is undoubtedly a large proportion 
of the population affected with chronic vascular disease. If to this there be 
added those who suffer from correlated cardiosclerosis (including cardio- 
renal, cardio-vascular, hypertensive diseases, arteriosclerosis, “senile” heart 
changes), the sum must certainly be very large. Unless and until statistics 
Chrome 
Hearl Disease 
Death RaJte per 100.000 
.Pneumonia. 
Pul rt\onar\^ 
T-u'bercu'los'iS 
0Carv cev 
Fig. 275.—Curves showing comparative death rates from chronic heart disease, pulmonary, 
tuberculosis, pneumonia and cancer in io registration states. 
more carefully individualize the type of heart disease that causes death, they 
can give only a general idea of the incidence of heart disease. Even thus, 
comparison with other frequent causes of death—pulmonary tuberculosis, 
cancer and pneumonia—shows that death from heart disease is commoner 
than from any of these (Fig. 275). Perhaps it is exactly our increasing 
knowledge of the correlation of kidney and vascular changes with myocardial 
289 290 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
disease, and their report as “heart disease,” that has caused this apparent 
increase during the last decade or so (see chart). During the draft examina- 
tions for the Great War a correlation of statistics showed an incidence of 
heart disease of 2 per cent, among those called for service. This seems to me 
higher than the actual facts warrant. It must be remembered, for example, 
that the medical examiners were themselves ill-prepared at the beginning 
and that many functional conditions, particularly functional murmurs and 
irregularities, were regarded as organic changes. Another evidence of unpre- 
paredness for proper cardiac examination was the marked differences in ratio 
in rejected candidates among the various local boards. From my own expe- 
rience in a local board where I examined several hundred men, I found very 
few who required rejection for actual heart disease. I have no statistics at 
hand, but the percentage of rejection was certainly not nearly 2 per cent. 
I therefore feel that an assumed incidence of organic heart disease of one in 
fifty young men called by draft boards probably overrates the actual preva- 
lence of heart disease in younger individuals. 
The etiology and pathology of heart disease have already been described 
(Chapters IV, V). For clinical purposes, I shall divide valvular endocarditis 
into rheumatic, bacterial, and chronic streptococcus viridans. Cardiac syph- 
liis and cardiosclerosis are discussed separately. 
RHEUMATIC ENDOCARDITIS 
Clinical phenomena accompanying acute endocarditis affecting any valve 
may be divided into the general rheumatic and the endocarditic manifesta- 
tions. The former include the well known joint and muscular symptoms: 
Chorea, tonsillitis, erythema nodosum, subcutaneous fibroid nodules, etc. 
These rheumatic manifestations, however, do not always run parallel with the 
degree of endocardial involvement: The rheumatism may be mild, the endo- 
carditis severe, or the reverse. I have, for example, noted the appearance of 
infections of the mitral valve following very mild catarrhal invasions of the 
upper air passages. One instance was that of a young, vigorous adult of 
twenty, suffering from mild pharyngeal catarrh. His highest temperature 
was 100.4°. After three days, a typical mitral lesion developed. Another 
instance is that of a young physician, age 32, who had recently passed satis- 
factory army tests with reference to his heart. A murmur was never present 
until it was accidently discovered some months later while being examined 
for life insurance. He never had rheumatism. Some weeks prior to the life 
insurance examination, he had pharyngitis lasting a few days. When I ex- 
amined him, I found a loud systolic murmur heard over the mitral area and 
in the left axilla, typical of a mitral regurgitant lesion. There was no cardiac 
enlargement nor cardiac symptoms. I have the impression that such loud 
murmurs are not indicative of severe pathological damage to the valve but RHEUMATIC AND BACTERIAL ENDOCARDITIS 
291 
are caused by mild valvulitis with dilatation of the mitral ring; probably it 
is the latter element which causes the loudness of the murmur in these cases. 
Endocarditic and myocardial manifestations depend upon physical signs, 
and upon the type, course and complications of the valvular infection. The 
physical signs of the various lesions have been described (Chapter XIII). 
Upon their discovery rests not only the diagnosis of valvulitis but also the 
possibility of damage to the myocardium. That this possibility is present 
in every case of acute or recurrent endocarditis has already been indicated. 
Frank decompensation from severe involvement of the myocardium is 
extremely rare in acute endocarditis. There are, however, several signs 
and symptoms which, when present, tend to confirm the suspicion of 
myocarditis. Muffled indistinct heart sounds (not due to a pericardial 
effusion) in which the first sound resembles the second (so-called embryo- 
cardia), is an important sign of muscle involvement. Slight dyspnoea not 
accounted for by fever, tachycardia or exhaustion, is another. Continued 
rapid heart action and occasional extrasystoles after the fever and endo- 
carditis have run their course are added hints of possible muscle disease. 
An important sign of myocarditis, only discoverable by electrocardiograms 
or polygrams, is the presence of prolonged conduction time from auricle 
to ventricle—partial heart block (Chapter X). 
Writers have classified endocarditis according to special features (fever, 
cerebral complications, etc.), the assumed pathological process (verrucous, 
warty and papillary endocarditis) or upon the results of blood culture. Since 
the various groups merge, and since bacterial invasions (e.g., streptococcus 
viridans) may complicate rheumatic endocarditis as a superadded bacteremia, 
sharp divisions are arbitrary and cannot be maintained. I propose therefore 
to describe the usual clinical type of simple rheumatic endocarditis, with such 
variations as are important. 
The one prominent sign of acute rheumatic endocarditis is fever. The 
course of the fever as such is not characteristic. Its duration likewise follows 
no general type. Depending upon the severity of the endocarditic infection, 
fever may last from days to weeks. When the general rheumatic manifesta- 
tions are still active, it may be impossible to trace the source of the fever, for 
it may then be due to rheumatism or endocarditis. When the rheumatic 
course becomes afebrile, and joint and muscular inflammation have ceased, 
any rise of temperature, especially if sustained, is extremely suggestive of 
an endocardial involvement. In other words, fever continuing after reces- 
sion of rheumatic signs in the joints and elsewhere, is strongly indicative 
of endocarditis. Louder murmurs and cardiac irregularities strengthen this 
suspicion. Fever may be so slight that the temperature may have to be 
taken frequently in order to establish a febrile rise. This is especially true 
in the mild type of endocarditis of adults. More often there is a rise of tem- 
perature of one or two degrees; its usual accompaniments—lassitude, anorexia 
and headache—are then present. Hyperpyrexia, due to endocarditis alone 292 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
is uncommon. An initial chill or rigor is rare. It occasionally happens that 
there is no rise of temperature during the entire course of the endocarditis; 
this of course does not preclude the possibility of fever before the patient 
came under observation. 
Certain prodromal symptoms following mild rheumatism or tonsillitis are 
suggestive of developing acute or recurring endocarditis, even in the absence 
of fever; this statement is particularly true in children. Such children, 
otherwise robust and healthy, complain of feeling tired and become anemic 
and less active. Epistaxis is by no means infrequent. These manifestations 
have no direct references to the heart, for the children are not especially 
dyspnoeic, and physical signs of endocarditis are not then present. It is 
only when mild rheumatic symptoms occur, such as fleeting pains in the 
limbs, that a slight rise of temperature for a few hours may be observed; with 
it, the physical signs of endocarditis often become evident for the first time. 
Between the very mild, almost non-febrile cases, and the commoner 
ones with moderate temperature, there exists all grades and types of febrile 
disturbances. 
The physical signs of acute endocarditis are inconstant; they usually 
vary with the intensity of the process. The latter may be slow and gradual 
so that only after a long time do frank physical signs of valvulitis appear. 
On the other hand, physical signs, especially in children, may be immediate 
and unmistakable. The difficulty of interpretation of apical murmurs, 
especially in the presence of fever, has also been alluded to (Chapter XIII). 
Once established, the ausculatory phenomena of the valvular affections are 
those already described (Chapter XIII). 
Other Symptoms and Signs of Acute and Recurrent Rheumatic Endo- 
carditis.—The first hint of endocardial damage may be slight acceleration of 
the pulse. In adults the rate may reach ioo; in children, 120 per minute. 
This pulse acceleration is commoner in children than in adults. It may precede 
the physical signs of endocarditis by several days. This occurred, for example, 
in a young woman of twenty-five with articular rheumatism and with no 
temperature at the time she came under observation. She suddenly devel- 
oped tachycardia; it was only several days after rheumatic manifestations 
had ceased that the physical signs of endocarditis first presented themselves. 
Next in frequency to moderate pulse acceleration are extrasystoles. Paroxys- 
mal tachycardia, auricular fibrillation and flutter are uncommon. Pro- 
longed conduction time is sometimes found; this is an evidence of myocardial 
rather than of endocardial involvement. In very rare instances myocardial 
involvement shows itself by atrio-ventricular heart block (Chapter XI). 
New or disappearing patches of localized dry pericarditis, usually at the apex 
or over the left base, are occasional physical evidences, and offer clinical hints 
of the probability of acute endocarditis. 
Subjective symptoms of various kinds are sometimes referred to the pre- 
cordium during the course of acute endocarditis. They consist of indefinite RHEUMATIC AND BACTERIAL ENDOCARDITIS 
293 
sensations of weight or pressure on the chest. Occasionally “thumping” 
sensations are complained of, although the heart rate is normal; this seems 
due to abnormally strong ventricular contractions. There are at times “ stick- 
ing” or “stitch-like” precordial pains (Chapter XXIII). Pain may be pres- 
ent not only over the precordium, but may radiate to the left shoulder and 
neck, and to the left intercostal spaces. In general, the pains are not severe; 
they are more common when tachycardia is present. 
Cardiac decompensation in any of its phases is very rare in simple acute 
rheumatic endocarditis. 
To Summarize.—Fever, anemia, arrhythmias, or precordial sensations 
constitute suggestive signs of the onset of acute rheumatic endocarditis. 
Definite physical signs of a valvular lesion are necessary in order to clinch 
the diagnosis. 
Exacerbations and recurrences of simple rheumatic endocarditis are, in 
general, marked by signs and symptoms similar to the original onset of the 
disease. Rheumatism, pronounced or obscure, is often present. In some 
respects however, rheumatic endocarditic recrudesence may differ from the 
primary attack. For example, pulse irregularities are more frequent. 
Tachycardia—simple pulse acceleration, or, more rarely, the paroxysmal 
type—-is particularly common. Extrasystoles occur next in frequency. 
Auricular fibrillation, present throughout the entire exacerbation or coming 
in attacks, is by no means rare; in this respect, especially, exacerbations differ 
from the original onset. Auricular flutter is occasionally observed. Subjec- 
tive precordial sensations are more common; they vary from sensations of 
pressure to frank attacks of precordial distress. The physical signs of the 
valvular lesions are more pronounced unless they are masked by rapid or 
irregular heart action. Mild disturbances of compensation—slight edema 
of the legs, enlarged liver, dyspnoea, etc.—begin to make their appearance. 
Chronic Rheumatic Endocarditis.—Depending on the duration and fre- 
quency of rheumatic exacerbations, the symptoms and signs of recurring 
endocarditis merge into those of chronic endocarditis, embracing as it does 
the great majority of cases of valvular heart disease. Patients with chronic 
endocarditis and perfect compensation may continue in good health for years; 
cardiac symptoms may never occur. These are the fortunate instances in 
which the disease has become quiescent, and the cardiac damage, especially 
to the musculature, has not been extreme. The chief symptoms of chronic 
rheumatic endocarditis are due to myocardial insufficiency and to decom- 
pensation. They have already been described in detail. It remains now to 
differentiate the special signs and symptoms constituting the syndromes of 
decompensation in chronic rheumatic valvular lesions, as well as some 
considerations regarding the special dynamics involved. 
Decompensated Mitral Regurgitation (Mitral Incompetency). Dynamic 
Considerations.—When the mitral valve is rendered incompetent in a lab- 
oratory model of the circulation, there is a rise of auricular and a fall of 294 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
arterial pressure; the venous system is over-filled and there is a decreased 
transfer of blood from the venous to the arterial side. With the “heart” 
(pump) rate unaltered, there is a decreased ventricular output and a fall of 
arterial pressure. The “pulse” becomes smaller in amplitude. In animal 
experiments, MacCallum and McClure have shown similar results: In the 
experimentally produced mitral leak, there is a fall of pressure in the systemic 
arteries and a rise of pressure in the left auricle. The pressure in the pul- 
monary artery may rise or fall, depending on the degree of mitral insufficiency 
produced. When the insufficiency is extreme, the pressure in the pulmonary 
artery falls; when slight, the pressure usually rises. In either case, there is 
pulmonary congestion. But important as these laboratory and experimental 
observations are in support of the older “back pressure” theory (in this 
instance, failure of the right heart) in relation to experimental valvular leaks 
and their consequences, they are not entirely comparable to what takes place 
in the human being. In animals and in laboratory models, the leak is 
a sudden operation and hence requires sudden accommodation on the part of 
the cardiovascular apparatus. In the human being, the pathological process 
is usually a slow and gradual one, so that the heart, and the systemic and 
pulmonary circuits can slowly accommodate themselves to changes of pressure 
and of blood output. It is none the less true that pulmonaty signs often 
represent the initial changes in decompensated mitral regurgitant lesions (see 
below), hence it seems probable that at least in some cases, “backpressure” 
plays a clinical role. It should be remarked that a small regular pu lse (thatis, 
one of small amplitude), often present in mitral regurgitation and regarded 
by some as significant of decompensation, does not necessarily imply a cor- 
respondingly lowered blood pressure, as can be readily shown by clinical 
blood pressure observation (Chapter XXV). 
Clinical Syndrome of Mitral Regurgitation.—With beginning heart fail- 
ure, venous stasis affecting the pulmonary circuit is often an early symptom; 
hence bronchitis is one of the first, sometimes the only early manifestation. 
Bronchitis may range from a short, hacking, unproductive cough to one with 
numerous soft, mucous rales and areas of sibilant breathing scattered over 
both lungs. This complex with its physical signs accurately resembles true 
bronchial asthma, from which it must be differentiated. The signs of 
endocarditis and heart failure are usually sufficient to make the differen- 
tiation. Hemoptysis or expectoration of blood mixed with muco-pus is not 
infrequent. Patients with mitral regurgitation and heart failure are as a rule 
cyanotic. When cyanosis is extreme, the lips and extremities are bluish; the 
conjunctivae, suffused and discolored. Even with marked cyanosis, dyspnoea 
may be mild when the patient is resting quietly. Severe decompensation 
is accompanied by the visceral congestion and dependent edema already 
described (Chapter XIV). The usual subjective phenomenon is a feeling of 
weight or pressure on the chest; severe precordial pains are rare. On the 
other hand, sensitiveness to pressure in the epigastrium is common with or RHEUMATIC AND BACTERIAL ENDOCARDITIS 
295 
without gastric phenomena. Somnolence with a fair output of urine in the 
extremely decompensated is probably due to cerebral congestion and edema 
(Chapter XIV). 
Moderate pulse acceleration is the rule, extreme pulse acceleration or 
paroxysmal tachycardia is exceptional. The usual cardiac irregularities are 
extrasystoles (commonly ventricular) and auricular fibrillation; extrasystoles 
are observed in the beginning, auricular fibrillation in the later stages of 
decompensation. 
Decompensated Mitral Stenosis. Dynamic Considerations.—In the 
circulatory model, mitral stenosis causes a rise of venous, and a fall of 
arterial pressure, with lessening of the amplitude of the pulse wave. Narrow- 
ing of the mitral orifice can be produced experimentally upon animals by plac- 
ing a ligature around the auriculo-ventricular groove, or by placing a small 
inflatable balloon within the left auricle. There follows a rise of pressure in the 
left auricle and pulmonary artery, and a fall in the systemic arterial pressure. 
It is commonly assumed that similar conditions occur in the human being: 
Namely, a rise of pressure in the pulmonary circuit; as a consequence, increased 
pressure in the right ventricle occurs, finally leading to dilatation of the tri- 
cuspid ring and functional regurgitation in that orifice. A murmur due to 
functional tricuspid regurgitation is not infrequent in clinical cases of decom- 
pensated mitral stenosis. (See Chapter XIII.)’ Besides purely mechanical 
considerations of pressure differences, there are probably important patho- 
logical factors involved (myocarditis) in the production of this type of tri- 
cuspid regurgitation in the human being. 
Clinical Syndrome of Decompensated Mitral Stenosis.—A subjective 
feeling of palpitation combined with slight tachycardia is one of the earliest 
symptoms. This is not due to moderate pulse acceleration alone, but also 
to increased violence of the heart action. Slight dyspnoea accompanies the 
palpitation. Cyanosis is a comparatively late symptom and marks the 
period of severe decompensation. An enlarged and distinctly pulsating liver 
may be present even when cardiac failure is not extreme. Sharp, precordial 
“sticking” pains are common; they usually accompany the tachycardia and 
are present without pericarditis. Paralysis of the vocal cord due to paralysis 
of the left recurrent laryngeal nerve occasionally occurs. 
Ortner in 1897 first described the connection between mitral stenosis and 
paralysis of the left recurrent nerve. Since then, reports of thirty-two cases 
have been collected from the literature by Cuisset up to 1912. The theories 
held accountable for the paralysis may be recapitulated as follows: 
I. Ortner’s Theory.—Recurrent paralysis is due to pressure of the 
enlarged left auricle upon the nerve. 
II. Kraus’ Theory.—The right ventricular dilatation present in mitral 
stenosis causes displacement of the heart to the right, with consequent drag- 
ging on the aortic ligament and arch, and resultant stretching and paralysis of 
the nerve. 296 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
III. Alexander’s Theory.—The pulmonary artery, either by its own 
enlargement or indirectly by enlargement of the left auricle, is pressed against 
the nerve and aortic arch. 
IV. The nerve may be compressed and caught between bands of pericar- 
dial and mediastinal adhesions. 
All these theories have had some necropsy support. Normally, the pul- 
monary artery is situated under, and divides immediately beneath, the aortic 
arch; below the pulmonary artery is the left auricle. It therefore seems 
improbable that the left auricle, even when extremely enlarged, can exert 
sufficient direct pressure to produce recurrent paralysis, unless the auricle is 
jammed between, or is adherent to, the pulmonary artery and aorta. This 
was the finding in one case which came to necropsy. In another case, the 
left auricle was the size of a small fist and was found pressing against the nerve. 
From careful anatomic studies of frozen sections, Fetterolf and Norris state 
that the effect of left auricular dilatation is pressure of the left pulmonary 
artery against the aorta, and of the left pulmonary vein against the pulmo- 
nary artery, thus forcing the latter against the aorta. They believe that 
direct pressure alone of the enlarged left auricle can scarcely produce paralysis 
unless the auricle is squeezed between or is adherent to the pulmonary 
artery and aorta. They conclude that anything which will dilate or force 
upward the left auricle, the left pulmonary vein, or left pulmonary artery will 
tend to produce paralysis, and that the latter must finally be caused by the 
nerve being “squeezed between the left pulmonary artery and aorta or aortic 
ligament.” This conclusion bears out the common knowledge of the normal 
close juxtaposition of pulmonary artery and aorta (Chapter I). A similar 
conclusion was reached by Frischauer, who, in a case at necropsy, found the 
nerve compressed between the left pulmonary artery and aorta by the pres- 
sure of the dilated left auricle and pulmonary vein. 
I had an opportunity to observe a patient with mitral stenosis in whom 
there was not only paralysis of the left recurrent nerve, but also a marked 
difference in the radial pulse. The history and the result of the examination 
in this case are as follows: 
Female, aged 25, married two years, no children or pregnancies, had a 
severe attack of inflammatory rheumatism thirteen years ago. There were 
no cardiac symptoms until three years ago; at that time palpitation began. 
During the last year, she had also become dyspnoeic. Hoarseness commenced 
six months ago. Examination of the larynx showed that, owdng to left recur- 
rent paralysis, the left vocal cord was immovable and somewhat shortened, 
and in the cardaveric position. The voice was indistinct and hoarse. The 
examination of the cardio-vascular system revealed the following: There was 
a noticeable difference between the right and left radial arteries on palpation, 
particularly when the arms were extended above the head. The systolic and 
diastolic blood pressure of the right brachial were respectively no and 80 
m.m. of mercury; of the left, 82 and 70 m.m. There was no perceptible dif- RHEUMATIC AND BACTERIAL ENDOCARDITIS 
297 
ference in the carotid pulsations. The pulse was regular, the rate, 100 per 
minute. There was vigorous visible precordial pulsation; a diastolic thrill 
was felt, and a loud rumbling, presystolic murmur was heard at the apex. 
The aortic sounds were normal. Over the pulmonary area there was a 
somewhat rough systolic murmur and an exceedingly accentuated snappy 
second sound; the sharp click of the pulmonary valve closure was also evident 
on palpation. A dry pericardial friction rub was heard over the lower ster- 
num; three weeks later, there was evidence of fresh pericarditis over the 
pulmonary area. There was no systolic apical retraction. Orthodiascopic 
Fig. 276.—Orthodiascopic tracing of a case of mitral stenosis with paralysis of the left 
recurrent nerve. 
A, aortic outline; P.A., enlarged pulmonary artery; L.A., left auricle; L.V., left ventricle. 
examination (Fig. 276) revealed a short aortic bulge (A). The outline of the 
aorta was apparently encroached upon by the very much dilated pulmonary 
artery (P.A.). The left auricle (L.A.), though not enlarged in the tracing, 
was seen in the fluoroscope to overlap the pulmonary artery to some extent. 
The left ventricle (L.V.) and the right side of the heart were also somewhat 
enlarged. The electrocardiogram showed a negative S III, and a notched and 
enlarged P in the first lead. 
In this case, the fluoroscope showed no evidence of abnormal right ventricu- 
lar enlargement; the heart was dilated chiefly to the left. This evidence of 
left ventricular enlargement tends to discredit Kraus’ theory as to the 
etiology of recurrent paralysis in mitral stenosis. The orthodiascopic 
findings and the physical signs over the pulmonary artery in my case leads to 
the conclusion that the recurrent nerve paralysis was due to dilatation and 298 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
pressure of the pulmonary artery against the aorta; whether or not the left 
auricle was a factor in pushing up the pulmonary artery, it is impossible to 
state. Lian and Marcorelles insist upon the presence of old thrombosis of 
the left auricle, or of a mediastinitis as contributory causes. Pericarditis 
was present in my patient; it was at first confined to the precordial area over 
the lower sternum; later it involved the area over the pulmonary artery. 
This may have been an added factor in binding down the dilated pulmonary 
artery. 
A unique feature of the case was the marked difference in the right and 
left radial arteries, and in brachial blood pressures. This, in conjunction 
with paralysis of the vocal cord, formed a striking resemblance to 'the 
clinical syndrome of aortic aneurism. The difference in brachial pressure 
seemed due to the dilated pulmonary artery being wedged under the aortic 
arch opposite the origin of the left subclavian artery, with a pressure sufficient 
to produce interference with the circulation of the subclavian, and, conse- 
quently, of the left brachial. 
Attacks of paroxysmal tachycardia are comparatively frequent in 
decompensated mitral stenosis. Emboli produce occasional complications. 
Hemiplegia and aphasia may follow cerebral emboli. As an instance, one of 
my patients, a woman aged 50 with a mitral stenotic lesion, had aphasia for 
ten years from a cerebral embolus. A large artery of the extremity may be 
plugged by an embolus and cause gangrene. This happened in a patient of 
forty with mitral stenosis and finally led to amputation of the leg; the patient 
recovered. Hemoptyses from pulmonary emboli are not uncommon. Such 
cases must be carefully distinguished from the hemorrhage of pulmonary 
tuberculosis. The physical signs of mitral stenosis, and the site and nature of 
the pulmonary signs usually make the differentiation easy. Emboli do not 
necessarily,occur with symptoms of recurring endocarditis, nor can they be 
regarded as evidence of cardiac failure in the true sense. Indeed, they usually 
antedate severe dyspnoea, edema and visceral congestion by months or 
years. These embolic “accidents” seem in the main due to mechanical 
breaking off of vegetations on the mitral valves from overforceful and 
abnormally rapid heart action. Another frequent characteristic of mitral 
stenosis, already described (Chapter XVIII), is its susceptibility to nervous 
influences of various sorts. It is probably this which causes disturbances of 
heart action from various sources. Indeed, it is apparently this nerve 
lability which causes various referred disturbances of the gastro-intestinal 
canal. The gastric syndrome is that usually associated with hyperacidity 
or even of gastric ulcer. It is therefore extremely important to study such 
gastric phenomena from the cardiac aspect, otherwise patients are unneces- 
sarily rigidly dieted and put upon ulcer treatment. 
Severe decompensation in mitral stenosis usually occurs with the onset 
of auricular fibrillation, with the signs and symptoms already described. 
The arrhythmia, once established, often remains permanently. Occasion- RHEUMATIC AND BACTERIAL ENDOCARDITIS 
299 
ally, however, fibrillation occurs with each fresh exacerbation of endocarditis. 
Auricular fibrillation is found much oftener in mitral stenosis than in any 
other valvular disease. 
Aortic Stenosis—Dynamic Considerations.—In the circulatory model, 
aortic stenosis causes a marked increase of intra-ventricular pressure during 
systole, and a fall of arterial pressure during both systole and diastole. The 
“pulse” wave shows a slow ascent and a rounded top (pulsus tardus, Chapter 
VII). Similar observations have been made upon the experimental ani- 
mal; when a marked degree of aortic stenosis is produced, the rise of intra- 
ventricular pressure is correspondingly marked. The time of systole is 
prolonged, however, so that the amount of blood ejected into the circulation 
is not much decreased. 
Clinical Syndrome of Heart Failure in Aortic Stenosis.—As already 
mentioned, aortic stenosis as an isolated valvular lesion is rare. The 
symptoms of heart failure depend chiefly upon the degree of ventricular 
hypertrophy with its implied lowered cardiac efficiency. Marked decom- 
pensation is a late symptom, and is found only when hypertrophy becomes 
extreme. Congestion and auricular fibrillation occur only in the terminal 
stages. Among earlier symptoms are those due to cerebral anemia (dizziness 
and faintness). Other beginning manifestations consist of a subjective 
feeling of palpitation and of moderate tachycardia. Embolic infarcts in the 
viscera or extremities are occasional complications. 
Decompensated Aortic Regurgitation—Dynamic Considerations.—In 
the laboratory model the production of aortic regurgitation is followed by a 
fall of the diastolic pressure in the arterial system; there is no constant change 
in systolic blood pressure. Similar results have been obtained in animal 
experimentation. The cause of the fall of diastolic pressure, however, is still 
in dispute. According to the older assumption, the diastolic fall of pressure 
is massive back flow of blood during ventricular diastole. More recent 
observations (Stewart, Wiggers) demonstrate that the amount of back flow 
is after all but a small fraction of the amount ejected during systole. This 
was shown by cardiometer experiments and by the fact that the rate of ven- 
tricular relaxation (Chapter III) remained unaltered. Stewart attributed 
the diastolic fall of arterial pressure to reflex dilatation of the peripheral 
vessels. As the result of studies of subclavian and intraventricular pressure 
curves, Wiggers maintains that peripheral dilatation is not a factor in this 
diastolic fall but that it must be attributed to a “ back leak of pressure into the 
ventricle with or without an appreciable back flow of blood.” 
The clinical application of these facts seems to be that the amount of 
blood regurgitating into the ventricle is probably very slight and that “ back 
pressure” becomes a factor only when for any reason the muscular efficiency 
of the left ventricle becomes subnormal. 
Clinical Syndromes of Decompensated Aortic Regurgitation.—The 
patients are characteristically prone to suffer from attacks of tachycardia 300 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
(often paroxysmal), and from very severe precordial pains. Pains, dyspnoea 
and tachycardia frequently occur in nocturnal attacks. Mechanical inter- 
ference with the coronary flow by the aortic lesion may be a cause of some of 
these attacks. The pains are usually severe, sometimes agonizing (q. v. 
Cardio-vascular Clinics). Their favorite site is the precordium; they may 
radiate to the arms, neck, abdomen, and even to the legs. Fright, excite- 
ment, over-exertion, or nervous strain may be sufficient to initiate an attack 
of pain or of tachycardia, especially when ventricular hypertrophy is far 
advanced. Such attacks may also represent the only evidence of fresh 
endocarditis. Susceptibility of the heart to nerve influences of the most 
varied kinds, a condition common in aortic regurgitation, depends chiefly, I 
believe, upon continued mechanical “insults” from aortic hyperactivity to 
branches of the cardiac plexus surrounding the root of the aorta (Chapters 
I, XVI). This may well produce an altered state of nerve tone and of 
nerve control, leaving the heart readily susceptible to extraneous influences. 
Hemoptyses occasionally occur with the tachycardial attacks; they seem 
due to acute pulmonary congestion from rapid heart action. More rarely, 
hemoptysis may be the result of a pulmonary infarct. Another occasional 
complication of aortic regurgitation consists in periods of somnolence merg- 
ing into stupor. In one patient, a girl of 17 with a typical rheumatic regurgi- 
tant lesion and tremendous left ventricular hypertrophy, these cerebral 
manifestations were usually ushered in by fever up to 103°, and by paroxysms 
of auricular fibrillation. Cyanosis was not present. The dyspnoea during 
these attacks was not more marked than usual. The fever and fibrillation 
seemed due to recrudescence of endocarditis. Meningitis could be excluded. 
The accompanying somnolence, and later, stupor, in this and other attacks, 
could scarcely be accounted for by the fever alone or upon the supposition of 
a toxemia, for the patient had had a severe and long continued pneumonia 
with higher fever, without any cerebral manifestations. In patients with 
well marked aortic regurgitation, cerebral anemia from disturbed circulation 
in the brain is perhaps the underlying cause for such attacks of somnolence 
and semi-stupor. 
Visceral congestion, edema, and permanent auricular fibrillation represent 
late stages of decompensation in aortic regurgitation. 
Decompensation with rheumatic disease of the pulmonary and tricuspid 
valves is not described because rheumatic endocarditis affecting these 
valves is very rare, especially as isolated lesions. 
Therapy of Rheumatic Endocarditis without Decompensation.—During 
the acute stages, aside from the specific action of drugs of the salicylate group, 
we possess no medication that can influence the pathological process affecting 
the endocardium and valvular structures. Therefore in acute rheumatic 
endocarditis, or in endocarditic exacerbations accompanied by general rheu- 
matic. manifestations, the salicylates, preferably salicylate of soda, are 
indicated. Clinical observation has shown that the salicylates often control RHEUMATIC AND BACTERIAL ENDOCARDITIS 
30! 
rheumatic manifestations; it is therefore assumed that they may control the 
rheumatic poison affecting the heart. I prefer to give the salicylate of soda 
in 15 grain doses hourly until tinnitus occurs, or until six doses have been 
taken; thereafter, the same dose should be given three times daily. The 
futility of sera and vaccines is discussed later (Chapter XX). When fever 
is present the diet should be bland, mainly fluid. As fever decreases and 
the patient’s appetite returns, semi-solid and finally ordinary diet may be 
permitted. I find no special value in the restriction of the amount or kind 
of meat when the gastro-intestinal and kidney functions are normal and when 
the patient craves food (Chapter XX). Rest in bed should be enjoined 
during the period of the acute endocarditic attack. The plan, sometimes 
followed, of keeping patients in bed many weeks or even months after the 
acute stage has passed, possesses no value in aiding the circulation or in 
preventing reinfection (Chapter XXII). From three to five weeks I con- 
sider the average time for rest in bed after the acute manifestations have 
passed. In those with rapid heart action or with precordial discomfort, an 
ice bag should be placed over the heart; it should be kept in a proper sling 
so that the patient is not continually annoyed by its slipping. The length 
of time that ice is to be applied depends chiefly upon the patient’s feelings. 
I have occasionally found more relief from hot applications (hot water bag, 
electric pad) than from cold. If tachycardia is marked, or if patients are 
restive, luminal in one and one half grain doses, the bromides alone in fifteen 
grain doses, or bromides combined with small doses of morphine, are indi- 
cated. Occasionally such hypnotics as chloral and veronal are required. 
Digitalis is rarely indicated, for decompensation does not often occur in acute 
endocarditis. An exception may be the presence of tachycardia with acute 
dilatation and dyspnoea, a condition more frequent in children than in 
adults. 
In chronic rheumatic endocarditis, when no decompensation exists, 
drug medication intended to affect the heart and circulation is not indicated. 
Here, questions regarding proper exercise, vocation and occupation, play 
important roles (Chapter XXII). The therapeusis of decompensation in 
chronic endocarditis is described, to a great extent, in another chapter 
(Chapter XIV). Although medication is in general the same for the various 
valvular lesions it should again be emphasized that the same therapy is not 
followed by uniform results. The most beneficial results are derived from 
digitalis alone or in conjunction with quinidin sulphate (Chapter XX) when 
employed in decompensated mitral stenotic lesions with auricular fibrillation. 
In the heart failure of aortic disease with marked hypertrophy, digitalis has 
little or no effect in relieving decompensation, even in the presence of auric- 
ular fibrillation. The influence of foci of infection—teeth, tonsils, etc.—is 
elsewhere described (Chapter XXII). 302 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
PROGNOSIS IN RHEUMATIC ENDOCARDITIS 
It is naturally impossible to give categoric rules which will infallibly 
guide one in the prognosis. It is always necessary to study the disease 
in all its various aspects, as well as how it affects the individual patient. In 
chronic cases, the following general statements may be permitted, namely; 
prognosis depends more upon the condition of the cardiac musculature than 
upon the valve that is affected; and the greater the amount of hypertrophy, 
the worse the prognosis, especially as regards longevity. 
For clinical purposes the question of prognosis in rheumatic endocarditis 
may be divided into the acute and subacute, the quiescent and the chronic 
stages. The first two are here grouped together because they overlap so 
frequently that a sharp distinction is impossible. 
In the acute and subacute stages, the main prognostic problem is to deter- 
mine, if possible, the virulence of the infection. Although, as before stated 
(Chapters IV, V), a few observers claim to have isolated the specific organism 
from the blood of patients suffering from rheumatic endocarditis, this has 
not been substantiated by other bacteriologists; hence blood examina- 
tion for bacteria cannot at present be used to gauge the severity of the 
infection. In addition to information gained from physical signs, most 
reliance regarding the degree of virulence in rheumatic valvular infections 
must be placed upon such clinical manifestations as the acuteness and severity 
of the onset, the frequency of chills, the presence of hyperpyrexia, vomiting, 
leucocytosis, severe anemia and delirium, and upon such complications as 
pericarditis and pleurisy with effusion. If both the aortic and mitral valves 
are affected, the acute and subacute stages are apt to last a longer time than 
when one valve alone is diseased, and the prognosis'is correspondingly worse. 
Patients with aortic lesions are somewhat more prone to complications arising 
from the virulence of the infection than are those with mitral lesions. During 
the time that systemic rheumatic manifestations are present, the endocarditis 
cannot be regarded as quiescent, even if there be no clinical manifestations of 
recrudescence. However, more direct evidence of fresh endocarditis may be 
found in increased intensity and harshness of endocardial murmurs, tempo- 
rary arrhythmias, precordial “sticking” pains, and, occasionally, in embolic 
infarcts in the brain, lungs or kidneys. Slight rises of temperature, if not 
otherwise accounted for, are to be regarded as probable signs of the continua- 
tion of the endocarditic process. Another highly suggestive evidence is 
anemia, severe or moderate, not responding to the usual treatment. 
Occasionally the infection is mild, fever and other inflammatory manifes- 
tations cease, the valvular lesion quickly becomes quiescent, and indeed 
soon eludes all signs of ever having been present. Such cases usually occur 
in children and young adults, and apparently represent instances in which 
healing begins soon after the mild endocardial infection has run its course. 
The existence of such cases has been corroborated by necropsy findings. RHEUMATIC AND BACTERIAL ENDOCARDITIS 
303 
If the physical signs and clinical phenomena indicate an active endocardi- 
tis lasting for a month or longer, the outlook for a “quiescent” period, and 
therefore for a favorable prognosis, becomes correspondingly poor. These 
patients may die of embolic infarcts, or of superadded bacteremias, such as 
pneumococcemia or streptococcus viridans infections. Decompensation 
usually plays a minor role. 
Quiescent Stage.—In the fortunate cases, this stage represents uninter- 
rupted convalescence from the acute and subacute, with complete cessation 
of active signs of endocarditis. These patients with their recurrences and 
exacerbations comprise the great class of chronic rheumatic heart cases. 
Conceiving the quiescent stage as convalescence from the acute, decompensa- 
tion is rare, while the chances of the lesion becoming “chronic” and remain- 
ing quiescent are good. The prognosis then depends upon that of chronic 
endocarditis. 
In chronic quiescent cases, the cardinal point in prognosis is the con- 
sideration, not of the number or varieties of murmurs present, but the 
extent and damage to the myocardium, factors usually decided by a study of 
the muscular and circulatory efficiency of the heart. If myocardial efficiency 
and cardiac reserve are good, a correspondingly good prognosis may be given. 
Regarding prognosis from the standpoint of longevity, the above observations 
must be combined with a general knowledge of the average duration of life in 
the various types of valvular lesions; but each case must nevertheless be 
studied individually in the attempt to gauge the probable span of life. 
It has been demonstrated statistically that patients with mitral insuffi- 
ciency live longest; individuals with this lesion living to ripe old age are not 
uncommonly encountered. The usual duration of life in mitral stenosis is 
much less; one of the reasons for this is that such cases are prone to develop 
auricular fibrillation, and with it, the usual train of symptoms and dangers 
arising from decompensation. In aortic regurgitation, massive ventricular 
hypertrophies (cor bovinum) are common; yet years may elapse until death 
occurs from decompensation, emboli or from some superadded acute infective 
process. In general, however, the chances for longevity with this lesion 
correspond somewhat to the degree of ventricular hypertrophy; where this 
is marked or extreme, patients are not apt to live beyond middle age. 
Acute Bacterial Endocarditis.—Other terms for this infection are malig- 
nant, ulcerative, infectious and septic endocarditis. Bacterial endocarditis 
as an acute process engrafted upon a chronic valvular lesion is not here 
included. It has already been pointed out that, although not proven, 
rheumatic endocarditis is probably of bacterial origin. But acute bacterial 
endocarditis differs so markedly from the rheumatic type, and even from 
streptococcus viridans infection (itself a bacteremia), that it deserves indi- 
vidual description. 
Acute bacterial endocarditis is almost always a secondary process; 
its presence as a primary lesion has indeed been denied by several writers. 3°4 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
It may complicate erysipelas, pneumonia, puerperal fever; in fact, any bac- 
teremia. It is occasionally present as a terminal infection. Although 
the course of acute bacterial endocarditis is essentially acute, occasional 
cases of comparatively long duration have been described. In acute staphy- 
lococcic infections, the portal of entry is the skin or an osteomyelitic focus; 
in streptococcus pyogenis, the mucous membrane of the throat or uterus. 
Gonococci, also streptococci and staphylococci, may enter the general circula- 
tion from the genito-urinary tract; pneumococci, from the respiratory tract. 
The clinical picture of acute bacterial endocarditis is essentially that of a 
more or less virulent bacteremia, with all its protean and manifold charac- 
teristics. The disease rarely lasts more than four weeks. There are often 
no cardiac manifestations; no murmurs, pain, dyspnoea or other signs of car- 
diac involvement. 
The clinical manifestations are sometimes divided into the typhoid, 
septicemic, cerebral, etc. These varying characteristics depend upon the 
virulence of the invading organism, and upon the underlying cause of the 
bacteremia (erysipelas, puerperal septicemia, etc.). 
The course of bacterial endocarditis is usually marked by high fever; 
daily chills are common; long remissions of temperature are rare. Sweating 
is often profuse. The onset of the endocarditis may be marked only by an 
intensification of the fever from the original source of infection, or by an ini- 
tial rigor. Added hints of its onset may be found in sudden increased pulse 
rapidity, in sticking pains over the precordium, in the friction rub of dry 
pericarditis. When pericarditis is present, there is usually endocardial 
involvement as well. 
Septic infarcts into various organs mark the stormy progress of the disease. 
Thus, cerebral infarcts may produce paralysis and unconsciousness, or, occa- 
sionally, purulent meningitis; symptoms from the latter may then dominate 
the clinical picture. Hematuria, sometimes abundant, may follow a renal 
infarct; pneumonia, an infarct in the lungs. Of frequent occurrence are 
petechise. They are usually numerous, especially upon the oral and con- 
junctival mucous membranes. The petechias sometimes contain pinpoint 
pustules in their centers. Occasionally, patchy erythematous areas in the 
skin, resembling urticaria, may be found. Various joints, especially the 
larger ones, may be involved in a purulent or sero-purulent inflammatory 
process. 
The usual general manifestations of sepsis, or of a septic (typhoid) condi- 
tion are common. The patients may be actively delirious, or be stuperous 
and comatose. There may be coma vigil with a dry and coated tongue. 
As a rule the left heart alone is affected. It is, however, not unusual to 
have the right heart also affected, or even the right heart to the exclusion of 
the left. 
Medication, including sera and vaccines, possess no value. The treat- 
ment is symptomatic only. RHEUMATIC AND BACTERIAL ENDOCARDITIS 
305 
SUBACUTE AND CHRONIC STREPTOCOCCUS VIRIDANS INFECTIONS 
I have made no attempt to divide the disease into two distinct stages, 
for the terms “subacute” and “chronic” depend chiefly on differences of 
duration rather than of symptomatology. The usual duration is from a 
month to one year or more, hence either term may be appropriate in individual 
cases. 
Pathological Features.—Of the bacterial infections of the heart, that of 
the streptococcus viridans has been most exhaustively studied. The process 
is almost always engrafted upon a chronic rheumatic infection. Occasion- 
ally, congenital lesions form the nidus. The pathological process consists 
of vegetative proliferative masses of grayish, greenish or pink color. Their 
main site is the mitral valve. Here they may form a few soft, friable masses, 
or the valve may be encrusted with large polypoid lesions. The latter 
may then extend along the left auricular wall above, and the chordae tend- 
inae below. The process on the chordae tendinae occasionally leads to 
ulceration and rupture of these structures. Similar sequelae are sometimes 
found as the result of vegetations on the mitral. Proliferative lesions on 
the aortic cusps and walls are less common and less extensive than on the 
mitral. Mycotic aneurisms of the valves are occasionally found. 
Characteristic changes in the kidney depend chiefly on the presence of 
infarcts. When pyogenic, they give rise to numerous small congested 
areas containing minute purulent foci; these are readily seen when the capsule 
is stripped from the kidney. Non-pyogenic bland infarcts occasionally occur; 
they show the changes usual to anemic necrosis; the infarcted areas are wedge- 
shaped and may be several centimeters in depth. When they are recent, 
the cut surface is yellow; the color becomes paler with the process of organiza- 
tion. Another type of infarct, assumed as pathognomonic of chronic strep- 
tococcus viridans, is embolic focal nephritis. Some characteristic changes 
are then found in the glomeruli; a part of, or an entire tuft may be involved. 
The capillaries are congested, the glomeruli contain a fibrinous exudate, 
the glomerular epithelium becomes swollen, and finally desquamates. The 
adjacent parietal layers of Bowman’s capsule are often involved in the 
necrotic process, so that the entire necrotic area becomes semilunar in shape. 
The mass eventually organizes. There is a growth of epithelial cells from 
the healthy adjacent Bowman’s capsules; this growth finally covers the 
lateral surface of the mass. When healing is completed, the result is a hya- 
line area of pyramidal shape. 
The cerebral lesions consist chiefly of softening from emboli. Occa- 
sionally, cerebral hemorrhages from rupture of embolic aneurisms of the 
cerebral vessels have been observed. 
Clinical Features.—The pathological features enumerated, and the fact 
that streptococcus viridans infection is a bacteremia, made it apparent 
that the clinical complex varies considerably. The predominant clinical 306 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
features depend on the toxemia, on focal emboli in the various organs and 
viscera, and on the pronounced pathological changes in the heart and kidneys. 
The onset of the streptococcus viridans affection is usually insidious; the 
only complaint for days or weeks preceding the definite febrile period may be 
slight general malaise or mild anorexia. Sometimes the initial symptoms 
resemble those of other febrile invasions: rigors, chills, vomiting and fever 
between ioi° and 103°. Occasionally, the onset is even more acute, and the 
daily temperature reaches 104° or 105°, with remissions resembling malaria. 
Such initial symptoms usually betoken a stormy and comparatively short 
course for the viridans infection. When the disease is once established, it 
is usual to have a febrile period from one to three weeks, with afebrile inter- 
vals of about the same duration. Each new invasion, at its beginning, may 
be marked by severe chills and hyperpyrexia; temperature up to 1060 is occa- 
sionally encountered. The disease may thus continue for months until 
emboli or exhaustion produce death. 
Petechiae represent one of the most prominent and frequent manifesta- 
tions. They are due to small capillary emboli. On the mucous membrane 
they appear as small, isolated red spots, with pale centers surrounded by an 
area of congestion, and sharply defined from the normal mucous membrane. 
The favorite site of petechiae is the lower conjunctiva. Here they are 
characteristically found at the angulation of the vessels; the entire sac 
should be well exposed by pressing back the eyeball. Occasionally, pete- 
chiae are found, not in the lower but in the upper lid. They are also found in 
various parts of the oral and even the pharyngeal mucous membranes. In 
one of my patients in whom petechiae often appeared in crops on the skin 
as well as on the conjunctivae and buccal mucous membrane, I found in 
addition a few in the anterior urethra. 
Skin petechiae resemble those of the mucous membrane. They are usually 
small and punctate. Occasionally, they become somewhat larger. Very 
rarely they are surmounted by minute pustules. While isolated petechiae 
are the rule, it is not unusual to have them appear in crops over various parts 
of the body. Occasionally their appearance is attended by severe neuralgic 
pains in the area corresponding to the location of the rash. The cause of 
such pains is not apparent. The petechiae are not tender; they usually 
disappear within one week. They sometimes leave small pigmented spots 
for a few days; these must be carefully distinguished from other pigmenta- 
tions, especially freckles. 
In addition to petechiae, other skin manifestations are not uncommon in 
this infection. Painful erythematous nodules, slightly red and somewhat 
tender (Heubner’s nodes) may occur in the terminal phalanges, especially 
of the fingers. The nodules, usually multiple, disappear within a few days; 
they are probably of embolic origin. Pyogenic emboli in the deeper dermal 
arteries may produce skin gangrene or necrosis. This occurred in one of my 
cases and finally resulted in sloughing of the entire scrotum. Emboli are RHEUMATIC AND BACTERIAL ENDOCARDITIS 
307 
sometimes scattered, shower-like, through the smaller arteries of the extremi- 
ties, producing numerous small areas of deep or superficial gangrene, and 
necrosis in fingers and toes. This was well illustrated in a woman aged 50 
with streptococcus viridans and a decompensated double mitral lesion. She 
developed gangrenous areas on several digits and toes, and on the dorsum 
of both hands. She died one week later. 
The hematological finding in streptococcus viridans infections is some- 
times of great importance. While a mild secondary anemia with moderate 
leucocytosis and a high polynuclear count is the rule, anemia may become so 
marked as to overshadow the clinical picture, even leading to the erroneous 
diagnosis of non-organic, hemic instead of organic, endocardial murmurs. 
Occasionally, the blood picture and the hemoglobin percentage so closely 
resemble pernicious anemia that patients have been treated for the latter 
disease; only at necropsy has the correct diagnosis been established. 
Splenic enlargement is quite common; it may vary from moderate in- 
crease in size to one reaching several inches below the free border of the 
ribs. At necropsy, infarcts of various sizes are almost regularly found in 
this organ. 
Changes in the Urine.—A trace of albumin and a few casts are frequently 
found. More significant, when traced to the kidney as its source, is the 
presence of a microscopic amount of blood. Macroscopic hematuria is 
rarely present. The streptococcus viridans can only occasionally be cul- 
tured from a catheterized urine specimen. In exceptional instances renal 
signs and symptoms predominate the clinical picture, as in one of my patients. 
There was unilateral renal colic and bleeding. A blood culture taken at 
that time was sterile. A nephrectomy was done; the affected kidney was 
found twice the normal size and riddled with infarcts. The patient died two 
weeks later. Another blood culture, taken two days before death, showed the 
streptococcus viridans. At necropsy, valvular lesions characteristic of 
streptococcus viridans were found. 
Nervous manifestations are frequent. They depend on one or several 
factors, all of which must be etiologically considered. Stupor, for example, 
may be due to toxemia, hyperpyrexia, meningitis, cerebral infarcts or to 
uremia. An instance of the difficulties with which the etiology of this one 
symptom may be surrounded is that of a woman aged 45, admitted to the 
hospital in semi-stupor. A double mitral lesion, auricular fibrillation, and 
irregular fever were present. The urine showed microscopic hematuria and 
a few renal elements. Two blood cultures were negative. A spinal tap was 
unsatisfactory. Semi-stupor finally merged into coma and death. Clini- 
cally, the symptoms seemed due to meningitis. At necropsy, a double 
mitral lesion, splenic infarcts and the glomerular kidney changes of strepto- 
coccus viridans were found. Meningitis was not present. Toxemia was 
the apparent cause of stupor and coma. The most common cerebral lesions 
in streptococcus viridans infections are hemiplegias; monoplegias are rare. 308 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
Occasionally pareses, not paralyses, occur, but disappear during the course of 
the disease. Meningitis is usually a terminal event; its clinical signs may 
be disguised by toxic symptoms. 
Pneumonic complications are not often found in chronic streptococcus 
viridans infections. Enterorrhagia from an intestinal infarct is occasionally 
met with. Retinal hemorrhages sometimes occur. 
Cardiac symptoms (precordial discomfort, decompensation, etc.) are not 
regularly present, and then but late in the infection. Even when valvular 
vegetations are extremely exuberant, decompensation may not occur during 
the entire disease. On the other hand, physical signs of a valvular lesion 
are usually frank and unmistakable. This is because of a pre-existing 
valvular lesion, and because the streptococcus viridans usually produces 
abundant valvular vegetations. Occasionally, when the mural instead of 
the valvular endocardium is chiefly involved, murmurs may be faint and not 
characteristic. Arrhythmias, especially auricular fibrillation and extra- 
systoles, are not uncommon. When found during the active febrile periods, 
they are apparently caused by endocardial, rather than by myocardial, 
involvement, for they usually cease with the disappearance of fever. When 
present during decompensation, cardiac irregularities are probably due to 
myocardial degeneration, or are indicative of myocardial insufficiency. 
The study of blood cultures is naturally of extreme diagnostic importance. 
When properly made and a sufficient length of time (one week) is allowed 
for the appearance of the growth, the organism has been recovered in a 
great majority of cases. Sometimes numerous blood cultures are necessary 
before the organism can be isolated. 
The clinical course of some cases in which the coccus has not been recov- 
ered during life, and the presence at necropsy of glomerular lesions character- 
istic of viridans infections, make it probable that some cases heal, or at least 
remain quiescent over a long period of time. The quiescent interval may 
last several years. These patients have been grouped as being in the “ bac- 
teria free stage” (Libman). The following cases are illustrative of this 
condition: 
Male, aged 21, had scarlet fever, followed by severe endocarditis when 
seven years old. A double aortic and a mitral regurgitant lesion resulted. 
For many years there was no decompensation or other symptom except 
occasional attacks of hematuria. A few months before death the patient 
developed chills and fever; the streptococcus viridans was then found in the 
blood. In the light of our present knowledge this case seems to belong to the 
category just described. The intervals between the attacks of hematuria 
probably represent long remissions or “bacteria free stages.” 
Male, aged 40, entered the hospital with fever. He had a mitral and an 
aortic lesion. Blood cultures on two occasions showed the streptococcus vir- 
idans. The fever remained high for three weeks, during which time the 
patient was delirious. The temperature then gradually became normal. RHEUMATIC AND BACTERIAL ENDOCARDITIS 
309 
The patient was not seen again for one year. In this interval he said that 
he had been quite well. He was readmitted to the hospital with pneumonia 
of embolic origin. The physical signs of valvular disease were the same as 
upon first admission. Blood cultures were negative. The patient made a 
good recovery from the pneumonia. 
The extent and frequency of bacterial reinvasions (i.e., the duration 
of the bacteria-free interval) are at least partly governed by certain physical 
characteristics of the vegetations. If the latter be covered by a firm, par- 
tially organized fibrin layer, bacteria are not as apt to invade the blood 
stream; while if the fibrin layer be thin or be so situated that the blood stream 
impinges with full force against it, the bacteria are much more likely to be 
washed into the blood current. The amount of fibrin covering the vegeta- 
tions probably depends upon the virulence and the proteolytic digestive 
power of the invading organism. 
Besides symptomatic treatment, therapy consists in the use of vaccines, 
preferably autogenous, and of horse serum sensitized to various strains 
of the streptococcus viridans. An occasional cure by these methods has been 
reported. In view of the exceptionally long remissions, sometimes for years, 
without the use of vaccines, final judgement regarding “cures” by serum or 
vaccine treatment should for the present be withheld. In my own cases I 
have observed no effect on the course of the disease from serum or vaccine 
therapy; nor was there any evident arrest of the pathological process. This 
was shown by the examination of such hearts at necropsy. For example, in 
one case in which the diagnosis of streptococcus viridans infection was 
established by blood culture four days after the initial chill, not only did 
autogenous vaccines and sensitized horse serum administered for months 
have no effect on the symptoms or course of the disease, but the postmortem 
examination showed exuberant and fresh masses of vegetation literally plas- 
tering the mitral valves, the left ventricle and left auricle. Unfortunately, 
therapy of all kinds, including intravenous injections of silver salts (Chapter 
XX), must at this time be regarded either as futile or as purely in the experi- 
mental stage. The wisdom of prophylactic vaccination against viridans 
infection in those cases in whom its later occurrence is feared deserves careful 
consideration. Blood transfusions are only of value in combating existent 
anemia. I have seen no good effects from transfusions in other stages of the 
disease, even when the blood is transfused from an immunized donor. 
Baehr, G.: Glomerular Lesions of Subacute Bacterial Endocarditis. Journal of Experi- 
mental Medicine, 1912, XV, 330. 
Barringer, T. B., Jr.: Studies of the Heart’s Functional Capacity. Archives of Internal 
Medicine, 1917, XX, 829. 
Barringer, T. B., Jr. and Teschner, J.: The Treatment of Cardiac Insufficiency, etc., with 
Dumb-bells and Bars. Archives of Internal Medicine, 1915, XVI, 795. 
Graeupner: Die Funktionelle Bestimmung, etc., des Herzmuskels. Deutsche Medezin. 
Wochenschrift, 1906, 1028. 
REFERENCES 3ro 
RHEUMATIC AND BACTERIAL ENDOCARDITIS 
Harrop, G. A., Jr.: The O and CO2 Content of Venous and Arterial Blood in Heart Disease 
Journal of Experimental Medicine, 1919, XXX, 241. 
deHeer: Die Dynamik des Saeugetierherzens im Kreislauf. Archives f. d. ges. Phys- 
iologic, 19x2, CXLVIII, x. 
Heiberg, H.: Ein Fall von Endocarditis Ulzerosa, etc., Virchow’s Archiv fuer Pathologische 
Anatomie und Physiologie, 1872, LVI, 407. 
Herz: Eine Funktionspruefung des Kranken Herzens. Deutsche Medezin. Wochensch., 
1905, XXXI, 215. 
Horder, T. J.: Infectious Endocarditis. Quarterly Journal of Medicine, 1908-1909, II, 
289. 
Jochmann: Ueber Endocarditis Septica. Berliner Klinischer. Wochenschrift., 1912, 
XLIX, 1, 436. 
Jores, L.: Wesen und Entwickelung der Arteriosklerose. Wiesbaden, 1903. 
vonjuergensen, T.: Endocarditis. Nothangel’s Encyclopedia, American Edition, 1908. 
Krehl, L.: Die Erkrankungen des Herzmuskels, 1913. 
Lewis, T.: Observations on Ventricular Hypertrophy, etc., Heart, 1913-1914, V, 367. 
Libman, E.: A Study of the Endocardial Lesions of Subacute Bacterial Endocarditis, etc. 
American Journal of Medical Sciences, 1912, CXLIV, 313. 
Litten, M.: Die Endocarditis und ihre Beziehungen zu anderen Krankheiten. Verhand- 
lungen d. Kongresses fuer Innere Medizin, 1900, XVIII, 97. 
Luederitz: Versuche ueber den Ablauf des Blutdruckes bei Aortestenteneoe. Zeitscheift f. 
Klinische Med., 1892, XX, 373. 
Lundsgaard and VanSlyke: Studies of Lung Volume. Journal of Experimental Medicine, 
1918, XXVII, 65. 
MacCallum and McClure: On the Mechanical Effects of Experimental Stenosis and 
Insufficiency. Johns Hopkins Hospital Bulletin, 1906, XVII, 260. 
Mackenzie: Diseases of the Heart, p. 74. 
McLean: The Numerical Laws Governing the Rate of Excretion .of Urea and Chlorides in 
Man. Journal Experimental Medicine, 1915, XXII, 366. 
Meltzer, S.: Edema: American Medicine, 1904, VIII, 19. 
Mendelsohn: Die Erholung ala Maas der Herzfunction, Verh. d. XIX, Kong, f. Innere 
Medezin. Weisbaden, 1901, XIX, 200. 
Moritz: Eine Methode, etc., Orthodiagraphie. Meunchener Med. Wochenschrift, 1900, 
XLVII, 992. 
Osier and McCrae: Modern Medicine, Volume IV. 
Peabody: Cardiac Dyspnoea. Harvey Lectures, 1916-1917. 
Peabody: Clinical Studies on the Respiration. Archives Internal Medicine, 1917, XX, 
433- 
Peters, J. P., Jr.: Carbon Dioxide Acidosis, etc., the Cause of Cardiac Dyspnoea. Ameri- 
can Journal of Physiology 1917, XLIII, 113. 
Plesch: Hemodynaemesche Studien. Zeitsch. f. Expt. Path. v. Ther., 1909, VI, 380. 
Poynton and Paine: Researches on Rheumatism. 
Rapport: The Systolic Blood Pressure Following Excercise, with Remarks on Cardiac 
Capacity. Archives of Internal Medicine, 1917 XIX, 981. 
Romberg: Krankheiten des Herzens u. der Blutgefaesse, 2nd. Ed. 82. 
Stengel: Paroxysmal Pulmonary Edema. American Jonrnal of Medical Sciences, 1911, 
CXLI, 1. 
Stewart, H. A.: Experimental and Clinical Investigation of Pulse and Blood Pressure 
Changes in Aortic Insufficiency. Archives of Interdal Medicine, 1908, I, 102 
Stone, W. J.: The Differentiation of Cerebral and Cardiac Types of Hyper-arterial Ten- 
sion, etc. Archives of Internal Medicine, 1915, XVI, 775. 
Welch: Arch. f. Anatomie u. Physiologie, 1878, LXXXI, 375. 
Wells, H. G.: Chemical Pathology, Edition 1918. 
Wiggers: Circulation in Health and Disease. CHAPTER XVI 
CARDIAC SYPHILIS—AORTITIS—ANEURISMAL DILATATION OF 
THE AORTA—SACCULATED AORTIC ANEURISMS—NON- 
SYPHILITIC AORTIC ANEURISMS 
Syphilis rarely attacks the heart during its secondary stage. A few 
instances however have been reported in which the myocardium alone was 
involved during this stage. These involvements may be sufficient to pro- 
duce symptoms of myocardial insufficiency such as dyspnoea on exertion, 
indefinite precordial distress and pain, precordial sensitiveness to pressure, 
slight pretibial edema, sometimes also a faint systolic murmur at the apex. 
The vast majority of cardiac syphilis occurs during the tertiary stage. 
The symptoms and pathological changes depend upon the degree, extent 
and admixture of muscular, valvular and endocardial involvement. 
In occasional cases, isolated luetic valvulitis of the mitral or tricuspid 
has been found. In most instances, however, the aortic valves bear the 
brunt of the endocardial infection. In addition to the cusps, there is often 
widespread destruction of the aortic walls, finally resulting in aneurismal 
dilatation and in true aneurisms. Accompanying the aortitis are changes 
affecting the myocardium, the remainder of the endocardium, and the 
coronaries. Together they comprise a composite picture often similar to that 
found in non-luetic cardiosclerosis (Chapter XVII). 
In the absence of a history of veneral infection or of other signs of syphilis, 
the presence of a strongly positive Wassermann blood reaction is of paramount 
importance in the diagnosis of cardiovascular syphilis. More than one blood 
examination may be necessary, or provocative injections of mercury or of 
small doses of salvarsan (arsphenamin) may be required to obtain a positive 
Wassermann reaction. If the blood Wassermann remains negative, the 
chemical and cytological examination of the spinal fluid may indicate the 
presence of syphilis, for it has been found that the spinal fluid sometimes 
shows definite evidence of syphilis when the blood does not. Thus tested 
by routine and other methods, the diagnosis of cardiovascular syphilis can be 
substantiated in the great majority of suspected cases. It must be remem- 
bered that cardiac syphilis is often a latent process and that cardiac manifes- 
tations usually occur only ten to twenty years after the initial lesion. Most 
cases therefore, are first seen by the physician in early middle fife. 
From the clinical standpoint, the characteristic symptomatology and 
signs of tertiary cardiac lues depend mainly upon the presence of aortitis 
alone, or upon aortitis as part of the picture of cardiosclerosis. It should be 
here remarked that syphilitic aortitis is not always accompanied by enlarge- 
311 CARDIAC SYPHILIS 
312 
ment of the aorta. In the exceptional instances in which the myocardium 
alone is affected, the diagnosis usually rests on the ordinary manifestations 
of severe myocarditis. The presence of gummata in the myocardium must 
also be considered. They add to the possibility of the occurrence of a myo- 
malaceous focus, or, when involving the conduction system, to the occurrence 
of heart block. 
Aneurismal Dilatations of the First Part and Arch of the Aorta.—A cen- 
tury ago Hodgson made the fundamental distinction between sacculated 
and “dilatation aneurisms.” He defined the latter as a “preternatural 
permanent enlargement of the cavity of an artery.” The former is definite 
protrusion of only one side of its wall and may include a small or large part 
of the arterial caliber. This distinction is of clinical importance in aortic 
disease. The French still apply the term “Maladie de Hodgson” to aneuris- 
mal dilatations of the aorta associated with valvular insufficiency. Aortitis 
of the ascending and transverse aorta is now known to be of luetic origin in 
the great majority of instances. The pathology and mechanism of aneurismal 
dilatations of these parts of the aorta have been described in detail by Thoma, 
who had studied ninety-two cases. He ascribes their fundamental cause to 
lessened resistance to the arterial walls, and categorically states that “such 
weakened condition is not found in the descending thoracic aorta,” which 
showed no change macroscopically. 
The orthodiascopic picture of dilatation of the first portion and arch of 
the aorta has already been described (Chapter XII). On auscultation 
the normal first sound at the right base is accompanied or replaced by a soft 
blowing murmur, usually not transmitted beyond the first and second right 
interspaces. Occasionally the first sound is faint or absent. The second 
sound is accentuated, of varying quality, and is best described as bell-like, 
metallic or tinny. When typical it has a peculiar twang-like character, almost 
pathognomonic of dilatation of the first portion of the aorta. The first sound 
is often followed by a soft diastolic murmur, indicative of aortic insufficiency. 
The accentuated and metallic quality of the second sound is not always due 
to extreme hypertension, for it is frequently present with normal or very 
slightly raised systolic blood pressure. The factor most responsible for the 
abnormal second sound is, I believe, aortic dilatation which acts acoustically 
as a sounding box in reflecting and thus changing the character of the sound. 
In marked aneurismal dilatation, especially of the arch of the aorta, 
there is often visible aortic pulsation in the jugulum. When not visible, 
it may be felt by insinuating the finger behind the manubrim sterni. In 
cases of aneurismal dilatation of the first part of the aorta, there may be more 
marked right than left carotid pulsation, a fact determined by placing the 
finger deeply behind the respective clavicles. At the apex, there is frequently 
a soft systolic murmur, probably due to relative mitral insufficiency; 
or there may be a loud murmur due to thickening of the mitral cusps and 
mural endocardium, with consequent regurgitation. If the aneurismal dilata- CARDIAC SYPHILIS 
3X3 
tion is accompanied by left ventricular hypertrophy and by hypertension,, 
there may also be a reduplicated apical impulse or a somewhat accentuated 
first, as well as a slightly metallic second sound at the apex. 
Aneurismal Dilatation of the Descending Thoracic Aorta.—Reports 
of aortitis are almost entirely confined to disease of the ascending or trans- 
verse aorta, with fragmentary or no reference to the descending thoracic. 
McCrae, Allbutt, Osier and others consider aneurismal dilatation of the 
descending thoracic aorta extremely infrequent, a statement apparently 
based on postmortem findings, for no symptomatology was mentioned nor 
had a clinical diagnosis been made. I shall, however, indicate, through 
illustrative cases the comparative frequency, diagnosis and symptomatology 
of aneurismal dilatations of the descending aorta, and present its claim 
to a clinical entity. 
W. W., male, aged 69, has never been seriously ill previous to his present 
complaint. He had been a heavy smoker and had suffered from a venereal 
infection forty years ago, for which he had received many subcutaneous 
injections (presumably of mercury). His present illness began two years ago 
with exceedingly mild symptoms: Very slight precordial pains when lying on 
the left side, and slight dyspnoea when climbing stairs. At examination, the 
patient looked well preserved, the carotid pulsation on both sides was some- 
what exaggerated, there was a belt of small dilated capillaries over the lower 
part of the chest. The cardiac thrust at the apex and the systolic impact at 
the right base were somewhat exaggerated. The cardiac area seemed normal 
to percussion. At the base there was a double murmur—a rough systolic 
and a softer diastolic—transmitted and best heard to the left of the middle 
third of the sternum; a definite sensation of heaving impulse was imparted 
to the examining hand placed over the same area. Similar but fainter mur- 
murs were heard at the apex. Both radial pulses were alike; the average 
systolic blood pressure was 170 m.m., the diastolic 70. Neurological and other 
examinations revealed no abnormalities. There was slight pretibial edema. 
The Wassermann reaction was negative. The roentgenogram (Fig. 264) 
showed a long fusiform dilatation of the entire descending thoracic aorta. 
The electrocardiogram presented evidence of left ventricular preponderance, 
i.e., negative S III. Treatment consisted of one salvarsan and many 
mercurial injections; iodide of potash in moderate doses was administered in 
alternate periods of two weeks. Tincture of digitalis was given for one week 
until edema of the legs disappeared. The patient has been under my 
observation for many years and is quite comfortable, with no pains for the 
last three years; the physical signs along the middle third of the sternum have 
markedly receded. 
Female, aged 47 years, married sixteen years, had never been pregnant. 
Prior to the present illness she complained of dyspnoea on exertion, and of 
nocturnal palpitation accompanied by pain in the lower precordium. She 
had lost about forty pounds since her illness began. One week before admis- 314 
CARDIAC SYPHILIS 
sion to the hospital her legs became edematous. The patient was emaciated, 
the right pupil was somewhat larger than the left, both reacted sluggishly 
to light but normally to accommodation; the knee reflexes were diminished; 
Romberg’s sign was absent. The patient was dyspnceic even when at rest. 
There was vigorous visible carotid and jugular pulsation; the aortic thrust 
could be plainly felt by pressing the finger tip behind the manubrium. By 
placing the eye on a level with the patient’s chest, two distinct areas of 
impact were discernible; one corresponding to the apical region, the other to 
an area slightly to the left of the lower half of the sternum. The latter 
impact was also palpable by sinking the fingers in the lower left intercostal 
spaces, and also by auscultating with the stethoscope over this area in the 
routine manner. There was no precordial tenderness. The apex was felt 
most distinctly in the sixth interspace, a considerable distance (14 c.m.) from 
the midsternal line. Over the base, and particularly to the left of the mid- 
sternum, there was a rough systolic murmur and a somewhat accentuated 
second sound merging into a soft murmur occupying the entire diastole. 
Friction sounds indicative of dry pericarditis were present at the base and 
apex. There was slight edema of the legs. The Wassermann reaction was 
negative upon first examination; some months later it became positive. The 
systolic blood pressure ranged between 200 and 180 m.m., the diastolic 
between 100 and 40 m.m., the pressure in both arteries was equal. The urine 
was normal. The roentgenogram (Fig. 265) showed fusiform aneurismal 
dilatation of the entire descending thoracic aorta; orthodiascopic examination 
corroborated this finding. The electrocardiogram presented evidence of left 
ventricular preponderance. The patient refused treatment. She has since 
reentered the hospital, with signs of severe cardiac failure. She received 
iodide of potash and mercurial injections, with marked improvement. 
Male, aged 38, a vigorous and healthy looking man, has complained 
during the last six months of slight dyspnoea upon climbing stairs, but none 
when at rest. He was a heavy cigar smoker. He had gonorrhea twenty 
years ago and denied any other illness. The blood pressure was normal. 
There was vigorous carotid pulsation at the root of the neck. There was no 
pain on precordial pressure. The apex beat was strong and was felt best in 
the fourth interspace, 11 c.m. from the midsternal line. A soft systolic mur- 
mur was heard at the apex. At the base the first sound was impure; the 
second sound was not accentuated but was prolonged and somewhat liquid 
in character, and occupied the entire diastole. These abnormal sounds were 
heard loudest and most distinctly along the middle left sternal border. The 
eye placed on a level with the chest could discern a slight systolic heave over 
the latter area, apparently distinct from that at the apex. The other organs 
were normal. The Wassermann reaction was negative. The roentgeno- 
gram showed dilatation of the upper part of the thoracic aorta, the latter 
being visible as a somewhat denser shadow behind the ventricles. The 
orthodiascope confirmed this. The electrocardiogram was normal. The CARDIAC SYPHILIS 
3i5 
patient was given salvarsan, 0.3 gms. intravenously, and many bichloride 
injections combined with iodide of potash. The dyspnoea disappeared 
entirely; the abnormal sounds at- the base and left sternum were much less 
pronounced than at the first examination. 
Differential Criteria of Aneurismal Dilatation of the Descending Thoracic 
Aorta.—It is important to distinguish the aortic impacts to the left of the 
sternum from those found in patients with marked left ventricular hypertro- 
phy or in healthy individuals with over-acting hearts and thin chest walls. 
In these individuals, the auscultatory signs above described are then absent. 
Although there are many refinements of percussion methods used in the 
attempt to delicately outline the dilated arch and the ascending aorta (for 
example, threshold and auscultatory percussion, Chapter XIII), their value 
in dilatation of the descending aorta seems nil because the aorta is deep seated 
and most of the enlarged area is situated behind the ventricles. Examination 
of the posterior chest wall also fails to reveal any difference from the normal 
physical signs. In three of my cases in whom a tentative diagnosis was made 
before fluoroscopy, all methods of percussion failed to reveal any enlargement 
of the descending aorta. To clinch the diagnosis, examinations by means 
of the fluoroscope, or roentgenograms are essential. As in examination for 
suspected disease of other portions of the aorta, the patient should be fluoro- 
scoped in several lateral positions. Fluoroscopy must be practiced carefully 
in order to reveal and distinguish the darker silhouette of the dilated descend- 
ing aorta behind the left ventricle. Roentgen-ray plates must also be care- 
fully scrutinized for the same reason. It is important in this connection to 
again indicate the difference in shadow areas between orthodiascopic fluoro- 
scopy and roentgenograms of the heart and aorta. It has been my experi- 
ence that the former produces very little distortion in the size of the cardiac 
and aortic areas, because the X-ray tube and screen move together (Chapter 
XII), thus approximately parallel rays reach the observer. In the roentgeno- 
grams the rays are always divergent and there is an increased cardiac shadow. 
Comparisons between the orthodiascopic tracings and roentgenograms in 
my series of cases occasionally showed marked discrepancies in the size of the 
dilated aorta and heart by these two methods. 
Because of its importance I shall summarize the clinical complex of aneu- 
rismal dilatation of the descending aorta as I have observed it. The Wasser- 
mann test was done in four of the five cases. It was positive in two and 
negative in two. One of the latter gave a definite history of luetic infection. 
Three cases had slight symptoms when treatment was begun; these were 
clinically cured. One, with severe heart failure, was much improved. In 
three the correct diagnosis was made by the presence of an impact area to the 
left of the sternum at its middle third, and by prominent localization of the 
murmurs over this' area. Electrocardiograms were taken in four cases; 
three showed complexes of left ventricular preponderance, the fourth was 
normal. The physical signs of the cases were most marked when the symp- 316 
CARDIAC SYPHILIS 
toms—dyspnoea, pain, or cardiac failure—were present; the signs became 
markedly less with improvement. 
Symptomatology of Aortic Dilatations—Aortitis.—There is no distinguish- 
ing characteristic in symptomatology between dilatation of the various aortic 
divisions: They are therefore grouped in this description. Sharp, continuous, 
gnawing pains such as those often associated with sacculated aneurisms are 
not prominent features of dilatation of the descending aorta. When present, 
substernal pains or those referred to different parts of the chest, neck or head 
are most apt to occur with exercise or following physchic and emotional 
disturbances. It is difficult to state the exact etiology of these pains. They 
are probably not due to pressure of the dilated aorta upon the surrounding 
structures (esophagus, ribs, dorsal vertebra, intercostal nerves, etc.). In one 
of my cases, pain may have been due to esophageal stricture rather than to 
aortic pressure. In general the contour of the aneurismal dilatation would 
in itself argue against pressure upon, or erosion of surrounding tissues. The 
rich nerve and ganglionic plexus surrounding the root of the aorta, and the 
nerve fibers and isolated nerve cells which have been found in the connective 
tissue of its middle coat, may explain how various grades of inflammation in 
the aorta and how differences of aortic pressure and dilatation can give rise 
to these referred pains. In addition, peri-aortitic inflammation with possible 
involvement of the neighboring nerve structures can also cause neuralgic 
symptoms. Similar nerve involvement has been found in dilatations of the 
ascending aorta and arch. The assumption of inflammatory exacerbations 
within or without the aorta is corroborated by the occasional rapid subsidence 
of the pains following salvarsan injections. This result is probably ascribable 
to control of these inflammatory recurrences, although Vaquez and Laubry, 
and Vaquez and Bordet claim that there is sometimes a reduction in size of 
sacculated aneurisms after several salvarsan injections. The writer has not 
been able to determine any difference in the size of the dilated aorta as the 
result of therapy. In addition to the aortic disease it must be remembered 
that concomitant coronary sclerosis and myocarditis can also produce cardiac 
pains. Another causal factor of pain is involvement of the coronaries in the 
luetic process. Precordial pain from this source is similar to that usually 
found in coronary disease (Chapter XXIII). Sudden overdistention of the 
ventricle from increase in intraventricular pressure by blood regurgitated 
from the aorta may be another cause of severe attacks of precordial distress. 
It is conceivable also that the coronary supply may be mechanically inter- 
fered with by tension of the diseased and dilated aorta, this again giving rise 
to precordial or substernal pain. 
Dyspnoea is a common symptom, especially in advanced aortitis, even 
without extensive myocardial changes. It is often paroxysmal and nocturnal 
in character. Some of these attacks may be due to pulmonary congestion or 
edema. Others are undoubtedly of an entirely different nature; it is to these 
that I wish to call particular attention. They have already been emphasized CARDIAC SYPHILIS 
317 
by others (Longcope, Lamb). These attacks are neither pulmonary nor 
cardiovascular but are in the nature of bronchial asthma. Indeed, the 
physical signs are exactly those of the latter condition. There is an emphy- 
sematous note on percussion; there is typical sibilant and sonorous breathing, 
there is wheezing inspiration and prolonged expiration'. The two subjoined 
cases well illustrate the clinical picture. 
M. C., aged 38, married and father of several healthy children, entered 
the hospital with what appeared to be afoudroyantattackof typical bronchial 
asthma: There was sibilant and sonorous breathing, with an emphysematous 
percussion note over the entire chest. Dyspnoea was extreme and alarmingly 
violent. The heart sounds could not be accurately made out because of the 
difficulty in breathing. Nonetheless definite systolic and diastolic murmurs 
could be heard over the right base. The next day there was skin crepitation 
over the entire chest from rupture of the pulmonary vesicles. The Wasser- 
mann blood reaction was 4 plus. The skin emphysema rapidly disappeared. 
The asthmatic condition only slowly receded during the patient’s hospital 
stay of several months, despite vigorous antiluetic treatment, iodides, adrena- 
lin and atropine. With partial recession of the asthma, there were typical 
signs of a luetic aortic lesion with aortic regurgitation. The X-ray showed 
but slight enlargement of the arch of the aorta. The patient has been under 
my observation for several months subsequent to his discharge from the 
hospital. At no time were cardio-vascular symptoms present. Therapy 
indeed was almost continuously directed to the asthma. The usual mixture 
given contained iodide of potash, tincture of belladona and chloral hydrate. 
When sibilant breathing and wheezing were not extensive or marked, the 
patient’s condition was comfortable, there was correspondingly less dyspnoea 
and he was partially able to attend to his work as a piano maker. When 
asthma was more prominent, breathing was again difficult. Of late months, 
the asthma has gradually subsided, so that for the present at least the patient 
is practically symptom-free although the physical and X-ray signs of the 
aortitis are exactly as before. 
A. F., male, aged 52, a flutist, was always very active physically, and 
prided himself upon his physical stamina. Eight months prior to my first 
examination, he was suddenly attacked with violent cough, oppression and 
pain in the chest. Since then the main complaints have been cough and some 
substernal discomfort especially when walking. Examination revealed the 
signs of aortic dilatation over the right base, a rough systolic and a diastolic 
murmur. This was confirmed by X-ray, which showed aneurismal dilata- 
tion of the first portion of the arch of the aorta. Further physical examina- 
tion of the chest showed typical emphysematous and asthmatic breathing, 
there was no evidence of pulmonary congestion or edema. The patient was 
given an asthmatic mixture containing iodide of potash and tincture of bella- 
donna. Intramuscular mercurial injections and intravenous neosalvarsan 
injections were also begun. Within two weeks there was marked improve- 318 
CARDIAC SYPHILIS 
ment in his condition. The sibilant breathing had almost entirely disap- 
peared, he could walk two miles fairly comfortably in windy weather along a 
country road. At the end of two months, the sibilant and asthmatic condi- 
tion had disappeared, the patient considered himself well. X-ray and phys- 
ical examination of the chest however revealed the same condition of the 
heart and aneurism as before. 
These two cases give undubitable proof, I believe, of a distinctly bron- 
chial asthmatic type, but have no reference to the size of the aortic dilatation; 
for in one case, the aorta was practically normal in size (and this was the 
severe case) and in the other there was the usual marked aneurismal dilata- 
tion. Nor have these cases any direct relation with assumed pulmonary 
stasis or with a tendency to heart failure. Both of the patients, for example, 
considered themselves well when the asthmatic condition came under control, 
although the cardiac condition remained the same. It seems that instances 
of bronchial asthma with aortitis are explicable only upon the supposition of a 
bronchial spasm resulting from reflex disturbances initiated in a diseased 
aorta. It has already been pointed out that the aorta is surrounded by many 
nerve plexuses and ganglia (Chapter I). There exists experimental evidence 
that certain manipulation of the inner surface of the aorta may also evoke 
this reflex, with resultant bronchial spasm. These facts and the clinical 
evidence make it highly probable that disturbance of innervation by aortic 
disease can likewise produce a spasmodic asthmatic condition in the human 
being. In luetic aortitis, the primary instigating factor seems to be a periaor- 
titis, which when controlled or controllable by proper remedies, causes reces- 
sion of the bronchial spasm and relief of the asthma. 
Another group of symptoms of aneurismal dilatations is that due to car- 
diac decompensation. This is not necessarily a marked clinical feature; in 
fact, it may only consist of slight dyspnoea upon exertion. Its presence seems 
due to accompanying cardio-vascular disease rather than to the aortic dila- 
tation itself. Edema is usually slight and confined to the legs; it is extreme 
only late in the disease or in neglected cases. Dyspnoea is of the usual car- 
diac type; it is generally most marked on exertion; it is continuous in the 
severe cases with cardiac failure. Left ventricular hypertrophy of varying 
degrees is usually present. The heart is occasionally hypertrophied before 
cardiac failure sets in. It is a mistake, however, to assume that ventricular 
hypertrophy is present in every case of syphilitic aortitis, for occasionally 
the cardiac chambers are not appreciably enlarged. 
Sacculated Aneurisms.—As already mentioned, the physical charac- 
teristic of sacculated as distinguished from dilatation aneurisms is that the 
former is a protrusion of “only one side of the caliber of an artery and may 
include a small or large part of the arterial caliber.” The pathological proc- 
ess is similar to that found in dilatation aneurisms except that the damage is 
not general but is localized in portions of the artery, thus causing localized 
weakness of the arterial coats, with gradual bulging and the final formation CARDIAC SYPHILIS 
3i9 
of a sac. The site of the aorta most frequently affected is its first or ascend- 
ing portion, but any part including the abdominal aorta may become the site 
of a sacculated aneurism. Although one sac is the rule, as many as nine 
different sacs have been described. Depending chiefly upon the area and 
degrees of weakness of the arterial wall, the aneurismal sac may have the 
most diversified shape and size. It may be saucershaped, pearshaped, oval, 
pedunculated, circular, etc. It may be so large as to occupy an entire half 
of the chest. 
The physical signs to some extent resemble those of dilatation aneurisms 
and are indeed sometimes identical with them. Depending chiefly upon 
such gross characteristics as the size of the sac and its nearness or adherence 
to the chest wall, thrills, murmurs and visible pulsations are apt to be more 
prominent than in dilatation aneurisms. Percussion may be of value if the 
sac is near to the chest wall. It is important to emphasize, however, that 
sacculated aneurisms, even fairly large ones, may give rise to no physical signs 
at all, and unless the patient is fluoroscoped, the diagnosis may be missed. 
It is clear that an aneurism which has eroded bony and soft structures, 
or has pushed the latter aside so that the sac forms an easily visible pulsating 
tumor, can be readily diagnosed. Our diagnostic difficulties occur with deeper 
sacs with unclear, masked, and equivocal physical signs, so that either the 
aneurism is not suspected, or if suspected, it may be difficult to distinguish it 
from a mediastinal or pulmonary tumor. In all instances when examining 
for aneurisms, inspection of the bared chest is of special importance. This is 
usually best practiced with the patient in a recumbent position, in a good light, 
and the observer’s eye on a level with the chest wall. In this manner 
pathological pulsatile heaves of various portions of the aorta in its relation to 
the chest wall may be distinguished. It is of course necessary to be familiar 
with the normal impacts and pulsations, especially those due to the aorta and 
left ventricle (Chapter XIII) in order to diagnose those abnormal ones caused 
by a sacculated aneurism. It is also necessary to scan the patient’s back 
carefully, for occasionally the aneurism bulges posteriorly. Palpation should 
be as carefully practiced as inspection, especially over the assumed site of the 
tumor. This is best carried out by pressing the flattened fingers well into the 
intercostal spaces. Auscultation usually reveals a rough systolic murmur 
over the pulsatile area, especially if the tumor be large and near the chest 
wall. Under such circumstances, the murmur is also plainly audible in the 
carotids. Depending upon the size of the sac and the degree of dilatation 
of the aortic ring, there may be an accentuated or twang-like second sound, 
or a variably distinct diastolic murmur. In one instance that I observed—an 
aneurism of the transverse arch protruding into the anterior chest wall— 
there was a reduplicated second sound to be heard and felt, apparently due 
to asynchronous closure of the aortic cusps. 
The heart may be pushed laterally or downward, depending upon the size 
and direction of growth of the aneurismal sac. Such misplacement is 32° 
CARDIAC SYPHILIS 
often mistaken for cardiac hypertrophy. Hypertrophy however, is by no 
means invariable with aneurism; the sac indeed may be very large, and the 
heart itself be normal in size or only slightly hypertrophied. 
In addition to the physical evidence of sacculated aneurism derived as 
above outlined, there are other concomitant signs which may help to clinch 
the diagnosis, or make us suspect aneurism when more direct signs are lacking. 
Tracheal tug is frequently mentioned as one of these. It is by no means invar- 
iably present and is found only when the sac is adherent to the trachea. 
Over-pulsatile carotids are frequently associated with sacculated aneurisms: 
They are of course present in many other abnormal cardiac conditions (Chap- 
ter XIII). If by palpation and inspection it is determined that there is a 
distinct difference in the carotid throb on both sides of the neck, importance 
is lent to the probability of aneurism. Inequality in the radial pulses and 
in brachial blood pressure is common in arotic aneurisms. Usually the right 
radial is smaller than the left because of involvement and narrowing of the 
innominate artery. Inequality of the pupils is fairly constant. Suffusion 
of the facies and swelling of one or both upper extremities may occur as 
the result of pressure upon the veins at the root of the neck: This is usually 
a late sign. The superficial venules and capillaries of the skin of the chest 
may be dilated for a similar pressure reason. 
In modern practice, no examination for suspected aneurism is complete 
without an X-ray examination. An X-ray plate should always be supple- 
mented where possible by a careful fluoroscopic examination. For instance, 
a photograph or plate may show only a questionable enlargement of some por- 
tion of the aorta, while fluoroscopy may show overpulsatile expansion and 
excursion of the suspected area, thus aiding in clinching the diagnosis. The 
patient should be fluoroscoped in several lateral positions in order to render all 
parts of the aorta visible. 
Symptomatology of Sacculated Aortic Aneurisms.—Small aneurisms 
that do not cause pressure are not apt to give rise to symptoms. Inflamma- 
tory exacerbations (peri-aortitis) may give rise to pain, especially sub-sternal 
in distribution. Concomitant coronary disease is another frequent cause of 
pain. Pressure against various nerve and bone structures, especially in 
aneurisms with erosive tendencies, naturally cause pains of various distribu- 
tion. Finally, continuous and excruciating pains may be present. Pres- 
sure upon the phrenic nerve may produce hiccough; upon the sympathetic, 
unilateral dilatation of the pupil, and sweating and flushing of the face. 
Pressure upon the recurrent laryngeal nerve as it curves around the aortic 
arch usually produces a brassy or croupy cough; in other cases the voice is 
altered so that it sounds cracked. Pressure against the esophagus produces 
dysphagia; ultimately ulceration of the esophagus may result. Pressure 
against the trachea and bronchi, when mild, gives rise to an irritating cough; 
with severe pressure, there may be actual bronchial stenosis, a condition 
which may mask the actual disease. CARDIAC SYPHILIS 
321 
Therapy of Luetic Aortitis.—What follows under this heading applies 
to all types of aortic syphilis, aortitis, and aortic dilatations with and without 
sacs. Treatment may be conveniently divided into three parts: That of 
the underlying disease, of the decompensation, and of the pains. Salvarsan, 
(arsphenamin) was originally considered contraindicated by Ehrlich in car- 
diac lues because of the fear of overwhelming the system with spirochetes 
(Herxheimer reaction); but experience has shown that the drug judiciously 
administered is definitely indicated in cardiac syphilis. The safest method 
is to begin with several intramuscular injections of mercury and the adminis- 
tration of iodide of potash. This is folio vved by intravenous injections of 
arsenic compounds. In the majority of cases, the best routine procedure is 
the intravenous injection of 0.2 gms. of salvarsan or arsenphenamin (or 0.45 
of neosalvarsan) every ten days until three doses have been given; then if 
indicated, it may be repeated in 0.6 gms. doses a month or two apart. A 
course of several intravenous injections is again followed by mercurial injec- 
tions and the iodides. Usually these procedures render a previous plus 
Wassermann negative. If the luetic changes in the aorta are such that 
calcification and scar-tissue formation are -extensive, and the myocardium 
is the seat of advanced disease, the treatment can naturally be of little or no 
avail. The degree and extent of such pathological changes cannot be 
diagnosed accurately enough by our present methods, although Vaquez 
and Bordet claim to have observed with the fluoroscope calcified areas in the 
ascending and transverse aorta, and the diminution of these areas after 
salvarsan injections. Since the treatment outlined is often efficacious and is 
followed by marked improvement, I believe it should be carried out in all 
cases unless there be marked heart failure. When luetic aortitis is strongly 
suspected, even if the Wassermann reaction is negative, the same therapy 
should be instituted, because in any case salvarsan is only rarely followed by 
serious results. An occasional case, however, may be encountered in which 
even small doses of arsenphenamin, carefully given, do damage, apparently 
by lighting up dormant pathological processes. 
Cardiac failure requires the same treatment as that from any other 
cause. A reliable preparation of digitalis should be given (Chapter XX). 
I prefer digitan tablets or the tincture administered undiluted in 15-drop 
doses three times daily. If the case be urgent, and very little or no digitalis 
had previously been given, 1 c.c. of a 1 per cent, solution of strophanthin can 
be slowly injected intravenously. The objection that digitalis in therapeutic 
doses raises blood pressure has been sufficiently disproved by many careful 
investigations (Chapter XX). Digitalis had no effect upon the blood pres- 
sure in any of my cases; the pressure was as often lowered as raised during its 
administration. Symptomatic treatment of the pains occasionally requires 
codein or morphine, but pains are frequently relieved by the antiluetic 
treatment which acts by controlling the inflammatory exacerbations of 
aortitis and periaortitis. 322 
CARDIAC SYPHILIS 
Prognosis.—Patients with aneurismal dilatation who seek advice before 
severe decompensation sets in, and in whom vigorous anti-luetic treatment 
can be instituted, may live in comparative comfort, for the aortic disease is an 
index of the general cardiovascular mischief rather than in itself the cause of 
cardiac failure. In those with sacculated aneurisms, the ultimate prognosis 
depends largely upon the size of the sac, its adherent and erosive tendencies, 
and the pressure it produces. When the sacs are large, protuberant and 
adherent to the chest wall, the patients usually live, at the utmost, but a 
few years; in exceptional instances, however, many years may elapse before 
death ensues. 
Cure, in the sense of a return of the aorta to its normal state, is impossible; 
but, as in other organs, the luetic disease can be arrested and controlled, so 
the heart and aorta, although still crippled, may be sufficiently restored to 
make the patient comfortable. Rupture of a dilatation aneurism is extremely 
infrequent. Unless the luetic disease is confined to a small area, this 
accident seems less likely to occur in the descending aorta because of its 
greater length and because the dilatation occupies a larger area. In the 
sacculated varieties, one massive bleeding, or smaller hemorrhages through 
the skin or into the bronchus are by no means rare. Hemothorax, caused by 
aneurismal rupture into the pleura is another occasional late accident. 
Mention should be made of various operative procedures intended to 
obliterate the sac, especially the introduction of wire. The object is to have 
layers of fibrin deposits from the blood clot separate out, thus diminishing 
the calibre of the artery. A recent method has been to introduce very fine 
wire into the sac, and then to send an electric current through the wire in 
order to induce electrolysis. I have observed two cases treated by this 
method. In one, the end of the wire perforated the chest wall and gave rise 
to hemorrhages from which the patient finally succumbed. The other lived 
several months after the operation. 
Aortic Aneurism and Aneurismal Dilatation Due to Rheumatism.—Klotz 
in particular has called attention to the possibility of rheumatism as an 
etiological factor of aortic aneurism. When aortic aneurism is present in 
children, an occasional occurrence, congenital syphilis must be definitely 
excluded before rheumatism is considered in a causal relation. However, the 
role of articular rheumatism as the causative factor of aortic aneurisms 
in the middle-aged and old has perhaps received insufficient consideration, 
because attention is usually focussed upon frank valvular defects in those 
with a rheumatic history and because in the arterio-sclerotic aneurisms of 
the old (q. v.), a definite and unmistakable rheumatic history is long since 
forgotten or overlooked. In occasional instances, however, the clinical 
correlation between articular rheumatism and aortic aneurism seems unmis- 
takable. The following is an example. 
Mrs. R. D., aged 65, no history of any serious acute illness until thirteen 
years ago. She then had a typical attack of inflammatory rheumatism last- CARDIAC SYPHILIS 
323 
ing several weeks. There were no cardiac symptoms until one year ago, 
when her present complaints began. These are chiefly dyspnoea, tachy- 
cardia and occasional pains in the left arm. Examination revealed a systolic 
blood pressure of 160, diastolic, 100. There was a palpable thrill over the 
right base. There was hyperactivity of the carotids and of the aorta in the 
jugulm. There was a rough systolic murmur and a slightly accentuated 
second sound over the right base, and a rough systolic murmur over the mit- 
ral area. The X-ray showed marked aneurismal dilatation of the first por- 
tion and arch of the aorta. The Wassermann reaction was negative. 
This case emphasizes the fact that rheumatism can occasionally act as 
a vascular and not only as a valvular poison. 
The physical signs, pathological picture and symptoms of rheumatic 
aortic aneurisms and aneurismal dilatation are no different from those of 
arterio-sclerosis aneurisms. (See below.) 
Atheromatous and Arterio-sclerotic Aneurisms and Aneurismal Dilata- 
tions.—These conditions are by no means unusual in the old and senile. 
They rarely occur without associated cardio-sclerosis (Chapter XVII). The 
murmurs they cause are sometimes quite loud and are heard over large areas. 
The diseased process first attacks the intimal coat and produces various 
degrees of arterial thickening, and in advanced cases, calcified placques. At 
this stage the aorta is not necessarily enlarged. It is only when the media 
becomes affected that, similar to aortic syphilis, the aortic walls weaken and 
give rise to aneurisms and aneurismal dilatations. These do not as a rule 
reach the enormous size of luetic aneurisms, although I have seen some in the 
X-ray which involved the first portion and arch of the aorta and reached con- 
siderable proportions. The physical signs are those of syphilitic aortitis 
(q. v.) except that the rather distinctive twang-like second sound at the 
right base is usually absent. The condition is commonly only part and 
parcel of cardio-sclerosis (Chapter XVII), hence generalized arterio-sclerosis 
is a frequently concomitant. 
REFERENCES 
Adami and Nicholls: Principles of Pathology, 2nd Edition, 178. 
Allbutt’s System of Medicine, VI, 658. 
Brooks, H.: The Heart in Syphilis; N. Y. State Journal of Medicine, 1916, XVI, 185. 
Einthoven, W.: Weiteres ueber das Elektrokardiogram; Archiv fuer die gesammte 
Physiologie, 1908, CXXII, 517. 
Frank, Francois: Aortic Reflex; Archives de Physiologie, 1890, Series V, n, 508, 547. 
Gruber, G. B.: Ueber die Doehle-Hellerische Aortitis. 
Held, I. W.: Aortitis Syphilitica; Medical Record, 1913, LXXXIV, 1105. 
Hodgson, J.: Treatment of Diseases of the Arteries and Veins, 1815. 
Klotz: Rheumatic Fever and the Arteries; Transactions of the American Physician, 19x2, 
XXVII, 181. 
Klotz: Arterial Lesions Associated with Rheumatic Fever; Journal Pathology and Bac- 
teriology; 1913-1914, XXV, 1819. 324 
SARDIAC SYPHILIS 
Kraus, F.: Ueber die Aortenerweiterung bei der Heller-Doehleschen Aortitis; Deutsche 
Medizinische Wochenschrift, 1914, XL, 577. 
Lamb: Aneurisms of the Aorta; Nelspn Loose Leaf Medicine, IV, 538. 
Lewis, T.: Observations on Ventricular Hypertrophy, etc.; Heart, 1914, V, 367. 
Longcope, T. W.: Syphilitic Aortitis—Its Diagnosis and Treatment; Archives of Internal 
Medicine, XI, 15. 
McCrae, T.: Dilatation of the Aorta; American Journal of the Medical Sciences, 1910, 
CXL, 469. 
Mackenzie, J.: Digitalis; Heart, 1910-1911, II, 284. 
Manoelian, Y.: Recherches sur le Plexus Cardiaque, etc.; Annalen de l’lnstitut Pasteur, 
June, 1914, 579. 
Osier’s System of Medicine, IV, 457. 
Price, F. W.: Some Investigations on the Action of Digitalis on the Blood Pressure in 
Man; British Medical Journal, 1912, II, 689. 
Thoma, R.: Untersuchungen ueber Aneurismen; Virchow’s Archiv, 1888, CXI, 89. 
Vaquez et Bordet: Le Coeur et L’Aorte. 
Vaquez, H., et Laubry, C.: Sur le Traitment Specifique des Aortitis, etc.; Archives des 
Maladies du Coeur, 1912, V, 561. CHAPTER XVII 
ACUTE MYOCARDITIS—SYMPTOMATOLOGY, PHYSICAL SIGNS, 
DIAGNOSIS AND PROGNOSIS OF CHRONIC MYOCARDITIS AND 
CARDIO -SCLEROSIS—THE HEART IN CHRONIC EMPHYSEMA- 
FATTY HEART 
Because the pathological changes found in myocarditis vary considerably in 
extent and degree (Chapter IV), it becomes apparent that its symptomatology 
must be a varied one, and to a great extent, must depend upon the type and 
extent of the pathological process. 
Acute Myocarditis.—It should be emphasized that while many infectious 
diseases are undoubtedly accompanied by some inflammatory change in the 
myocardium, chiefly cloudy swelling (Chapter IV), such changes are so fleet- 
ing in character or are so slight, that they give no clinical evidence of their 
existence. Hence myocardial damage found at postmortem, unless wide- 
spread and severe, does not necessarily imply that the patient suffered from 
the clinical evidences of myocarditis during life. On the other hand, cardiac 
death may be the result of a severe toxemia as in pneumonia, yet the heart 
may show comparatively little damage at autopsy, either macroscopically or 
microscopically. Such and similar instances no doubt rest upon the fact 
that important cardiac functions (especially contractility and conductivity) 
may be interfered with by poisons elaborated by various diseases during life 
and yet comparable actual visible pathological changes may not be found 
postmortem. It has already been indicated in various connections (Chapter 
V) that some diseases (especially rheumatism and diphtheria) are particu- 
larly apt to be accompanied by clinical evidence of acute myocarditis. The 
clinical symptomatology and signs of these conditions have been elsewhere 
described (Chapters XI, XXVI). 
Acute myocarditis is probably extremely rare as a primary affection. 
It is usually secondary to endo- and peri-carditis and to invasion of the blood 
stream by bacteria and toxins. 
Chronic Myocarditis.—The pathological features of chronic myocarditis 
and cardio-sclerosis have already been detailed (Chapter IV). Chronic 
myocarditis as an isolated lesion is very rare; and its diagnosis as an isolated 
lesion may be extremely difficult or perhaps impossible. The presence of 
definitely correlated infectious factors in the patient’s history, especially 
acute rheumatism and diphtheria, aid considerably in the diagnosis. 
The physical signs of chronic myocarditis as an isolated entity may be 
limited to some definite evidence of enlargement of the heart, shown prefer- 
325 326 
MYOCARDITIS AND CARDIO-SCLEROSIS 
ably by X-ray rather than by percussion. In advanced cases with severe 
degeneration, there may be a weakened and diffuse apical impulse, as well as 
weakness of the first sound at the base and apex, and weakness or entire 
absence of the second sound, especially at the base. However, it may not 
be possible to venture more than a guess as to the extent, or even the presence, 
of any myocardial damage from the physical examination alone. But when 
the entire clinical picture is correlated and considered, with its positive and 
negative data:—a definite etiological factor; an increase in the size of the 
heart; normal palpable arteries; absence of valvular disease; the presence of 
muffled and indistinct cardiac sounds; moderate tachycardia and dyspnoea; 
electrocardiograms indicative of myocarditis (Chapter IX); the subjective 
and objective phenomena indicative of myocardial insufficiency and heart 
failure (Chapter XIV); then, it may be possible to diagnose with a fair degree 
of accuracy not only the presence of chronic myocarditis as an isolated lesion, 
but even the extent of myocardial mischief. On the whole, it is clear that 
the diagnosis must often be established inferentially and by exclusion. 
Cardio-sclerosis, also called the arterio-sclerotic and senile heart, pre- 
sents a composite pathological picture (Chapter V) in which chronic myo- 
carditis of varying degrees is almost always present. 
Although the general subject of arterio-sclerosis is beyond our scope, it is 
necessary to indicate its importance in cardio-sclerosis. While arterioscle- 
rosis is usually general, insufficient emphasis is laid upon the fact that it is 
often an arteriolar rather than an arterial disease, and that the arterioles are 
by no means equally diseased throughout the cardio-vascular-renal system. 
We do not know the cause of this uneven distribution of the diseased process, 
but it is upon this basis of selection that one organ rather than another, pre- 
sents the predominantly clinical syndrome. Indeed, arteriolar disease may 
be so selective that the coronaries alone may bear the chief clinical brunt of 
the disease. If the process be confined mainly to the smaller arteries of the 
brain, symptoms and dangers become chiefly cerebral; if in the coronaries, 
the pathology and symptomatology is that of cardio-sclerosis; if in the 
coronaries and aorta, the pathology and symptomatology is that of 
aortitis and cardio-sclerosis; if in the kidneys, especially in the glomeruli, 
varying types of renal sclerosis with their symptomatology come prominently 
in the foreground; if in the retinal vessels, there are correspondingophthalmo- 
logical changes. It may be mentioned parenthetically that careful examina- 
tion of the eye backgrounds often offers corroborative, indeed sometimes the 
only objective diagnostic proof of the probable existence of more or less gen- 
eralized arterial or arteriolar disease. This fact does not usually receive the 
clinical importance it deserves. This brief summary of selective vascular 
disease also indicates the frequent clinical overlapping of the diseased process 
various vital parts of the cardio-vascular renal system. Often it tries 
the skill of even a broadly trained clinician to decipher and properly group 
the complex clinical picture and to apportion the pathological damage. MYOCARDITIS AND CARDIO-SCLEROSIS 
327 
Physical Signs.—If cardiosclerosis is at all advanced, it is readily diag- 
nosed from physical signs. Prominent among these are the signs of aortitis. 
If the latter be accompanied by simple or aneurismal dilatation of the arch 
of the aorta (Chapter XVI), there may be on inspection, a broad expansile 
rise of the tissues in the suprasternal notch, due to the vigorous overaction 
and enlargement of the arch. In advanced cases of arteriosclerosis, not only 
the radial and temporal arteries but also the carotid vessels may be tortuous 
and thickened, and may pulsate very vigorously with an accentuated thrust. 
If the first part of the aorta be especially involved in the atheromatous 
process, this carotid phenomenon may be more marked on the right than on 
the left side. In a thin chested individual, with the patient lying prone, and 
with the eye of the observer on the level with the patient’s chest, it is some- 
times possible to see pulsatile rises of the tissues over the right second inter- 
space in simple or aneurismal dilatation of the aorta. 
Corresponding to the physical signs discovered by inspection, on palpa- 
tion, one can feel a marked thrust by lightly insinuating the finger behind 
the sternum; a similar thrust may be found over the carotids. Systolic 
expansion over the right base may likewise be felt by snugly applying the 
fingers laid flatly in the second and third right interspaces near the sternum. 
The auscultatory signs of typical aortitis are characteristic and readily 
recognized. The first sound is rough and harsh; the second, accentuated and 
in some instances, metallic and tinny in character. The latter has usually 
been interpreted as due to hypertension, a frequent accompaniment of 
aortitis. It is fairly frequent, however, when hypertension is not present. 
The roughened and harsh murmur over the right base is sometimes trans- 
mitted to the aortic arch and may be plainly heard by placing the bell of the 
stethoscope in the jugulum over the pulsating arch; transmission of the 
murmur depends partly on the extent of the aortic enlargement and partly 
on the height of the arch. The murmur is likewise occasionally propagated 
along the carotids. Following the second sound, a diastolic murmur of 
varying duration and intensity may be heard over the right base. It is 
usually transmitted downwards along the right sternal border; on rare occa- 
sions it is heard best over the third interspace and along the left sternal 
border. 
Although the physical signs above described are characteristic and typical 
of aortitis, there is scarcely a cardiac lesion which produces more varied or 
atypical auscultatory phenomena. For example, the sounds may be per- 
fectly normal at the right base, the first or second sound, or both may be 
extremely faint or entirely absent. Upon what changes in the aorta or in the 
heart itself such differences depend it is at present impossible to state. 
The sounds that are heard at the apex are rarely significant in the diag- 
nosis of aortitis. They apparently vary with the state of efficiency of the circu- 
lation, and, to a lesser extent, with the state of hypertension. For example, 
the first sound may be muffled or scarcely audible. Occasionally, in hyperten- 328 
MYOCARDITIS AND CARDIO-SCLEROSIS 
sion with or without left ventricular hypertrophy, the second sound at the 
apex takes on characteristics similar to that at the right base, that is, it 
becomes metallic in tone. In conjunction with a weak or absent first sound, 
the cardiac impact also may be weak or scarcely palpable. I was able to 
prove at necropsy one instance characteristic of these findings. The patient 
complained of severe epigastric pains, especially on walking. The cardiac 
examination showed a muffled first sound over the right base and a scarcely 
perceptible first sound at the apex. Polygraphic tracings showed heart block. 
The orthodiascopic tracing showed enlargement of the first part and arch of 
the aorta, and an enlarged left ventricle. The patient died suddenly. 
At necropsy, there was diffuse dilatation and thickening of the aorta up to, 
and including the upper abdominal aorta; spirochetes were isolated from the 
aortic wall. There was moderate left ventricular hypertrophy; the myocar- 
dium was riddled with scar tissue. 
While physical signs like those described are indicative of myocarditis 
and aortitis, these lesions can be present and yet sounds at the apex and base 
be perfectly normal. A faint systolic murmur may accompany the first 
sound; this, however, possesses no diagnostic value, for such impurities are 
by no means rare in normal hearts (Chapter XIII). Of much more signifi- 
cance is the presence of a loud, rough systolic murmur heard most promi- 
nently at the apex and sometimes transmitted to the left. These murmurs 
are probably caused by fibrous or calcareous valvular thickening with con- 
sequent mitral regurgitation. In old individuals with marked senile arterio- 
sclerosis and widespread aortic and valvular changes—a cardiovascular 
condition also found occasionally in the middle-aged—a very loud, rough, 
systolic murmur is sometimes heard over the entire anterior part of the 
chest. This murmur is transmitted to the left, and may even be heard 
posteriorly between the upper part of the scapulae. In its harshness, loudness 
and area of transmission, it is extremely suggestive of aneurism. However, a 
diastolic murmur is rarely encountered and the roentgenograms of the cases 
that I have studied have not regularly shown abnormal aortic enlargement. 
This loud systolic murmur is apparently the result of the coalescence of two 
components: An aortic systolic and a mitral regurgitant murmur. The 
aortic factor is due either to atheromatous change in the aortic valves produc- 
ing stenosis, or to the impact of the impinging blood stream over the rough- 
ened sclerotic aortic wall; both causes sometimes operate together to produce 
this aortic component. The mitral component of the murmur is due to 
sclerotic changes in the mitral cusps. The intensity of the combined murmur 
seems to depend on the state of myocardial efficiency. I have found it excep- 
tionally loud only in those who were compensated, or in whom there was but 
slight cardiac failure. The mechanism of the murmur with illustrative cases 
is described in detail in Cardio-Vascular Clinics. On the other hand, a 
murmur may be absent in those who clinically or at necropsy show 
advanced cardio-sclerotic changes. Such an instance is the following: MYOCARDITIS AND CARDIO-SCLEROSIS 
329 
A robust man of 44 complained chiefly of substernal pains upon slight 
exertion. There were occasional attacks of nocturnal dyspnoea. The 
only abnormality upon auscultation was slight muffling of all the cardiac 
sounds. Several Wassermann blood tests were negative. The patient 
finally died of heart failure. At necropsy, encrusted calcareous deposits were 
found on all the valves. The coronaries were thickened and impermeable, 
the aortic arch was markedly atheromatous, the myocardium contained 
many fibrous patches. As already suggested, the absence of loud, harsh 
murmurs in this case was probably due to failing circulation. 
An extremely valuable hint regarding the degree of cardio-sclerotic change 
is sometimes given by the presence of pericardial adhesions. These are 
found most frequently over the right base or in the apical region. Superficial 
creaking sounds or pericardial rubs are then heard at the end of long inspi- 
ration, or with cardiac systole. The importance of diagnosing these old 
localized adhesions lies not so much in the fact that they add embarrassment 
to the circulation, but because they are found only when the cardio-sclerotic 
changes are advanced. Some of these adhesions may be due to localized 
pericarditis covering myocardial infarcts from advanced coronary disease. 
Thus far, most stress in the diagnosis of cardio-sclerosis has been laid 
upon the auscultatory signs. Other important diagnostic data may be 
gained by examination for ventricular hypertrophy, hypertension, and 
palpable and audible reduplicated first sounds at the apex. The significance 
and bearing of all these phenomena are more fully described in other connec- 
tions (Chapter XIII). 
Symptomatology of Cardio-sclerosis.—As the morphology of cardio- 
sclerosis is a varied one, so its symptomatology depends on the pathological 
factor that is clinically predominant. It is evident that it is often impossible 
to group these patients into one class, for the symptoms produced by the various 
underlying pathological changes frequently overlap. It has already been 
pointed out that arteriolar and capillary fibrosis may be a generalized patho- 
logical process, or may attack individually the arterial system of the heart, 
the kidneys, or the brain. In such types, the symptoms are predomi- 
nantly cardiac, renal, or cerebral, respectively. We shall here concern our- 
selves only with those individuals in whom the cardiac symptoms form 
the chief complaint. 
As with other cardiac patients, the earliest subjective symptom of cardio- 
sclerosis usually is dyspnoea. Its onset is gradual; it is evident at first only 
after severe exertion. Later, the dyspnoea occurs upon slight exertion. 
It is frequently associated with a sense of weight or oppression on the chest, 
at first transient, later, constant. Such sensations must be differentiated 
from other types of precordial pain and distress (Chapter XIV) from which 
these patients also suffer. Precordial pains may be slight and localized, or 
severe and radiate to the left axilla and arm, to the neck, interscapular region, 
or occasionally to the right arm. At first the pains occur only after exertion; 33° 
MYOCARDITIS AND CARDIO-SCLEROSIS 
later, they may appear in attacks which rouse the patient from a sound sleep. 
Slight hemoptyses occurring after exertion sometimes antedate the subjective 
symptoms for months or even years. An enlarged congested liver, smooth 
and globular in outline, is another objective sign which may be found before 
the patient complains of dyspnoea. It is not uncommon to feel the edge 
of the liver several inches below the free border of the ribs. Epigastric 
sensitiveness to pressure is fairly frequent. It is found even when the liver 
is not enlajged. The cause is usually assumed to be congestion of the gastric 
mucous membrane; in another connection, (Chapter XIV, XXIII) I have 
pointed out that it is probably of neurogenic origin, the result of reflex excita- 
tion of the gastric nerves. 
Pulmonary examination often reveals crepitant rales at both bases. Their 
presence is prognostically suggestive of subsequent attacks of pulmonary 
edema. The latter may be mild and occur frequently, or a very severe attack 
may suddenly take place after unusual exertion or excitement. Hydro- 
thorax, usually right-sided, may also be present. Edema of the legs is slight 
in the beginning and is present only when the patient is up and about; when 
the process is far advanced, general anasarca may supervene. 
The types of arrhythmias encountered in cardio-sclerosis are of some 
clinical significance. When decompensation is not far advanced, the pulse is 
regular. Extrasystoles are usually the first arrhythmia to appear; they are 
mostly of the ventricular variety. The next most frequent irregularity is 
auricular fibrillation. Heart block is usually found only in advanced cases. 
In isolated instances, attacks of paroxysmal tachycardia alone or alter- 
nating with auricular fibrillation, are found. In one case, for example, 
a man of 54 with moderate hypertension, mild cardiosclerosis and slight 
precordial pain, there was an attack of paroxysmal tachycardia lasting one 
week; thereafter the patient felt well for several months. He then developed 
auricular fibrillation, again accompanied by but slight precordial discomfort. 
This attack lasted four days. The patient was feeling quite comfortable and 
his condition was progressing favorably. While sitting in a chair he suddenly 
died. In neither attack was dyspnoea a severe or prominent symptom. In 
some patients the cardiac irregularities change suddenly and apparently 
capriciously, from one type to another, especially from extrasystoles to 
auricular fibrillation, or the reverse. Such variability I have found of 
ominous prognostic import. 
There exists a small group of patients in whom digitalis does not relieve 
decompensation, but produces diverse arrhythmias in rapid succession; these 
are chiefly sinus arrhythmia and extrasystoles, either isolated or coupled. 
Here, too, I have found that the occurrence of such varied arrhythmias may 
portend a fatal outcome within a few weeks or months. 
In patients with typical “senile” cardio-sclerosis—that is, those who have 
in addition to cardio-sclerotic changes, palpably thickened and tortuous arteries 
—auricular fibrillation is very common. One of my hospital services consists MYOCARDITIS AND CARDIO-SCLEROSIS 
33i 
of old people with cardio-vascular disease; among these there is a large propor- 
tion of fibrillators. In those who are compensated, the cardiac rate is between 
70 and 80 per minute, most of the beats are effective and reach the wrist. 
In those who suffer from severe decompensation the cardiac activity is rapid 
and quite irregular, with many frustrane beats (pulse deficit). The course 
of the disease of the elderly cardio-sclerotic patient is essentially afebrile, 
unless disturbed by complications. The most frequent complication is pneu- 
monia, chiefly of hypostatic or embolic origin. 
Prognosis in Cardio-sclerosis.—Under this caption are included those non- 
rheumatic chronic cases of heart disease which show various degrees of involve- 
ment of the myocardium, and atheromatous changes of the endocardium, the 
coronaries, the valves and the aorta. With perhaps the exception of syphilis, 
the etiological factor, whatever it may be assumed to be, has long since 
reached the quiescent stage; the pathological process, however, apparently 
continues insidiously and slowly. Clinical and pathological proof of this 
is usually lacking, since the slow progress of the damage can scarcely show 
itself except by careful clinical observation of the same patient over a long 
period of time, or by occasional necropsies of patients in whom the disease 
has been watched and studied since its incipiency. 
The kind and frequency of complications found in cardio-sclerosis are, in 
the main, different from those in rheumatic endocarditis. Prognostically, 
much depends upon the type of disease which dominates the clinical ensemble. 
For example, if the uremic element predominates, the prognosis will revolve 
upon that; cerebral hemorrhage or acute uremia are then apt to be the 
commoner ways in which the disease will terminate. If the arteriosclerotic 
syndrome predominates, the terminal accidents are prone to be hemiplegias 
or monoplegias. But the arterio-sclerotic syndrome itself can occasionally 
be clinically subdivided into that affecting the aorta and the coronary cir- 
culation, and that involving the myocardium; the prognosis must then be 
studied from these separate standpoints. 
General Prognosis.—“Acute accidents” which may occur and which may 
immediately change the entire prognostic picture will be discussed later. 
Aside from these, the general prognosis depends on an attempt to gauge the rate 
of development and the extent of cardio-sclerotic damage, and the actual 
degree of myocardial insufficiency. The first is only derived from careful 
and patient inquiry into the onset of cardio-vascular symptoms, and from tan- 
gible evidence of an underlying infective process. From these the duration 
of the disease may be estimated. Thus, in one instance of severe myocar- 
ditis with decompensation, in a physician of 55, I was definitely able to 
establish the commencement of the disease as a mild nephritis following grippe 
infection some twenty years previously. The patient had entirely over- 
looked the nephritis as an etiological factor. Very slight cardiac symptoms 
began fifteen years ago and consisted of slight dyspnoea and occasional 
hemopty ses. Acute symptoms of decompensation appeared only a few months 332 
MYOCARDITIS AND CARDIO-SCLEROSIS 
prior to my first examinations; they usually occurred after rapid walking or 
after coitus. The fact that cardiac symptoms began so long ago, and the 
present status of widespread cardio-sclerosis as revealed upon examination, 
made it appear that the pathological damage must have long antedated the 
symptoms. The entire history bespoke a steady though very gradual con- 
tinuation of the pathological mischief. 
This case well illustrates the meaning conveyed, and the information to 
be gained, by a careful clinical history, in an attempt to roughly approximate 
not only the degree of cardio-vascular disease but the length of time required 
to reach the condition found when the patient first presents himself for 
examination. The degree of myocardial insufficiency is gauged not alone 
by physical signs, but also by its usual clinical manifestations; chiefly dysp- 
noea, precordial distress, and a sense of exhaustion after effort. 
It will be noted that the amount of cardiac hypertrophy and of hyper- 
tension has not been emphasized, because these are more concerned with 
sudden heart failure and cerebral accidents than with the question of “ general 
prognosis.” Thus, specimens of extremely hypertrophied and diseased 
hearts have been removed from patients who lived to ripe old age, and in 
whom the disease had doubtless been present for many years. So, too, 
clinicians have for many years followed patients with severe aortic and myo- 
cardial involvement; yet during this long period there may have been no 
marked discomfort, and almost negligible subjective symptoms from the 
cardiac disease. 
With our present knowledge, we cannot state why some tremendously 
hypertrophied hearts carry their circulatory burdens fairly well for many 
years, while other more nearly normal hearts suffer from early circulatory 
failure. I believe that the activity and the degree of progress in the patholog- 
ical process play important roles. The system may accustom itself to a 
gradual curtailment of its circulatory reserve, while a more acute though less 
widespread pathological change might be attended by quick cardiac exhaus- 
tion in a heart already working at or near its maximal energy. 
In order to study myocardial insufficiency from the standpoint of prog- 
nosis, it is further necessary to evaluate roughly not only the amount of patho- 
logical damage to the cardio-vascular system, but also the amount of fairly 
healthy tissue that remains. For this purpose, and in addition to careful 
physical examination, the cardiac reserve power should be estimated in order 
to determine whether any “factor of safety” remains. Functional efficiency 
tests (Chapter XIV) may be of some value in this connection. More readily 
applicable and of greater aid are the facts already mentioned, which can be 
determined by the ordinary methods of clinical examination. These include 
the investigation of the result of effort and exercise upon the heart rate; the 
patient’s subjective sensations when reacting to effort; the size of the 
liver, the presence of dyspnoea, edema, hydrothorax and precordial 
distress. MYOCARDITIS AND CARDIO-SCLEROSIS 
333 
To study ideally the degree and rate of progress of the pathological dam- 
age requires a knowledge of the patient over a long period, but this opportu- 
nity is rarely vouchsafed us. We therefore, shall have to depend in the 
main upon the data and history furnished by the patient. Of great importance 
prognostically are the frequency, type and duration of attacks of decompensa- 
tion, and the manner and rapidity with which they yield to proper therapy. 
These considerations are often glossed over or entirely disregarded; yet from 
them, in addition to other data, one is frequently guided correctly as to the 
ultimate “general prognosis.” Much will depend naturally upon the individ- 
ual opinion as to what is “proper therapy.” If, for example, decompensa- 
tion is infrequent and has been relieved, and diuresis has been promoted by 
diet, digitalis and some caffeine derivative (theobromin, theocin, caffeine), the 
“general prognosis” regarding longevity is correspondingly enhanced. On 
the other hand, if decompensation is frequent, severe and is refractory to 
treatment, the “general prognosis” is poor. 
Knowledge of the prognostic features included under the term, “Acute 
Accidents,” depends upon the fact that, in the pathology of cardio-sclerosis 
there is an admixture of myocardial, arterial and valvular disease in varying 
proportions; and it requires not only laboratory tests and detailed examina- 
tion, but also clinical acumen and broad experience to decipher and properly 
apportion the damage to the heart, kidneys, arteries and brain. Thus 
aneurismal dilatations of the aorta may be confined to its first portion, the 
arch, or to the descending thoracic aorta, while the coronaries and myo- 
cardium may be healthy. In other patients with cardio-sclerosis, the corona- 
ries and their branches are only slightly involved, while the brunt of the 
disease affects the myocardium and produces myofibrosis and hypertrophy. 
Conversely, coronary disease may be widespread and include subsidiary 
branches of the second and even third order, yet the main mass of the myo- 
cardium may remain comparatively healthy. Again, an arterio-sclerotic 
process may spend itself chiefly upon the circle of Willis, and produce symp- 
toms of cerebral softening. All these instances show how necessary it is to 
search out the lesion which is symptomatically and pathologically pre- 
dominant; for in this manner alone can a fairly scientific prognosis be 
grounded, and “acute accidents” foretold and possibly guarded against. 
For the purpose of studying acute accidents prognostically, patients with 
cardio-sclerosis may be roughly grouped into those with predominant arterio- 
sclerotic, uremic, or cardiac symptoms. In cases with general atheroma 
without marked hypertension (usually found in the “senile”), the more 
common causes of sudden death are cerebral hemorrhage, pneumonia or 
pulmonary stasis. The latter produces bubbling or crepitant rales at both 
bases. Such signs may be present for weeks or months before an “acute 
accident” occurs; they help presage probable pulmonary edema or a terminal 
pulmonary infection. 334 
MYOCARDITIS AND CARDIO-SCLEROSIS 
A fairly definite hint of cardiac failure or of impending death is furnished 
by the presence of arrhythmias, the type of which change, apparently 
capriciously, hourly or daily. Thus, at various times, extrasystoles, auricu- 
lar fibrillation, or tachycardia may alternate with a regular pulse. This 
heightened ventricular irritability is not necessarily associated with any 
demonstrable change in the clinical symptoms. It seems to be due to some 
profound change in cardiac nutrition dependent on severe sudden focal myo- 
cardial damage from coronary emboli or infarcts. The following cases will 
serve to illustrate the clinical picture. 
Male, aged fifty-five, was suffering from mild nephritis and cardio-sclerosis 
with moderate hypertension. The main complaint was slight dyspnoea 
upon climbing stairs. He improved under therapy and felt comparatively 
well for one year. His pulse had always been regular until one day he 
complained of constant “fluttering” in his heart. Clinical examination and 
electrocardiograms showed a simple tachycardia; the rate was 160 per 
minute. His condition was accompanied by very slight dyspnoea. There 
was no precordial pain. The tachycardia lasted two days. For a period of 
three months he again felt well, his pulse remained regular. Then, suddenly, 
during the night he complained of feeling faint and of a very slight “ uneasi- 
ness” in the chest. Again slight dyspnoea was present. Examination 
showed auricular fibrillation with rapid and irregular heart action; the cardiac 
rate was 150 per minute. He was given digitalis and later was allowed to 
sit out of bed. The fibrillation continued, but the patient said that he felt 
very much better. Despite apparent improvement and absence of pain, a 
diagnosis of probable coronary infarct was made, and a guarded prognosis 
given regarding the outcome of the attack. After four days, while the 
patient was sitting quietly at the table and reading, he gasped and died 
within two minutes. 
Female, aged sixty-seven, well preserved, had been complaining of sub- 
sternal pain for one year. More recently, she began to have attacks of 
dyspnoea and of pains lasting about one hour and radiating to the back. At 
such times, the pulse became irregular (auricular fibrillation); between 
attacks, it remained regular. Upon examination, the systolic blood pressure 
was 168, the diastolic, 80; there was slight pretibial edema. Fluoroscopic 
examination showed a somewhat dilated aortic arch. The urine contained 
neither casts nor albumen. The electrocardiographic tracing showed a few 
ventricular extrasystoles. A diagnosis of probable coronary sclerosis was 
made and sudden death prognosticated, mainly because of the arrhythmia 
which accompanied the attacks of dyspnoea. Two months after the first 
examination, the patient had an attack of dyspnoea and precordial pain, and 
died within a few minutes. 
Prognosis in Cardio-sclerosis with Coronary Disease.—Where disease of 
the coronaries is assumed to be the main cause of the symptoms (Chapter 
XXIII) the prognosis depends on the severity of the precordial attacks and MYOCARDITIS AND CARDIO-SCLEROSIS 
335 
on the extent of concomitant cardiac damage; in other words, on the state 
and amount of preservation of the undamaged cardio-vascular apparatus. 
If compensation is good, the precordial distress mild and yields to therapy, 
the patient may continue a fairly comfortable existence for years; in such 
cases, fair but somewhat guarded prognosis regarding longevity should be 
given. Widespread coronary disease may show itself clinically in several 
ways: By severe attacks of precordial distress (angina pectoris, Chapter 
XXIII), in any one of which the patient may die from edema of the lungs, 
coronary infarct, or embolus; by attacks of dyspnoea; by vomiting which has 
no relation to the ingestion of food and is often wrongly ascribed to indiges- 
tion and hyperacidity; or by slight febrile disturbances combined with 
tender areas over the precordium. Apparently the latter are due, at times 
at least, to focal myocardial or even to myomalaceous areas from an infective 
or embolic process in a secondary coronary vessel. Such a process may run 
its course in a few days or weeks; the heart becomes permanently affected, 
but the damage is not necessarily incompatible with life or with a fair amount 
of cardiac comfort. The prognosis in such cases depends on the severity 
of the infection as judged by the temperature and rigors, the duration, and 
especially by the frequency of the attacks. When the clinical manifestations 
are mild, with but occasional recurrences, the prognosis is fair, for the 
chances are that the myocardial damage occurring with each infection will 
only gradually cripple the heart, and that symptoms of myocardial insuffi- 
ciency will supervene only after a long period of time. The chief danger is 
the possibility of embolic infarcts into some vital organ as, for example, the 
brain. 
The main right or left coronary artery may be suddenly plugged by 
an embolus, or its lumen closed by an infarct (Chapter XXIII). This is 
usually accompanied by intense precordial distress, dyspnoea and gastric 
symptoms. Signs of acute cardiac failure rapidly supervene, and death 
usually occurs within 24 hours. Such cases have been corroborated by nec- 
ropsy examinations. 
Ventricular fibrillation (Chapter X) is probably another type of sudden 
death occurring in patients with cardio-sclerosis. As far as our knowledge 
goes, this arrhythmia is almost immediately fatal.1 It seems most likely 
to occur in patients who receive digitalis (Chapter XX) and who, immediately 
preceding the presumed fibrillation attack, are in a fair state of compensation 
and are apparently progressing favorably. Attacks of ventricular extra- 
systoles (ventricular tachycardia) may occasionally presage a fatal attack of 
ventricular fibrillation, for we possess experimental knowledge that ventricu- 
lar tachycardia can lead to ventricular fibrillation and death. Death from 
ventricular fibrillation may account for some necropsy reports in which neither 
1 Robinson, however, reported a case in which the patient lived several weeks after the 
onset of ventricular fibrillation. 336 
MYOCARDITIS AND CARDIO-SCLEROSIS 
the heart, brain, nor any vital organ shows an embolic cause of death, and 
yet the patient dies quite suddenly of advanced cardiac disease. 
The degree of cardiac hypertrophy has a certain influence in increasing the 
probability of “acute accidents,” especially after a first attack of decom- 
pensation. The cardiac reserve power is then apt to be quickly exhausted, 
even after restoration of compensation. Lack of cardiac reserve may evi- 
dence itself by dyspnoea, slight edema, visceral congestion, or by arrhyth- 
mias, especially extrasystoles. The usual terminal stages consist in edema of 
the lungs coming on in attacks, or in steadily increasing pulmonary engorge- 
ment. 
Prognostically, hypertension forms an extremely important factor in the 
possible causation of cerebral hemorrhage. There is, however, no definite 
method of foretelling these apoplectic attacks. In many cases the blood 
pressure is high for months and years, and cerebral hemorrhage does not 
supervene; in others, hypertension is only moderate and hemorrhage does 
occur. The reason for this probably lies in the fact that this lesion depends 
not only on the degree of hypertension but also on the extent and type of the 
arterio-sclerosis. Where brain symptoms are absent, we possess no definite 
means of determining the extent of cerebral arteriolar disease. 
Uremia is another frequent form of death in cardio-sclerosis. It is com- 
monly reported that the diastolic pressure (Chapter XXV) is of great sig- 
nificance in determining the probability of uremic complications. A dia- 
stolic pressure of 130 m.m. or over is regarded as a danger signal; the higher 
the diastolic, the greater the chances of uremia, with all its symptoms 
and complications. I have not been able to definitely corroborate the 
assumption of a high diastolic pressure with impending uremia. Briefly, 
the symptoms are vomiting, nausea, headache, oliguria, dyspnoea and pallor. 
The special prognostic features of each of these manifestations are beyond 
the scope of this chapter. 
To summarize, although the question of prognosis in cardio-sclerosis 
is complicated and entails many cardio-vascular, cardio-renal, arterio-cerebral 
and cardiac factors, it is possible to make a fairly accurate general prognosis 
in many cases. Although the time of incidence of an acute accident can be 
foretold in only the rarest instances, a correlation of physical data and symp- 
tomatology helps in the prediction of the probability of its occurrence. 
Fatty Heart.—Fatty heart in the sense of an accumulation of fat pads 
around the heart (Chapter IV) does not of itself give rise to symptoms. 
It is simply one of the many local deposits common in very obese individuals. 
Fatty infiltration of the myocardium (Chapter IV)—a more important 
clinical type—is also a general phase of obesity. It is questionable whether 
such infiltrations alone can cause myocardial insufficiency and heart failure. 
It seems more likely that heart failure in obese individuals is due to the usual 
causes—myocarditis and coronary disease—producing cardiac symptoms 
perhaps more quickly because of the fatty infiltration and because the heart MYOCARDITIS AND CARDIO-SCLEROSIS 
337 
muscle partakes of the flabbiness of the general skeletal musculature. The 
symptoms in heart failure (Chapter XIV) of this type differ in no wise from 
those already described. Physical signs, however, are apt to be masked 
because of abnormally fat chest walls and because the heart itself is encased 
in a fatty layer. 
The Heart in Chronic Emphysema.—This presents a type of clinical 
myocarditis not infrequent, especially in men between 50 and 60. Emphy- 
sema seems to be the primary factor. The degree of myocarditis does not 
seem to be clinically severe. There is usually moderate cardiac enlargement; 
because of the emphysema or cardiac weakness or both, the heart sounds at 
the apex are distant. There is often a soft murmur at the apex; in advanced 
cases, the murmur of functional tricuspid regurgitation (Chapter XIII) is 
heard over the xiphoid. The arteries are soft. Hypertension is not the rule. 
iVrterio-sclerosis is not a prominent feature. Physical signs over the lungs 
are the usual ones of emphysema. There is constant cyanosis of varying 
degrees, from slight venous stasis and suffusion to definite bluish coloration. 
It increases markedly upon exercise, especially upon bending the head 
sharply and low. When the process is not extreme, the usual complaint 
of the patient, in addition to shortness of breath, is a feeling of heaviness 
and oppression in the chest upon exercise. Severe precordial distress is rare. 
Edema of the legs is a late complication. 
I have not been able to study these hearts postmortem, so that I cannot 
speak of the actual amount of myocarditis. If present, it is probably due to 
insufficient arterial blood supplied to the heart because of interference with 
the pulmonary circuit. Clinically, myocardial insufficiency seems the pre- 
dominant factor, whether it be due to actual myocarditis or to right heart 
failure from continuous distention of these chambers. 
Therapy is the usual one for heart failure. Special treatment should be 
directed to the emphysema. The results are often disappointing because 
the primary cause of emphysema can rarely be controlled. CHAPTER XVIII 
CARDIAC NEUROSIS'—GENERAL CONSIDERATIONS —“WEAK” 
HEART — IRRITABLE HEART IN CIVIL AND MILITARY 
PRACTICE, WITH COMPARATIVE OBSERVATIONS—GOITROUS 
HEART 
The role of nervous disturbances such as shock, fright, and other emotions 
in patients with organic disease has already been described (Chapter XIV). 
Other phases of cardiac neurosis such as paroxysmal tachycardia, arrhythmias 
and precordial pains of reflex origin are dealt with in their appropriate con- 
nections. Cardiac overstrain as a factor in initiating the symptoms found in 
“ irritable heart ” has been alluded to (Chapter XIV). One can therefore com- 
prehend that emotional instability and cardiac overstrain, alone or combined, 
can in various ways be of great importance in causing cardiac symptoms in 
those without organic disease, especially if there already exists an underlying 
neurotic tendency, environmental or constitutional. The physiological control 
of the cardiac inhibitors and accelerators has been previously dealt with 
(Chapter I). It will be shown clinically that abnormal excitation of either 
the inhibitory (vagus) or accelerator mechanism, especially the latter, is 
responsible for much of the symptomatology of cardiac neurosis, and par- 
ticularly of “irritable heart.” Many illustrative cases of various types of 
cardiac neurosis are given in Cardio-vascular Clinics. 
Distinct group divisions of cardiac neuroses cannot indeed always be made 
because symptoms and physical signs frequently overlap; I neverthless have 
found the following generic subdivisions of distinct clinical advantage, 
especially from the symptomatological standpoint. There is what may be 
designated as the Vaso-motor group (“weak” heart); the mildest of the neu- 
roses; next in severity comes the Irritable Heart; and finally, the Goitrous 
Heart. The subject will therefore be described under these three captions. 
VASO-MOTOR NEUROSIS—“WEAK” HEART 
Clinical Symptoms.—“Weak,” “asthenic,” “neurotic,” 1‘neurasthenic” 
hearts, X-disease (Mackenzie), are some of the terms more or less loosely 
applied to various ill-defined conditions in which I believe the salient feature 
to be an unstable state of the vaso-motor mechanism. I shall not here 
include a discussion of the arrhythmias which in themselves are sometimes 
regarded as evidence of a “ weak ” heart. The fact that arrhythmias of various 
kinds may be purely functional in origin has already been frequently empha- 
33 8 CARDIAC NEUROSIS 
339 
sized (Chapter XI). As indicative of a “weak” heart, stress is often laid upon 
the presence of a soft, faint, systolic murmur over the apex, only slightly or 
not at all transmitted. The murmur itself is very inconstant: Some days, or 
at some examinations it is present; at others it is absent. Moderate hypoten- 
sion (Chapter XXV) is also common in these individuals. Such findings are 
often interpreted as organic. Actually, however, they offer not the slightest 
evidence of organic cardio-vascular disease. There is never any sign of 
actual heart failure or of myocardial insufficiency. Subjectively the patients 
complain of tiring very easily; if the occasion demands it, however, they can 
undergo long-continued physical exertion with no sign of strain upon the 
circulatory system. Such physical stress, however, is often accompanied 
by long continued fatigue. The patients also complain of feeling faint and 
dizzy; sometimes indeed they actually lose consciousness. Their faces and 
hands easily redden or blanche, with a corresponding feeling of warmth or 
cold in these parts. These changes are due to vaso-motor instability, to 
alterations in what has come to be called the “peripheral heart,” and not at 
all to a “weak” heart. This is further shown by the fact that these patients 
never suffer from edema or visceral congestion, or from any of the signs found 
in decompensation. 
Aside from symptoms and physical signs referable to the circulation, these 
individuals sometimes suffer from ill-defined gastric complaints of non- 
organic nature, often associated with referred intercostal and precordial 
pains. By some, such pains are called “vaso-motor angina,” a very inapt 
term (Chapter XXIII) in my opinion. It is because of these pains that one’s 
attention is frequently drawn to the heart as the presumed offending organ. 
Nervous strain, joy, worry, excitement, and physical fatigue quickly elicit 
many of the symptoms I have referred to. The same factors seem occasion- 
ally to exercise an influence upon the apical murmur, which at such times 
becomes somewhat louder. The cause of the increased intensity of the mur- 
mur is not clear; it may consist in some disturbance of muscular tone of the 
ring at the mitral opening, allowing regurgitation. 
The patients as a class are usually regarded as neurasthenic, because, 
although frequently of robust appearance, little or no physical basis for their 
symptoms can be found. Many have been fluoroscoped in search for some 
abnormality in the size and shape of the heart in order to account for the 
instability of the peripheral circulation. “Drop” hearts (Chapter XII) and 
abnormally small hearts (so-called microcardia) have been found in some of 
these individuals. I have studied a number of cases of “weak” hearts 
fluoroscopically. In some I have found the abnormal orthodiascopic types 
above referred to; in others, I have found the heart of normal size and 
contour, or with the left ventricle lying quite broad and flat upon the 
diaphragm. In other words there was no orthodiascopic picture that I 
could definitely correlate with “weak” heart. Indeed, I have made the 
fluoroscopic observation that some of these “weak-hearted” individuals 340 
CARDIAC NEUROSIS 
show particularly vigorous and strong ventricular contractions. It is 
therefore clearly evident that there is no constant parallelism between the 
vaso-motor symptoms and the muscular power of the heart. 
A few brief illustrative clinical histories and findings will serve to typify 
some of these characteristics. 
A buxom woman of 45 had been told for years that her heart was “weak.” 
There was no history of any previous serious illness. She had had two 
children who died. Very soon after the death of the last child, there began a 
series of symptoms consisting of giddiness, nausea, and flushing or pallor of 
the face. These symptoms have been intensified since her menopause two 
years ago, so that, in addition, she often feels faint and, in fact, actually 
fainted several times. There is a very soft systolic murmur at the apex, 
the orthodiascopic tracing shows an outline slightly broader than the normal, 
the blood pressure and all the other physical findings are normal. There is no 
evidence of any organic cardio-vascular disease. This patient has been under 
my observation for several years. She has undergone a severe operation for 
appendicitis with no effect upon her circulation. When I last examined her, 
most of the evidence of vaso-motor disturbances had disappeared. 
A vigorous woman of 40, married and the mother of two children, while 
abroad was suddenly called home by illness in her family. She became 
worrisome, and complained of feeling fatigued; her hands and face readily 
became cold; she complained of severe pains across the chest upon exertion. 
There was a faint systolic murmur at the apex; orthodiascopic examination 
revealed a somewhat broad left ventricle; otherwise the cardio-vascular and 
general examination revealed nothing abnormal. Upon being assured that 
her heart and other organs were normal, she soon recovered her mental poise. 
She began taking active exercise and now walks several miles daily without 
cardiac or other complaints. 
A tall, narrow-chested and somewhat anemic youth of 20 complained 
of frequent flushes and a feeling of “ heat ” in the face. The lungs and cardio- 
vascular system were normal. The only abnormal finding was a narrow, 
pendulous heart. Upon being told after the examination that there was no 
lesion of any kind in the heart or lungs, he began leading a more normal and 
athletic life with rapid disappearance of the vasomotor symptoms. 
I believe it is worth while emphasizing the fact that the fundamental 
abnormality of this entire group of patients lies in an instability of the vaso- 
motor mechanism, the cause of the irregular flushes, pallor, dizziness and a 
faintness. Nerve shock of any kind is often the culminating factor initiating 
the more acute symptoms. From the neurosis standpoint, most of these 
individuals can be classified under the term of fatigue neurosis with predomi- 
nating vaso-motor symptoms. They should be sharply differentiated from 
the cardiac hypochondriac, a term to be applied to those with purely imagina- 
tive cardiac complaints arising chiefly from an abnormal, intense introspective 
tendency. CARDIAC NEUROSIS 
34i 
To a great extent, therapy in those with vasomotor neuroses lies in assur- 
ing the patients that there is no organic disease, and that the symptoms can 
be cured or at least greatly alleviated. It is a diagnostic and therapeutic 
error to dismiss these individuals by telling them they are “ nervous,” for 
the symptoms are real and usually beyond their control. The treatment 
sometimes requires patience and, always, careful individualization. The 
patient should never follow any form of exercise, no matter how slight, to 
the point of fatigue. A rest cure for a longer or shorter time may be a pre- 
liminary requirement. Patients too intent upon business must decrease the 
number of hours and the intensity of their work. At no time should these 
individuals feel hurried at their work or even at their pleasure. Rest in 
the reclining position, getting up late, having breakfast in bed, long rest at 
night, mild balneotherapy; later, graded calisthenics, or exercise in the open 
(walking, swimming in shallow water, even tennis) are measures which, 
appropriately applied and carefully selected, are of great aid to the patient in 
helping him regain his vaso-motor equilibrium and in finally enabling him 
step by step to return to his accustomed duties. In women at the menopause, 
endocrine disturbance doubtless plays an important, sometimes indeed the 
chief part in the etiology. I have tried various organic extracts alone or in 
combination, in order to make up the assumed deficiency in the endocrine 
system. In most cases, the extract of suprarenal gland in one or two grain 
doses three times a day, is of benefit. Organotherapy in these individ- 
uals has not gotten much beyond the stage of clinical experimentation; 
but I believe the latter is warranted because it is harmless when carefully 
prescribed although it is often disappointing in results. 
When gastric disturbances are present, appropriate treatment should be 
advised. Among drugs I have found atropine sulphate (grains 3d200 to Moo) 
and nitroglycerin (grain to 3d5o)> three times a day before meals, of 
value. When hypotension is present, suprarenal extract is sometimes of 
benefit; indeed, it is often of value even when the blood pressure is normal, 
for it seems to stabilize the vaso-motor mechanism. Strychnine may also be 
helpful. If symptoms are intensified at the menopause, ovarian extract 
(corpus luteum) may be tried. All in all, it must be stated, that because of the 
type of the fundamental disorder—instability of the vasomotor mechanism— 
the effect of treatment is sometimes disappointing to the physician and dis- 
couraging to the patient. This is especially true in those with rather severe 
precordial pains (Chapter XIV). 
THE IRRITABLE HEART IN CIVIL AND MILITARY PRACTICE, WITH 
COMPARATIVE OBSERVATIONS 
Because the “irritable heart” is so well exemplified among soldiers, I have 
thought it best to describe and compare it with the similar condition found 
among civilians, thus emphasizing the fact that the fundamental etiology 342 
CARDIAC NEUROSIS 
is the same. It has the further advantage of showing how the various 
grades may merge. 
During and shortly after the Great War, medical literature abounded 
with various descriptions of the soldier’s and recruit’s heart. Indeed, so 
much had been written that, with but a superficial knowledge of, or interest 
in cardiology, the impression gained was that a new and distinct entity charac- 
teristic of warfare had been discovered, and that it is never, or but extremely 
rarely, encountered in civil life. This impression was heightened by the fact 
that similar conditions in civil life had scarcely been alluded to in the numer- 
ous reports, and that new and more or less confusing names had been given 
to this symptom-complex. To mention a few: The soldier’s heart; effort 
syndrome; neurocirculatory asthenia; neurocirculatory myasthenia; disor- 
dered heart action and hyperthyroidism. From the broader viewpoint of 
clinical medicine; from an intensive study of the condition in cardiologic 
practice for many years, from the examination of hundreds of candidates 
before the draft board, and from observation in camp hospitals, I believe the 
term “irritable heart” or even “cardiac neurosis” best fits the syndrome. 
Either appellation applies to all types of instability and irritability of cardiac 
innervation both in civil and military practice in which there are assumed 
to be no organic cardio-vascular changes. These terms, irritable heart and 
cardiac neurosis, are admittedly generic. They should be so, I believe, 
because the condition may have different underlying etiological factors and 
varying clinical manifestations. For those seeking more specific appellations, 
perhaps vaso-motor cardiac neurosis or accelerator cardiac neurosis would 
more accurately define the general types. 
Probably because of the early intensive cardiologic work in the late war, 
the fundamental relationship between the irritable “soldier’s heart” and a 
similar condition in civil life was missed entirely or was not emphasized 
sufficiently. Various theories were at first propounded to explain its fre- 
quency in soldiers. For example, infection was assumed to play a fundamen- 
tal role. But the numerous cases occurring in American camps among recruits 
who had never seen active service and who had had no infection tended to 
upset this theory. The fact that diminished blood alkalinity (acidosis) was 
found in a certain number of the cases studied abroad was also given as a 
tentative explanation. It seems possible that in such individuals the “ acido- 
sis” and change in the buffer salts in the blood may have been the result, not 
the cause, of the cardiac neurosis from circulatory disturbance and conse- 
quent interference with proper elimination of toxic products. 
Intensive military training took men from civil life without regard to their 
previous occupations, and immediately exposed them to the stress, exertion 
and fatigue of camp life. I am not criticizing this procedure because the 
exigencies of war demand haste. Besides, it may perhaps have been wise 
to discover as soon as possible those recruits who were totally unfit for 
actual war service. Concomitant with unwonted muscular exertion, espe- CARDIAC NEUROSIS 
343 
dally in those from sedentary life, there is a certain amount of nerve fatigue, 
perhaps best expressed by the common term “fag.” Nerve fatigue, psychas- 
thenia and neurasthenia are admittedly somewhat vague terms and are open 
to wide variances in meaning, but they define a tendency to quick exhaustion, 
inability to properly coordinate somatic and even cerebral functions, and 
irritability and restiveness of these functions. This nerve fatigue and insta- 
bility often characterize patients with irritable hearts. In addition, there is 
the important emotional factor, the mental attitude of the recruit toward the 
war. Is he cowardly by nature? Does he fear warfare? Can the natural 
diffidence against war in a peaceloving people be overcome rapidly enough by 
instillation of the martial spirit, of military morale? Can the recruit’s mind 
readjust itself rapidly enough to the vital necessity of risking life and limb for 
country? How far are such questions related to the nerve stamina of the 
individual? Does the recruit coipe of nervous stock? Has he shown any 
neurotic manifestations in civil life? Have venery and sex ideas played a 
large share in his thoughts? Questions like these undoubtedly play impor- 
tant roles in the mental and nerve poise of the individual, may retard or 
induce, considerably influence, or even cause the advent of the irritable heart. 
Such are some of the important crass neurologic and psychiatric factors in 
camp training. These are tremendously intensified by actual warfare and 
combat; the nerve tension, perhaps of weeks, before actual combat; the dread 
of injury or death in the clash of battle; the nerve exhaustion following 
it; fright in all its phases—these are here the outstanding factors. 
Is there any correlation between the irritable heart under camp and war 
conditions, and that found in general practice? I believe the two conditions 
are comparable, and that its infrequency in civil life is due to the relative 
rarity of the factors just mentioned. Besides, in general practice I believe 
we do not delve sufficiently into possible etiological data. We are prone to 
weigh the patient’s story too lightly because there is no tangible, corrobora- 
tive physical evidence to be seen, heard or felt. Neurotic individuals, espe- 
cially those with cardiac neuroses, have frequently told me that they felt 
anger and excitement “in the heart,” while others with gastric disturbances 
feel similar emotions “in the stomach.” It may appear unscientific to 
believe such statements when no method of examination is open to us to prove 
or disprove them, but, measured by our own personal experiences, I am sure 
that there are physicians who, at some time, under special emotional stress 
such as fright or anger, have referred their sensations to the heart or the 
abdomen; and I need but recall poetic and romantic literature which abounds 
in examples of pangs of jealousy and rage being referred to the heart. 
Illustrative cases of cardiac neurosis are given in Part II, Cardio-vascular 
Clinics. 
The salient feature of the symptom complex of individuals with cardiac 
neurosis is instability of the vaso-motor or of the accelerator mechanism, 
or of both. I believe that all the symptoms as well as the abnormal physical 344 
CARDIAC NEUROSIS 
signs are attributable to these fundamental disturbances. Giddiness, 
flushes, pallor, dermatographia, swooning, fainting are patently due to vaso- 
motor disturbances. They are found very frequently, for example, in many 
types of gastric disorder without cardiac symptoms. The tachycardia in 
irritable heart ranges from simple pulse acceleration to gradual or sudden, 
sharp increases in rate following exercise, emotion or unknown causes. The 
sudden, sharp increases in rate and in forcefulness of heart action are found 
oftenest in the irritable heart of soldiers. To use a simile derived from 
physiology, the threshold for the abnormal excitation varies considerably. 
The cause of the various types and degrees of precordial sensation, such as 
heaviness, pressure, pain, skin and deep sensitiveness, is still obscure because 
nerves of sensation have not been discovered in the heart, and because the 
reflex arcs involved are still matters of surmise. But the clinical fact, already 
alluded to, that some people in anger or fright refer the first sensation to the 
heart, and Head’s theory of sensitized spinal segments indicate how a diseased 
or improperly functionating organ can cause various local referred sensations. 
The abnormal physical sign of irritable heart to which most importance is 
attached is a thrill-like palpable systolic impulse and the thrill-like, split, or 
broken first sound at the apex. Soft apical murmurs that are not transmitted, 
slightly accentuated second pulmonic sounds, and the occasional reduplicated 
second sound over the pulmonary artery, the aorta or at the apex, may be 
dismissed because they are not characteristic of the “irritable heart” and are 
sufficiently common in other conditions. When present, the thrill at the 
apex in the irritable heart with tachycardia is systolic in time; its degree and 
transmission seem to depend upon the violence as well as the rapidity of heart 
action. A thrill, for example, is infrequent in the regular heart action of 
paroxysmal tachycardia, in which the heart beats at the rate of from 150 to 
200 per minute. It is quite common, however, in exophthalmic goiter, even 
when the cardiac rate is as low as 100 to no per minute. I believe it is the 
violence of the heart action, rather than its rapidity, that accounts for the 
abnormal systolic thrill, for theoretically at least, it seems probable that 
blood, suddenly and forcefully ejected by ventricular systole, can produce 
impingeing countercurrents and whorls against the inner ventricular surface; 
to the ear and touch these are interpreted as broken, almost cog-tooth-like 
interruptions of the normal systolic sound and thrust. This receives some 
support from the observation I have frequently made that if the cardiac 
rate and hyperactivity can be controlled by having the patient take a long, 
deep breath and holding it a moment, the thrill often diminishes or disap- 
pears, almost commensurate with corresponding decrease in ventricular 
hyperactivity. 
The close etiologic and symptomatic relationship between the irritable 
heart in civil and military practice are shown by the case histories with their 
comments. (See Cardio-vascular Clinics.) In the soldier’s heart, tachy- 
cardia, especially following effort (effort syndrome), is the most common CARDIAC NEUROSIS 
345 
sign; vasomotor symptoms alone are less common, while in civil practice, 
the vasomotor symptoms predominate. It must be remembered and empha- 
sized that patients frequently complain of “palpitation” without tachycardia, 
that is, they have a subjective feeling of palpitation. In a few instances, 
I have been able to discover with the aid of the fluoroscope that such patients 
had particularly strong ventricular contractions; the left ventricle was decid- 
edly diminished in size with each systole. This may perhaps be the physical 
explanation of subjective “palpitation” in some of these cases. 
I have tabulated a list of the commoner symptoms, physical findings and 
etiological factors as I have observed them in the neurotic heart in civil 
practice, and have arranged each column, as far as possible, in the order of the 
importance of the various factors. 
Symptoms 
Abnormal precordial sensations (pain, sensi- 
tiveness, oppression). 
Vasomotor symptoms (giddiness, flushes, 
dermatographia, faintness). 
Dyspnoea (actual and subjective). 
Extrasystoles producing subjective sensa- 
tions. 
Tachycardia following slight effort. 
Constant tachycardia. 
Sudden changes of heart rate. 
Etiological FACTORsr 
(Causing hyperirritability of the accelerator 
branch of the sympathetic nervous sys- 
tem:) 
Previous history of shock, fright or emo- 
tional strain. 
Reflex excitation from gastro-intestinal canal. 
Physical fatigue with insufficient rest. 
Insufficient recuperation following acute 
infections. 
Disturbance of the organs of internal secre- 
tions (thyroid?, adrenals?). 
Irritable Heart in Civil Practice 
Physical Findings 
Normal sized heart; thrill-like, split systolic 
impact and first sound over the mitral 
area. 
Systolic murmur over the lower precordium; 
rapid regular heart. 
Normal rate with occasional extrasystole. 
Sudden changes, of heart rate. 
Slow heart action with powerful ventricular 
contraction. 
Therapy 
Reassurance. 
Short rest periods. 
Retraining, especially through graded 
games; bromides and luminal in the 
beginning or in severe cases. 
Suprarenal gland extract (especially for 
vaso-motor symptoms). 
Some of the headings require additional comment; others have been 
discussed in the description of the case histories or elsewhere. 
Dyspnoea as stated may be actual, for example in patients who develop 
tachycardia as the result of exercise. At other times, especially in patients 
with vasomotor symptoms, the dyspnoea seems purely subjective, for there 
is no increase in the rate or depth of respiration. In rare instances tachypnea 
—rapid shallow breathing—results. 346 
CARDIAC NEUROSIS 
The size of the heart, as mapped out by ordinary methods of clinical 
examination, gives the impression of enlargement. This impression, how- 
ever, is the usual one in almost all cases of violent, rapid heart action (Chapter 
XII). I have had occasion to fluoroscope many cases of tachycardia that 
had no organic cardiac disease. The orthodiascopic tracing revealed no 
characteristic change from the normal in the size or configuration of the 
heart. I have rarely found the drop or pendulous heart (Chapter XII), that 
is, a narrow organ resting lightly on the diaphragm along a small part of its 
under surface. 
Among etiological factors of the irritable heart, a fundamental one 
is an “emotionally unstable, neurotic individual.” (See Table.) Some of 
the patients give definite histories of a nervous taint in either parent, or in 
closely related member of the family. I believe, however, that while such 
taints may be common, they are not the actual exciting or impelling causes of 
the neurotic heart. Some great emotion such as fright, dread and shock, 
is usually the direct antecedent cause of the outbreak of the cardiac symptoms. 
Reflex excitation from the gastro-intestinal canal is the next most frequent. 
In other words, the cardiac nerves of hereditarily disposed individuals react 
more readily, more continuously and in a more exaggerated fashion to a neu- 
rogenic “insult” than do those of an individual with normal poise. 
Cause of Irritable Heart.—Having alluded to some illustrative cases 
and various attendant symptoms, physical findings and etiological factors, 
the question arises, is there some basic underlying excitation to account for 
the irritable heart? Careful analysis of all the various phases of the irri- 
table heart, especially facts elicited by careful history, lead me to the belief 
that it is probably fundamentally due to hyperexcitation of the sympathetic 
nervous system. In his classic paper on the irritable heart of soldiers, 
DaCosta ascribes many of the symptoms to stimulation of the sympathetic 
system. Recent observations of the same subject show that there exists 
hyperirritability of the accelerator reflex arc and probably also of the vaso- 
motor mechanism. No diminution of the vagal tone was found, as judged by 
atropin experiments. Experimental observation demonstrates that fear and 
dread in cats, for example, are accompanied by erection of the fur, by exceed- 
ingly rapid heart action, by profuse perspiration and by staring eyes. These 
are all evidently due to hyperexcitation of the sympathetics. Such symp- 
toms have their analogies in man. Fright and terror can be the immediate 
cause of exophthalmic goiter. Authentic causes of this type have been 
reported. I myself have observed at least two such undoubted cases. 
One of these was that of a young girl, who, while riding in a passenger elevator, 
saw a man killed before her eyes. On reaching home, she went to bed with 
rapid heart action, and within a few weeks, developed all the classical signs 
of exophthalmic goiter. In war recruits, the development of typical exoph- 
thalmic goiter has been occasionally observed. On the other hand, the de- 
velopment of rapid heart action, tremor and other signs and symptoms of the CARDIAC NEUROSIS 
347 
irritable heart, without the type of goiter found in exophthalmic goiter, has 
been regarded by some as evidence of hyperthyroidism. Some of these 
individuals had soft goiters. But changes in the thyroid, especially cystic 
degeneration, are by no means regularly accompanied by cardiac or nervous 
symptoms. The subject of hyperthyroidism brings up for discussion 
the involved question of the endocrine glands. Are we justified in assuming 
hyperthyroid activity without the typical eye and thyroid signs of exophthal- 
mic goiter? I do not believe that the present state of our knowledge allows 
us to go thus far. Besides, I think that the symptoms of hyperthyroidism 
so-called in the recruit and soldier can be understood better and more rationally 
on the broader and more fundamental basis of hyperirritability of the sym- 
pathetic system. It is probable that this supposition can even explain why 
an occasional case of irritable heart develops all the classical signs of actual 
exopthalmic goiter, for the endocrine glands themselves, especially those 
with rich nerve supply are presumably subject to varying influences of nerve 
excitation and nerve tone. This has been proven experimentally for the 
adrenals. The entire subject is further complicated by the probability that 
the endocrines themselves are mutually influenced by the action of hormones. 
This was illustrated in a case I saw at one of the war camps in which the 
development of a constant tachycardia was one of the prominent features. 
The man had gained about 50 pounds in weight within a few weeks; his 
breasts had taken on female characteristics; sexual desire had disappeared 
entirely for several months. The thyroid was not enlarged; there was no 
exophthalmos or tremor. Despite the rapid heart action, he looked the typ- 
ical example of hypopituitarism. According to our present terminology, the 
case would probably be classed as dyspituitarism. 
Hyperexcitation of the sympathetic system can undoubtedly produce 
rapid heart action, tremors and sweating; and as already stated, symptoms 
starting thus, may, in some instances, finally eventuate in actual exophthal- 
mic goiter. In several polygraphic tracings of undoubted cases of exophthal- 
mic goiter, I observed that the conduction time from auricle to ventricle 
(the a-c interval) was diminished even when tachycardia was not marked 
(Chapter X). This may offer some clinical corroboration of the experimental 
observation that one of the effects of stimulation of the sympathetic is a 
decrease of this interval. Only recently it was pointed out that the thyroid 
is subject not only to hyper- and hypo-, but also to dysfunctions, a fact 
which may account for some of the vagaries and apparent contradictions in 
the clinical syndrome of exophthalmic goiter. 
The physiologic antagonism between the sympathetic and vagus systems, 
between the accelerators and inhibitors is of course well known. In an 
abnormal antagonism between these two controls, I believe that even when 
inhibition is normal, its power can be nullified by hyperirritable and hyper- 
active accelerators. In other words, the inhibitory tone, as tested by 
atropin, may be normal, yet its power can be nullified by hypertonic accelera- 348 
CARDIAC NEUROSIS 
tors. This is perhaps explicable by the physiological fact that, tested 
electrically, there is normally no quantitive relationship between these two 
systems (Chapter I). Sympathetic excitation, therefore, can apparently 
upset the nice balance of cardiac nerve control, with consequent lack of the 
normal inhibitory process. 
From a review of the data I believe we may assume that the “irritable 
heart” is due fundamentally to sympathetic hyperexcitation, unopposed or 
insufficiently opposed by the inhibitory apparatus, and that therefrom 
arises the cardiac syndrome and vaso-motor symptoms at one extreme, and 
the actual goitrous heart at the other. 
The fact I again wish to emphasize is that the soldier’s irritable heart is no 
new complex, but is the same syndrome seen in civil life, intensified and 
multiplied by training and war conditions. Suspense and fright intensify 
latent and dormant symptoms and tendencies, and cause nerve instability in 
those temperamentally unfit, by heredity or otherwise, “to carry on.” 
Therapy.—On the continent, the original treatment of the soldier’s heart 
had narrowed itself to a comparatively short period of rest, and then graded 
restraining in camp routine: Mild exercise at first, routine marches, light 
packs, heavy packs, etc. In this way a fair percentage again became fit 
for active duty. Digitalis was found to be of no value, as indeed was to be 
expected, for the patients did not suffer from decompensation, nor was there 
any evidence of organic valvular or muscular disease. At the beginning 
there was no attempt to attack the problem of the irritable heart from the 
psychologic or psychotherapeutic viewpoint. Mental and physical relaxa- 
tion, especially in the form of games, and later, sports, was not then 
attempted. More recently, especially in the United States, games and farm- 
ing have been used therapeutically. In private practice, where these matters 
can be individualized better, I have found that, if after a careful examination, 
patients could be assured that they had no “heart disease,” and that all the 
symptoms were the result of “upset nerves,” the cure was tremendously 
hastened. An explanation, not too scientific, but which offers a sufficient 
cause for the symptoms, is also of distinct benefit, especially to intelligent 
patients. What such patients dread most is sudden death from heart disease. 
With a satisfactory explanation for their symptoms they are usually re- 
lieved, sometimes permanently, of this fear. For the purpose of mental 
relaxation, as well as gradually increasing the amount of exercise, I suggest 
billiards, croquet, bowling, golfing, light farming and, in cases that are 
improving, rowing and even swimming in shallow water. Re-education of 
the tone of the cardiac nerves in order to regain stability is oftimes a slow 
and tedious process. Sudden sharp exercises should be avoided. The prac- 
titioner should never omit praise, even exaggerated praise, for good work 
done on the patient’s part in overcoming his timidity to exercise, and 
especially in continuing exercise and play, despite the presence of such minor 
symptoms as moderate tachycardia and slight precordial pain. CARDIAC NEUROSIS 
349 
Medicinally, I have found luminal, mixed bromids and suprarenal gland 
extract the best drugs. The bromids or luminal given in large doses at first, 
lessen mental irritability and anxiety. My usual procedure is to give luminal 
tablets of one and one-half grains twice daily, or one gram of the mixed 
bromids well diluted in water, three times a day after meals. Depending on 
the progress of the case, the dose is correspondingly diminished and finally 
stopped. In cases that are annoyed by sleeplessness, I add ten grains of 
chloral hydrate or eight grains of veronal every night for a few nights. I 
have seen no bad effects on the heart or on the individual from these proce- 
dures. The suprarenal gland I prescribe in one or two grain tablets, to be 
taken only when symptoms such as tachycardia or precordial distress become 
annoying. Paradoxical as it may seem, I prescribe this extract even when 
hypertension is present. Its beneficial effect seems to depend on its power to 
temporarily stabilize and decrease vasomotor instability by its action on 
the vasomotor center; it thus counteracts the cause of many of the symptoms. 
The effect of the drug is only temporary, hence with recurrence of symptoms, 
the dose should be repeated if necessary several times a day. 
To Summarize.—The irritable heart as observed in civil practice is 
similar to that found in soldiers. Vasomotor symptoms are more pro- 
nounced in the former. The etiological factors are similar, but because of 
training and war conditions, dormant and latent neuroses crop out oftener 
and are more readily evoked; consequently the cardiac syndrome is more 
violent and lasts longer. Infection is a factor only in so far as it induces 
and produces nerve and muscular fatigue, and psychasthenia. There is no 
pathologic change in the cardio-vascular system. The fundamental cause of 
cardiac neurosis with its various manifestations seems due to hyperexcita- 
tion of the sympathetic nervous system, either of its accelerator or vaso- 
motor arc, or both. 
It may be here remarked that in civil life many of the febrile respiratory 
affections, especially when epidemic as in influenza, are followed by cardiac 
neuroses. These are often regarded as due to a toxic myocarditis from 
the infection. Such respiratory affections, however, are extremely rarely 
followed by actual organic changes in the heart. The fundamental cause 
of the cardiac neurosis seems to rest upon conditions of general nerve fatigue 
incidental to sharp febrile invasions with their crises, and possibly also to 
disturbances of cardiac functions from the toxemia. 
THE GOITROUS HEART 
I shall consider only the circulatory phases of the goitrous heart, with its 
symptomatology, physical signs and medicinal therapy, and shall emphasize 
especially those features which have a bearing upon the general subject of 
cardiac neurosis. 
From the immense literature of the subject it is clear that etiological 
factors of the most diverse kinds can produce exophthalmic goiter, and, 350 
CARDIAC NEUROSIS 
with it, the goitrous heart. It may be of interest to briefly mention some of 
these factors; thus: Drinking waters, pregnancy, menstruation, climacteric 
and other endocrine disturbances, infectious diseases, change of type of a 
cystic goiter, sudden emotional disturbances, thyroiditis from direct inflam- 
matory continuity from a neighboring inflammatory focus, have all had their 
advocates. Although it is not known in what manner exophthalmic goiter 
is actually brought about, it seems proven that, once established, hyperthy- 
roidism from overproduction of toxic products or from their abnormally 
rapid absorption (thyrotoxicosis) is one of the important fundamental 
elements in the symptomatology. 
The goitrous heart may occur without the usual syndrome of exophthalmic 
goiter; the reverse occurs much more rarely. The characteristic finding 
in typical instances of the goitrous heart is violent, overforceful and rapid 
heart action. Similar to the physical sign already described in irritable 
heart (q. v.) but more pronounced and more constant in occurrence, is a rough 
palpable thrill not only at the apex but over the entire mitral area. This 
is commonly combined with an overforceful throb and impact of the ventricles 
against the chest wall. To a lesser degree there is a throb-like impact of 
the aorta and pulmonary artery against the examining hand flatly applied to 
the chest wall. The overaction of the great vessels and of the ventricles 
is often visible as well as palpable. Upon auscultation one hears a systolic 
thrill, or a split, cog-tooth-like first sound over the mitral area. The murmur 
and thrill are often transmitted to the carotids and to the axilla. The 
auscultatory and palpatory phenomena so resemble valvular disease that 
they are often mistaken for the latter; as a matter of fact, however, endo- 
carditis in the sense of vegetations is an extremely rare autopsy finding. An 
occasional autopsy instance of myocarditis, apparently the result of thyro- 
toxicosis, has been reported. The abnormal sounds and thrills over the 
mitral area are apparently due to vibrations of the valves from racing intra- 
ventricular blood-currents and whorls, in combination with violent ventricu- 
lar impact against the chest wall. A systolic murmur of varying intensity 
is also often heard over the aorta in the second right interspace. 
The violence and impact of the heart action frequently give the impres- 
sion of extreme enlargement; but with the exception of advanced cases with 
decompensation, orthodiascopic examination shows no marked difference in 
the size and form of the heart from the normal. Slight enlargements, 
however, apparently due to ventricular dilatation and dilatation of the aorta 
and pulmonary artery, are by no means infrequent. 
While tachycardia with a regular pulse rate of from ioo to 120 is the rule, 
pulse rates of 100 and under occasionally occur. In a few of the latter, I 
found a slightly shortened conduction time (Chapter X) from auricle to 
ventricle. In isolated instances there are brief periods of comparative 
slowing followed by similar periods of rapidity of the heart action, as if the 
heart came under alternate cyclic control of the vagus and accelerators, CARDIAC NEUROSIS 
35i 
respectively. Extrasystoles occasionally occur with the goitrous heart. 
Of comparatively frequent occurrence is the complete irregularity of the pulse 
(auricular fibrillation). The arrhythmia often occurs in attacks, especially 
in those in whom the heart rate is already rapid. The attacks may last 
several hours; they seem to bear no relationship to the general neurotic or 
other symptoms present. In those with permanent auricular fibrillation, the 
clinical phenomena of heart failure are apt to play an important part in the 
symptomatology. That this is not always the case, however, is demonstrated 
by a patient, a female of 54 with exopthalmic goiter who has auricular fib- 
rillation and who has been under my observation for several years. Despite 
the fibrillation she has had hardly any cardiac symptoms. She attends to 
household and other duties with scarcely any dyspnoea or palpitation. The 
only definite sign of decompensation was edema of the legs when she first 
came under my observation; this has gradually disappeared under digitalis 
therapy. 
Hypertension is a frequent accompaniment of the goitrous heart; systolic 
blood pressures of 180 and over are sometimes encountered. It is apt to 
vary considerably, however, from day to day. The usual pathological 
changes found in the kidneys in hypertension are absent. Apparently 
the fundamental cause of the hypertension is hyperirritability and instability 
of the vasomotor mechanism. 
Dyspnoea, often mild, is common. From the circulatory standpoint 
patients with goitrous hearts are usually incapable of severe exertion because 
the latter increases the violence and rapidity of cardiac activity. Emotional 
excitement is also very apt to have the same effect. 
Treatment will be discussed from the circulatory standpoint alone, 
although it is recognized that the cardiac symptoms are but part of the clinical 
syndrome. When in advanced cases the usual signs and symptoms of 
cardiac failure are present—dyspnoea, edema, pulmonary congestion, etc., 
the same regime of bed rest and cardiac remedies (Chapter XX) as in cardiac 
failure from other causes should be employed. In those with attacks of 
auricular fibrillation, I have found that digitalis neither curtails their duration 
nor does it have any effect upon the rate or violence of the cardiac arrhyth- 
mia. In those with permanent auricular fibrillation, also, digitalis does 
not exert its usual beneficial effect. Some years ago, for example, I observed 
a patient for some weeks with auricular fibrillation and a goitrous heart. The 
patient was severly decompensated. Thorough digitalization had not the 
slightest effect upon the irregular heart action, the cardiac symptoms or 
the clinical course of the case. The patient became progressively worse and 
died. Perhaps quinidine sulphate may be of use in these cases. Except in 
one instance, I have had no personal experience with it in the auricular 
fibrillation of exophthalmic goiter. Digitalis has no effect in lessening the 
tachycardia and violent heart action when the pulse is regular. One may 
perhaps surmise that the usual cardiac remedies cannot have their accus- 352 
CARDIAC NEUROSIS 
tomed effects until the basic etiological factor causing the goitrous heart can 
be controlled. Caffein and its derivatives (Chapter XX) are sometimes of 
value when edema is present. The bromides given in large doses occasion- 
ally have the power of reducing the cardiac hyperactivity, thus rendering 
the patient more comfortable: The drug has very little power in reducing 
the cardiac rate. When tachycardia disturbs the patient’s rest at night, 
veronal in 5 to 10 grain doses alone or in addition to a bromide mixture is 
of value. Luminal in 1 to 3 grain doses at night may also be tried. For 
flushes and other vasomotor symptoms, the extract of the suprarenal gland 
in one grain doses is beneficial even in the presence of hypertension. If 
the sensation of cold be a pleasant one to the patient, an icebag to the 
heart is occasionally of use in controlling the tachycardia. CHAPTER XIX 
CONGENITAL HEART DISEASE 
In previous chapters (Chapters I, II, IX) the various congenital mal- 
formations and their embryological characteristics, as well as their electro- 
cardiograms were described. The clinical findings and physical signs of the 
commoner and more important of these defects will now be discussed. In 
order to understand the special signs in individual lesions, it will be necessary 
to detail some of the general characteristics of congenital heart disease. 
Cyanosis (morbus ceruleus) is the most prominent obvious sign of congenital 
cardiac affections. It is by no means invariable; it is found especially in 
those in whom the defect has produced marked interference with circulation. 
Cyanosis, when typical, is present from birth, the infants are known as “blue 
babies.” It is most apparent in the fingers, toes, nose and ear lobes. 
Cyanosis, however, may not be present until several days or months after 
birth; even then, it may only make its appearance when the child cries vigor- 
ously. Both in infancy and later, cyanosis is increased by any factor which 
embarrasses the pulmonary circulation. Various degrees and extremes of 
cyanosis are encountered in congenital heart disease, from a slight bluish tint 
evident only on exertion, to a deep violaceous, bluish purple hue of the skin. 
The mucous membranes are then similarly discolored: The conjunctivas are 
deeply cyanotic, the buccal mucus membrane may be almost black. While 
the amount of cyanosis follows no definite rule regarding types of defects, it 
may be said that deepest cyanosis is found in pulmonary atresia and trans- 
position of the arterial trunks (Chapter II) while next in degree is congenital 
pulmonary stenosis. Cyanosis is moderate in biloculated and triloculated 
hearts. Cyanosis is least evident or indeed may be absent in patent foramen 
ovale, in patent ductus arteriosus and in septal defects, except in the ter- 
minal stages or upon exertion. Polycythemia is frequently present as a con- 
comitant of cyanosis. The red cell count may vary from 6,000,000 toas much 
as 9,000,000 in severe cases; the hemoglobin from 100 to 130 per cent. 
The cause of cyanosis in congenital heart disease has been in dispute for 
many years. It has been variously explained as due to mechanical admixture 
of venous and arterial blood resulting from abnormal communication between 
arterial and venous chambers or blood vessels; to interference with the return 
flow of venous blood in the pulmonary and systemic circuits or to insufficient 
aeration in the pulmonary circuit. While any one factor cannot always be 
singled out as the controlling one, it seems probable that the cyanosis depends 
fundamentally upon insufficient aeration, whether brought about by too 
353 354 
CONGENITAL HEART DISEASE 
much venous blood in the arterial circuit or by obstruction in the venous pul- 
monary circuit. Apparently also the circulation can accommodate itself to a 
varying degree of lack of aeration (that is, to lack of oxygen) without causing 
cyanosis: When oxygen deficiency reaches a certain limit, cyanosis results 
(Abbott). 
Clubbing, especially of the fingers, less of the toes, is another prominent 
sign of congenital cardiac defects. The terminal phalanges are the ones 
particularly affected, they appear somewhat flattened, the nails become 
convex. 
Dyspnoea is usually an early and prominent symptom in severe cases, 
whether cyanosis be present or not. Though dyspnoea be present in the 
cyanotic cases, it should be emphasized that cyanosis and dyspnoea do not 
necessarily go hand in hand. Cyanosis is often marked yet dyspnoea may 
be comparatively slight. Dyspnoea occurs in attacks, especially in the 
extremely cyanotic group. 
Hemoptysis is frequent in those with marked cyanosis. It may vary 
from slightly blood-tinged sputum to massive pulmonary hemorrhages. 
The latter, when occurring, may be a very alarming symptom and become 
immediately dangerous to life. 
GENERAL PHYSICAL SIGNS OF CONGENITAL DEFECTS 
The general physical signs, especially murmurs and thrills, vary not only 
with the type and degree of the cardiac defect and anomaly, but they also 
vary considerably with the state of cardiac compensation. With these lim- 
itations, and remembering that murmurs and thrills of congenital anomalies 
are neither characteristic nor constant (indeed, they may be absent), some of 
the typical murmurs will be described. 
Typical congenital pulmonary stenosis and patent interventricular sep- 
tum produce rough harsh systolic murmurs and thrills; in pulmonary steno- 
sis, the latter are more prominent over the upper left interspaces; in patent 
interventricular septum, over the midsternum. 
When present as isolated anomalies and of only moderate size, individuals 
with patent foramen ovale or interauricular septal defects rarely present 
clinical signs or diagnostic symptoms. Based upon necropsy evidences, it is 
apparent that patients even with large defects present no physical or clinical 
signs during life upon which a correct diagnosis might have been based. 
Cyanosis is rarely present; only occasionally are systolic or diastolic murmurs 
heard over the left third interspace. Orthodiascopic tracings present nothing 
characteristic. 
PATENT DUCTUS ARTERIOSUS (PATENT DUCTUS BOTALLI) 
This congenital defect is not rare. Cardiac symptoms are not always 
present; but when they are, the history usually shows that the patients were CONGENITAL HEART DISEASE 
355 
born cyanotic. The cyanosis is increased by crying, by exposure to cold, and 
in older children, by exertion and exercise. Upon percussion, a slight exten- 
sion of cardiac dullness in the second left interspace (Gerhardt’s area of dull- 
ness) can sometimes be mapped out. A rough systolic thrill is felt, and a loud, 
rough systolic murmur is heard most intensely over this area. The murmur 
is usually transmitted over the entire precordium and into the carotids. In 
addition, there is a loud diastolic murmur most prominent in the left upper 
interspaces near the sternum; the double murmur thus produced is called a 
“machinery murmur.” The presence and intensity of the diastolic murmur 
apparently depend upon the amount of blood which regurgitates through the 
Fig. 277.—Orthodiagram of a boy of 16 with patent ductus arteriosus. The curve of the 
pulmonary artery (P.A.) is extremely enlarged and flattened. 
patent duct, and, in its mechanism, resembles aortic insufficiency; indeed, 
capillary pulsation has been described as an occasional accompaniment of this 
lesion. The orthodiascopic picture in typical cases of patent ductus arterio- 
sis is that of a vigorously pulsating aortic arch, increased in size, beneath 
which is found an enlarged, flattened or protuberant overacting pulmonary 
artery. The duct itself is rarely visible because of its small size and of its 
frequent involvement in pericardial adhesions. This condition was found in 
two autopsy specimens I have seen. 
The following is an illustrative case, with clinical and orthodiascopic find- 
ings. Male, aged 16, tall and spare, was born a “blue baby.” He had 
scarlet fever when seven years old. He has never been able to play actively 
or to run. He frequently complains of palpitation; he has a productive 356 
CONGENITAL HEART DISEASE 
cough and has had hemoptysis. His face and extremities are cyanotic, his 
lips almost black, his fingers markedly clubbed. There are vigorous carotid 
and jugular pulsations, and a strong visible ventricular impulse; the apex is 
most prominent in the fifth interspace. A strong systolic pulsation is seen in 
the second and third left interspaces just outside the sternal border. There 
is a marked palpable carotid thrill felt almost up to the angle of the jaw. 
There is also a rough thrill most prominent in the second, third and fourth 
left interspaces, less marked in the second and third right interspaces. A 
definite (Gerhardt’s) area of dullness can be mapped out by percussion. 
Upon auscultation, a loud systolic murmur is heard over the entire precor- 
dium, and over the chest posteriorly. The murmur is especially loud and 
rasping over the second and third left interspaces and over the manubrium 
sterni. The fluoroscope reveals a vigorously overacting aorta and pulmo- 
nary artery; the latter is extremely enlarged and flattened (Fig. 277). The 
electrocardiogram shows a negative S deviation in the first and second leads, 
a marked evidence of right ventricular preponderance. 
PATENT INTERVENTRICULAR SEPTUM 
This congenital anomaly very rarely exists as an isolated defect. Cyano- 
sis is the most prominent clinical sign; its degree depends on the size of the 
interventricular aperture and on the presence of other congenital defects— 
usually pulmonary atresia. The extremities are clubbed, there is a marked 
coarse systolic thrill to be felt, and a corresponding rough murmur to be heard 
over the entire precordium; the maximum intensity of the murmur and thrill 
is over the lower sternum and xiphoid and occasionally over the epigastrium. 
There is also vigorous epigastric pulsation. In the orthodiagram the left 
auricle and ventricle are hugely dilated and rounded, the heart is also enlarged 
to the right; because of atresia of the pulmonary artery, its pulsation may be 
slight or absent. 
The following case illustrates a fairly well compensated patient with a 
patent interventricular septum. 
F. M. female, aged 9, the youngest of three children was born a “blue 
baby.” Her face was always duskier when she cried. She carl now walk 
fairly well and can even climb stairs slowly without dyspnoea. The child is 
well nourished and well developed. Inspection of the neck reveals no hyper- 
activity of the carotids or jugulars. There is moderate cyanosis of the hands 
and lips, and slight clubbing of the phalanges. Inspection of the chest shows 
slight overaction of the apical region. Upon palpation a rough systolic thrill 
is felt over the mitral area; this is not transmitted to the carotids. Upon 
auscultation, a loud rough systolic murmur is heard chiefly over the mid- 
sternum and to its left; from here it is transmitted, although much less 
intensely, over the entire anterior surface of the chest: It is heard CONGENITAL HEART DISEASE 
357 
faintly posteriorly. Orthodiascopic tracing revealed slightly enlarged 
aortic and pulmonary curves, and a somewhat hypertrophied left ven- 
tricle. Slow walking caused neither dyspnoea, tachycardia nor increase 
in cyanosis. 
A unique instance of patent interventricular septum in a child with con- 
genital dextrocardia also came under my observation. The history and 
findings are as follows: 
Male, age years, was the youngest of nine children; he had measles 
and pertussis when two years old. The mother said the child had always 
been “blue” and “short of breath,” but never sufficiently dyspnoeic to be 
Fig. 278.—Orthodiagram of a child with congenital dextrocardia and patent inter- 
ventricular septum. It shows an enlarged and broadened aortic curve and enlarged 
“right” (see footnote p. 358) auricular curve, coalescence of enlarged and knob-like “left” 
auricular and ventricular curves, and absence of pulmonary prominence. 
bed-ridden. The child appears well nourished. The extremities, lips, face 
and conjunctivae are cyanosed; the conjunctival blood vessels are congested; 
there is distension of the superficial veins of the chest and abdomen. The 
fingers and toes are clubbed. There is a vigorous, heaving systolic impulse 
in the right axillary line and in the epigastrium. A strong, marked systolic 
thrill can be felt over the entire precordium; it is roughest and most prominent 
at the lower end of the sternum and in the epigastrium. Over the former there 
is a loud, rough systolic murmur, tailing away over the remainder of the chest, 
anteriorly and posteriorly. The murmur is transmitted along the carotids. 
There is no Gerhardt’s area of dullness in the second and third right inter- 358 
CONGENITAL HEART DISEASE 
spaces. The liver and spleen are not transposed; the gastro-intestinal canal, 
as shown by bismuth roentgenograms, is in its normal position. Fluoroscopy 
of the chest reveals an enlarged and vigorously pulsating aorta. Beneath it, 
the usual pulsating curve representing the pulmonary artery, is absent. In 
its stead, there is a tremendously dilated, prominent and knob-like “left”* 
auricle. The “left” ventricular shadow is also very much enlarged; its area 
cannot be definitely separated from the superimposed auricle, although 
their non-synchronous pulsation can be readily determined. The “right” 
auricle is enlarged; beneath it, the beginning of the “right ventricular” 
shadow is seen deeply depressing the 
diaphragm during inspiration. From this 
finding, it is probable that the “right” 
ventricle is enlarged. The orthodiagram 
(Fig. 278) shows a greatly dilated aorta, 
rounded and prominent, and coalescence of 
the “left” auricular and “left” ventricular 
curves. The “right” auricular curve is 
also considerably enlarged. The electro- 
cardiogram shows the typical downward 
deviation of the P, S, and T waves in the 
first lead, pathognomonic of congenital 
dextrocardia (Chapter IX). A diagram- 
matic representation of the probable circu- 
lation in this case is shown in Fig. 279. 
Fig. 279.—Diagram of probable 
cardiac circulation in the patient 
DL. Solid arrows = main circula- 
tion; dotted arrows = minor circula- 
tion. R.A., right auricle; R.V., 
right ventricle; L.A., left auricle; 
L.V., left ventricle; P.D.A., patent 
ductus arteriosus; P.C., pulmonary 
circulation; S.P.A., stenosed pul- 
monary artery. 
CONGENITAL AORTIC STENOSIS 
Extreme narrowing of the aorta at the 
isthmus (a physiologically narrow area 
about one inch above the root of the aorta) is not an unusual congenital 
anomaly; occasionally aneurismal dilatation of the aorta finally results. 
Congenital aortic stenosis sometimes forms the nidus for a later streptococcus 
viridans infection. Thus, a young man of 21 had had “heart trouble” 
following a severe scarlet fever infection in childhood. For years, he had no 
cardiac complaints. He had occasional mild attacks of hematuria. Shortly 
before I saw him, he had fever and indigestion for a few days. Examination 
revealed loud systolic murmurs over the aortic and mitral areas. Fluoro- 
scopic examination (Fig. 280) showed a pulsating aneurism of the first portion 
and arch of the aorta, and an enlarged left ventricle. The Wassermann 
reaction was negative. The diagnosis of probable streptococcus viridans 
infection affecting the aorta and mitral valves was made. The aneurism was 
* To avoid confusion in the description of this case of congenital dextrocardia, “left” 
and “right” are used in the sense as usually applied to the normal heart in its normal 
position; that is, “left” will refer to the larger, and “right” to the smaller ventricle, with 
their corresponding auricle. •CONGENITAL HEART DISEASE 
359 
accounted for as probably due to congenital narrowing of the aortic isthmus. 
Later, streptococci were found in the blood. An autopsy was obtained. The 
aortic and mitral valves were thickly covered with typical viridans vegeta- 
tions, there was a moderate congenital stricture of the aorta at the isthmus. 
Fig. 280.—Orthodiagram of a patient with streptococcus viridans infection, a double 
mitral lesion and aortic aneurism. At autopsy, moderate congenital aortic stenosis was 
found. CHAPTER XX 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
The question of occupation for cardiacs is discussed in a succeeding 
chapter (Chapter XXII). The subject of special types of diet in cardio-renal 
disease is also subsequently described (Chapter XXI). I shall here limit 
myself to diet in valvular disease. Since persons with severe cardiac failure 
rarely have much appetite, it is as a rule safe to follow the patient’s modest 
wishes regarding food and drink. In those with moderate heart failure the 
general dictum should be laid down that it is better to give food and drink 
frequently (about every 2 to 3 hours) instead of the usual three meals, and 
that the food should be bland. Special restrictions regarding salt and fluid 
intake are required only when edema and kidney complications are present 
(Chapter XXI). Bland food consists in the main of milk, cereals, gruels, 
clear soups, soft, boiled, coddled and poached eggs, boiled chicken, lamb 
chops, white meat of fish boiled or broiled, fresh and stewed fruits, thin cocoa, 
potatoes, creamed carrots, custards, white bread and butter, plain cake. 
The question of tobacco, coffee and alcoholic drinks and diet in obese car- 
diacs is discussed in succeeding chapters. 
Intravenous 10 per cent, solution glucose injections have recently been 
advised in heart failure, on the theory that they assist cardiac nutrition by 
producing a hyperglycemia, a procedure which presumably restores the 
proper sugar balance in the cardiac tissue, particularly in the junctional 
tissues (Chapter I). The amount injected is from 200 to 300 c.c. A few 
favorable reports have been published. I have had no personal experience 
with this method. 
The usual list of drugs used in cardio-vascular disease includes some which, 
upon careful clinical and pharmacological investigation, have been found of no 
or only problematical value. Only those of recognized value will be here 
described. 
DIGITALIS 
Digitalis or foxglove was used empirically for very many years. Our 
knowledge of its action has recently been enhanced by the use of graphic 
tracings. There still exists some difference of opinion as to the method of its 
action. According to the most reliable clinical and experimental data, 
digitalis action may be divided into several components: (1) A direct effect 
upon the cardiac contractile power, which increases the pumping or driving 
force of the heart. There is good ground for the assumption that this is due 
360 DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
361 
to direct action upon the cardiac musculature. (2) A marked inhibitory effect 
on the nervous mechanism of the heart by vagal action on the cardio-inhibi- 
tory center. (3) Effect upon the specialized junctional tissues (the atrio-ven- 
tricular conduction system). This threefold action makes it difficult to decide 
at times how digitalis produces the arrhythmia often found when the drug is 
given in full therapeutic doses. Thus, digitalis can slow the whole heart 
(auricles as well as ventricles) and can cause prolonged conduction time from 
auricle to ventricle by its primary inhibitory vagal affect. It may slow the 
ventricles alone in one or two ways, either by vagus inhibitory effect (thereby 
producing various grades of heart block (Chapter XI), or by some direct 
action upon the ventricular musculature. Extrasystoles occasionally 
induced by digitalis therapy are probably caused by the drug acting as an 
excitant of cardiac irritability. Auricular fibrillation can also be caused by 
digitalis. Unique instances of auricular standstill due to digitalis have been 
described. Blocked auricular beats and alternation represent other types of 
digitalis arrhythmias. Some of these digitalis irregularities can be made to 
disappear by the use of atropine subcutaneously, an evidence that they are 
due to abnormal vagus excitation. Some patients are hypersensitive to the 
neurotropic action of the drug and very soon develop cardiac irregularities. 
Thus, a young man of 23, with a typical rheumatic mitral regurgitant lesion, 
entered the hospital with the usual signs of decompensation. His pulse was 
regular. Several courses of digitalis were required to restore compensation. 
Each time, the beneficial effects of the drug were coincident with the inception 
of auricular fibrillation and coupled rhythm. After digitalis had been dis- 
continued for a few days the pulse again became rhythmical. Of added 
interest is the fact that this patient complained of such extreme hunger and 
hunger pangs with the fibrillation attacks that he could not rest unless fre- 
quently fed during the night. In another connection, I have pointed out that 
such symptoms are probably due to vagus excitation. They are of practical 
importance because the advent of these peculiar symptoms is a warning 
that sufficient digitalis has been given. Such manifestations must be differ- 
entiated from the nausea and vomiting common in digitalis poisoning. 
Hunger and hunger pangs precede the usual vomiting by two or three days; 
hence vomiting can be avoided by discontinuing medication in those rare 
instances in which hunger symptoms follow the administration of digitalis. 
As already indicated, the apparently contradictory effects of digitalis are 
explicable on the basis of its twofold action: That upon the neurogenic control 
of the heart, thus affecting the rhythm; and that upon the contractile power. 
Although these effects are usually coincident, the former may precede the 
latter by one or several days. In other words, arrhythmias occasionally occur 
before decompensation is relieved. I do not regard such early appearance of 
digitalis arrhythmias as any contraindication to further digitalis medication. 
The circulation is only rarely affected by these irregularities; the drug should 
be pushed in the usual fashion until the beneficial effects upon the 362 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
circulation are noted. If then the drug be stopped the arrythmias soon 
disappear. 
Digitalis in Auricular Fibrillation and Flutter.—The drug exerts its great- 
est influence clinically on the irregular ventricular action commonly met with 
in auricular fibrillation; this seems due to a vagus effect upon the auriculo- 
ventricular junctional tissue whereby many of the discordant auricular 
impulses are blocked. As a result, ventricular action becomes steadier, 
slower and more regular, changes which are indicated by the pulse. In 
auricular flutter (Chapter XI), digitalis is employed with a double object; to 
benefit the cardiac failure which is usually present, and to attempt to change 
flutter to auricular fibrillation. When the latter is accomplished, the drug 
is stopped; normal rhythm is then often resumed. Many instances of the 
final change of flutter to sequential rhythm after the use of digitalis have been 
described. However, I have observed one case of auricular flutter accom- 
panying acute rheumatic endocarditis without decompensation, in which the 
drug did not have this effect. The flutter appeared and disappeared several 
times pari passu with the febrile rheumatic manifestations. It finally 
remained absent with the subsidence of the rheumatism. One year later the 
pulse was still rhythmical. In other words, digitalis in large doses had no 
effect on the arrhythmia nor on the restoration of normal rhythm. Such 
negative result might have been anticipated in this instance, for the effect of 
digitalis in changing auricular flutter to normal rhythm probably depends 
chiefly upon the relief of decompensation, a marked feature in most cases of 
flutter. 
With reference to auricular fibrillation occurring in cardiac decompensa- 
tion , it remains to be added that the patient must be kept under the influence of 
digitalis for months or even years, in order to attain proper control of ven- 
tricular action and pulse rate. In this manner, individuals can be kept in a 
good or fair state of compensation for many years. Properly supervised, 
this long continued medication can be carried out with no harmful after- 
effects. 
Digitalis in Heart Block.—-If cardiac failure co-exists, complete heart 
block in itself is not a contraindication to the use of digitalis, for the drug 
cannot increase the dissociation already present. As an instance, I have 
reported a case of complete heart block in which the cause of the dissociation 
could not be ascertained during life. Digitalis was administered several 
times until vomiting resulted. There was no change in the dissociation, 
the only effect of the drug being a subjective thumping sensation in the chest. 
In incomplete heart block digitalis has been regarded as contraindicated 
because of the danger of development of complete heart block. This conver- 
sion has been reported in two cases. One came to autopsy. Lesions involv- 
ing the conduction system and part of the sino-auricular node were found; 
but similar pathological changes in an instance of auricular fibrillation and 
heart block, lasting many years, have been described, and digitalis played no DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
363 
role in the arrhythmia. The second case was one of severe, long-continued 
decompensation. Digitalis was given for several days; heart block and auric- 
ular fibrillation occurred and continued until death a few days later. These 
two reports do not offer sufficient evidence that digitalis alone was the cause 
of the block. In neither case was there clinical evidence of any ill effects 
from the presumed induction of complete heart block by the drug. It 
appears to me that the possible danger of changing an incomplete to complete 
block with digitalis may be averted by the judicious administration of 
atropine. The latter should be given in full physiological doses, administered 
as frequently as the digitalis, but about one half an hour before it; for example, 
atropine may be given before, and digitalis, after meals. 
In one of my patients with complete heart block, in whom, through 
a nurse’s inadvertence, digitalis had been continued for a long time, auricular 
fibrillation and coupled rhythm were produced in addition to the dissociation. 
These arrhythmias were not followed by any demonstrable change in the 
clinical condition. 
Digitalis and Alternation.—Alternation (Chapter X)—alternate weak 
and strong pulse beats occurring in a rhythmical pulse—is usually indicative 
of a badly impaired myocardium. Thorough digitalization is indicated. 
Pulse alternation itself is also occasionally caused by digitalis. Because of 
its usual serious prognostic import when not produced by drugs, digitalis 
alternation might a priori be considered as contraindicating its further use. 
However, the following shows its seeming harmlessness, when alternation is 
produced by digitalis. A case has been reported by Mackenzie in which 
alternation and extrasystoles were the result of digitalis; despite this, the 
drug was continued and the patient showed gradual improvement. In other 
words, alternation so produced is apparently not dangerous and in itself does 
not warrant discontinuance of the drug. 
Digitalis and Extrasystoles.—When extrasystoles are of functional origin 
and are not associated with cardio-vascular disease, digitalis is not indicated, 
although occasionally so employed on account of its power to increase vagus 
inhibition. When extrasystoles accompany cardiac failure, they apparently 
depend upon some profound nutritional disturbance of the cardiac muscula- 
ture. Digitalis is then definitely indicated, for with restoration of compensa- 
tion, the extrasystoles often disappear. This favorable action may directly 
depend upon improvement of the intracardiac circulation with consequent 
improvement of cardiac nutrition. 
Coupled Rhythm and Digitalis.—Coupled rhythm is a cardiac irregularity 
in which every normal beat is followed by an extrasystole (Chapter X). 
Coupled rhythm—an occasional result of digitalis medication in auricular 
fibrillation—is usually regarded as a definite warning to stop the drug. 
In order to decide this question for myself, I kept several patients under 
the effects of the drug for a varying length of time after coupled rhythm had 
been induced. Most of the patients were elderly individuals with cardio- 364 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
sclerosis. In each case, digitalis in moderate doses was continued for several 
weeks after the beginning of coupling. The patients were allowed to walk 
about. They all felt quite comfortable, there were no ill effects. Improve- 
ment was particularly noticeable in one individual who was under treatment 
for a second severe break in compensation. Besides cardio-sclerosis, he had 
had emphysema with profuse expectoration for years. The typical gross 
pulse irregularity of auricular fibrillation was present. Digitalis produced 
coupled rhythm within five days. Medication was continued for two weeks 
longer, although the ventricular rate fell to 40 per minute. Cyanosis dis- 
appeared, expectoration ceased; the patient stated that he had not been so 
free from cough and expectoration for years. Digitalis was then discontinued; 
coupled rhythm and improvement remained; the patient passed from obser- 
vation a few weeks later. 
Digitalis Vomiting. Administration of Atropin with Digitalis.—Digitalis 
vomiting has been ascribed to irritation of the gastric mucosa, but this scarcely 
explains the marked variations in susceptibility to the emetic action of the 
drug. Some patients vomit almost immediately, others only after massive 
doses have been given. A very suggestive explanation is found in experiments 
in cats in whom the alimentary tract was removed; none the less, all the accom- 
panying manifestations of emesis occurred when digitalis bodies were injected 
intravenously. These experiments strengthen the belief that digitalis vomit- 
ing is probably due to central nerve action and not to peripheral irritation. 
This fact is of practical clinical importance because, in susceptible patients, 
small initial doses of digitalis may be advantageously combined with atropine 
sulphate in doses of 3<L50 of a grain; subsequently the digitalis dosage may be 
increased gradually to the usual maximum. In this manner I have succeeded 
in administering digitalis to some patients in whom even small doses ordi- 
narily produced vomiting. Details of the combined administration of digi- 
talis and atropine are given in the following illustrative cases: 
Male, age 60, suffered from chronic bronchitis, dyspnoea and asthmatic 
attacks for many years. The patient was cyanotic; physical signs of chronic 
bronchitis, emphysema and myocarditis were present; the pulse was com- 
pletely irregular (auricular fibrillation). The tincture of digitalis and Karrell 
diet (q. v.) were given. At the end of one week he was very much im- 
proved; digitalis was discontinued because of vomiting. After two weeks the 
drug was again given with the same result. On the third administration it was 
combined with atropine sulphate, grain later, grain given sub- 
cutaneously. In this manner digitalis was administered continuously for 
several weeks without inducing vomiting and with excellent clinical results. 
Female, age 27 years, had auricular fibrillation, a double mitral lesion 
and a decompensated heart. Fifteen minims of tincture of digitalis, three times 
a day were prescribed. Upon three occasions, after three days administration, 
medication was discontinued because of nausea and headache. On two subse- 
quent occasions digitalis was combined with atropine sulphate. Once, one- DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
365 
fiftieth of a grain was given subcutaneously when nausea was already present, 
and continued in doses of H50 grain three times a day. Upon the second 
occasion, atropine and digitalis were given uninterruptedly for two weeks 
without nausea. Decompensation was relieved. 
Female, age twenty-six, had a rheumatic mitral regurgitant lesion. 
There were cardiac pains and broken compensation for several months. 
Tincture of digitalis, one drachm daily in divided doses, was given. Usually 
after a few days’ medication was discontinued because of vomiting and head- 
ache, and the decompensation which had been temporarily relieved, soon 
recurred. Caffeine, digipuratum and tincture of strophanthus were substi- 
tuted for the tincture of digitalis without effect. Finally the latter was 
combined with atropine sulphate, grain given internally, three times a 
day. This was continued in two weekly periods, with interruptions, for 
many months, and the patient showed improvement. Her appetite remained 
good. She finally decompensated again and died. 
Digitalis and the Kidneys.—It is now definitely known that the diuretic 
action of digitalis in clinical conditions in man is due directly to the relief 
of heart failure and to an improvement of the general circulation in which the 
kidneys take part. Digitalis does not cause increased diuresis in normal 
individuals nor in circulatory failure without edema. Furthermore, it 
causes no increased urine output in kidney disease, with or without edema, 
in which the heart itself is not implicated. Since, however, myocarditis is 
often associated with kidney disease (Chapter XVII), the beneficial effects 
of digitalis as a diuretic can be readily appreciated. 
The preparation and dosage of digitalis have long been matters of dispute. 
I prefer the tincture, or an infusion freshly prepared from potent leaves. A 
good tincture kept in a properly stoppered bottle will retain its strength 
for several months. The objection to the infusion is that it must be freshly 
prepared, requires large dosage, and is more unpalatable than the tincture. 
The tincture and infusion are therapeutically I have also found 
digipuratum or as they are now called, digitan tablets an excellent and reliable 
preparation; it is standardized in frog heart units. One tablet of one and 
one half grains each is equivalent to fifteen minims of the tincture. It some- 
times seems more efficacious than the tincture, especially when administered 
in chronic cardiac disease. Another excellent preparation is the powdered 
leaf given in two to four grain doses four times daily. Recently, Hatcher has 
divided digitalis into a chloroform-soluble and a non-chloroform-soluble 
fraction. The latter is thick, tarry and much less active than the former. 
The chloroform-soluble fraction (now also called the purified tincture) has 
shown very active digitalis properties when used experimentally in animals; 
it has also shown quick absorbability and powerful digitalis action when used 
in man. The dose and preparation, however, have not yet been standardized. 
Variability in absorption is no doubt a large factor in variability of the 
action of digitalis when given by mouth. By the effect of digitalis on the 366 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
T wave (flattening or inversion of the T wave in Leads I and III, Chapter IX) 
it has been shown that beginning digitalis action may occur even within a few 
hours of the administration of the drug. Digitalis dosage should be regulated 
by the degree of cardiac failure and by the type of cardiac disease. In 
general, very little if any good is accomplished by beginning with doses very 
much below the average, partly because small doses pass so readily out of 
the system. The usual total amount of the tincture required for a full thera- 
peutic effect varies from one to one and a half ounces taken over a period of 
about one week. The average daily amount is one drachm given in fifteen or 
twenty minim doses. It is best administered undiluted because it has 
been found that the admixture of water may interfere with absorption. If 
urgency demands it or if one wishes to digitalize more rapidly, very much lar- 
ger initial amounts can be safely given. Eggleston, for example, has given 
initial doses of several drachms of the tincture with great benefit and with no 
untoward symptoms except occasional nausea and vomiting. In urgent 
cases I have also often administered the tincture in drachm doses four or five 
times daily; no ill effects were observed. The usual dose of the infusion is 
from one half to one ounce given three or four times daily. This amount can 
likewise be considerably increased if quick effects are desired. 
The therapeutic effect of digitalis in patients with rhythmical heart 
action becomes evident rather by improvement in the signs of decompensa- 
tion (lessened dyspnoea and edema, increased urine output) than by any 
marked slowing of the pulse. In auricular fibrillation with a completely 
irregular and rapid pulse, the therapeutic action is shown in addition, by 
the elimination of the irregular and weaker ventricular contractions, the frus- 
trane ventricular activity which produces no pulse beats (so-called pulse 
deficit). In consequence, ventricular rhythm becomes steadier and slower, 
and the pulse tends to become correspondingly regular. Some observers 
advise discontinuance of the drug or decrease of its dosage when this result 
has been achieved. This advice should be followed only if the drug has 
produced some degree of intoxication such as nausea or vomiting, if decom- 
pensation has been relieved, or if the usual amount of digitalis (about one 
ounce of the tincture) had already been taken; for it occasionally happens 
that the typical discordant arrhythmia of auricular fibrillation comes under 
sudden control after a few doses, while signs of heart failure continue or 
quickly recur if digitalis is then stopped. In other words, with the exceptions 
noted, the administration of the drug should be continued until decompensa- 
tion is restored. 
In decompensated cases with a rhythmical pulse and moderate tachy- 
cardia, the latter is sometimes reduced to normal rapidity with gradual 
restoration of compensation by the administration of digitalis. This is 
occasionally brought about by the inception of such digitalis arrhythmias 
as sinus slowing, sino-auricular block and blocked auricular beats. As 
already indicated, a moderately slow pulse rate is in itself no contraindica- DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
367 
tion to the further administration of the drug, although the type of digitalis 
arrhythmia under discussion is apt to be coincident with the full therapeutic 
effect. 
Older patients with cardio-sclerosis and decompensation usually require 
larger and longer-continued digitalis doses than younger individuals with 
cardiac failure. The former are often comfortable with ventricular rates 
between 45 and 50. Such elderly individuals should be kept under full digi- 
tal effects by giving them several courses of the medication over a series of 
weeks. This is best accomplished by giving one ounce of the tincture (about 
one drachm daily) for the first week; it is then discontinued for the following 
week. In the third week about one half ounce of the tincture will be required. 
It should then be again discontinued for a week. In the succeeding weeks 
somewhat smaller doses are adequate. In this manner, the heart can be 
safely saturated with digitalis and the patient kept under its influence for a 
long time. 
Much has been written about the cumulative effect of digitalis and the 
dangers therefrom. Variability in gastric absorption may be one of its 
causes. Unless the usual mild toxic symptoms are meant—headache, nausea, 
arrhythmias—digitalis cumulation is an infrequent phenomenon, and its dan- 
gers have undoubtedly been exaggerated. Perhaps the “ cumulative effect ” 
is best explained by our present knowledge of the persistence of digitalis 
action, described below. Digitalis has been administered in innumerable 
instances for weeks and months, and even years, with no dangerous effects. 
In only one instance did I observe symptoms which might be interpreted as 
due to an actual cumulative effect. A woman of 40 with a double mitral 
lesion, orthopnoea, anasarca, cyanosis and auricular fibrillation entered the 
hospital in extremis. Infusion of digitalis in one half ounce doses was given 
every four hours. After three ounces had been taken, the patient’s condi- 
tion improved. Vomiting, a drop of ventricular rate to 60, and cold face 
and extremities suddenly developed. Hypodermic injections of strychnine 
and caffein had no effect upon this condition. Despite these apparently 
alarming symptoms, the patient felt quite comfortable, orthopnoea temporarily 
disappeared, cyanosis decreased, and the urinary output markedly increased. 
The patient died two days later from cardiac failure. 
„ As shown electrocardiographically by the action on the T wave the per- 
sistence of the action of digitalis in a thoroughly digitalized subject lasts two 
weeks or more after its discontinuance. This persistent action seems due 
to fixation of a small amount of the drug in the cardiac tissue (Eggleston). 
It substantiates the clinical observation that, after thorough digitalization, 
the effects of the drug can be maintained by giving much smaller doses. 
It is conceivable that there is one possible danger in administering digitalis 
in unnecessarily large doses over long periods; that is, the production of ven- 
tricular fibrillation (Chapter IX), an arrhythmia which, so far as we now 
know is universally fatal. We possess neither experimental nor definite clini- 368 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
cal grounds for the assumption that ventricular fibrillation may be caused by 
digitalis. I predicate it upon the power of digitalis to incite all types of 
cardiac irregularities, and upon the occasional clinical observation that 
patients who are apparently improving under full digitalis dosage sometimes 
die quite suddenly, with no sufficient cause at autopsy for the sudden fatal 
termination. Some of these deaths are assumed to be due to ventricular 
fibrillation. 
The Use of Digitalis in Valvular Lesions.—Dogmatic distinctions were 
formerly made regarding the various types of valvular lesions in which digi- 
talis was indicated or contraindicated. Abundant clinical experience has 
shown that, although not followed by equally good results, digitalis may be 
given in all forms of cardiac failure, regardless of the valve affected. In 
rhythmically beating hearts, digitalis is not usually followed by the same 
rapidly beneficial effects as in auricular fibrillation. Its chief value in the 
former lies in the occasional reduction of the cardiac rate and particularly 
in strengthening ventricular contractions. In aortic lesions with decompen- 
sation and left ventricular hypertrophy, digitalis is not as beneficial as in 
mitral lesions. This may depend upon several factors: In aortic lesions there 
is less systemic congestion and edema, except in the final stages of decompen- 
sation; the cardiac rate is very susceptible to neurogenic and other influences 
which cause tachycardia (Chapter XV); finally, digitalis may not exert 
its full action upon the fibers of an extremely hypertrophied muscle. In 
mitral lesions, tachycardia is not as common; congestion and edema more 
common, conditions more readily influenced by digitalis through increase of 
the cardiac contractile power. 
The value of digitalis in cardio-sclerosis with hypertension and coronary 
disease has often been questioned; indeed, for many years, hypertension was 
regarded by many as a distinct contraindication to digitalis. Careful clinical 
study has shown, however, that digitalis, in therapeutic doses does no* gu- 
larly raise the blood pressure; when occasionally increased, the increase bears 
no relation to the time of administration or dosage of the drug. I have treated 
patients with hypertensive disease, many of whom had a systolic blood pres- 
sure of over 200 m.m. of mercury, and I have never observed any pressure 
increment which could in any way be correlated with digitalis administration. 
In fact, in those in whom cyanosis and dyspnoea were the chief manifestations, 
and in whom digitalis gave relief, the blood pressure was often lowered. This 
may be because cyanosis itself acts as an excitant to the vaso-constrictor 
center and thus raises blood pressure. This disturbing factor is eliminated 
by the beneficial effect of digitalis upon the general circulation. 
Coronary disease had previously been regarded as a contraindication to 
the use of digitalis, upon the assumption that it caused coronary spasm. 
There is no actual experimental evidence of this. Clinically, I regard some 
types of coronary disease with precordial pains as especially amenable to 
digitalis therapy because of the necessity of increasing the intra-cardiac DIET, DRUGS AND OTHER THERAPY IN CIRCULATORY DISEASE 
369 
circulation. While often disappointed in its results because of the probable 
occluded lumen of the coronaries (Chapter XXIII), I have seen no harm from 
its use. 
Another important consideration in digitalis therapy is the question of its 
use in endocarditis and pericarditis during the acute stages. When the heart 
rate is increased as the result of these acute inflammatory processes, digitalis 
has no effect in diminishing the pulse rate. This is also true of other febrile 
diseases, such as pneumonia, grippe, etc. Hence the use of digitalis for the 
persistent tachycardia of inflammatory conditions is very apt to be followed 
by disappointing results. 
In this connection I wish to point out one reason for the futility of digi- 
talis in chronic pericarditis with dense and extensive adhesions. The latter 
act mechanically like a vise, hindering normal systole and diastole. I 
observed one instance in an adult who had rheumatic arthritis and irregular 
temperature for several weeks. Auricular fibrillation was present. The 
obscure physical signs—a scarcely audible or palpable apex beat—pointed to 
myocarditis as the probable cardiac lesion. A roentgenogram of the chest 
showed a somewhat enlarged cardiac shadow. Digitalis was given for several 
weeks with no effect upon the slowly increasing heart failure or upon the 
fibrillation. At necropsy the valves were normal, the myocardium not exten- 
sively diseased, there was a tightly adherent pericardium that encircled and 
fixed the entire heart. In another instance, a young adult male, dyspnceic 
and cyanotic, with polyserositis of unknown origin, X-ray plates showed 
definite, sharply defined calcareous plaques in the pericardium. Auricular 
fibrillation with a fairly regular and slow ventricular rate was present. The 
cardiac impulse and sounds were weak. Here, also, it seemed probable that 
the vise-like action of an adherent and thickened pericardium was an impor- 
tant etiological factor in the cardiac failure and cyanosis. Digitalis had no 
influence upon the symptoms or arrhythmia. 
Speaking from a broad clinical aspect, in decompensated valvular and 
cardio-vascular disease in which infection is either quiescent or non-existent, 
I have found the following classification of value from the viewpoint of the 
probable effect of digitalis medication: 
1. Mitral lesions with rhythmic hearts: Improvement slow unless in the 
presence of marked visceral congestion. Rest is apparently the largest factor 
in the improvement. 
2. Mitral lesions with auricular fibrillation: Unless decompensation is 
extreme or long continued, improvement is very rapid under digitalis. The 
irregular cardiac activity is quickly controlled, and, with it, decompensation is 
usually promptly relieved. 
3. Aortic lesions with slight or moderate ventricular hypertrophy: The drug 
is not of much value, rest is the important factor. 
4. Aortic lesions with extreme ventricular hypertrophy: Reaction to 
digitalis not good, possibly because there is not sufficient healthy cardiac 370 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
muscle upon which the drug can act. Even if auricular fibrillation be present, 
digitalis is not apt to be followed by beneficial results. 
5. Cardio-sclerosis with decompensation: Those with cardiac failure and 
edema, with or without hypertension, are apt to react well to Karrell diet, 
(q. v.) and digitalis and theobromine sodium salicylate administered on alter- 
nate days. In cardio-sclerosis and hypertension with uremia and no edema, 
digitalis has very little effect in the relief of decompensation. 
Summing up the effect of digitalis medication, the following conclusions 
seem warranted: 
1. The best single criterion of the amount and duration of digitalis 
administration is its clinical effect. 
2. The beneficial effect of digitalis in rhythmically beating hearts depends 
chiefly upon producing increased contractile power of the cardiac musculature. 
3. The gradual production of arrhythmias is usually coincident with full 
clinical effects. 
4. If decompensation demands the continuance of digitalis, the rapid 
onset of arrhythmias does not contraindicate its further use. 
5. Atropine sulphate, grains to three times a day, given inter- 
nally or subcutaneously at the beginning of medication, occasionally prevents 
nausea and vomiting in susceptible individuals. 
6. The hypertension of cardio-vascular disease does not contraindicate 
the use of digitalis. 
7. To derive clinical benefits quickly, digitalis should be given in full 
therapeutic doses. In urgent cases, very large initial doses can be given. 
8. When digitalis acts promptly in small doses, the effect is likely to be 
temporary. For permanent improvement, thorough digitalization is required. 
9. Digitalis occasionally produces epigastric sensitiveness and hunger 
pangs which appear to be due to heightened vagal tone. These symptoms 
precede vomiting by one or two days, and indicate a full therapeutic digitalis 
effect. 
10. The effect of digitalis on the T-wave of the electrocardiogram has 
been described in another connection (Chapter IX). It should be emphasized 
here that the effect is simply electrocardiographic evidence of action of the 
drug upon the cardiac musculature and is not by any means necessarily 
concomitant with the full clinical effect of the drug. The inverted or flat- 
tened wave produced by digitalis does not invalidate any of the above 
conclusions. 
Tincture strophanthus.—This possesses no advantages over the tincture i 
of digitalis. Its disadvantage is that it varies considerably in strength, as I 
well as in absorbability; hence it may occasionally produce a sudden unex- 
pected toxic effect, even when given in ordinary therapeutic doses. 
Crystalline Strophanthin is a most powerful digitalis glucoside. The best 
preparation is that put up in glass ampoules containing 1 c.c. of a 1 per cent, j 
solution. The dose is from 10 to 15 minims; this should be slowly injected, ! DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
371 
preferably intravenously. It is of remarkable efficacy, particularly in the 
acute heart failure of auricular fibrillation. Within a very short time, some- 
times even after one hour, the injection may be followed by slower and more 
regular ventricular activity, with a correspondingly good effect upon dyspnoea 
and cyanosis; frustrane beats may quickly disappear, edema show some 
evidence of clearing up, and diuresis increase. If the urgency of the case 
demand it, the injection may be repeated at the end of 24 hours. In other 
words, these injections in a remarkably short time can produce the effect 
which only occurs after several days of the usual method of digitalis adminis- 
tration. On the other hand, the effect is more evanescent; hence, in the 
decompensation of cardiac disease, it is necessary to follow up these injections 
by digitalis given in the usual manner. Strophanthin is also indicated in 
acute cardiac failure from cardio-renal disease, especially if pulmonary edema 
is present. There is one caution necessary respecting strophanthin; namely, 
it is contraindicated, or should be used very sparingly, if the patient is already 
digitalized, otherwise very serious toxic symptoms may immediately follow. 
For example, in a patient with mitral regurgitation, extreme decompensation 
and rhythmical pulse, who had already been thoroughly digitalized, this 
precaution was not heeded by the physician in attendance; an injection of 1 
c.c. of strophanthin was immediately followed by auricular fibrillation, a 
condition which lasted until death a few days later; strophanthin undoubtedly 
hastened the fatal termination. 
Tincture of Squills.—In doses of 15 to 30 minims this drug has an action 
on the circulation similar to digitalis. Like the latter, it may produce sinus 
arrhythmia and heart block, apparently by increased vagal inhibition. 
Given in large doses, it has an effect upon auricular fibrillation and upon the 
T-wave similar to digitalis. It possesses no advantages over digitalis, and is, 
in addition, irregular and uncertain in action. Squills is often prescribed in 
pill form as a diuretic. 
Apocynum.—Apocynum or Canadian hemp, given in fluid or solid extract, 
has been studied to a slight extent; it has no regular or marked effect in 
improving the circulation. 
Quinidine.—Quinidine is a quinine derivative, a stereo-isomer of quinine. 
Quinidine or its more soluble salt, quinidine sulphate had found its way in 
medicine because there had been occasional sporadic clinical observations 
that quinine had the power of restoring the normal rhythm in cases of auricular 
fibrillation (Wenckeback). Frey, in 1918, was the first to study the subject 
systematically. More recent reports (Levy, Lewis and others) deal with 
quinidine from the experimental and clinical standpoints with the aid of the 
electrocardiograph. As a result, the following conclusions of the effects 
of quinidine sulphate seem warranted. One effect is directly on the auricular 
musculature by which it lowers the sino-auricular rate, depresses and prolongs 
the conduction time from auricle to ventricle, and lengthens the refractory 
period of the auricular musculature. The second effect is a neurogenic one 372 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
upon the vagus; the drug paralyzes, releases or decreases vagus control. 
It thus appears that in this regard digitalis and quinidine have opposite 
effects, for, as already noted, digitalis increases vagus inhibition. 
Auricular fibrillation is now regarded as basically due to blocking of a 
continuous “circus” wave of excitation (Chapter XI), the normal method of 
the spread of impulses through the auricles. Although the circus wave con- 
tinues on in its circuitous path, its blocking depends upon differences and 
defects in conductivity, irritability and refractory periods (Chapter III) of 
various portions of the auricular musculature: The consequence is what we 
know clinically as auricular fibrillation (Chapter XXI). When quinidine is 
administered in auricular fibrillation, its most important effect in restoring 
the normal rhythm is its power to lengthen the refractory period in the 
auricles. The mechanism of auricular fibrillation may perhaps be aptly com- 
pared to a circuit whose path has been irregularly interrupted by hurdles of 
all kinds and sizes; the hurdles represent the blocking and breaking up of a 
single wave into fibrillatory waves (auricular fibrillation). Quinidine removes 
these by allowing a sufficient interval for the refractory phase to pass off, so 
that the circus wave may again re-enter and pass on smoothly across the 
gaps. 
It has been shown by electrocardiograms with leads taken directly from 
the chest (that is, electrodes fastened directly over the precordium instead 
of to the extremities in the usual way) that one of the first effects of quinidine 
is to partially regularize the fibrillatory waves; the latter have a tendency 
to become more regular and slow, somewhat similar to what is seen in impure 
flutter (Figs. 159, 161), indeed actual flutter may result. Before normal 
rhythm is restored by quinidine in auricular fibrillation the first clinical 
evidence of its action is usually a preliminary phase of increase of the ven- 
tricular rate, an increase of tachycardia; in fact tachycardia sometimes 
persists even after the normal rhythm has been restored. This effect of 
quinidine seems due to release of vagus inhibition. Occasionally the tachy- 
cardia is violent, with the natural result that cardiac output is decreased and 
dyspnoea results. This, and the fact that quinidine can cause gastrointes- 
tinal disturbances—nausea, vomiting and diarrhoea—show that the drug has 
its dangers. Another occasional occurrence coincident with the restoration of 
normal rhythm is cerebral embolism from auricular thrombosis due to sudden 
slowing of the circulation in the auricle. Finally, quinidine exceptionally 
produces a shower of ventricular extrasystoles—ventricular tachycardia. 
These do not always occur at the beginning of quinidine medication nor is 
there any clinical method of detecting them except by electrocardiograms. 
Since we know from animal experiments that ventricular tachycardia is 
sometimes a forerunner of death from ventricular fibrillation (Chapters 
X, XI), and since in clinical auricular fibrillation, we are already dealing 
with a disordered rhythm and a diseased heart, caution is demanded in the 
use of quinidine. Indeed, I feel that the more extended and safe use of DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
373 
quinidine in general medicine, and not in hospitals alone to which its use is 
now practically limited depends upon some method of knowing in advance 
which patients are likely to react by ventricular tachycardia, a dangerous or 
possibly even fatal arrhythmia. 
Patients present favorable and unfavorable drug susceptibility (idio- 
syncrasy) to quinidine as indeed they do to almost all powerful drugs. Thus, 
with some, normal rhythm is restored after a comparatively small dose. 
Others again show the bad effects—especially, significant increase of tachy- 
cardia and dyspnoea—after small dosage. As a rule, normal rhythm is 
restored on the day succeeding the quinidine therapy. Sometimes the 
rhythm remains regular for a day or two, and then fibrillation recurs. In 
favorable cases, the normal rhythm remains permanently; “permanent’” 
is here used in a limited sense of months, since the drug has not been employed 
for a sufficient length of time to use “permanent” in its true sense. Fairly 
frequently, the normal rhythm is disturbed by occasional extrasystoles; 
electrocardiograms show that they are usually auricular (Chapter X) in type, 
an evidence of the selective action of quinidine on the auricular musculature. 
Clinical Observation and Dosage (see also Cardio-vascular Clinics).— 
Before quinidine sulphate is used, the first all-important step is to properly 
digitalize the patient where decompensation is present and digitalis had not 
yet been employed. When the full effects of digitalis have been induced, 
and not until then, quinidine sulphate administration may be begun. I have 
tabulated the results of quinidine sulphate in some 40 cases of auricular fibril- 
lation in hospital and consultation practice. Of these about one half were 
old individuals with marked cardio-vascular and cardio-renal changes, some 
with, others without hypertension (q. v. Cardio-vascular Clinics). Many 
were decompensated. The net result of quinidine administration was restora- 
tion of the normal rhythm for a day or two in a few of these old people. A 
few complained of nausea, one or two vomited. Several exhibited an 
increase of tachycardia but none to an alarming extent. Some of the patients, 
had two or three courses of quinidine but the results were the same. I had not 
expected permanent restoration of normal rhythm in these advanced cases of 
cardio-sclerotic disease, for it was my clinical impression that quinidine was of 
most value in younger individuals with valvular disease and without far 
advanced degeneration of the heart muscle. 
Quinidine is administered in various doses and intervals. My own rou- 
tine consists in giving six 5 grain capsules as follows: The first capsule is 
given early in the morning. If at the afternoon visit, there is no contra- 
indication two other capsules are given an hour apart. The patient is again 
visited the same evening. If then normal rhythm has not been restored or if 
there are no untoward symptoms—no vomiting, diarrhoea, undue tachycardia 
or dyspnoea, 5 grain doses in hourly intervals is repeated for three more doses. 
Thus 30 grains are given. I have found this method and dosage satisfactory, 
and up to the present, have observed only an occasional alarming effect from 374 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
the drug thus administered. The method seems safe because any important 
drug idiosyncrasy (except possibly a shower of ventricular extrasystoles) will 
show itself with the first 5 or 15 grains, a dose which seems well within 
conservative limits. 
I have also tabulated my results in eight patients whom I saw in con- 
sultation but who remained at home under the care and supervision of their 
own family physician. I felt that the risk was justified, for unless quinidine is 
used more widely by the general practitioner, it can have only a limited use in 
medicine. Besides, it is often impossible in private practice to demand 
hospitalization for a few days in order to test the efficacy of a drug; indeed, 
the request alone is apt to frighten off many patients. The family atten- 
dants in the eight cases to which I refer were physicians of average ability, none 
of whom had any special knowledge of cardiology. When necessary, first 
digitalis and then quinidine were given according to the method just out- 
lined. The physician was told to visit the patient after the first and after the 
third dose (i.e., after 5 and again after 15 grains had been taken). The 
special possible dangers—significant increase of tachycardia, dyspnoea, vom- 
iting, nausea and diarrhoea—were emphasized. An exceptional case of 
cerebral embolism with regularization of the rhythm may naturally occur 
both in private and in hospital practice; hence this in itself is no contra- 
indication to its use in private practice. Not more than 30 grains was 
administered. 
Of the eight cases in private practice thus supervised and treated, most 
were middle aged: Six had mitral disease; two had cardio-sclerosis. The 
rhythm was permanently restored in three, temporarily in two; it had no 
effect on the remaining three. In none did the quinidine have any serious 
untoward effect. In one, two courses of quinidine were necessary in order 
to restore the normal rhythm permanently. 
Where normal rhythm has been restored and occasional extrasystoles 
occur, it offers definite clinical evidence that the quinidine is beginning to lose 
its effect. In such individuals, quinidization should be continued. There is 
here no established method of dosage or procedure. Depending upon the 
number of extrasystoles, my present practice is to give the drug in 5 grain 
doses two to four times weekly. 
Since many patients with auricular fibrillation when properly digitalized, 
are comfortable, sometimes for years, it is a fair question to ask why quinidine 
should be given at all. First, the patients lose the annoying sense of palpi- 
tation, almost always present in fibrillators. Furthermore, it is a clinical 
fact that if the normal rhythm be restored, most patients have much more 
cardiac reserve and can be more active without becoming uncomfortable. 
Thus, in one of my cases, tachycardia and dyspnoea continued despite rest 
and several courses of large doses of digitalis. The patient was practically an 
invalid and was scarcely out of the house for months. When the rhythm 
became regular, the patient was soon enabled to take up her old activities, DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
375 
including household duties, climbing stairs, walking in the open, etc. The 
rhythm has now been normal for several months. 
As a summary of indications and contraindications to quinidine, the 
following seem permissbile in our present knowledge. 
Patients with comparatively recently established auricular fibrillation 
and with valvular disease in whom there is no or but moderate cardiac 
enlargement react best to quinidine. 
Patients with advanced hypertrophy from valvular or cardio-sclerotic 
disease do not react favorably. The normal mechanism is rarely 
restored. 
Patients who complain early of cardiac discomfort, and in whom none-the- 
less, quinidine is pushed, are especially prone to develop more serious com- 
plaints—embolic infarcts, more severe tachycardia, showers of extrasystoles 
(R. I. Levy). 
Patients whose decompensation has not been relieved by properly 
directed therapy because of their cardiac muscle exhaustion, are prone to 
develop mural thrombi in the auricles under quinidine, and hence also 
embolic infarcts in various organs (R. I. Levy). 
Signs of peripheral venous thrombosis should be looked for in the veins of 
the lower limbs of individuals to whom quinidine is to be given. Such throm- 
boses indicate a tendency to intravascular clotting, hence the drug is contra- 
indicated in such patients. 
There are three chief dangers to the use of quinidine. (i) Auricular 
thrombosis with cessation of fibrillation and consequent slowing of the blood 
current. Some clinical indications of patients in whom this is likely to 
occur have been given. 
2. Significant tachycardia with precordial discomforts. Quinidine regu- 
larly produces a preliminary, though slight tachycardia. When tachycardia 
is marked it contraindicates further use of the drug. 
3. Ventricular extrasystoles (premature contractions) during the time 
that the auricles are still fibrillating. Unfortunately, there is no clinical 
method of detecting these; they require graphic control for their detection. 
The danger lies not in isolated extrasystoles, but because they come in runs 
and showers (ventricular tachycardia) and thus possibly presage ventricular 
fibrillation and death. 
Caffein and Its Derivatives.—Caffein produces vasoconstriction by its 
action upon the vasomotor center; it also has a slight effect upon the heart 
itself. Its main therapeutic value rest upon action on the kidneys. Since 
cardio-vascular disease includes the kidneys, a discussion of caffein and its 
derivatives is important. 
Caffein acts primarily as a diuretic, thereby increasing the output of 
urine. The manner of its action is still in dispute; some ascribe it to an 
irritating effect upon the renal epithelium, others to an effect upon the renal 
circulation. Caffein increases principally the watery constituent of the 376 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
urine; there is also an increased output of solids, especially of sodium chloride, 
and to a lesser degree, of the nitrogenous constituents. 
The best method of caffein administration is in the form of caffein sodium 
salicylate, a readily soluble salt. A 20 per cent, solution of this salt in 
distilled water lends itself admirably to hypodermic administration; the dose 
is from 15 to 30 minims. 
Theobromine Sodium Salicylate.—This salt produces more marked diure- 
sis than caffein and is in general preferable to the latter. Another advantage 
is that it has no effect upon the vasomotor center, and hence does not produce 
blood pressure changes. The drug is administered in 7 to 15 grain (0.5 to 
1 gm.) doses three or four times daily, well diluted in water. Because of its 
unpleasant taste, it can be given in wafers. If the medication upsets the 
stomach, it may be given in smaller doses more frequently. It can also be 
administered by rectum by the Murphy drip method. Finally, it can be 
given intravenously according to a method which I developed. 
The intravenous method seems of importance because the drug is par- 
ticularly indicated in uremic conditions with vomiting, delirium and distur- 
bances of the sensorium in which theobromin cannot be given by mouth, 
or if so given, the amount absorbed is very slight or nil. I use a 5 per cent, 
solution, the percentage ordinarily used in animal experimentation. Pharma- 
cological examinations show that the specific gravity of a 5 per cent, solution 
at 2o°C. is 1.0228, and its alkalinity equivalent to that of a 2.4 per cent, solu- 
tion of sodium bicarbonate. Sodium bicarbonate in this concentration, or even 
stronger, is sometimes given intravenously in diabetic coma. A 5 per cent, 
theobromin sodium salicylate solution heated in a closed vessel at 96°C. 
for one hour, and then for another half hour shows slight yellowish discolora- 
tion and a very slight loss of alkalinity, but remains perfectly clear. Sterili- 
zation does not alter the solution. The dose I usually employ is 15 grains, 
i.e., 20 c.c. of 5 per cent, solution. In one instance, 30 grains (40 c.c. of the 
solution) were given in a single dose. The stock solution should be resteril- 
ized by boiling immediately preceding each injection. If the entire solution 
enters the vein, there is no local reaction. If a few drops find their way into 
the subcutaneous tissue, some induration, ecchymosis, or slight pain lasting 
a few days sometimes follows. In one instance, through a misunderstanding 
by one of the house staff, the solution was injected subdermallv; a local skin 
slough and ulcer resulted. The injections are never followed by systemic 
reactions. The solution is readily prepared and sterilized. While 20 c.c. of 
a 5 per cent, solution is a convenient standard, the dosage can be modified 
to suit individual requirements. The ordinary dosage can be given intra- 
venously daily for several days. 
It is known that the diuretic function of the kidney becomes fatigued by 
long-continued theobromine administration, hence it is advisable to give the 
drug in the customary oral method in courses of two or three days with 
intermissions of similar periods. Theobromine sodium salicylate (diuretin) DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
377 
is particularly indicated in the dropsy of cardio-renal disease. Given on 
alternate days with digitalis, it often enhances the action of the latter, not 
only in cardio-renal but also in purely valvular disease. As an adjuvant, 
theobromine is often combined with the Karrell diet. Because of its impor- 
tance, this diet and the method of its administration require detailed 
description. 
The Karrell Diet consists in daily administration of 800 to 1000 c.c. of 
milk; it is preferably given in glassfuls of six ounces every three hours. 
This is usually termed a “Karrell day.” On Karrell days the patient 
should be in bed or at rest. The milk should be sipped slowly. Patients 
rarely complain of thirst, but occasionally become so hungry that they suffer 
from hunger pangs and faintness. Under these conditions, I allow them 
dry toast, crackers, perhaps also an apple or orange in amounts just sufficient 
to curb extreme hunger. An excellent routine procedure in moderately severe 
edema of cardio-renal origin is Karrell diet and theobromine sodium salicylate 
for two days, alternating with digitalis, and an appropriate renal diet (Chap- 
ter XXI) with somewhat restricted fluid intake for the succeeding two days. 
In most cases, I believe it advisable to continue theobromine therapy and 
Karrell diet at intervals, long after edema has disappeared and the patient 
feels well. These intervals should be gradually lengthened; for example, 
Karrell diet and theobromine may be given for a day, at first twice 
weekly, then once weekly, then once monthly. In this manner it seems 
possible to retain and to continue for months, and occasionally for years, the 
improvement gained by the initial, more intense therapy. In some instances 
of cardio-renal disease with extreme anasarca, the intensive treatment out- 
lined—digitalis, theobromine and Karrell diet—yields remarkable results: 
Losses of from 10 to 15 pounds during the first week, and from 20 to 40 pounds 
in several weeks, are not exceptional. Coincident with reduction of edema, 
other serious symptoms such as semistupor, dyspnoea, cyanosis and manifes- 
tations of hypertension often decrease or disappear. Beneficial results 
derived from this therapy are most marked in those in whom myocardial 
insufficiency is a prominent clinical feature. 
As a modification of the Karrell diet and as a method of promoting diure- 
sis in patients in whom the urinary output is approximately normal in 
amount, I have occasionally restricted the fluid intake to but 500 c.c. daily. 
The liquids allowed are water, sweetened or unsweetened lemonade, and 
coffee and tea with very little milk. When necessary, only sufficient solids 
of the kind above mentioned are added to control severe hunger. Patients 
rarely complain of thirst; when present, it is partially relieved by small 
quantities of cracked ice, or by rinsing the mouth with water. I give this 
restricted and modified Karrell diet for two days, with theobromine sodium 
salicylate in 7 to 15 grain doses to the amount of 45 grains daily. Then 
follow two days of digitalis with appropiate cardio-renal diet and a slightly 
restricted fluid intake. By this method, I have occasionally achieved results 378 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
which did not follow the ordinary Karrell diet. Older patients with long- 
standing edema frequently voided from 60 to 80 ounces, and occasionally 
ioo ounces, on the day succeeding the second theobromine day, the usual 
time of most marked diuretic action. Coincidentally, edemas quickly 
cleared up, and cyanosis and especially dyspnoea very rapidly and markedly 
improved. These secondary results may be due not only to the elimination 
of water, but also to simultaneous elimination of toxic substances. 
Strychnine.—In animal experiments, strychnine has been shown to have a 
vaso-constrictor influence, and hence has been assumed to be of value in low 
blood pressure and shock. However, careful observations of its effect on the 
circulation in health and in cardiac disease have shown no influence upon the 
urinary output, edema, blood pressure or heart rate—the usual criteria of 
any effect on the circulation. The claim, formerly made, that in some 
intangible way strychnine acts as a circulatory “tonic” by its influence upon 
the nervous system is not substantiated by any clinical evidence. It may, 
however, act as a “nerve tonic” in the sense of promoting a feeling of 
well-being and of lessening the fatigue that often accompanies cardiac 
disease. 
Vasodilators.—These consist mainly of nitroglycerin, nitrate of potas- 
sium and sodium, amyl nitrite, erythrol tetranitrate and mannitol hexani- 
trate. Amyl nitrate is the emergency drug of this class. Nitroglycerin, the 
drug most often prescribed, acts as a peripheral arteriolar dilator. The 
usual dose is 3-foo grain three times daily. It may be given hypodermically 
or by mouth. In circulatory disease it is chiefly used for lowering blood 
pressure in hypertension and for the relief of precordial pains. It is believed 
that the latter is accomplished by the relief of spasm of the coronary arteries. 
In some cases of hypertension I have administered as much as of a grain 
of nitroglycerin subcutaneously three times daily with little or no effect 
upon hypertension or precordial symptoms. These and other inconstant 
results following nitroglycerin may be accounted for by the various amounts 
of arterial thickening and consequent variations in dilatability of the arteri- 
oles. In edema of the lungs and in hypertension and nephritis, nitro- 
glycerin in large doses (from to 3-fo gr- hypodermically), combined with 
the usual cardiac remedies, occasionally relieves the overburdened heart by 
its effect upon the peripheral circulation. 
Nitroglycerin is of most value in cardio-sclerosis with moderate hyperten- 
sion and labile vasomotor mechanism (Chapters XVII, XXIII). Its 
administration may then result in fairly long continued lowered blood pressure 
and in relief of symptoms. If the use of nitroglycerin be limited to such cases, 
it becomes a very valuable drug. If, however, it is used in continued hyper- 
tension with advanced coronary disease, nitroglycerin is apt to be followed 
by disappointing results for reasons already mentioned. Erythrol tetrani- 
trate and mannitol hexanitrate have a slower and more continued action 
than the others of the vasodilator group. DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
379 
Aromatic spirits of ammonia in teaspoonful doses, Hoffman's anodyne, 
in one half teaspoonful doses on sugar or in water, and benzyl benzoate in one 
half teaspoonful doses in water are drugs of occasional value in combating 
some of the troublesome flushes and occasionally also some of the precordial 
pains found in those with hypertension and vasomotor symptoms. 
Camphor.—This drug, especially in the form of camphor in oil, given 
hypodermically, has been a favorite circulatory remedy for many years, 
especially on the continent. Careful clinical observation, however, has 
shown that it has no demonstrable influence upon the circulation, for it 
exerts no influence on diuresis, blood pressure or pulse rate. In animal experi- 
mentation there is a slight effect upon the pulse pressure. The use of spirits 
of camphor in depression of the nervous system, as, for example, in fainting 
spells, is sometimes of value because of its reflex action emanating from the 
local effect of camphor on the gastric mucosa. 
Alcohol.—Discussion of alcohol is here limited to its effect upon the 
circulation. In animals, alcohol slightly increases cardiac contractility. 
When given in large quantities in human beings, alcohol produces a marked 
fall of blood pressure by its depressant action upon the vaso-constrictor center 
and upon the heart muscle. Small quantities of alcoholic beverages occa- 
sionally seem to augment cardiac contractility in decompensated cardiac 
disease, but the effect is slight and inconstant, and its value problematical. 
Aconite.—Recent investigations have shown that the strength of the 
tincture of aconite, the preparation usually used, varies considerably, and 
that, even when properly standardized, the dose ordinarily administered 
is much too small. Aconite does not slow the heart rate in cardiac disease. 
Its presumed therapeutic value is based upon experimental investigation in 
animals in which cardiac rate, contractility and blood pressure are lowered 
as the result of a central vagus effect. When given in very large doses, the 
drug sometimes increases ventricular irritability. This has been shown by 
the production of extrasystoles by pressure over the pneumogastrics in 
patients who had been given the drug. 
Sparteine.—This drug is the alkaloid of the common broom. Formerly 
it was used as a cardiac tonic because it was presumed to have an action like 
digitalis. When injected into animals, it slows the heart and slightly raises 
the blood pressure. Clinically, these effects have not been observed; it must 
be added that careful investigation of its action is lacking. The dose advised 
ranges from % to 5 grains; probably two grains of sparteine sulphate is a 
safe dose for an adult. 
Suprarenal Extract—Adrenalin.—Its vaso-constrictor action, especially 
when given intravenously, is well known. It may be used in circulatory col- 
lapse accompanied by a sharp fall of the systolic blood pressure, or in hyper- 
tension with rapidly falling blood pressure, the latter indicating myocardial 
insufficiency. Injection of the drug in these conditions is sometimes followed 
by decided, though temporary improvement. I have found the drug of 380 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
special value in various types of vasomotor instability with or without 
tachycardia. Adrenalin has also been advised in so-called constitutional 
hypotension (Chapter XVIII), a condition in which cardiac failure is absent. 
The main symptoms in these individuals are those referable to vasomotor 
disturbances. The hypotension itself rarely requires medication, but the 
accompanying symptoms may be relieved by adrenalin. The best method 
of administration is the standard sterile solution in the strength of i to 1000; 
the dose is from 15 to 30 minims given internally, or, preferably, hypoder- 
mically or intravenously. The drug may also be given in tablet form in 
one grain doses. 
Morphine.—This drug produces slowing of the heart rate by its effect 
upon the medullary center. Injections in dogs are sometimes followed by 
complete heart block. In man, morphine is a cardiac “stimulant” only in 
the sense that, by its effect on the central nervous system, the patients 
become less restive and irritable. Thus regarded, it is often an excellent 
aid to other drugs in such acute circulatory conditions as paroxysmal tachy- 
cardia, acute onset of auricular fibrillation, and sudden cardiac failure with 
dyspnoea. It should then be given hypodermically in full therapeutic doses. 
Morphine is almost invaluable in the pulmonary edema that accompanies 
attacks of coronary occlusion. 
Bromides.—These are indicated in tachycardia from any cause, or in 
those in whom extrasystoles cause subjective sensations. In the former, 
where morphine may also be indicated, the bromides enhance and prolong 
the morphine effect. Even though the bromides do not reduce the cardiac 
rate, they are sometimes effective in relieving the patient of many of his 
subjective sensations. 
Luminal.—This is a new synthetic drug. I have used it frequently to 
control restlessness and sleeplessness in cardiac disease as well as in annoying 
tachycardia from any cause. The usual dose is one and one half grains, given 
in tablet or powder form once or twice daily. I have also employed luminal 
sodium in doses of one and one half grains hypodermically in various cardiac 
conditions accompanied by dyspnoea and tachycardia in which hypnotics 
like morphine or codeine did not seem indicated. On the whole the results 
were gratifying. One may also increase and prolong the quieting effect of a 
small dose of morphine by combining the latter with sodium luminal: Two 
separate injections must then be given. 
Other sedatives which may be employed to combat restlessness and sleep- 
lessness are chloral hydrate and veronal (barbitol); they may be given alone 
or in combination with small doses of morphine or codeine, or with the bro- 
mides. Contrary to the usual opinion, chloral hydrate and barbital have not 
a sufficient depressant action on the circulation to contraindicate their 
use. 
Acetate of Potash and Soda.—Their diuretic action is usually slight 
and depends upon the non-metallic salt—the acetate—for its effect. The DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
381 
dose is from 15 to 30 grains, given in solution every two or three hours. It 
is occasionally of advantage to alternate these drugs with the more active 
diuretic, theobromine sodium salicylate. 
Saline Cathartics.—Brisk catharsis is sometimes of value in starting diu- 
resis. The best saline for this purpose is the sulphate of magnesia. 
Calomel.—The drug is sometimes of benefit in cardiac dropsy; it is of less 
value in edema of renal origin. The dose generally recommended is the 
heroic one of three grains three times daily for two to four days. After an 
interval of a few days, unless some contraindications exists, it may be repeated 
in the same dosage. Its action is acribed to direct stimulation of the renal 
epithelium. I have had no experience with calomel given in this manner. 
Venesection.—This procedure has a limited sphere in plethoric cases with 
cyanosis, dyspnoea and threatened or actual pulmonary edema. It possesses 
a double advantage: From the circulatory standpoint, its chief advantage 
probably lies in a reduction of venous pressure, for the latter is usually 
abnormally high in the type of patients just cited. Bleeding also removes 
toxic products. The amount to be withdrawn must be individualized; the 
usual amount if 400 to 600 c.c. 
Multiple Skin Puncture.—This procedure is sometimes of great value 
when massive general anasarca exists for a long time and does not respond to 
the usual therapeutic measures. The procedure is as follows: The skin of 
the leg is cleansed with soap and warm water and then washed with a bichlo- 
ride of mercury solution. For the punctures a rather large-sized, triangular 
surgical needle (glover’s needle) is used. The needle and the physician’s 
hands should be sterile. The needle should be firmly grasped with the fingers 
one half inch from the needle point. It should then be quickly plunged into 
the skin, especially of the leg and dorsum of the foot up to the level held by 
the fingers. From 50 to 100 punctures in each extremity should be made. 
The punctures must be made very rapidly and should not take more than 
about two minutes. The legs should then be swathed in large, clean bath 
towels. It is surprising to see how much fluid can be drained off in this 
manner. The patients are relieved not only locally but also from the general 
circulatory standpoint. The skin punctures often give cardiac medication 
a better change for therapeutic results. To emphasize a necessary modifica- 
tion of the procedure, two cases deserve mention. In one, massive drainage of 
fluid from both extremities was followed by semi-stupor lasting twenty-four 
hours; in the other a similar semi-stupor developed into unconsciousness and 
death in three days. In both, the loss of the fluid per se (oligemia) seemed 
accountable for the symptoms. I would therefore advise, where anasarca 
and decompensation are marked, that there be an interval of several days 
between puncture of the two extremities. 
Paracentesis of the thorax and abdomen for hydrothorax and ascites 
respectively has its appropriate place for the removal of pleural and perito- 
neal exudates when these are due to cardiac failure and cannot be removed by 382 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
circulatory drugs. The removal of such accumulated fluid by paracentesis 
often gives drugs a much better chance for beneficial results. 
Autogenous and Stock Vaccines, and Sensitized Sera.—I have employed 
autogenous vaccines in a number of cases of endocarditis due to the strepto- 
coccus viridans (Chapter XV), but have not been able to discern any benefit 
from their use. There was no effect upon the temperature or toxic symptoms, 
nor was there any change in the clinical course of the disease. In a few cases 
that came to necropsy in which this therapy was employed, nothing was 
found to indicate that the vegetative process on the valves was checked in 
in the slightest degree. 
I have also administered stock vaccines in a small number of cases of 
endocarditis which seemed clinically of streptococcic origin but in whom the 
organism was not isolated from the blood. Although I observed no ill effects 
from the injections, they had not the slightest therapeutic result. 
In a number of instances of streptococcus viridans infections, I employed 
serum derived from horses sensitized to the coccus. The effect of such injec- 
tions was also entirely negative. 
Blood Transfusions.—Except for the temporary relief of anemia, I have 
seen no lasting beneficial effects of transfusions in streptococcus viridans 
infections either in the fever or the clinical course of the case. My experi- 
ence with transfusions from donors immunized with the streptococcus viri- 
dans is limited; in the few cases I observed, there was no appreciable benefit. 
Colloidal Silver Preparations.—Interest in the use of silver salts in septic 
conditions has been revived by the administration of various colloidal silver 
salts in the treatment of acute rheumatic and bacterial endocarditis. I have 
observed a few cases in which the silver colloids were injected intravenously. 
In one, a streptococcus viridans infection, twenty injections were given at 
two and three day intervals without benefit; the patient died with the symp- 
toms of cerebral embolism. In another case, a child with acute rheumatic 
endocarditis, a few injections were followed by a rather sharp fall in tempera- 
ture. In the same ward, I had under observation at the time a male adult 
of twenty who suffered from an acute rheumatic outbreak, and from acute 
endocarditis and pericarditis with effusion. The cardiac involvement ran a 
very stormy course: The temperature reached 105° and remained between 
104° and 105° for one week; dyspnoea, chiefly due to the very large amount 
of pericardial exudate, was extreme. The patient received neither silver 
injections nor serum therapy of any kind. After one week the temperature 
fell suddenly, signs of pericardial effusion quickly disappeared, the patient 
rapidly convalesced with the physical signs of a permanent aortic lesion. 
Thus are contrasted two cases of an acute endocardial infection both of 
whom rapidly convalesced, one with colloidal silver injections, the other 
without any attempt at specific therapy. The inference is clear that there 
is no proof in the first case that the injections caused a recession of the acute 
endocarditis. In the enthusiastic reports regarding the use of colloidal DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
383 
silver in endocarditis, I have found no instance of “ cure ” which could not be 
explained upon the basis of an acute endocarditis which had quickly run 
its febrile course, or upon the basis of a longer duration with the usual 
remissions. In other words, I do not believe that the intravenous use of 
silver preparations is warranted in any type of endocardial infection. 
Massage—Passive Motion.—As a result of careful observation of many 
cases of cardiac disease, it is my conviction that patients are allowed in bed 
or at absolute rest too long after compensation has been restored or after an 
inflammatory process in the heart has run its course (Chapter XXII). 
Two or three weeks after the quiescence of inflammatory symptoms and after 
restoration of compensation constitute, I believe, the average time for com- 
plete rest. After that period the judicious use of massage, active and passive 
motion, and exercise aid the circulation by slowly increasing heart work, and 
produce a more rapid return to normal circulatory conditions. No form of 
exercise or massage should be pushed far enough to cause dyspnoea, dis.ress, 
rapid heart action or unpleasant subjective symptoms. Massage and passive 
motion also have some value as added therapeutic aids in long continued 
cardiac decompensation in bedridden patients. The chief contraindication 
in such individuals is extreme continued dyspnoea. In such cases, massage 
should be limited to the extremities and to the muscles of the back; the 
abdomen and the anterior part of the chest should not be included. When 
edema and venous stasis are present, it may be of advantage to stroke the 
limbs in the direction of the venous and lymphatic current, i.e., from the 
periphery to the trunk. This sometimes decreases the local engorgement. 
The kind of massage to be employed in cases of restored compensation 
must be individualized. Usually light superficial massage alone is tolerated. 
Deep vigorous massage and kneading of the muscles produces discomfort and 
pain, and, by exciting the patient, may cause rapid heart action and dyspnoea. 
The amount of passive motion must be similarly studied in every individual 
case. Flexion and extension of the smaller joints—fingers, wrists, ankles and 
toes—should at first be practiced gently once daily; subsequently the larger 
joints (knees, elbows, hips and shoulders) should be flexed and extended. If 
these procedures are not followed by pain, cyanosis, tachycardia, exhaustion 
or dyspnoea, more vigorous and oft-repeated passive motion is indicated. 
This does not necessarily require the services of a trained attendant; in any 
case, however, it should at the outset be carried out under the direct super- 
vision of the physician, so that he can carefully observe any possible ill 
effects following its use. 
Calisthenics—Medical Gymnastics—Resistance Exercises.—These are 
occasionally indicated while the patient is still in bed. They require the more 
active cooperation of the patient and make more demands upon the circula- 
tory reserve. Rapid breathing, dyspnoea, increased and prolonged pulse 
rapidity, or subjective feelings of faintness and exhaustion are the best clinical 
guides that gymnastics or exercise have exceeded safe limits and have caised 384 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
marked diminution of the cardiac reserve power. It should be emphasized 
that these treatments are only added therapeutic aids, and cannot replace 
therapeutic drugs when indicated. The use of dumb-bells and of carefully 
graduated exercises as measured by the ergostat are also of value. Resis- 
tance exercises may also be practiced in suitable cases. These consist in the 
well-known flexion and extension of the wrist, elbow and shoulder joints of the 
upper, and of the ankle, knee and hip of the lower extremities. Perhaps 
the Zander apparatus used in various types of joint and neurological disease 
(mechano-therapy) may also have a special therapeutic application in some 
forms of cardiac disease. It should be remarked that all types of calisthenics, 
gymnastics, etc., should be graded and only slowly increased in duration and 
strength. 
Walking is the best, simplest, and most accessible of all the forms of 
more active exercise. Some years ago, a system of carefully planned and 
graduated hill climbing with interspersed resting benches was popular on the 
continent (Oertel treatment), but arbitrary insistence upon fixed distances 
to be covered or the hills to be climbed leaves out of consideration the only 
safe and cardinal guide of circulatory endurance, namely, the patient’s 
cardiac reserve power as measured by his subjective sensations, a constantly 
varying factor. On the other hand, walking at a moderate pace on the level 
or up a slight incline for a distance or length of time well within the patient’s 
circulatory power is a much safer and more elastic rule, and approaches more 
nearly the normal demands and mode of life that the individual will later 
follow. 
Hydrotherapy.—The usual hydrotherapeutic procedures consist in tepid 
baths, sponging with tepid water followed by a quick cool or cold sponge 
over the entire upper parts of the body, tepid or cool shower baths, needle 
baths, or sprays of water of varying temperatures applied to various portions 
of the body. Except for very warm baths, after the patient is properly 
inured to them, the above measures are applicable to any type of cardiac 
disease in which compensation has been well established. These measures 
have their special application, however, in a large group of patients who 
suffer from marked neuropathic tendencies in addition to their organic dis- 
ease. These individuals are apt to have vasomotor instability, such as hot 
or cold extremities, frequent flushed, etc. They may suffer from dyspnoea 
of purely subjective origin not correlated with exercise or with any dis- 
cernible cardiac change. They complain of indefinite pains in the chest, 
neck or arms. They frequently suffer from headache and anorexia. In 
other words, this type of patient, well compensated, suffers from that train of 
cardiac symptoms found in the so-called cardiopathic individuals, in whom 
there is no organic disease (Chapter XVIII). Doubtless the knowledge 
of the presence of organic trouble plays a role in unduly directing the patient’s 
attention to otherwise trivial symptoms. To some extent, also, I have found 
that this neuropathic tendency has been caused by consultation with physi- DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
385 
dans who have exaggerated the importance of the physical ailment and have 
not sufficiently relieved the mental disquietude and fear of sudden death which 
exists in many patients with cardiac disease. Naturally, where pathological 
changes are present, it will require careful discrimination between the 
so-called neurotic symptoms and those emanating from the organic lesion 
(Chapter XIV). In those in whom the diagnosis of an added neurotic 
ailment has been established, the hydrotherapeutic measures already out- 
lined exercise a very favorable influence. Regarding the special procedure to 
be employed in individual instances, it is necessary to remember that in no 
case should early treatments be so brusque or vigorous as to frighten or in 
any way upset the patient. Tepid baths or sponges should be employed at 
first; later, more vigorous measures—-cool sprays and showers—may be 
used. In this manner the neurotic symptoms, which are very real and dis- 
heartening to the patient, may gradually disappear. 
Hot baths race the heart, hence they should not be used therapeutically 
in any type of valvular disease in which there is actual heart failure or any 
tendency to decompensation. There are, however, many stabilized cardiac 
cases who (carry on) as well as normal individuals. For these, ordinary hot 
baths have no more than the usual effect in normal people. 
Carbon Dioxide and Oxygen Baths—Nauheim Baths.—In a different 
therapeutic category belong those baths in which the water is naturally or 
artificially charged with carbon dioxide or oxygen. Carbon dioxide is the 
gas usually used. The gas bubbles surround the body of the patient, pro- 
duce a sensation of warmth and cause dilatation of the superficial vessels. 
The claim is made that by the use of these gas impregnated baths, congestion 
is relieved, the pulse rate slowed, dyspnoea decreased, and the overburdened 
heart correspondingly benefited. There are conflicting reports regarding the 
effect of these baths upon blood pressure; it is raised according to some, lowered 
according to others. In those I have observed, there was no constant rise or 
fall of the systolic blood pressure following the baths. There seems little 
room for doubt, that, when taken at spas and health resorts, gas impregnated 
baths are of benefit. However, this is not so much because of their direct 
effect upon the circulation, but because of the difference in environment; the 
enforced rest from business and worry; the more moderate diet, and because 
of the more regular and physiological mode of living. The baths act upon 
the circulation in the same manner as any mild stimulating exercise, and, in 
my opinion, on this alone rests their efficacy on the circulation. Their use 
should therefore be limited to well-compensated patients or to those with but 
mild disturbances of compensation. Even here, the baths should not be 
prescribed universally, but only to those in whom observation has shown a 
good reaction during and following the bath. Cold extremities, a sense of 
exhaustion, rapid breathing, accelerated pulse rate, dyspnoea, constitute dis- 
tinct contraindications. I regard the possible effect upon the blood pressure as 
of less importance. 386 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
The usual routine of a series of carbonated baths given at Nauheim con- 
sists of a first immersion lasting from five to seven minutes in a bath of the 
temperature of 95°F. The temperature of the succeeding baths is gradually- 
reduced to about 86°F.; the immersion time is slowly increased to 20 minutes. 
The bath is omitted every third or fourth day. A full course consists of two 
series of twenty baths each, with an interval of three or four weeks. Oxygen 
and “Nauheim” carbonated brine baths can be prepared at home by dissolving 
salts, producing oxygen and carbon dioxide gas respectively, in the proper 
quantity of water. A simple method is as follows: A tub is filled with a 
sufficient amount of water at a temperature of 98°F., ten pounds of ordinary 
salt and four pounds of bicarbonate of soda are separately dissolved in a suffi- 
cient quantity of hot water. These are added to the bath. The patient 
then enters the tub. A well stoppered eight ounce bottle containing four 
ounces of hydrochloric acid is then held by the attendent at the bottom of 
the tub and as far as possible away from the patient’s lower extremities. 
The bottle is then slowly uncorked under water so that the patient is not 
burned by the escaping acid. In this manner a Nauheim bath may be 
safely and readily prepared at home. Naturally the greatest disadvantage 
of such home baths is that there is no change of environment, with all its 
attendant and important beneficial features. However, in the group of 
cardiac patients already described who suffer largely from neurotic in addition 
to organic complaints, gas impregnated baths, even when taken at home, may 
be followed by excellent results. 
Types of Patients Suitable for Spa Treatment.—The question frequently 
and insistently arises in private practice as to the class of cardiac patients 
who should be sent to the continent for “Nauheim” treatment. Nauheim is 
mentioned because it is the most popular and best known among patients 
themselves. Until some American health resort becomes as popular and can 
offer the same or similar well-balanced facilities for restful environment and 
medical supervision, the question must be fairly met and intelligently con- 
sidered. The answer must depend, not upon the type of valvular lesion or 
cardio-vascular disease nor upon the degree of hypertension, but chiefly upon 
the state of cardiac compensation. Patients severely decompensated—for 
example, those suffering from marked edema, cyanosis and dyspnoea— should 
be advised against taking a trip for Spa treatment. They are more benefited 
by proper treatment at home. There are some patients, however, otherwise 
intelligent, who will go to almost untold risks and expense to achieve what 
they conceive to be a life saving cure, and this directly against medical advice. 
I have observed several such patients who returned home worse than when 
they left; very few were improved. One of those not benefited was a 
physician with marked cardio-sclerosis, edema and cyanosis, who left for 
Europe against advice; he returned home a few months later in extremis. 
The patients I have found most improved were those who, besides mild decom- 
pensation, were nervous, high strung, or worried, and who at the Spas were DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
387 
able not only to have enforced rest and quiet, but also to quickly divorce 
their minds and thoughts from domestic and business cares. It is to indi- 
viduals of this type that Spa treatment should be recommended with the great 
probability that it will be followed by good results. 
REFERENCES 
Adler and Krehbiel: Orthodiascopic Observations Concerning a Certain Type of Small 
Heart, etc.; Archives of Internal Medicine, 1912, IX, 346. 
Barringer, T. B., Jr., and Teschner, J.: The Treatment of Cardiac Insufficiency, etc., with 
Dumb-bells and Bars; Archives of Internal Medicine, 1915, XVI, 795. 
Brooks, H.: Hyperthyroidism in the Recruit; American Journal of Aledical Science, 156, 
726, 1918. 
Buedingen, T.: Grundzuege der Ernaehrungsstoermgen des Herzmuskels und ihr Behand- 
lungen mit Traubenzuckerinfusionen; Deutsche Medizin. Wochensch., 1919, XLV, 64. 
Cohn, A. E., and Fraser, F. R.: Certain Effects of Digitalis on the Heart; International 
Medical Congress, 1913, Section 6, Part II, 258. 
Cohn, A. E.: Present Status of the Electrocardiographic Method in Medicine; American 
Journal of the Medical Sciences, 19x6, CLI, 529. 
Cohn, A. E., and Lewis, T.: Auricular Fibrillation and Complete Heart Block; Heart, 
19x2-1913, IX, 17. 
Cotton, Rapport and Lewis: Observation on Atropin; Heart, 1917,VI, 295. 
Cotton, Slade and Lewis: Observation on Pilocarpin Nitrate; Heart, 1917, VI, 299, 310. 
Cushny, A. R.: Pharmacology and Therapeutics of the Action of Drugs. 
DaCosta, J. M.: On Strain and Overaction of the Heart. Third Toner Lecture May, 
1874; American Journal of Medical Science, January, 1871, p. 40. 
DaCosta, J. M.: Cardiac Asthenia or Heart Exhaustion; American Journal of the Medical 
Sciences, 1894, CVII, 361. 
Eggleston, C.: Digitalis Dosage; Archives of Internal Medicine, 1915, XVI, 1. 
Eggleston, C. and Hatcher, R. A.: The Emetic Action of the Digitalis Bodies; Journal of 
American Medical Association, 1913, LX, 499. 
Eggleston, C.: Some Newer Conceptions of Digitalis Therapy; American Journal of 
Medical Sciences, 1920, CXL, 625. 
Eyster and Fahr: Quinidine Sulphate in Auricular Fibrillation; Archives of Internal 
Medicine, 1922, XXIX, 60. 
Frey, W.: Ueber Vorhofflimmern bein Menschen . . . und Quinidine; Berliner Kl. 
Wochensch., 1918, LVI, 849. 
Frey, W.: Weitere Erfahrungen ueber Quinidine; Berliner Kl. Wochensch., 1918, LVI, 849. 
Hatcher, R. A.: Some Observations on the Pharmacology of a Digitalis Body; Journal of 
American Medical Association, 1920, LXXV, 460. 
Janney, N. W.: Studies in Thyroid Therapy; Archives Internal Medicine, 1918, XXII, 187. 
Levy, R. L.: Restoration of the Normal Cardiac Mechanism in Auricular Fibrillation by 
Quinidine; Journal American Medical Association, 1922, LXXVI, 1289. 
Levy, R. L.: Clinical Studies of Quinidine; Journal American Medical Association, 1922, 
LXXIX, 1108. 
Lewis, Drury, Iliesen and Wedd: Quinidine Sulphate; Heart, 1921, IX, 55. 
Mackenzie: Disease of the Heart; Second Edition. 
Medical Research Committee, Special Report Series No. 8, 1917, Report upon Soldiers 
Returned as Cases of “Disordered Heart Action” (D. H. A.) or “Valvular Disease of 
the Heart” (V. D. H.). 
Neuhof, S.: Intravenous Injections of Theobromine Sodium Salicylate; New York Medical 
Journal, Oct. 25, 1913. 388 
DIET, DRUG AND OTHER THERAPY IN CIRCULATORY DISEASE 
Pardee: Notes on Digitalis Medication; Journal American Medical Association, 1919, 
LXXIII, 1822. 
Price, F. W.: Some Investigations of the Action of Digitalis on the Blood Pressure in Man; 
British Medical Journal, 1912, II, 689. 
Rothberger, C. J., and Winterberg, H.: Arch. f. d. ges. Physiol., 1910, CXXXV, 506. 
Rudolph, R. D., and Cole, C. E. C.: The Effects of Medical Doses of Aconite upon the 
Pulse Rate; American Journal of Medical Sciences, 1912, CXLIV, 788. 
von Schroeder, W.: Ueber die diuretische Wirkung des Kaffeins, etc.; Arch. f. Exptl. 
Path, und Pharmakologie, XXIV, 85. 
Schlayer, C.: Verhandlungen des XXVII ten Kongresses f. innere Medizin, 1910, 744. 
Taussig, A. E.: Complete and Permanent Heart Block Following the Use of Digitalis in 
Auricular Fibrillation; Archives of Internal Medicine, 1912, X, 335. 
Turnbull, H. H.: Cardiac Irregularities Produced by Squills; Heart, 1910-1911, II, 15. 
White, P. D.: Auricular Standstill: An unusual Effect of Digitalis upon the Heart, etc.; 
Boston Medical and Surgical Journal, 1916, CLXXV, 233. 
White, Balboni and Vike: Clinical Observations on the Digitalis-lijce Action of Squill; 
Journal American Medical Assn., 1920, LXXV, 971. 
Wilson and Merrman: Cerebral Embolism Following Arrest of Auricular Fibrillation by 
Quinidine; Journal American Medical Assn., 1922, LXXVIII, 865. 
Windle, J. D.: Heart Block from Drugs of the Digitalis Group; Heart, 1911-1912, III, 1. CHAPTER XXI 
TOBACCO—DIET—RENAL AND BLOOD TESTS IN CARDIO-VASCU- 
LAR DISEASE 
Tobacco.—The effect of tobacco as a possible causative factor of organic 
cardio-vascular disease has already been dealt with (Chapter V). It prob- 
ably produces a fleeting rise of blood pressure. When precordial pains 
(Chapters XXIII, XXIV) are a feature of the disease for which the patient 
seeks relief, and smoking has been immoderate, it should be stopped entirely. 
When precordial pains are infrequent and not severe, and the patient feels 
the interdiction of smoking a hardship, smoking of an occasional cigar or a 
few cigarettes daily or an occasional pipe may be permitted. When the organic 
disease is stabilized and quiescent and is not accompanied by precordial pains, 
I am in the habit of allowing the patient a moderate amount of tobacco. One 
should not be unnecessarily arbitrary in chronic diseases but should individ- 
ualize and weigh comforts from the patient’s standpoint against an assumed 
hastening of the valvular, cardio-sclerotic or arterio-sclerotic process from 
tobacco, a questionable arterial “poison” at best, especially when tobacco 
is used in moderation. 
From the dietetic standpoint, and because of the frequent correlation of 
cardiac with renal disease, it is necessary to make a clinical distinction between 
purely cardiac cases with no or very slight secondary renal involvement, and 
those in whom renal involvement is the primary or predominant feature. 
It is also necessary in both types to remember that we are dealing with 
chronic conditions, and that the dietetic regime will have to be carried out 
for months and even years. Hence the diet should not be unnecessarily 
harsh or restricted, and consideration should be given, as far as possible, to 
personal idiosyncrasies and tastes. 
In patients with compensated valvular disease with or without hyper- 
trophy, without renal involvement or hypertension, it is not necessary to 
make any radical change from the usual dietary of balanced rations of an 
individual in health. There is no necessity for strict observance of any special 
diet, nor for the limitation of fluids. On the other hand, there should be 
sensible restriction about excesses of any kind of food or drink. 
The Use of Coffee, Tea and Alcoholic Beverages, in Cardio-sclerosis.— 
To patients who are accustomed to small amounts of alcohol in the form of 
beer or light wines, I am in the habit of allowing a small amount of these 
beverages, provided observation shows no deleterious effects upon the pulse 
rate and blood pressure. I limit the amount to one glass of beer or to a 
small glass of light wine taken at the principal meal. I have observed such 
patients for years, and have found no ill effects upon the cardiac condition 
389 39O 
DIET—RENAL AND BLOOD TESTS IN CARDIO-VASCULAR DISEASES 
ascribable to this practice. Some patients, especially the elderly, find that 
they fall asleep more readily if they take a small amount of whisky or wine 
at bedtime. Here also I rarely stop this practice unless I find definite con- 
traindications, either from the cardio-vascular or gastro-enteric systems. 
Similarly, if patients are in the habit of taking tea or coffee without any ill 
effects, a cup of weak tea or coffee may be allowed daily. When patients 
demand much coffee, various types of caffein-free coffee may be substituted. 
Diet in the Obese.—In obese individuals with cardio-vascular disease, 
a systematic although gradual attempt should be made to reduce weight. 
Since these individuals as a rule eat too much, indeed, they often eat glutton- 
ously, it is sometimes sufficient to simplify and lessen their dietary so that 
it becomes sub-caloric, especially with reference to fats, sweets, pastries and 
other carbohydrates. If these simple restrictions are not sufficient, saccha- 
rine for sweetening purposes, may be used instead of sugar. It should be 
remembered, however, that some patients have always been fat even though 
they eat but sparingly. This probably depends upon some endocrine dis- 
turbance or idiosyncracy of metabolism. Such individuals should not be 
reduced much unless there exists some definite indication from the cardio- 
vascular standpoint (for example, edema, pulmonary or hepatic congestion). 
The general problem of reduction is much simpler in purely valvular 
cases than is those with hypertension or cardio-renal disease. In the latter, 
there may be metabolic changes which may require serious restriction of the 
caloric intake of proteins, so that if carbohydrates and fats are also restricted, 
there may result not only a loss of weight but also a considerable loss of 
strength. In such individuals it is therefore necessary to study the case from 
all angles—functional kidney tests, examination of the blood, etc. (q. v.)—* 
before reduction is attempted. 
When digestion is good, the following vegetables are suggested as sub- 
stitutes for carbohydrates and fats: Cabbage, spinach, onions, salad (lettuce, 
romaine, etc.), beans, carrots, mushrooms. 
Those with myocardial insufficiency and dyspnoea without edema are 
usually too ill to relish a normal amount of solid food, so that the patient’s 
own limitations and dietetic inclinations are usually sufficiently safe guides. 
But in view of the possibility of visceral stasis and of edema, the fluid intake 
should be somewhat restricted; about 500 c.c. in addition to solid and semi- 
solid nourishment is a safe limit. In cases of myocardial insufficiency with 
edema, pleuritic transudates or marked visceral congestion, a strict Karrell 
diet for several successive days or in courses of several days each, as already 
outlined (Chapter XX), is an excellent aid to drug therapeutics. The Karrell 
diet reduces the salt intake to a minimum. Even after disappearance of 
edema, and when comparison of the salt intake with its output in the urine 
demonstrates a normal relationship and no chloride retention, only a moder- 
ate amount of salt should be allowed in order to overcome any tendency to 
edema by salt retention. DIET—RENAL AND BLOOD TESTS IN CARDIO-VASCULAR DISEASES 
391 
In those cardio-renal cases in which the kidneys demand special attention, 
a brief account of some of the modern methods of kidney study and diagnosis, 
and their correlation with diet and therapy is required. In addition to the 
routine examination of the urine for normal and abnormal chemical and 
microscopical constituents, other methods have come into use to estimate 
renal function and efficiency; these depend on the power of elimination of 
certain substances or foods taken internally or given subcutaneously. The 
status and value of some of these tests and their correlation with clinical data 
have not yet been definitely fixed. Two of these tests consist in the study of 
iodide of potash excretion, and of the elimination of lactose injected intra- 
venously. Both of these have been discarded. The first test requires a 
long time for its completion and gives inaccurate results; the lactose test 
is too cumbersome and is likewise inaccurate. Probably the most important 
method at the present time consists in the estimation of the excretion percent- 
age in the urine of a dye which is injected subcutaneously. The dyes 
formerly employed were methylene blue, indigocarmine and rosanilin. Phe- 
nolsulphonephthalein is now almost universally chosen for this study. Briefly, 
the method is as follows: 
Twenty minutes to one half hour before the injection, the patient is given 
200 to 400 c.c. of water. The patient is then catheterized, the time noted, 
and the catheter kept in place. Then one c.c. of a carefully prepared 
sterile solution, containing 6 m.g. of the dye (phthalein) is injected intra- 
muscularly in the lumbar region. The urine is allowed to drain into a test 
tube which contains a drop of a 25 per cent, sodium hydroxide solution, 
and the time of appearance of the first pinkish tinge is noted. The catheter 
is then withdrawn and the patient is asked to void into two different recep- 
tacles at the end of one and two hours respectively. Sufficient 25 per cent, 
sodium hydroxide solution is added to make the urine decidedly alkaline. 
This changes the yellowish or orange color of acid urines to a brilliant pur- 
plish red. Sufficient water is now added to each specimen to make 1000 c.c. 
The solution is mixed; a small portion is then filtered and compared with 
the standard color. In those patients seen in office consultation where the 
phthalein test seems of value, I have employed the following routine: The 
patient is asked to void; he is then given a glass of water and the dye is injected. 
He is sent home, or follows his usual occupation, and is asked to void 
his urine two hours after the injection; this specimen is then examined for 
the percentage of dye excretion. I have found this method sufficiently 
exact for ordinary purposes; it obviates the necessity for catheterization, 
and requires very little time. In addition, it gives information of dye 
excretion during the time the kidneys are under normal strain, for the patient 
is about and not resting in bed. I consider this a very important considera- 
tion in ambulatory cases. 
As colorimeters the Dunning, Hellige or Duboscq may be used; or 
one can manufacture a practical and sufficiently accurate colorimeter by 392 
DIET—RENAL AND BLOOD TESTS IN CARDIO-VASCULAR DISEASES 
using a series of bottles or tubes which contain the solution of phenolsul- 
phonephthalein in multiples of 5 per cent.; the tubes are sealed and their respec- 
tive percentage labeled; these may then be used as the color standards. If the 
dye first appears in the urine within fifteen minutes of the time of its injec- 
tion, and 40 to 60 per cent, is excreted within two hours, the test is regarded as 
normal. For clinical purposes, the two hour excretion test alone is suffi- 
cient; this saves catheterization. In renal congestion secondary to circula- 
tory disturbances and in contracted kidney with hypertension the percentage 
and output in two hours is usually decreased. It requires clinical examina- 
tion to determine which of the two factors—renal congestion or primary 
nephritis—is the cause of the decreased phthalein output. 
For the purpose of testing quantitatively for urea, salt and water output 
in the urine, a balanced diet containing a measured amount of solids (starches, 
sugar, fats, proteids and salts) and of fluids (milk, water, tea) is given. 
Schlayer’s diet or some modification may be employed. An excellent and 
well-balanced ration is that of Mosenthal for testing the renal function. 
It is as follows: 
Nephritic Test Diet 
All food is to be salt free. 
Salt for each meal is furnished in weighed amounts.* 
All food or fluid not taken must be weighed or measured after meals, and charted. 
Allow no food or fluid of any kind except at meals. 
Note any mishaps or irregularities that occur in giving the diet or collecting the specimens. 
Breakfast, 8 A.M. 
Dinner, 12 Noon 
Meat soup, 180 c.c. 
Beefsteak, 100 gm. 
Potato (baked, mashed or boiled), 130 gm. 
Two slices of bread (30 gm. each). 
Butter, 20 gm. 
Green vegetables, as desired. 
Boiled oatmeal, ioo gm. 
Sugar, % teaspoonful. 
Milk, 30 c.c. 
Two slices of bread (30 gm. each). 
Butter, 20 gm. 
Coffee, 160 c.c. 
Sugar, 1 teaspoonful 
Milk, 40 c.c. 
200 c.c. 
Tea, 180 c.c. 
Sugar, 1 teaspoonful 
Milk, 20 c.c. 
200 c.c. 
Milk, 200 c.c. 
Water, 200 c.c. 
Water, 250 c.c. 
Pudding (tapioca or rice), no gm. 
Two eggs, cooked in any style. 
Two slices bread (30 gm. each). 
Butter, 20 gm. 
Supper, 5 P.M. 
Tea, 180 c.c. 
Sugar, 1 teaspoonful 
Milk, 20 c.c. 
200 c.c. 
Fruit (stewed or fresh), 1 portion. 
Water, 300 c.c. 
*One capsule of salt, containing 2.3 gm. of sodium chloride, is furnished for each meal. 
The salt which is not consumed is returned to the laboratory, where it is weighed, and the 
actual amount of salt taken is calculated. DIET—RENAL AND BLOOD TESTS IN CARDIO-VASCULAR DISEASES 
393 
8 A.M.—No food or fluid is to be given during the night or until 8 o’clock 
the next morning (after voiding), then the regular diet is resumed. 
Patient is to empty bladder at 8 A.M. and at the end of each period, as 
indicated below. The specimens are to be collected for the following periods 
in properly labelled bottles: 
8 A.M.—io A.M.; io A.M.—12 N.; 12 N — 2 P.M.; 2 P.M.;—4 P.M.; 
4 P.M.— 6 P.M.; 6 P.M.— 8 P.M.; 8 P.M.— 8 A.M. 
The amounts, specific gravity, and sodium chloride content, and the urea 
determination by the hypobromite method, or preferably the nitrogen content 
by the Kjeldahl method are separately determined for each two hour speci- 
men, and also for the night specimen. In other words, there are six deter- 
minations for the day, and one for the night. In this manner, besides other 
data, a comparison of the amounts and specific gravity of the day and 
night urine is made. If the specific gravity is low and shows only slight 
variations in the different specimens, and the night urine is larger in amount 
than that voided during the day, it speaks for the presence of a chronic inter- 
stitial nephritis. A less exact, yet fairly accurate method consists in measur- 
ing together the amounts and specific gravity of the 12-hour day and the 12- 
hour night specimens. Conclusions similar to the above may be drawn 
even from this simple procedure. 
Outside of hospitals, as in sanatoria or at home, a similar dietetic regime 
can be carried out if, instead of quantities measured in grammes and cubic 
centimeters, their known equivalents in cupfuls, glasses and teaspoonfuls can 
be substituted. This is a modification which I have carried out where careful 
weighing of the various food constituents could not be done, and I have found 
the results sufficiently accurate for clinical purposes. 
Because of evaporation by the lungs and elimination of water by the skin 
and intestines, the amount of urine is normally less than the fluid intake. 
Approximately all sodium chloride, and about 90 per cent, of the nitrogen 
ingested is excreted by the urine. Thus, the chemical urine tests described 
give valuable information regarding the retention of salt and nitrogenous 
products in the body. 
In order to determine which of these functional tests is of most clinical 
value, I made a correlated study of the non-protein nitrogen in the blood, 
the estimation of carbon dioxide tension of the expired air by means of the 
Fredericia apparatus, and the phthalein output in a small series of cases. I 
also observed the alkali tolerance of the urine by giving the patient measured 
amounts of bicarbonate of soda until the urine became alkaline. Although I 
have not arrived at any definite conclusions, I believe that a very careful 
study of the clinical phenomena, of the amount and concentration of the night 
urine, and of the ordinary examination of several specimens of urine taken 
within 24 hours, will often allow us to judge and foretell with fair accuracy, 
what the chemical blood examination (see below) will show with reference 
to the amount and type of the retained excrementitious products, namely, 394 
DIET—RENAL AND BLOOD TESTS IN CARDIO-VASCULAR DISEASES 
non-protein nitrogen and uric acid. In other words, clinicians may soon hope 
to reap the advantages of the careful scientific work of the laboratory by com- 
parison of its results with ordinary bedside methods. 
Chemical examination of the blood has assumed great importance, espe- 
cially since simpler and accurate methods have replaced the former cumber- 
some and less accurate determinations. The important constituents sought 
for are non-protein nitrogen, creatinin and uric acid. The knowledge thus 
gained is not yet fixed or positive, but there seems to be a correlation between 
an abnormal amount of non-protein nitrogen retained in the blood, a decreased 
phthalein output, and clinical evidence of a severe nephritis of a predomi- 
nantly vascular type. Of special importance are the facts recently brought 
out that an increase of uric acid in the blood seems to offer an early diagnostic 
sign of incipient nephritis; that a blood creatinin of over 5 milligrams per 100 
c.c. is fatal within a comparatively short time, and that blood acidosis as 
determined by the Van Slyke method is a valuable index of nephritis both 
from the diagnostic and therapeutic view points (Chase and Meyers). Not 
only has our diagnostic and prognostic knowledge been enhanced by these 
blood examinations, but the dietary of nephritis has assumed a less rigorous 
and more rational and scientific aspect. The subject of salt restriction has 
already been mentioned. In nephritics with abnormally increased amounts 
of non-protein nitrogen in the blood, a low protein and high carbohydrate diet 
is indicated. The amount of fluid should be restricted if urine measurements 
show decreased elimination of water. If the amount of urinary excretion is 
normal, it is advisable occasionally to allow large quantities of fluids—as 
much as several liters within 24 hours—in the attempt to flush the system and 
thus get rid of toxic products. 
In nephritis with excessive and abnormal amounts of non-protein nitrogen 
in the blood, attempts have been made to therapeutically attack the disease 
upon a chemical basis. Sugar solutions have been administered intraven- 
ously or by the Murphy drip. In cases of lessened blood alkalinity (so-called 
acidosis), I have occasionally given intravenous injections of 500 c.c. of 
a 5 per cent, solution of bicarbonate of soda. One instance was that of a 
patient of 64 with cardio-nephritis, regular pulse, hypertension, general 
anasarca and nocturnal dyspnoea, who had been ill over one year. Therapy, 
consisting of digitalis, theobromin, appropriate diet and occasional Karrell 
days over a period of several weeks had only a very slight influence upon the 
symptoms and course of the disease. 500 c.c. of blood were withdrawn by 
venesection and the same amount of a 5 per cent, bicarbonate of soda solution 
injected. Within twenty-four hours improvement began and continued 
uninterruptedly. At the end of two weeks, edema and dyspnoea had entirely 
disappeared. In another case, a man with cardio-vascular disease, a systolic 
blood pressure of 250, aortitis, very marked left ventricular hypertrophy, 
and attacks of nocturnal dyspnoea relieved only by morphine, a similar proce- 
dure was employed. The injection was followed by improvement for several DIET—RENAL AND BLOOD TESTS IN CARDIO-VASCULAR DISEASES 
395 
days. In less urgent cases I have tried venesection combined with a 10 per 
cent, bicarbonate solution per rectum given by the Murphy drip. In all 
therapeutic attempts of this type to combat acidosis it must be remembered 
that relief may be only symptomatic and temporary because the underlying 
kidney condition is often uninfluenced and because abnormal chemical con- 
stituents may be present not only in the blood but they may be locked in the 
tissues themselves. 
REFERENCES 
Chase, A. F., and Myers, V. C.: The Value of Recent Laboratory Tests in the Diagnosis 
and Treatment of Nephritis; Journal American Medical Assn., 1916, LXVII, 929. 
Folin, O., and Denis, W.: On the Creatinine Content of the Blood; Journal of Biological 
Chemistry, 1914, XVII, 487. 
Folin, O., Denis, W.. and Seymour, M.: The Non-protein Nitrogenous Constitutents of the 
Blood in Chronic Vascular Nephritis, etc.; Archives of Internal Medicine, 1914, XIII, 
224. 
Foster, N. B.: Increase of Extract of Nitrogen in the Tissue with Chronic Nephritis; 
Archives of Internal Medicine, 1919, XXIV, 242. 
Mosenthal, H. O.: Renal Function as Measured by the Elimination of Fluids, etc.; Archives 
of Internal Medicine, 1915, XVI, 733. 
Rowntree, L. G., and Gerarghty, J. T.: An Experimental and Clinical Study of Phenol- 
phthalein in Relation to the Renal Function; Archives of Internal Medicine, 1912, IX, 
284. 
Schlayer, C.: Verhandlungen des XXVII ten Kongresses f. innere Medizin, 1910, 744. CHAPTER XXII 
SOCIOLOGICAL ASPECTS OF HEART DISEASE—FOCAL INFECTION 
—PROPHYLAXIS—GENERAL MANAGEMENT—OCCUPATION 
FOR “CARDIACS”—CARDIAC CLINICS 
Including cardio-vascular disease in the term heart disease, it is acknowl- 
edged that heart disease is widespread and is responsible for a large propor- 
tion of deaths in the community (Fig. 275). Statistics vary but it is evident 
that valvular disease is prevalent even at the school age, and that cardio-vas- 
cular disease is especially prevalent from the 40th to the 60th years. The 
etiological factors may be grouped generically under infections, intoxications 
and improper mode of living. This phase alone of the subject presents many 
aspects and angles. A few of the etiological factors may perhaps be intelli- 
gently combatted; others are unknown or are recognized only after the 
damage has been done to the circulatory apparatus; again, others have 
given rise to the most diverse, diametrically opposed opinions.- I shall 
briefly sketch some of the practical difficulties of the problem, indicating some 
controllable, some debatable, and some of the unknown causative agencies. 
We know, for example, that both lead poisoning and syphilis (Chapter V) 
especially the latter, can cause cardio-vascular disease. Progress has already 
been made through educational campaigns in schools, factories, shops, 
amid lead workers, etc., which have probably tended to decrease the ravages 
of these factors. This is especially true of lead; but much more educational 
work will certainly be necessary before syphilis can be classed as a definitely 
controllable factor. Improper food, especially an improperly balanced, 
high protein diet, may have a certain influence in causing arterio-sclerosis; 
but in spite of some experimental evidence, further intensive, exhaustive 
and long-continued clinical study will be required before we have positive 
evidence that improper feeding alone is one of the fundamental causes of 
cardio-vascular disease. Alcoholism can undoubtedly cause cardiac disease, 
especially myocarditis. As already pointed out (Chapter V), its role in this 
respect has been exaggerated. There are hopes that alcoholism, even if not 
entirely eradicated, will gradually become an increasingly minor cause of 
heart disease. Diphtheria was undoubtedly a frequent cause of cardiac 
disease and death. Fortunately, toxic cases are now infrequent, and the 
immediate use of diphtheria antitoxin cures even some of these. Hence 
diphtheria has dwindled to a small etiological factor of heart disease. Scarlet 
fever, whether directly or because of the accompanying tonsillitis, may be 
taken as the type of a frequent infectious cause of valvular disease. We 
possess no specific remedy that can lessen the probability of the poison 
396 SOCIOLOGICAL ASPECTS OF HEART DISEASE 
397 
affecting the heart; our efforts are practically limited to the usual routine 
hygienic and symptomatic procedures which need not be discussed here. Yet. 
after all, the danger to the heart in scarlet fever is but a small phase of 
the larger problem of communicable diseases with which preventive and epi- 
demiological medicine must cope. Overcrowding, sanitation, education of 
the native-born and foreign population represent some of the sociological 
aspects of the same problem. 
Rheumatism (Chapter XV)—especially the acute, articular variety— 
and chorea and tonsillitis are undoubtedly the largest and most important 
causes of cardiac disease in the middle-aged and young. Here, likewise, 
we possess no specific remedy which, so far as known, will minimize the 
danger of endocardial involvement. It is not necessary to enter again into 
the extremely debatable question of the bacterial origin of the disease. 
Even assuming this etiology, we have no anti-bacterial remedy. We 
possess many drugs for the control of the rheumatic articular manifestations, 
but for the present we can only assume that these drugs thereby lessen the 
liability to rheumatic endocarditis. Attention of the public should be called 
to the dangers of rheumatism, they should become acquainted with such 
simple measures as we possess to prevent rheumatism; these consist chiefly in 
proper clothing, and protection against rain and snow in the changeable 
climate of the temperate zone. It may even be necessary to suggest climatic 
changes in order to obviate rheumatic recurrences. It is not alone the 
marked cases of rheumatism but also the so-called “growing pains” of 
children which, in educational campaigns, should be emphasized as evidences 
of actual rheumatism. The connection between rheumatism, and the tonsil 
and teeth will be discussed later. 
Tonsillar Infections and Tonsillectomy.—The inflamed tonsil is the 
next most frequent etiological factor of endocarditis. Only a short half 
dozen years ago, the tonsils were eradicated upon the slightest evidence of 
rheumatism or suspicion of endocarditis. The views at present are not 
quite as radical. Tonsillectomy has assumed much importance since the 
demonstration that the tonsils are often the portals of entry for endocardial 
infections. It is extremely difficult to follow dogmatic rules regarding 
tonsillectomy in the attempt to prevent the recurrence or occurrence of 
endocarditis. I have found it necessary to individualize, although I do 
follow certain general principles. Thus tonsils which are enlarged, ragged 
and interfere with breathing should be removed: These represent grossly 
diseased tonsils. If a patient with heart disease be harrassed with frequent 
tonsillitis, tonsillectomy should be advised, no matter what the size or appear- 
ence of the tonsil, or whether the submaxillary glands at the angle of the jaw 
be enlarged or not. I mention these glands because some assume that these 
are a sign of chronic tonsillar infection. Maxillary glands become infected 
from so many other causes, particularly from nasal catarrh, that I do not 
consider them a valid index of tonsillar disease. If a patient has small, 398 
SOCIOLOGICAL ASPECTS OF HEART DISEASE 
normal looking tonsils, and has only infrequent attacks of tonsillitis, and the 
valvular disease has reached a quiescent stage, I advise against tonsillectomy. 
I do not believe that removal of the tonsils prevents valvular reinfection in 
such individuals. This view is not invalidated by the fact that tonsils which 
look normal in the throat show, upon removal, various pathological changes, 
both macro- and microscopically. Because of their function as filtering 
agents and because of their constant contact with, and exposure to, bacteria, 
the tonsils can scarcely ever represent normal lymphoid structures. On the 
whole, it is still a moot question whether recrudescences of endocarditis have 
been prevented by the routine and radical practice of tonsillectomy in all 
children with valvular lesions. Thus, in one excellent report, such tonsillec- 
tomies did not affect the frequency of recurrences, nor the course of the 
disease. 
It is important to emphasize that, if possible, the time chosen for tonsil- 
lectomy should be during the quiescent stage (Chapter XV) of the cardiac 
disease. I have seen distinct harm, indeed, recrudescence of the disease, 
caused by untimely tonsillectomy (see Cardio-vascular Clinics). There are 
cases, however, in which sore throats—either frank tonsillitis, nasopharyngeal 
catarrh and so-called rheumatic sore throats—follow each other so quickly 
that tonsillectomy cannot wait for a quiescence of the endocarditis. In such 
individuals tonsillectomy, especially in children, is sometimes followed by 
exceptionally favorable results not only upon the endocarditis but also upon 
the general condition of the patient. Murmurs may become less loud, their 
area of transmission decreases, tachycardia and dyspnoea disappear, and 
what is most remarkable the patients gain rapidly in weight. I have, for 
example, seen children gain from io to 15 or even 20 pounds, so that their 
appearance changes from frail, anemic children to healthy, robust youngsters. 
Tonsillectomy here seems to check the infection radically and at once. 
Thorough enucleation is the ideal method for removal of the tonsils, 
so that one can be sure that no tonsillar tissue remains to cause possible 
reinfection. 
Tooth Infections.—The teeth have been found to harbor and act as foci 
of infection in the production of some types of muscular and joint rheumatism, 
especially in the adult. There have been vigorous campaigns launched both 
among the laity and physicians to eradicate these foci of infection, and thus 
prevent rheumatism and heart disease, or, when already present, to prevent 
their further spread. X-ray examinations of the teeth have been brought 
as witnesses to show how widespread dental infection may be. It perhaps 
may be parenthetically, yet pertinently remarked, that dentists can only 
indicate which teeth are diseased and the type of disease. It remains for 
the physician to determine the correlation, if any, between the dental 
infection and the disease in question, and to decide upon the advisability 
and time of removal of the dental infection. As a matter of personal observa- 
tion, I believe that diseased teeth as a primary cause of endocarditis is SOCIOLOGICAL ASPECTS OF HEART DISEASE 
399 
extremely rare. In the very few I have seen, there was dental caries and 
septic osteomyelitis of the jaw with general septicemia, endocarditis and 
death. As the result of careful and long-continued observation, I believe 
that endocarditis in itself does not warrant more radical or more careful 
dentistry than is usually required for diseased teeth and purulent foci in 
otherwise normal individuals. Dentistry here, as elsewhere, should follow 
sane lines. As with tonsillectomy, I regard routine extraction for the pre- 
vention of endocarditis as uncalled for. Extensive extractions upon the 
supposition that exceedingly small pus foci frequently produce endocarditis 
is in my opinion unwarranted by general clinical experience and by the nega- 
tive results following such practice in patients with endocarditis. 
The role of pyorrhea has already been discussed (Chapter V). 
Focal Infections.—The general subject of removal of foci of infection 
as a prophylactic of, or a curative measure in, heart disease has aroused the 
medical mind. It is undoubtedly true that a “focus of infection” anywhere 
in the body, e.g., the inflamed gall bladder, is a potential cause of endocardi- 
tis and hence is an etiological factor to be reckoned with. I believe, how- 
ever, that its frequency as a factor has been tremendously overstated. It 
is one thing to diagnose a focus of infection; it is another to state dogmat- 
ically that its removal is going to benefit the patient. As a matter of fact, 
it can scarcely affect a cure, for, when the diagnosis of circulatory disease 
is made, the pathological damage has been done. At best, therefore, eradi- 
cation of infected foci can either bring only relief or quiescence of the dis- 
ease. In some older individuals with cardio-renal disease and infected teeth, 
I saw no effect of any kind from the wholesale extraction of teeth. In other 
words, prophylaxis against cardio-vascular disease or the presence of the 
latter rarely calls for more radical surgical intervention and eradication of 
infected foci than that focus ordinarily demands. To do otherwise is to 
lose one’s clinical balance and to practice medicine by simple rule of thumb 
rather than by mellowed clinical judgment. 
Occupation and Exercise for the Cardiac.—Aside from diet and therapy, 
other questions regarding the management of compensated and decompen- 
sated cases of cardio-vascular disease arise. Some of the commoner of these 
are: Shall a patient return to work? What type of work should he follow? 
Shall medication be continued and, if so, how long? 
With respect to these questions, no matter what the type of lesion there 
are two preliminary fundamental considerations to be determined, namely: 
(i) The degree of compensation, and (2) the activity or state of quiescence 
of the disease. With quiescent compensated lesions, valvular or myocardial 
in nature, the main restriction regarding exercise should be the kind, rather 
than the amount, provided always it be well within the patients’s cardiac 
reserve power. This statement requires some modification, however, for the 
type of cardiac disease plays a role which requires some individual discrimina- 
tion. For example, patients with tremendousjiypertrophic left ventricles 400 
SOCIOLOGICAL ASPECTS OF HEART DISEASE 
from aortic valvular lesions are scarcely able to maintain long-continued 
effort without soon encroaching upon their cardiac reserve. In general, 
it may be stated that even quiescent compensated cases should avoid all 
exercises which call for competition or for sudden or sharp exertion, as swim- 
ming a long distance, running and tennis playing. On the other hand, golf 
is an excellent form of moderate exercise. It entails the necessity of being 
away from business and of being out in the open for a number of hours, 
considerations which in themselves are very desirable. All things considered, 
walking is the best and simplest form of exercise. In exercise as well as in 
work it should be emphasized that patients should keep well within their 
individual limits of fatigue. 
The question of occupation and vocation for patients with cardiac disease 
has recently received wide consideration from the lay as well as from the 
medical standpoints. It is now generally recognized that many individuals 
with cardio-vascular disease are not thereby necessarily precluded from 
attempting to earn a livelihood, and that, if proper work be chosen, they may 
become self-sustaining members of the community. Occupations and voca- 
tions at which patients sit or stand are preferable to those which require walk- 
ing or stair climbing. Positions in counting houses, clerical work, draftsman- 
ship, light manufacturing industries, working at lathes or small machinery, 
watchmen, are examples of the work which these patients may safely follow; 
but just because of these sedentary and easy occupations, exercise out in the 
open, chiefly walking, should be advised. It is, I believe, a therapeutic error 
to attempt to avoid all circulatory strain by having these patients pass an 
almost muscularly inert existence, for it is only by mildly stimulating the 
circulation by appropriate gentle exercise that the heart and circulatory 
apparatus are kept at their proper individual level of efficiency. In this 
respect the heart does not differ from other weakened muscles whose strength 
is enhanced by moderate, well-planned and individualized exercises. Mild, 
appropriate dumb-bell exercises and other calisthenics, and breathing exer- 
cises should be advised when walking is not feasible, or as additions to the 
latter. 
It has been found that when those with cardiac disease (so-called “car- 
diacs”) find employment, the fact that they are handicapped and hence can- 
not cope with other workmen in efficiency and earning power does not depress 
them; on the contrary, they find happiness and satisfaction in being able to 
earn something which will help them toward becoming independent and self 
supporting. It is, on the whole, difficult for cardiacs themselves to find the 
proper type of employment. Hence, in the larger cities, bureaus are estab- 
lished for the poorer and needier, through which appropriate employment 
may be found. Under such circumstances, the bureau head seeks infor- 
mation from the medical chief of the cardiac clinic and from the social service 
department (q. v.) in order to determine the functional capacity, the state 
and type of cardiac lesions, and the home surroundings of the individual. In SOCIOLOGICAL ASPECTS OF HEART DISEASE 
401 
this manner, some individuals have been given suitable employment and have 
been made earning members of the community. In an excellent report on 
employment for the cardiac by I. M. Duggan, the following was given as a 
partial list of employments in which cardiacs had been placed: 
Fountain pen factories (male) 
Grinding pens 
Polishing barrels 
Assembling 
Jewelry (wholesale) 
Chasing (men up to 30) 
Filing 
Soldering 
Carding (women up to 50) 
Matching and stringing pearls 
Architect’s office 
Draughtsman 
Filing blue prints 
Figuring plans 
Western Electric (only boys, mild cases) 
Taught business from beginning in each 
department 
Draughtsmen and mechanical engineers 
Hotels 
Door men 
Watchmen 
Elevator operators 
Kitchen and pantry 
Linen seamstress 
Assistant housekeeper 
Clerical 
Hand sewing 
Repairing expensive laces 
Finishing 
Publishing companies (male and female) 
Plain clerical 
Folding and inserting 
Information clerk 
Book binding (certain kinds) 
Wholesale grocers (female up to 25) 
Dictaphone operators 
Comptometer operators 
Plain clerical 
Tobacco companies (male not more than 
45) 
Stripping 
Packing 
Assistant engineer 
Auditor 
Telephone operator 
Yard man 
Timekeepers 
Vegetable man 
Painters 
Carpenters 
Moving pictures (male under 40) 
Inspector of reels 
Clerical 
Checking 
Detective and watchman (male up to 
60) 
Government property 
Steamship piers 
Private homes 
Hotels 
Construction companies 
Steamship companies 
Checkers on piers (must join union for this 
work) 
Lamp shades 
Hand sewing 
Frame making 
Wholesale meat hbuses 
Checkers 
Biscuit Co. (young girls) 
Light packing 
Tying cakes 
Piano factories (men up to 60) 
Assembling small parts 
Polishers 
Felt hammer department and gluing 
Tuners 
Can factories 
Tinsmith helpers 
Soldering 
In lithograph department 
Automobiles 
Salesmen, supplies 
Mechanic and construction department 
Placement for cardiacs has also this important medical aspect, that in some 
instances it may save patients from attacks of decompensation which are due 
to cardiac overstrain from improper and too laborious employment. To 402 
SOCIOLOGICAL ASPECTS OF HEART DISEASE 
that degree, it will decrease hospital admissions from this cause, and save 
hospital beds and money for other patients. 
Social Service Work and Cardiac Clinics.—Cardiac clinics are now estab- 
lished in some of the larger cities, not only for group treatment of cardiac 
disease but also to bring home to physicians and laity the importance and size 
of the problem involved. The cardiac clinic must not only be thoroughly 
organized from the medical standpoint, but other activities are necessary and 
must be organized in order to carry out important sociological work. These 
will be described first, the clinic itself, last. 
There is the social service department, an all important adjuvant to the 
clinic. Besides information regarding the financial status of the patient and 
his family, there is correlated socio-medical work as part of its domain. If, 
for example, the social service head be a trained nurse, she can readily control 
the group exercises of the cardiac, especially of the children; her medical 
knowledge is sufficient for her to observe beginning dyspnoea, rapid or 
overforceful heart action, etc. in those taking part in graded exercises and 
games. Follow-up work by means of which home conditions are studied, 
parents and relatives given proper information regarding ventilation, sani- 
tation, clothing, food and exercise (especially stair climbing) is also part of 
the work of this department. It is the most important link between the clinic 
and the home; without it, the clinician has no way of determining whether 
treatment and advice given by him can or will be carried out. If one is deal- 
ing with a child, the question of schooling and, with it, the advisability of 
special school classes must be considered; if with an adult, the problem of 
proper employment must be carefully discussed. These are but two 
instances of the vast number of questions upon which the work of the social 
department touches. When carried out in a kindly, unobtrusive way, this 
department tends to harmoniously bind the medical with the equally impor- 
tant social problems of the cardiac. In large cardiac clinics, more active 
educational work may be undertaken through talks given by medical and 
social attendants to mothers of cardiac children. These should, of course, be 
simple and should touch upon such topics as sanitation, ventilation, proper 
diet, rest, exercise, the hopeful aspect of many of the cases, the importance of 
operative treatment of the tonsils and teeth in appropriate cases, etc. 
In well equipped hospitals under whose auspices cardiac clinics are 
managed, there should exist helpful cooperation. Where possible, frequent 
consultations between cardiac and correlated departments should be the rule, 
in order to gain proper viewpoints and well balanced judgment regarding the 
necessity and type of operative treatment to be carried out. Unless unavoid- 
able because of crowded conditions, mere routine sending of patients to nose, 
throat and dental clinics is inadvisable. 
Where the proper hospital facilities are at hand, X-ray plates or 
fluoroscopic examination of the chest should be made in order to have 
data regarding the size as well as the activity of the heart. Electrocardio- SOCIOLOGICAL ASPECTS OF HEART DISEASE 
403 
grams are also of value, especially in fixing types of arrhythmias and in 
aiding the diagnosis of congenital lesions and of myocarditis (Chapter IX). 
In order to obviate the necessity of the cardiac child going home for lunch 
or climbing stairs at school, or even visiting the cardiac clinic, special cardiac 
classes are established in schools; lunches are supplied, rest periods regulated, 
and graded exercises and games carried out. When such special classes are 
not available, cardiac classes can be organized in health centers or settle- 
ment houses; under such circumstances a special teacher for educational 
purposes and a proper nurse are required. The physician can visit and 
examine the children in their class rooms and give such directions and 
instructions as he finds necessary. 
All these correlated activities are naturally predicated upon the proper 
formation of the cardiac clinic itself. A concerted attempt among cardiac 
clinics has been made to standardize and simplify the classification of cardiac 
disease. The following has finally been adopted: 
Class I. Organic (able to carry on habitual physical activity). 
Class II. Organic (able to carry on diminished physical activity). 
A. Slightly diminished. 
B. Greatly diminished. 
Class III. Organic (unequal to any physical activity). 
Class IV. “Possible” heart disease (doubtful murmurs: mainly accidental, possibly 
organic). 
Class V. Potential (predisposing history). 
One may perhaps cavil at the advisability of some of these groupings. 
For example, “potential” cardiacs—chiefly children that have had rheuma- 
tism, chorea and frequent tonsillar attacks—should undoubtedly be carefully 
examined from the cardiac point of view, but I fear that overlapping of func- 
tion can scarcely be avoided if “potential cardiacs” are grouped in the 
cardiac clinics. A simpler grouping of organic heart disease might perhaps 
be that of the quiescent, the mild, and the severe insufficiency cases. But 
for the sake of uniformity among cardiac clinics, the first mentioned classi- 
fication should be followed as adopted. Once graded, it becomes a compara- 
tively easy task to carry out appropriate treatment. Thus Class III, the 
severely decompensated, are not ambulatory cases. They belong at home 
or in the hospital. When again beginning to compensate, the questions of 
active and passive motion (Chapter XX), and the time for being allowed 
out of bed must be decided. The first class also—those with physical signs 
but no symptoms—are readily disposed of. Children and adults may 
follow the usual conservative daily routine of normal individuals. They 
may practice mild sports and games; but they should eschew violent sports 
such as football and should not participate in competitive games. When 
possible, laborers should choose a type of work that does not require constant 
extreme muscular exertion. One can only generalize by stating that all 404 
SOCIOLOGICAL ASPECTS OF HEART DISEASE 
patients with organic cardio-vascular disease should exercise, work or play 
well within their individual cardiac tolerance. I believe this warning 
justified in spite of the well known fact that cardiacs are found among 
laborers and athletes who have never shown any circulatory symptoms. In 
general, those with markedly hypertrophied hearts (usually aortic lesions) 
should be more conservatively advised regarding the type of sports and games 
and regarding such routine as stair and hill climbing. Next in the scale of 
conservatism are cases of mitral stenosis. One may be least conservative in 
those of this group (first class) who have quiescent mitral regurgitant 
lesions. 
Class II, the mild insufficiency group, is that which usually constitutes the 
majority of the ambulatory patients. They likewise offer the best oppor- 
tunity for improvement by means of graded games and exercises. I refer 
here to children alone: Adults of this group, if sufficiently improved, should 
seek suitable employment (p. 401). 
Exercise among children is best achieved by graded games and drills. 
Games that in addition give proper posture are of special advantage. Exer- 
cises should be supervised by .a doctor, trained nurse or specially instructed 
social worker. Various types of drills—all rhythmic—may be devised. 
The simplest are those in which, at the beginning, all may take part. In 
general, they correspond to mild setting-up exercises, leaving out sharp 
flexing of the abdomen. Upward and lateral movements of the arms, clap- 
ping hands above the head and in front of the body, lateral and forward, 
lateral and slight backward bending of the body on the trunk, bending of the 
knees and hips are some of the usual types of drill exercises. Military tramp- 
ing and shuffling steps, marking time and other exercises will readily suggest 
themselves. 
More active games may be devised for those who have shown no circula- 
tory strain as a result of the milder exercises. Breathlessness, prolonged 
tachycardia, overforceful and violent heart action, drawn and tired features 
are some of the more obvious, readily discernible evidences of such overstrain. 
Such games as hopping, pitching ball, rhythmic dancing, etc. are suggested 
as more active games in the better compensated cases. 
An excellent adjuvant to cardiac clinics is some form of convalescent 
country home. A sojourn in the country is especially advisable for those 
who have recently recovered from endocarditic reinfections, or who look 
pale, tired and undernourished. In the latter, overfeeding should be 
attempted. To bring these patients to normal weight is perhaps one means 
of strengthening the entire organism against the inroads of infection. The 
home should not be too far from the city so that the patients can be occasion- 
ally visited by relatives, thus forestalling nostalgia. Convalescent homes 
are especially appropriate for those with fair exercise tolerance. 
I have used the following scheme in my cardiac clinic. SOCIOLOGICAL ASPECTS OF HEART DISEASE 
405 
CARDIAC 
CLINIC 
o 
SOCIAL HISTORY 
w 
Name 
Age.... 
. . Address.. 
Living 
Health 
Alcoholic 
Working 
Occupation 
Wages 
Family income $ 
Intelligent? 
Responsive? 
Clean? 
Date 
For Child 
Mother 
Married 
Occupation 
Working 
Alcoholic 
Wages 
3 
Wife living? 
Husband living? 
< 
o 
Z 
>1 
Children: Number 
Ages. 
. Number working... 
tA 
Home: T.* 
P.H.* 
*Number rooms 
. .Number dark Rent $. . . .Boarders 
a 
<u 
Sanitary conditions: Neat 
Untidy 
Dirty Separate beds. . 
. . .Patient’s room 
ca 
Food: Sufficient? Yes 
No 
. .Fair. 
Bad 
5 
Needs 
Religion 
Church or settlement affiliation 
Immediate needs 
Sick benefits. . 
Insurance... 
LATER SOCIAL SERVICE REPORT 
Date. . 
r-19- 
Home: Improved? Yes No Food: Sufficient? Yes 
No Cooking: Good Fair Bad 
o 
Patients: T. 
P. 
R. 
Symptoms 
ft 
Treatment and advice. 
cl 
o 
« 
FIRST EXAMINATION- 
-CLINICAL 
NOTES AND TREATMENT 
Family History: Rheumatism. . . 
Chorea 
Cardiac disease 
. . . Alcohol 
Previous History: Rheumatic fever 
Tonsilitis. . . . 
. . Chorea 
Myalgia. . . . 
.. Purpura or Erythema.... 
Diphtheria. . 
.Venereal. .. 
Alcohol. . . . 
.Tobacco 
CA 
Sleep 
. Bowels.. . 
. Occupations 
CA 
O 
Other diseases and complications 
a 
bfl 
Patient feels. . 
. . Patient’s statement.. 
Ctf 
,p3 
Appetite 
Digestion. . 
B’kfast 
Dinner 
Supper 
>> 
Bowels: Move at 
. Between meals ... 
cS 
a 
C 
Sleep: In bed at 
Windows open? 
Rests? 
to 
to to 
Outdoors 
. School hours. . 
A.M. to 
P.M. Open air class 
a 
Exercise: Walking 
Running 
Playing 
Stairs: Flights a day. 
Flights at school. . 
. .Lives flights up 
Dvsoncea? 
Cough? 
Pain 
Paloitation: Subiective? Tachycardia? 
Edema: Where? When? 
Color: Good.. 
Cyanosed 
>» 
Nutrition—Weight: Stripped. . .. 
T 
P. 
R. 
T3 
Aspect: Calm— 
-Healthy.. . Quiet. 
. . . Active. 
Dyspnceic. . . 
.Sick. . . .Prostrated 
<D 
a 
Tonsils: Size.. 
Smooth.. 
. . . .Ragged Buried. . . .Crypts: Large. . . .Small 
e 
Removed: Completely? 
Incompletely? 
X 
w 
Lymph nodes: 
Cervical 
Size 
Teeth 
.Bad 
Pyorrhoea? 
• 
T. = 
Tenement. 
P.H. 
= Private House. 406 
SOCIOLOGICAL ASPECTS OF HEART DISEASE 
CARDIAC EXAMINATION 
Apical impulse: Circumscribed ? Diffuse ? 
j 
Forcible 
[ Weak 
Location of apex: Maximum in Interspace c. m. from M. S. L... 
! 
[ Heaving 
Borders: R. c. m. from M. S. L L. c. m. from M. S. L 
Auricular fibrillation? Sinus arrhythmia? 
Extrasystole ? 
Rhythm: Regular Irregular Tachycardia ? 
Heart block? 
Sounds: At apex I II 
At Rt. base, A. I II 
At Left base, P. I II 
Murmurs: Maximal site Transmission Time of occurrence. . . . 
Quality: Soft? Harsh? Blowing? Rumbling? Musical? 
Rough? 
Effect of inspiration Expiration 
Pulse rate: Standing Lying After exercise 
Character of pulse 
/ Systolic J Systolic 
Blood pressure: Brachial \ Diastolic Leg \ Diastolic 
Attacks of decompensation: Duration Date 
Chief symptoms 
Exercise tolerance 
Present attack: Time of onset Initial symptoms 
Dyspnoea Edema Pain Cough. .. 
/ Tachycardia? 
Disability Palpitation \ Subjective? Gastric symptoms.. 
Loss or gain of weight Color Urine 
Pericarditis: Dry Friction sounds Area Time of occurrence 
Effusion X-Ray 
Lungs 
Abdomen 
Spleen 
Type of lesion: Quiescent? Progressive? 
Electrocardiogram 
Prognosis 
Advice 
Group classification.—See 403. 
Duggan, Ida M.: Employment for the Handicapped, II; The Cardiac: Hospital Social 
Service Quarterly, 1920, II, 227. 
Emerson, H.: The Prevention of Heart Disease*—A New Practical Problem; Boston 
Medical & Surgical Journal, June, 1921. 
St. Lawrence, W. P., and Adams, L. A.: The Organized Care of Cardiac Children; Hospital 
Social Service Quarterly, 1920, II, 151. 
REFERENCES CHAPTER XXIII 
PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN—ANGINA 
PECTORIS—CORONARY DISEASE—ETIOLOGY, PATHOLOGY, 
CLINICAL COMPLEXES AND THERAPY 
Pains due to pericarditis are not included in this description. 
Pain in the chest, especially in the substernal region and in the left 
breast, is such a frequent accompaniment of all types of cardiac disease 
that, although but a symptom, it requires minute consideration. Precordial 
pains in all types of severe organic cardiac disease is probably due funda- 
mentally to some sudden disturbance in nutrition (as in coronary occlusion), 
to some added infection (as in rheumatism), or to some adverse mechanical 
factor (as in cardiac dilatation). These three factors may be summed up in 
the one that the basic cause of heart pain lies in some marked alteration 
of the myocardium by which it cannot contract and pump blood efficiently. 
Even here, the general qualifications are demanded that, as in all disease, 
different patients react to pain differently, and that psychic disturbances such 
as fright, excitement and strong emotions, can initiate symptoms of precor- 
dial distress (Chapter XIV). The etiological factor in psychic disturbances 
naturally varies, but fundamentally it consists in abnormal excitation starting 
from the cerebral centers; the effect upon the circulation, however, may be as 
disasterous and as pain-producing as the physical factors above enumerated. 
There is perhaps no single subject in the realm of cardio-vascular disease 
of greater clinical interest and importance than that of coronary disease, a 
common cause of precordial distress. Diagnosis is often difficult because of 
the many clinical complexes that coronary disease can produce. The diffi- 
culty is unfortunately enhanced by the many terms and types introduced 
by the older writers. Thus, Huchard has divided angina pectoris into true 
and false. Osier describes four types. False angina pectoris, angina sine 
dolore, angina vasomotoria, angina vera are terms handed down to us from 
older clinicians, and now are bandied about with no clear etiological or patho- 
logical picture in mind. If one excepts “ angina sine dolore ” (angina without 
pain), the common outstanding characteristic, whatever the nomenclature 
followed, is pain. It therefore seems more logical to retain cardiac, or better 
still, precordial pains as the predominent feature, and to specify the etiolog- 
ical factor which seems mainly or entirely concerned as the direct cause of the 
pain. Nothing can conduce to a clearer conception of this involved subject 
than a searching insight into the pathological possibilities of coronary disease; 
a good anatomical picture of coronary distribution; a general knowledge of 
the rich ganglionic nerve supply and plexuses surrounding the heart and 
407 408 
PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
aorta; the correlation and connection between the nerve supply of the heart 
and stomach; blood pressure estimation; a careful clinical history and urinary 
examination: These, the handy armamentarium of the thorough clinician, are 
the fundamental factors upon which diagnosis must be based. One should 
add, wherever possible, all the more modern methods of refined examination 
such as electrocardiographic and X-ray examinations, chemical examina- 
tion of the blood, phenolsulphonephthalein output, Wassermann examination. 
But often in consultation and general practice, one is suddenly confronted with 
an apparently unexpected attack of precordial pain of coronary origin, a bolt 
out of a clear sky, and one must arrive at a definite diagnosis, give an opinion 
and advise rational therapy with only ordinary clinical methods as our aids. 
Before dealing with the pains of coronary disease in detail, it will be 
advisable to call attention to some general salient features. 
i. Occlusion of Smaller Coronary Branches.—Regarding the coronaries 
themselves, they are no longer regarded as end arteries (Chapter I); there 
are numerous communications, especially deep intermuscular branches, 
by means of which collateral circulation can be maintained. As an obvicus 
consequence of this collateral circulation, partial occlusion of a larger coro- 
nary branch by embolism or thrombosis, or complete occlusion of a smaller 
branch need not necessarily completely cut off cardiac function of the affected 
part of the heart, for after a varying interval, collateral circulation may, 
at least for all functional purposes, restore the blood supply, and with it the 
vitality of the affected musculature. I emphasize the word “ necessarily ” 
because even a little thought will show that there are many factors involved 
in an assumed restoration of blood supply and function. One can readily 
conceive, for example, that a large embolus which completely and suddenly 
occludes a large coronary branch will immediately cause major and extremely 
serious symptoms with probable death. On the other hand, a cause operating 
gradually in a smaller coronary vessel—for example slow thrombus formation 
from chronic or subacute arteritis—will not produce sudden myocardial 
necrosis and will probably allow sufficient time for collateral blood supply, 
with a more or less complete restoration of cardiac function, despite the later 
formation of scar tissue at the thrombosed area. Again, sudden sharp 
occlusions of the main coronaries, by attacking and affecting large myo- 
cardial areas, are often accompanied by pericarditis. As will be later 
shown, this is of great diagnostic importance. 
It is known that patients who have recovered from cardiac pains have 
occasionally shown myocardial scars and other changes resulting from old 
infarcts. Huchard, in a summary of 145 necropsies of coronary disease with 
cardiac pains, found five due to embolism of the artery. Recently, several 
cases with necropsy reports of embolic infarcts of the main coronaries have 
been described; the patients died within a few days or hours with symptoms 
of intense precordial distress. I have observed several cases with inter- 
mittent pains lasting days or weeks, in which the symptoms were possibly PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
409 
caused by infarcts or emboli of the smaller coronary branches. Curschmann 
in 1891 first described this condition; he reported three cases with necropsies. 
Two patients died some years after the onset of symptoms. Both showed 
localized myocarditis. In one, there was an aneurismal dilatation confined 
to one sclerosed arteriole; in the other there was an obliterated coronary 
branch of the third order. The third patient, in whom the condition was 
correctly diagnosed, died suddenly; an embolus was found in a coronary 
branch of the second order. 
In addition to actual plugging of the vessels, there is again the much 
disputed question of coronary spasm. From experimental observations, we 
know that coronary spasm can occur. Upon clinical grounds, I believe that 
coronary spasm can occur in comparatively healthy vessels which are the 
subject of excessive nerve excitation. For example, I consider coronary 
spasm the chief cause of precordial pains in so-called “smoker’s heart” 
(Chapter XXVI). 
2. Pain.—So far as known, there are no nerves of sensation in the heart. 
Through the fundamental work of Sherrington, Head, and later, of Mackenzie, 
it is known that a viscus, though not possessed of nerves of sensibility, may, 
when irritated, excite the corresponding visceral segment of the spinal cord; 
the latter then sends abnormal centrifugal impulses to the muscles, glands, 
etc., which in the skin give rise to abnormal sensations usually felt and denoted 
as pain. In cardiac disease the area ordinarily affected is the precordium. 
Depending upon the nerves involved, upon the intensity of the irritation, 
or possibly upon the irradiation of centripetal impulses to other spinal seg- 
ments, pain may spread to the entire chest, to both arms (especially to the 
left), to the fingers, neck, head, the interscapular region, the epigastrium, 
the abdomen and even the thighs. Besides the precordium and left shoulder, 
the epigastrium is the favorite site for referred pains, a fact which often causes 
erroneous diagnoses, and mistakenly directs the therapy to the stomach. 
In severe cases, pain is usually sharp, lancinating or agonizing in character, 
and is combined with the oft-described feeling of impending death. In 
milder cases, it is dull and aching in character, or there may be merely a feel- 
ing of oppression of the chest. Head’s zones of hyperasthesia are sometimes 
present, usually over the precordium, more rarely in the epigastrium. Occa- 
sionally pressure even of wearing apparel, produces severe pain. The sensi- 
tiveness may be confined to the underlying intercostal muscles; deep pressure 
alone then elicits pain. It is sometimes possible in a general way to judge of 
the effect of therapy and of the progress of the disease by the amount of pain 
elicited upon superficial or deep pressure. When progress is favorable, 
sensitiveness to pressure is diminished. 
While pain is the most common and indeed a cardinal symptom, the 
patient may become so overwhelmed by other phases of the disease, for exam- 
ple, by vomiting, dyspnoea and pulmonary edema, that pain as a symptom 
may be either evanescent or of but minor importance. 410 
PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
3. Gastric Symptoms.—Vomiting is extremely common, indeed so 
much so that in every case of vomiting in an older individual, especially 
when combined with dyspnoea and with no evidence of any abdominal dis- 
ease, a coronary infarct should be suspected. The gastric symptoms aie 
usually attributed to a dilated stomach or to congested gastric mucosa, and 
the dyspnoea to the embarrassed heart action from pressure of a dilated 
stomach against the diaphragm and heart. My opinion is that, in the vast 
majority of cases, the cause of gastric symptoms is due to reflex excitation of 
the vagus nerve supply of the stomach. Indeed the gastric symptoms may 
mask the actual cardiac picture for years. For example, one of my patients 
had dyspeptic symptoms resembling severe hyperacidity for years. The 
chief hints of cardiac damage were some dyspnoea when out of doors, occa- 
sional severe pain in the left chest, and a low blood pressure. He finally died 
of a coronary occlusion attack. In this connection it is important to discuss 
the frequency of epigastric pains and of occasional epigastric Head’s zones 
found in heart disease. The former are usually ascribed to an enlarged 
liver or to congested gastric mucous membrane. However, the pains are 
present when the liver is not enlarged, and necropsy reports show that 
such patients often had no congestion or disease of the gastric mucosa. 
Besides, we possess no data which definitely correlate such presumed con- 
gestion with pain. From clinical manifestations, from disappearance of 
epigastric tenderness with disappearance of decompensation, and from 
the intimate correlation of the nerve supply of stomach and heart, it seems 
probable that this type of pain is chiefly, if not entirely, the result of referred 
nerve excitation from cardiac disease. 
Further, it should be remarked that the pains of cardiac disease are 
especially apt to be evoked in those who have actual gastro-intestinal or gall 
bladder disease. This is especially true of middle aged or older individuals 
with cardio-sclerotic or coronary disease. I do not believe that in the vast 
majority of cases, assumed intestinal toxemias play any role in the causation 
of these precordial pains. The etiological factor seems to be reflex excitation 
of cardiac innervation originating from disturbances of the gastric, intestinal 
or gall bladder nerve supply. 
4. Arrhythmias.—Cardiac irregularities frequently accompany attacks 
of coronary occlusion; the more severe the attacks, the longer the irregularity 
is apt to remain. Complete irregularity of pulse and heart action—auricular 
fibrillation—is the usual type of arrhythmia. Extrasystoles are also common. 
What I have always considered of special prognostic importance is the 
occurrence of frequent and apparently unaccountable attacks of arrhythmias: 
Auricular fibrillation, extrasystoles and paroxysmal tachycardia. Occurring 
with dyspnoea and accompanied by little or no pain in patients with cardio- 
sclerosis, they usually presage an attack of coronary occlusion which may end 
in sudden death. Such instances will be cited later. PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
411 
5. Acute Pulmonary Edema.—This very frequently accompanies the 
precordial attacks of coronary disease. It varies in degree, at times almost 
immediately causing the patient’s death. It is the chief alarming symptom in 
major attacks. While its cause is still speculative (Chapter XIV), it seems to 
be directly due to suddenly impaired and tremendously weakened cardiac 
function, in consequence of which there is pulmonary congestion as the first 
phase, and edema as its second and final phase. Often pulmonary edema is 
the symptom which requires immediate therapy. 
6. Transient Nephritis and Dependent Edema.—In some attacks of 
coronary occlusion, especially of the larger branches or main vessels, there is 
often a heavy trace or a cloud of albumen in the urine with many hyaline 
and granular casts. Hypertension, if previously high, usually decreases 
somewhat. The urinary condition seems due to general circulatory collapse 
following coronary failure, with consequent renal congestion. When the 
circulation improves, the edema and signs of nephritis rapidly clear up. If 
the coronary attack was not sufficiently typical to make a definite diagnosis 
from the usual signs and symptoms—precordial pains, pulmonary edema, 
arrhythmias, dyspnoea—one may venture the diagnosis upon the type of 
nephritis and edema above described. The treatment is that of the primary 
condition. 
7. Gastro-intestinal Paresis.—I have encountered this condition in several 
cases of coronary attacks when circulatory failure went from bad to worse. 
The patients are usually in coma or semi-coma. They regurgitate or vomit 
coffee-ground material; the abdomen is rotund, tympanitic, somewhat doughy. 
There is no local tenderness. The condition seems due to venous overfilling 
of the splanchnic reserve areas from cardiac failure, with consequent insuffi- 
cient oxygenation of the gastro-intestinal tract. Besides cardiac stimulation, 
gastric lavage, pituritin or adrenalin are especially indicated. 
8. Mottling of the extremities or actual venous thrombosis is sometimes 
observed in the terminal stages of coronary occlusion. The cause is venous or 
capillary stasis from circulatory collapse. 
I have sketched at some length these important and prominent general 
aspects of the subject in order to clarify the problem of diagnosis, differential 
diagnosis, prognosis and therapy. 
The commoner causes of precordial pains due to cardio-vascular disease, 
may be tabulated as follows: 
A. Organic cardio-vascular disease: 
1. (a) Hypertensive cardiovascular disease with myocardial insufficiency. (b) Hyper- 
tension with myocardial insufficiency and labile vasomotor mechanism. (c) Uremic 
group. 
2. Myocardial insufficiency without hypertension. 
3. Acute rheumatic endocarditis and rheumatic endocarditic exacerbations. 
4. Endomyocardial disease with general circulatory failure. 
5. Embolic infarcts in the main coronaries and their branches. 412 
PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
6. Cardiac syphilis. 
7. Premature arterio-sclerosis and cardiosclerosis. 
8. Senile arterio-sclerosis and cardio-sclerosis. 
9. Sacculated aneurysm. 
i. (a) Hypertensive Cardio-vascular Disease with Myocardial Insuffi- 
ciency.—The patients of this group probably represent the most frequent suf- 
ferers from precordial pains. The cause of hypertension has been ascribed by 
some to an increase of epinephrin in the blood, though careful experiments by 
Janeway and Park have not justified this assumption. Recent studies of 
blood metabolism have shown that chronic nephritis with hypertension is 
often accompanied by an increased amount of non-protein nitrogen in the 
blood, and by a diminution of blood alkalinity, (Chapter XXI)—facts which 
may in the future offer promising fields for therapy. The chief cardiac 
changes are ventricular hypertrophy, usually left, but sometimes also right; 
patchy, fibrous myocarditis; thickened aortic and mitral cusps; lime deposits 
on the first portion of the aorta; and atheroma and thickening of both 
coronaries. It must be remembered, however, that patients with similarly 
diseased hearts may have little or no precordial distress. 
A brief case description will serve to fix the type: A systolic blood pressure 
of 190 m.m.; a rough first and a sharply accentuated and bell-like second sound 
at the right base; evidence of marked left ventricular hypertrophy with a 
heaving apical impulse; urine with or without albumin or casts; very slight 
pretibial edema; dyspnoea on exertion or appearing suddenly at night; 
nycturia. The pains are usually dull, most marked in the precordium, 
and radiate to the neck and arms. 
Almost frantic therapeutic efforts are made, as a rule, to reduce the high 
blood pressure, while the fact that it is often a conservative, compensatory 
process seems to be entirely ignored. A mere enumeration of the long list of 
remedies is sufficient proof of their inadequacy. Vaso-dilators (nitroglycerin, 
amyl nitrite, erythrol tetranitrate), hot, Nauheim and oxygen baths, violet 
ray, diathermy and electric light baths are the most popular. There are con- 
flicting and contradictory reports regarding all. In some cases, I studied the 
effects of hypodermic injections of 1 per cent, solutions of nitroglycerin in 
doses up to one tenth of a grain, there times a day; they had no effect upon 
the symptoms and caused but an occasional temporary reduction of the blood 
pressure. The physical changes in the coronaries probably account for the 
futility of vasodilators to regulate the impoverished cardiac circulation and 
thus relieve the resultant precordial symptoms. While theories such as 
cardiac spasm and anemia have had vogue as the causes of the pain, it seems 
more probable that the underlying factor is nutritional cardiac disturbance 
either from inadequate coronary circulation or, possibly, from toxic products 
flowing in the general circulation. Acute violent pains call for morphine. 
Pearls of nitrite of amyl may also be of aid. With milder symptoms, nitro- 
glycerin occasionally gives some relief, especially if combined with atropine PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
4i3 
sulphate. Aside from temporary therapeutic measures, I have placed main 
reliance on digitalis, either the tincture in 15 drop doses, or digitan tablets 
three times a day. The drug should be given whether the auricles fibrillate 
or the pulse is rhythmic, and should be stopped when pains and other symp- 
toms improve, and then continued in smaller doses for a long period. A 
curb should be put on the patient’s physical activity. Mental excitement 
and stress should be avoided. The theoretical objection that digitalis may 
perhaps cause or increase coronary spasm has not been verified by clinical 
evidence in cases in which the drug has been given for months. In only one 
of my cases were precordial pains increased by digitalis, although even here 
there had been general improvement for several months. 
The importance of treatment of edema and other manifestations of cardio- 
vascular disease lies in their fundamental association with precordial pains. 
This is illustrated in the following case: 
A vigorous woman of 43, never pregnant, complained for three years of 
dyspnoea on walking, and of stabbing precordial pains radiating to the left 
shoulder. The Wassermann blood reaction was negative. The urine con- 
tained a trace of albumin and, occasionally, hyaline casts. There was slight 
tibial edema. Physical examination revealed typical signs of aortitis. The 
orthodiascopic tracing showed an enlarged left ventricle and a dilated aortic 
arch. The precordial area was tender to deep pressure. For the first few 
months she was put on digitalis, theobromin sodium salicylate, and occasional 
Karrell days (Chapter XX). Within two months the cardiac pains and 
pretibal edema disappeared. Later, when she became remiss about medi- 
cation and diet, dyspnoea and pain recurred. Under stricter surveillence and 
the same medication, combined with absolute rest at home on the Karrell 
days, twice weekly, she again slowly improved. This plan of treatment has 
been followed for several years. The blood pressure is still high; data 
revealed by physical and roentgen examinations are the same, but there 
is very marked clinical improvement; precordial pains and edema have 
entirely, and the dyspnoea almost entirely, disappeared. 
(b) Hypertension and Myocardial Insufficiency with Labile Vaso-motor 
Mechanism.—In a smaller group of cases, in which the highest systolic blood 
pressure was around 180 m.m., with marked diurnal variations of as much as 
30 m.m., precordial pains following exercise were the main symptoms. Neph- 
ritis was apparently not the main or the only cause of hypertension; emphy- 
sema and myocarditis were the chief pathologic conditions. Experimental 
subcutaneous injections of nitroglycerin in doses of one fiftieth grain three 
times a day had a marked temporary effect on the blood pressure and, 
usually, on the symptoms; in one instance, the injections were regularly 
accompanied by sudden relief of precordial pains, to be followed by giddiness. 
Such cases apparently represent examples of disturbed labile vaso-motor 
mechanism rather than hypertension due to marked vascular disease alone. 
Nitroglycerin or other vasodilators given at the onset of pain are apt to be 414 
PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
followed by great relief. Digitalis, though useful, is not as beneficial as in 
Group I. This is the group in which vaso-dilators are apt to be followed by 
beneficial results, apparently because coronary spasm plays an important 
role in the causation of symptoms. 
(c) Uremic Group.—Headache, nausea, vomiting, varying grades of 
anemia, attacks of paioxysmal dyspnoea and of precordial distress, high sys- 
tolic and, especially high diastolic pressures, nocturnal polyuria and changes 
in the retina, are the cardinal signs and symptoms. Kidney test meals, as 
advocated by Schlayer and others, usually show decreased salt, nitrogen and 
water elimination; and the blood shows retained non-protein nitrogen. The 
facial appearance in typical instances is characteristically pallid or ashy 
grey. 
The precordial pains are not relieved by nitroglycerin, digitalis or theo- 
bromin sodium salicylate. They are apparently caused by toxic products 
flowing in the general circulation and affecting cardiac nutrition. Dietetic 
measures, especially a diet low in protein and rich in carbohydrates, are of 
most value. When renal tests show no water retention, ingestion of large 
quantities of fluids is sometimes beneficial. For the relief of pain, occasional 
doses of morphine are necessary. On the theory of tissue acidosis, I tried the 
intravenous injection of 500 c.c. of a 5 per cent, bicarbonate solution in two 
cases (Chapter XXI). In one, there was marked relief of the precordial 
pains and other symptoms; in the other, the pain was relieved for a few hours 
only. Glucose solutions given by the Murphy drip or even intravenously may 
be of value. 
2. Myocardial Insufficiency without Hypertension.—The main complaint 
of these patients, usually men of sedentary habits between the ages of 50 and 
60, is slight precordial pain following exertion. The patients are well pre- 
served. The urine is normal or may contain a slight trace of albumin with a 
few casts. Physical examination reveals a slight impurity of the first sound 
at the apex, and a soft systolic murmur at the base. There is no evidence of 
severe cardio-vascular disease. The systolic blood pressure is around 160 
m.m., rarely much higher; there is no edema. The orthodiascopic tracing 
usually shows a slightly dilated aortic arch with the left ventricle lying broad 
and flat on the diaphragm; it is impossible to state if this ventricular contour 
is due to flabbiness or to hypertrophy (Chapter XII). It is interesting to 
note that these patients commonly give a history of having had painful 
gastric attacks in previous years, with symptoms pointing to gastric or duode- 
nal ulcer. Excellent results have followed the use of digitalis, given at first in 
large, and then in moderate doses, and continued intermittently for weeks or 
months. Small doses of atropine were sometimes added. At the beginning 
the patient’s activity was somewhat restricted; later, moderate exercise—golf 
or walking—was advised. Acidulous food and drink were interdicted, and 
some light form of nourishment between meals was prescribed. The 
following is an illustrative case: PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
4i5 
Male, age 60, for years has been careful about his diet, particularly in the 
avoidance of acids, because indiscretions were followed by epigastric pains. 
For several months he has complained of precordial, knife-like, paroxysmal 
pains on walking. Examination showed a well nourished man; there was no 
edema; the urine contained no albumin or casts; the average systolic blood 
pressure was 160 m.m. The orthodiascopic tracing revealed a somewhat 
enlarged left ventricle, the aortic outline was slightly broader than normal. 
There was an impure first sound at the apex and at the right base. There was 
no dyspnoea or decompensation. One digitan tablet was given, at first three 
times daily, and then continued in smaller doses for several months. Atro- 
pine sulphate, of a grain, three times a day, was also prescribed. The 
patient is now doing his regular work, has taken ocean baths during the 
summer, and has had no recurrence of precordial pains. 
3. Acute Rheumatic Endocarditis and Rheumatic Endocarditic Exacerba- 
tions.—These cases usually occur in young persons with definite rheumatic 
histories, with mild tachycardia, with no dyspnoea, and with marked ausculta- 
tory evidence of valvular disease (usually mitral stenosis). Slight irregular 
rises of temperature are common. The patients complain not only of the 
subjective feeling of palpitation, but also of “sticking” pains localized in the 
region of the heart. There are usually precordial Head’s zones of hyperasthe- 
sia. The cause of the rapid heart action and of the precordia.1 pains, even in 
the absence of abnormal temperature and other rheumatic manifestations, 
appears to lie in the irritative effect of fresh exacerbations of endocarditis. 
The best medication is sodium salicylate given in full therapeutic doses. 
My routine has been 15 grains hourly until six doses have been given or until 
tinnitus occurs; the dose is then decreased. Bromides in moderate amounts, 
and ice bags to the precordium, are also helpful. Moderate or absolute rest 
in bed may be necessary for some time. 
The following are typical instances: 
Female, unmarried, aged 18, under observation three years, gave a typical 
rheumatic history. There is a marked double aortic lesion and a tremen- 
dously hypertrophied heart. The Wassermann reaction and frequent blood 
cultures were negative. The systolic blood pressure was 180 m.m., the dias- 
tolic, 20 m.m. For months she has had many attacks of moderate irregular 
fever. On several occasions these were initiated by sharp precordial pains 
followed by tachycardia or auricular fibrillation, convulsive twitchings and 
tremors, and by loss of consciousness lasting several days. Latterly these 
attacks have become more severe and are followed by well localized Head’s 
zones. 
Female, unmarried, aged 20, gave a history of continued attacks of 
rheumatism and “heart trouble.” During the last few months she had two 
attacks similar to but not quite as severe as that with which she entered the 
hospital. There were continued agonizing pains and exquisite tenderness, 
even to the slightest touch, over the precordium, and radiating pains to the 416 
PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
shoulder and forearm. The temperature was 104°. A mitral regurgitant 
lesion was present. There was no edema. Breathing was frequent and 
shallow, apparently in the attempt to keep the chest at rest. After one 
week, high temperature, sharp pain, and rapid breathing disappeared; the 
patient felt comfortable, but precordial tenderness on firm pressure was 
still present when she left the hospital. 
Male, aged 40, with a double mitral lesion, gave a history of having felt 
well until three months prior to hospital admission. He then had an attack 
of mania (?) lasting three days. Subsequently pneumonia and pleurisy 
developed, accompanied by chills and high fever and by attacks of paroxys- 
mal auricular fibrillation. After several cultures, a non-hemolytic strepto- 
coccus was isolated from the blood. During several months of hospital 
observation there was a constant sensitive area near the cardiac apex. 
The characteristic of these three cases was not only the rise of temperature 
and evidences of active endocarditis, but also the progressive tendency of the 
disease, and the presence of local, tender precordial areas. Though these 
manifestations may have been due to the endocarditis alone, the distinct 
localized sensitive areas, and the clinical course, make it probable that, in 
addition, acute focal myocarditis was present. From clinical and physical 
signs, and from the progressive and probable bacterial nature of the endo- 
carditis, it seems fair to assume that such focal myocardial changes originated 
in embolic infarcts of the smaller coronary branches, accidents not neces- 
sarily incompatible with life. 
Necropsy findings will of course be necessary to establish the diagnosis 
in such cases. 
Two illustrative cases are given to show the diagnostic importance of dry 
pericarditis, as well as to indicate the difficulties of diagnosis. 
Mr. K. aged 80, a man of powerful physique, had always been well until 
two days before I saw him. He was then attacked by severe precordial 
pains which were almost continuous. Upon examination, there were found 
hypertension, thickened and tortuous arteries, loud systolic murmur over 
the mitral, a definite patch of dry pericarditis extending over the mitral 
area. The patient died of pulmonary edema after two days. 
Mr. S, aged 53, had chronic nephritis, hypertension and left ventricular 
hypertrophy for several years. Of late months he suffered from almost 
constant dyspnoea, from occasional slight attacks of pulmonary edema 
and from attacks of precordial pains. In at least three such attacks, as 
accompanying features, I was definitely able to localize areas of dry per- 
icarditis with typical friction rubs over the lower precordium. With the 
recession of these attacks of pain (which I ascribed to thrombosis in the 
smaller coronaries) the physical signs of dry pericarditis also disappeared. 
As I visualize the pathological process, each attack of coronary occlusion 
was accompanied by a patch of fibrinous exudate over the freshly invaded 
myocardium; the exudation again receeded either as the result of the estab- PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
4i7 
lishment of collateral circulation or because the acute inflammatory dis- 
turbances had run their course. 
4. Endo-myocardial Disease with General Circulatory Failure.—The 
fundamental cause of the pains in apparently nutritional disturbances from 
local circulatory failure in the heart itself. Precordial Head’s zones or inter- 
costal muscle tenderness are often present. The therapy for the relief of pain 
is the same as for decompensation. This ordinarily means vigorous and 
long-continued digitalis medication, and, for the relief of edema, theobromin 
and the dietetic regimen already outlined. If compensation is restored, 
cardiac pains and Head’s zones disappear. 
5. Cardiac Syphilis (Chapter XVI) is an extremely frequent cause of 
precordial pain. It is usually substernal, dull, boring and aching; it may, 
however, have the distribution and characteristics of the types already 
described. One can probably ascribe the frequency of these substernal 
pains to the almost invariable presence of syphilitic aortitis and periaortitis 
with consequent aoitic dilatation; to the fact that the root of aorta is sur- 
rounded by rich ganglionic and nerve plexuses; and to the varying degrees 
of aortic dilatability and pressure. Head’s zones are comparatively rare. 
There are apt to be acute attacks of precordial pains if the coronaries are 
also involved. Such attacks are frequently accompanied by decompensa- 
tion. Therapy consists in the treatment of the underlying disease (Chapter 
XVI). Although salvarsan was originally considered contraindicated in 
cardiac syphilis, abundant experience has since shown that, given first in 
smaller, later in larger doses, salvarsan combined with the usual mixed treat- 
ment is of great and definite value. The best routine method of administra- 
tion is 0.2 gim. of salvarsan or arsphenamin injected intravenously every 
week until 0.6 grm. is given; later, full doses may be given, the frequency 
depending on the cardiac condition. Salvarsan sometimes benefits and 
controls the pains immediately, apparently because of reduction in the syph- 
ilitic inflammatory exacerbations. Where the pathologic process in the 
aorta, the coronaries or in the myocardium has reached an extreme degree, 
salvarsan or any other treatment can be of little or no avail. Cardiac 
failure, if present, should receive its appropriate treatment, that is, digitalis, 
and if necessary, theobromin sodium salicylate. 
6. Premature Arterio-sclerosis.—This comprises a rare group found in 
young adults. Persistent precordial distress is often present for months. 
Gastric symptoms similar to those of hyperacidity occasionally dominate 
the clinical picture. Physical examination may give no hint of the severity 
of the pathological process attacking the entire cardio-vascular system, 
a process finally resulting in extreme changes throughout the aorta, coronaries, 
arterioles and endocardium. Indeed, such hearts may be pathologically 
identical with those of persons dying with senile cardiac changes. For 
months there may be no decompensation in the ordinary sense. The urine 
may be normal, the blood pressure not high, the heart sounds somewhat 418 
PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
distant, and the only indication of severe cardiac disease, besides the precor- 
dial pains, may be the presence of an arrhythmia, usually marked sinus 
arrhythmia or extrasystoles. Other occasional symptoms are dyspnoea 
and nocturnal attacks of precordial distress. 
An illustrative case with necropsy report follows: 
Male, aged 42, of athletic build, had been a heavy smoker. For four 
years he had suffered from gastric symptoms resembling hyperacidity; 
belching was particularly prominent. The gastric contents showed high 
values for free hydrochloric acid. He had frequent attacks of vasomotor 
disturbances; numbness, coldness and pallor of the hands. It was only late 
in the disease, when an attack of hemiplegia occurred, that attention was 
focused on the possibility of a generalized arterio-sclerosis as the underlying 
disease. Although several Wassermann tests were negative, salvarsan and 
mixed treatment were given; these were without effect. At necropsy, 
marked thickening and calcareous deposits were found on all the cardiac 
valves; the coronaries and their branches showed extreme thickening; the 
myocardium presented many fibrous patches; the entire heart was somewhat 
enlarged. Spirochetes were not found in the aortic tissue. The heart 
accurately resembled that of a very old person suffering for many years from 
severe generalized arterio-sclerosis and cardio-sclerosis. 
The cause of such presenile sclerosis is still undetermined. It is possible 
that unknown infections and toxemias are etiologic factors. In one of my 
patients the disease originated within two years of an obscure pulmonary 
infection of several months duration. For the present, one can only state 
that, from some unknown cause, the elastic tubing comprising the vascular 
system becomes prematurely defective and diseased. Except digitalis for 
temporary relief of dyspnoea, treatment is of no avail. 
7. Senile Arterio- and Cardio-sclerosis.—The clinical picture is usually 
clear. All the palpable arteries are tortuous and thickened; the blood 
pressure is normal or not very high; the heart, somewhat enlarged; the 
systolic sounds at the apex and right base are impure; the second sound at 
the right base is sometimes accentuated. Precordial pains usually occur with 
exertion; although sometimes intense, they are more often of mild character. 
Apparently they basically depend on coronary sclerosis. Because of the 
advanced pathologic changes, the patients can rarely be benefited by medi- 
cation. Digitalis and theobromin sodium salicylate sometimes help, the 
amount of relief seemingly depending upon the degree of healthy tissue still 
remaining to react to medication. The patients usually require prolonged 
periods of comparative rest. 
8. Sacculated Aneurisms (Chapter XVI).—In a general way, the pre- 
cordial pains depend on the size and position of the aneurism. If large, th( 
pains are those due to pressure on the surrounding structures (intercosta 
nerves, ribs, etc.). If small, and involving the first portion or arch of th< 
aorta, the symptoms are similar in character and etiology to those describee PRECORDIAL PAINS OF CARDIO-VASCULAR ORIGIN 
419 
under cardiac syphilis (Group VI). The therapy is also the same as that there 
indicated. My observation with wiring and the electric current treatment 
according to the method of Lusk is limited to two cases. In one, after 
some weeks, there occurred small frequent external hemorrhages due to 
perforation of the sac by the end of the wire; the patient finally died of ane- 
mia. In the other, the patient did not improve during his stay in the 
hospital; he died suddenly some weeks later; a necropsy was not obtained. 
REFERENCES 
Adler, I., and Hensel, O.: Intravenous Injections of Nicotine and Their Effects upon the 
Aorta of Rabbits; Journal of Medical Research, N. S. X, 229. 
Brooks, H.: The Tobacco Heart; New York Medical Journal, 1915, Cl, 830. 
Curschman: Angina Pectoris—Discussion; Kongress fuer Innere Medizin, 1891, X, 275, 
Foster, N. B.: Uremia; Archives of Internal Medicine, 19x5, XV, 536. 
Gy: L’lntoxication Tabagique chez l’Homme; Paris Theses, 1908-1909, 203. 
Head: Sensibilitaetsstoerungen der Haut, etc., 1898. 
Huchard: Diseases of the Heart, 1910, 50. 
Janeway, T., and Park, E. A.: Question of Epinephrin in the Circulation and Its Relation 
to Blood Pressure; Journal of Experimental Medicine, 1912, XVI, 541. 
Kent, A. F. S.: Some Problems in Cardiac Physiology; British Medical Journal, July 18, 
1914- 
Lewis, T., and Barcroft, J.: Further Observations upon Dyspnoea and Its Relation to 
Blood Reaction; Quarterly Journal of Medicine, 1914-1915, VIII, 97. 
Lucien, et Parisot: Quoted by Vaquez; Archives des Maladies du Coeur, 1915, VIII, 678. 
Mackenzie, J.: Symptoms and Their Interpretations. 
Mackenzie, J.: Diseases of the Heart, 2. 
Manouelian, Y.: Recherches sur la Plexus Cardiaque, etc.; Annales de L’lnstitut Pasteur, 
June, 1914, 579. 
Nothnagel, H.: Angina Pectores Vasomotoria; Deutsches Archiv f. klin. Medizin, 1867, 
V, 209. 
Oppenheimer, B. S., and Oppenheimer, A.: Nerve Fibrils in the Sino-auricular Node; 
Journal of Experimental Medicine, 1912, XVI, 613. 
Osier and McCrae: System of Medicine, IV, 449. 
Sherrington: Integrative Action of the Nervous System. 
Stein, R.: Angina Pectoris; Medical Record, 1915, LXXXVIII, 131. 
Wilson, J. G.: The Nerves of the Atrio-ventricular Bundle; Proceedings of the RoyaJ 
Society, 1909, LXXXI, Series B. CHAPTER XXIV 
PRECORDIAL PAINS OF EXTRA-CARDIAC ORIGIN 
Precordial pains are so frequently the result of disease and disturbances 
outside the heart, and are then so often attributed to some form of “heart 
trouble” that it is important to know the commoner extra-cardiac causes 
of precordial pains, and to indicate how they may be distinguished from the 
precordial pains of organic cardiac disease. 
Precordial Pains Due to Tabagism.—For reasons already given (Chapter 
V), I have classed the “tobacco heart” with the inorganic cardio-vascular 
diseases. The precordial pains may be dull and aching, or sharp and radia- 
ting ; occasionally, the first premonition is very sharp lancinating precordial 
pains radiating to the left shoulder and forearm, and accompanied by uncon- 
sciousness. As an instance, a healthy man of 40, a heavy smoker, while 
running for a train, was suddenly attacked by terrific precordial pain follow ed 
by unconsciousness for one hour. The cardio-vascular examination revealed 
nothing abnormal. For weeks after the attack, any slight movement, even 
turning in bed, brought on pains. The patient was finally able to be about 
and resume his usual occupation. At present, six years after the first fainting 
spell, he feels quite well. He again smokes, but moderately. 
The most frequent of the arrhythmias in smokers are extrasystoles, 
usually auricular. Other arrhythmias, however, are occasionally en- 
countered. Thus I have seen two cases of sino-auricular block (Chapter 
X), one of auricular flutter and one of auricular fibrillation. 
Most tobacco pains and arrhythmias cease when smoking is stopped. 
Occasionally both recur intermittently for years. In such instances nitro- 
glycerin given regularly or during pain, is of benefit. The bromides are of 
value in helping to control persistent arrhythmias. 
Gastric Disturbances.—Patients with gastric disturbances, particularly 
those in whom epigastric distress is marked, are apt to suffer from referred 
precordial pains. The clinical picture is that of hyperacidity, or of gastric 
or duodenal ulcer. Belching, loud and explosive in character, is usually a 
prominent symptom. The precordial pains are commonly sharp, neuralgic, 
fleeting, and inconstant in character; their distribution is usually along the 
fourth and fifth left intercostal spaces. Pain referred to the left shoulder is 
rare. Corresponding to the anterior distribution there may be a similar area 
posteriorly. A precordial Head’s zone is unusual; its area of distribution, 
inconstant. There may be a close association between gastric symptoms 
and precordial pains, particularly when “hunger pains” and belching and 
marked. There is no decompensation or dyspnoea. When gastric symptoms 
420 PRECORDIAL PAINS OF EXTRA-CARDIAC ORIGIN 
421 
are stormy, extrasystoles may occur. Treatment is naturally directed to the 
underlying disease. I have found most benefit from atropine given in full 
physiologic doses three times a day before meal's, and from an ant-acid pow- 
der containing equal parts of sodium bicarbonate, magnesium usta and 
oleosaccharated peppermint powder in half teaspoonful doses after meals. 
Appropriate bland diet given frequently and in small quantities is important, 
As already noted, gastric symptoms also accompany cardiac disease, so that 
the correlation and study of all the clinical data are necessary for a correct 
diagnosis. Unless extrasystoles are subjectively annoying, they require no 
medication; otherwise they may be partly controlled by bromides or luminal 
(Chapter XX). 
Cardiospasm with Temporary Hypertension and Precordial Pains.— 
The usual impression gained from the literature is that cardiospasm is con- 
stant, that it is accompanied by painful deglutition when food reaches the 
cardia, and that esophageal dilatation is frequent and often extreme. Only 
recently was I able objectively to verify my clinical impression that many 
mild cases of cardiospasm occur without any of the marked symptoms and 
signs above enumerated. The case was that of an unmarried girl of twenty- 
two whose appendix had been removed some months previously for dyspeptic 
symptoms apparently originating in a diseased appendix. Some dyspeptic 
symptoms still remained: These were chiefly^sudden distention, gas and eructa- 
tions after meals. Fluoroscopy of the stomach with a barium meal showed 
marked pyloric spasticity, so that only after long continued vigorous massage 
of the stomach was some of the barium mass seen to enter and fill out the 
duodenal cap. Of most interest to me was the fact that an added drink of 
barium in milk showed that it remained in the lower esophagus near the 
cardia, that slight anti-peristalsis took place and that when the barium mass 
finally entered the stomach, the cardia and lower esophagus formed one long 
spastic elongated tube filled with the barium. This introduction is of espe- 
cial importance for what follows. 
In a review of patients who sought relief for precordial pains, I was 
impressed by the comparative frequency of a group who, in addition to the 
pains, gave clinical evidence of mild cardiospasm. They sometimes com- 
plained of slight epigastric distress at the end of the act of swallowing: Their 
appetites were good; their only gastric complaint was a feeling of distention 
and a desire to belch after meals; if they could belch freely they were relieved. 
The only definite findings on abdominal examination was a varying degree 
of deep seated tenderness under the xiphoid, best elicited by pressing the 
finger in the epigastrium, not however toward the spinal column, but 
upward and under the xiphoid. The only definite abnormal physical finding 
upon thorough cardio-vascular examination was moderate hypertension, 
usually between 160 and 170. The heart, urine, phenolsulphophthalein, 
orthodiascopic and electrocardiographic examinations presented no devia- 
tions from the normal. There was no dyspnoea upon exertion, no edema of 422 
PRECORDIAL PAINS OF EXTRA-CARDIAC ORIGIN 
the legs. In addition to these symptoms, patients complained of precordial 
pains on walking, especially when first leaving their homes and encountering 
the fresh air; this was apparently due to vasomotor instability, a condition 
also found in precordial pains of organic organs (Chapter XXIII). The 
hypertension, the precordial pains, together with the fact that the individuals 
affected are usually of middle age make a clinical picture, which symptomatic- 
ally resembles actual coronary disease, hence the importance of making a 
differential diagnosis. 
Illustrative cases are as follows: 
E. N. 0., male, aged 50, was always a rapid irregular eater. For years 
he suffered from explosive belching and slight epigastric distress after eating. 
He never vomited. His appetite is always good. He is a moderate smoker. 
For one year he complained of precordial pains radiating to the left arm and 
hand, accompanied by tingling sensations in the fingers. At times the 
pains were so severe that he had to stop walking. He also had slight dizzy 
spells during the last six months. As the result of a thorough cardio- 
vascular and general clinical examination, including orthodiascopy and 
electrocardiography, the only definite abnormal findings are slight deep 
seated sensitiveness under the xiphoid, and moderate hypertension: The 
systolic blood pressure was 160, the diastolic 100. The diagnosis of cardio- 
spasm was made, the patient was put upon a bland ant-acid diet and regular 
meals. Thorough chewing of food was insisted upon. A good prognosis was 
given. An ant-acid powder to be taken after meals, and small doses of atro- 
pine before meals were prescribed. Within one week after therapy directed 
entirely to the stomach, the hypertension disappeared. The pains dis- 
appeared more slowly. Several weeks after the original examination, the 
patient felt entirely well, the systolic blood pressure was 120, the pains 
had not recurred, the patient was able to walk and to attend to his business 
without precordial discomfort. 
S. L. male, lawyer, aged 39, always stout, had been under treatment 
for hypertension and precordial pains for many months. The blood pres- 
sure varied from 160 to 180 systolic. He had been under a vigorous protein- 
free dietary regime during the same period. Inquiry elicited that the 
patient suffered from flatulence for years, that he was exceedingly busy 
and under nerve tension in his office work, that he ate very irregularly 
but voraciously, that he smoked 30 cigarettes daily. A fortnight before I 
saw him, he had an attack of sudden severe substernal pain after a heavy 
meal: The pain was aggravated by walking. The pains now radiate to both 
arms and occasionally even to the legs. There was no history of tonsillitis or 
rheumatism, there was no dyspnoea after exertion. The Wassermann blood 
test was negative: The urine, normal. The only abnormal finding upon 
cardio-vascular examination, including orthodiascopy and electrocardio- 
graphy, was slight hypertension. Abdominal examination revealed an 
obese abdomen; there was a small definite area of deep-seated sensitiveness PRECORDIAL PAINS OF EXTRA-CARDIAC ORIGIN 
423 
under the xiphoid. The amount of smoking was reduced. Regular and 
slowly eaten meals were insisted upon; a .bland ant-acid diet was ordered: 
Tablets containing grains of atropine sulphate and Hso of a grain of 
nitroglycerin before meals, and an ant-acid powder of equal parts of magne- 
sium usta, bicarbonate of soda and oleosacchorated peppermint powder after 
meals was prescribed. The pains and hypertension gradually disappeared, 
epigastric sensitiveness became less. During the summer the patient was 
able to swim, row and climb hills without any discomfort. I have seen the 
patient several times since then; the blood pressure has remained normal. 
I believe that in this group of cardio-spastic patients with hypertension, 
organic cardio-vascular disease whether of the heart, systemic arteries or 
kidneys, can be excluded because of the negative findings in the circulatory 
system after careful clinical investigation, and because they yield so readily 
to therapy directed to the affending organ, the stomach. It is known that 
the cardiac end of the stomach is richly supplied with nerve structures, 
mainly branches of the vagus. Upon clinical, physiological and thera- 
peutic grounds it seems to me that the hypertension as well as the precordial 
and referred pains are in some manner brought about by referred nerve 
excitation from a hyperirritable spastic cardia. The etiology of the cardio- 
spasm seems quite clear in the type of patients we are dealing with; namely, 
constant dietetic insults from irregular and improper eating, and from bolt- 
ing food. The individuals themselves are often not neurotic in the ordinary 
sense of that term: Indeed they are as apt to be phlegmatic. But once 
injury to the cardia is established, other reflex areas may be disturbed 
and produce the clinical syndrome outlined above. 
Precordial Pains from Esophageal Disease and Spasms.—Carcinoma, 
syphilis, ulceration and diverticula are the usual organic causes of referred 
intercostal and precordial pains of esophageal origin. In some cases, 
organic disease is absent; the symptoms may then be due to esophageal 
spasm, especially in the region of the cardia. The usual symptoms are an 
uncomfortable, conscious gulping effort on swallowing solids or fluid, accom- 
panied by sharp pains referred to the lower sternum; and radiating to the 
precordium or even to the upper and lower extremities. Such symptoms are 
occasionally mistaken for those due to aortic aneurism; the difficulty in 
swallowing, to aneurismal pressure on the esophagus. 
An illustrative case with therapy follows: 
Male, aged 48, stated that for seven years he had “choking sensations” 
in the larynx and severe substernal pains on attempting to swallow solid food. 
These pains occasionally radiated to the head, arms and legs. The symptoms 
became progressively worse. The neurologic and physical examinations 
revealed nothing abnormal; the fluoroscope showed a normal aorta. Wasser- 
mann reactions of the blood and spinal fluid were negative; the stools, urine 
and gastric contents were normal. Roentgenograms showed a pouch-like 
dilatation of the middle part of the esophagus. An esophageal bougie was 424 
PRECORDIAL PAINS OE EXTRA-CARDIAC ORIGIN 
arrested opposite the middle of the sternum. Finally a small bougie was 
passed. For purposes of dilatation, bougies of increasing caliber were 
employed. At first semisolid food was given. Atropine sulphate, Moo grain 
three times a day was administered. The pains gradually subsided and 
finally disappeared. The patient was taught to pass a stomach tube; this 
he did for some weeks after he left the hospital. An examination months 
later showed that esophageal symptoms and pains had disappeared, and that 
there had been considerable increase in weight. 
Precordial Pains Accompanying Crises of Acute Fulmcnary Affections.— 
Such attacks of precordial pain are fairly common with the crises of influenzal 
bronchitis and pneumonia, especially when sharp critical sweats are present. 
Head’s zones in the left nipple region, and arrhythmias (especially sinus 
arrhythmias and extrasystoles), are frequent, a combination suggestive at 
first sight of toxic myocarditis. Symptoms, however, last only a few days; 
except for pain and arrhythmia, the heart is normal; there is no decompensa- 
tion or edema. Examinations made months or years later show that the 
cardio-vascular system has not been damaged. 
The following is an example: 
A physician, aged 43, never had any prior cardiac complaint. He con- 
tracted pharyngeal and bronchial grippe. There was critical defervescence, 
sharp sweats, an irregular pulse, and sharp, stinging pains in the left breast. 
The patient feared that he had an infectious myocarditis, and carefully avoided 
any unnecessary exertion. Examination revealed a small Head’s zone 
confined to the left nipple region, and an arrhythmia which polvgraphic 
and electrocardiographic tracings showed to be due to auricular extra- 
systoles. Otherwise the cardio-vascular system was normal. The patient 
was reassured, told to get out of bed, and given atropine sulphate, Mso 
grain three times a day before meals, and bromides at night. He was sent to 
the country and advised to exercise as much as he chose. He was soon able 
to walk several miles daily. Within one week the extrasystoles and pain 
disappeared, and have not since returned. 
While types such as those described are apparently not due to any 
disease of the myocardium itself, they must be sharply differentiated from 
the occasional case in which precordial discomfort presumably arises from 
some mild toxic disturbance of the myocardium coincident with or following 
the infection. The usual characteristic, distinguishing features are tachy- 
cardia; slight dyspnoea; exceptionally, a soft systolic murmur at the apex; and 
a sense of oppression in the left chest rather than any severe precordial pain. 
The treatment consists of rest in bed until these acute manifestations 
disappear. 
Precordial Pains Accompanying Vasomotor Disturbances at the Meno- 
pause.—Women at the climacteric period with marked vasomotor distur- 
bances (flushes, heat flashes, cold extremities, etc.), frequently have 
persistent precordial pains without evidence of organic disease of the heart PRECORDIAL PAINS OF EXTRA-CARDIAC ORIGIN 
425 
or of neighboring organs. The pains occasionally radiate to the left arm 
and hand. They are possibly evidence of vasomotor circulatory distur- 
bances in the heart itself. The patients rarely react well to medication. 
Bromides and small doses of atropine and nitroglycerin are of most value. 
Ovarian extract (corpus luteum) and extract of suprarenal gland tablets 
are occasionally helpful. Hurry and excitement should be avoided. 
Precordial “Neuralgias” of Unknown Origin.—Under this heading 
is grouped a small number of individuals, usually young and apparently 
healthy and vigorous, without vicious habits, with no rheumatic manifesta- 
tions, in whom continued and frequent examinations of -the heart and 
other organs reveal nothing abnormal. Occasionally, sudden explosive 
belching or singultus occurs. In one of my cases, smoking some years 
previously might have been an etiological factor. The pains are apparently 
quite haphazard in their onset and duration, and in my experience defy 
medication and therapy. 
In this group may also be placed females who complain of indefinite 
chest pains and distress, and who, from other manifestations apparently 
suffer from a functional disorder of an internal secretory organ or organs 
(endocrine imbalance). These patients are occasionally relieved by medica- 
tion aimed at substituting the presumed secretory deficiency. The extract 
of suprarenal gland is of most benefit. 
Pott’s Disease, Mediastinal and Spinal Tumors, Tabes, Intercostal 
Neuralgia and Myalgia, Pleurisy, Pericarditis.—These are some of the 
additional obvious extracardial conditions and diseases producing precordial 
pain. They require mention in order to complete the subject. 
The etiology and types of precordial pains ennumerated and described 
are admittedly incomplete. Only those frequently encountered and clini- 
cally important have been discussed. It must be emphasized that the 
various groups sometimes overlap and that careful discrimination is 
necessary in order to distinguish precordial pain of organic cardiac disease 
from that due to extra-cardiac causes. CHAPTER XXV 
ARTERIAL BLOOD PRESSURE—VENOUS PRESSURE—CAPILLARY 
CIRCULATION 
Physiological Considerations.—Blood pressure observation has taken 
its place as a' routine method of examination in clinical medicine. Its 
value and importance in health and disease are based upon the results of 
experimental physiology, which demonstrated that various factors are 
concerned in the estimation of blood pressure. These are (i) Cardiac Energy; 
(2) Elasticity of the Arterial Wall; (3) Peripheral Resistance; (4) Venous 
System; (5) The Lymphatic System; (6) Volume of the Circulating Blood; 
(7) Viscosity of the Blood. 
1. Cardiac Energy.—From the physical standpoint, cardiac work 
depends on the amount of, and the velocity with which blood is pumped 
into the arterial system. This in turn largely depends on the amount of 
venous blood brought to the heart. If the amount of venous return is greatly 
diminished, as for example, by section of the splanchnics, ventricular filling 
and, consequently, systolic output are also considerably diminished. The 
dynamics of the cardiac cycle—systole, diastole and diastasis—as well as 
the effect of rapid and slow heart action upon the cardiac output have already 
been described, (Chapter VI). Others factors being equal, an increased 
volumetric output raises, a decreased output decreases, blood pressure in the 
aorta. In the normal animal, the pulse rate is retarded by raising arterial 
pressure, and accelerated by lowering it. This reaction does not usually 
occur after vagus section; hence it is probably due to action upon the vagus 
center, partly reflex and partly direct. In animals the centripetal nerve 
to this center is the depressor which sends terminal filaments to the ventri- 
cular musculature and probably also to the aorta (Chapter I). If this 
nerve is cut or stimulated peripherally, it has no effect upon the heart 
action or blood pressure. If its central end is stimulated, there follows a 
marked fall in blood pressure and heart rate. The depressor thus acts 
as a defensive mechanism against unduly high blood pressure. Its aortic 
filaments are stimulated by undue distention of that vessel. 
2. Elasticity of the Arterial Wall.—Because of their elastic distensibility, 
a large proportion of the force of ventricular systole is stored up in the larger 
arteries. By their stretching and elastic recoil, arteries act as a reservoir of 
power after systole has ceased. In this manner the strain of systole upon 
the cardiac musculature, as well as upon the arterial wall, is considerably 
diminished. If the arterial tree were a rigid system, the systolic blood 
pressure, and hence the force of the impact, upon the arteries would be greatly 
426 BLOOD PRESSURE 
427 
increased. The diastolic pressure would always be nil, hence there would 
always be a tremendous pulse pressure, thus again enormously increasing the 
cardiac load. 
3. Peripheral Resistance.—This has reference to resistance encountered 
in the capillaries and end arterioles. The capillaries and veins together act 
as a reservoir for the blood. They are under the influence of nerve tone, 
hence any profound factor which decreases this tone will cause an accumu- 
lation of blood in the capillary bed and venous reservoir. With other factors 
unchanged, the blood pressure is increased by greater peripheral resistance and 
decreased by lessened peripheral resistance. The tension of the normal 
artery depends on its tonus, which in turn chiefly depends upon the vaso- 
motor mechanism. To a lesser extent, this statement applies to the veins, 
for they too possess a certain amount of tone. Normal tone is governed by 
a proper balance between the vasodilator and vasoconstrictor mechanisms, 
as derived from the regulatory centers in the medulla. There are other 
subsidiary centers in the spinal cord, demonstrated by the fact that, after 
destruction of the bulbar center, the arteries gradually recover their tone. 
In the experimental animal, general vasomotor tone is readily influenced by 
distant and near reflexes. After stimulation of the depressor nerve the 
splanchnic vessels become dilated, and blood pressure falls, but stimulation 
of all the other centripetal nerves raises blood pressure. The abdominal 
vessels, innervated by the splanchnics, have the greatest effect upon the gen- 
eral blood pressure because they can contain a large amount of blood and 
are easily influenced reflexly. It is important in this connection to empha- 
size that reflex lowering or raising the blood pressure does not simultaneously 
affect vascular areas in the same way. 
4. Venous System.—It has already been indicated that venous tone 
exists and that the venous system, especially in the splanchic area, can con- 
tain a large part of the entire volume of blood. It is apparent that splanchic 
overfilling of the venous system would result in a lessened supply of blood to 
the heart, and hence would decrease the blood pressure. It would corre- 
spond to some phases of vasomotor shock (Chapter XXVI) in which patients 
are assumed “ to bleed into their own vessels. ” On the other hand when the 
large venous trunks leading to the heart become overdistended as a result of 
pulmonary or hepatic disease, or of circulatory disturbances, the right heart 
cannot properly empty itself. This undoubtedly affects venous pressure, 
although what effect it may have clinically upon the systemic blood pressure 
is not known. 
5. Lymphatic System.—The state of filling of the lymphatics is probably 
a factor in blood pressure by acting as a temporary regulator and distribu- 
tor of the fluid elements of the blood when, for any reason, the volume of the 
circulating blood is increased. 
6. Volume of the Circulating Blood.—The possible content of the arterial 
and venous systems is much larger than the actual amount of blood found in 428 
BLOOD PRESSURE 
the body. The disproportion is equalized by peripheral contraction and by 
the other factors described; hence normally, blood volume has only a very 
slight effect upon blood pressure. 
7. Viscosity of the Blood.—It is evident that the degree of viscosity may 
have some influence upon blood pressure. Up to the present time, however, 
there are no clinical or experimental data (except in shock (Chapter XXVI) 
which have any bearing upon the subject. 
All the above factors found in the experimental animal are also present in 
the human being. Their value and importance vary not only relatively but 
Pig. 281.—The Baumanometer—a mercurial sphygmomanometer, illustrating also the 
application of the instrument for the auscultatory method of reading the pressure. This 
instrument is accurate, portable, simple in construction and not apt to get out of order. 
The graduate tube is carefully calibrated. 
absolutely from time to time; the blood pressure is the resultant of these vari- 
ants. Although we posses no methods or instruments by which individual 
agencies making up the clinical blood pressure can be separately calculated, 
one should at least attempt to gauge them by careful examination and by 
such significant data as the thickness of palpable arteries, existence of ple- 
thora, state of venous distention, etc. 
Clinical Estimation of Blood Pressure.—The instruments which are used 
in the clinical estimation of blood pressure are called sphygmomanometers. 
The three types are the mercurial, the aneroid and the compressed air. Funda- 
mentally they depend on calculating the power exerted in partial or complete BLOOD PRESSURE 
429 
Fig. 282.—-Construction diagram of the Tycos Aneroid. (After Norris.) 
Fig. 283.—Oliver mercurial compressed air manometer. (After Norris.) 43° 
BLOOD PRESSURE 
obliteration of an artery in terms of a column of mercury, an aneroid pressure 
indicator or compressed air activating a fluid column, respectively. , 
An example of each is shown in the accompanying illustrations, (Figs. 
281-283) which serve to typify the numerous blood pressure instruments in 
clinical use, all based upon the three principles mentioned. 
In its clinical application,the brachial is the artery chosen for com- 
pression. This is accomplished by means of a standard 12 c.m. broad, 
flattened cuff placed upon the upper arm. To the cuff are attached two 
tubes: One connected with a small metal or rubber hand pump for the purpose 
of inflation, the other connected with the mercurial column or aneroid 
instrument. A great disadvantage of the latter is that the spring may lose its 
resiliency; as a result, the instrument becomes inaccurate. If standardized 
sufficiently often by comparison with a mercurial sphygmomanometer, the 
aneroid manometer is as useful for clinical purposes as the mercurial instru- 
ment. Its advantages are that it is made compactly, so as to be more readily 
carried about, and the dial can be read more conveniently than the millimeter 
markings in a column of mercury. In the compressed air manometer (Fig. 
283), pressure from the hand bulb forces the liquid (mercury or colored fluid) 
from the bulbous reservoir into the manometer tube, where the pressure can 
be read off. The advantages are compactness and ease of operation; the 
chief disadvantage is lack of sensitiveness. 
Arm cuffs are of two types: One stiff, made of leather; the other, soft and 
made of cloth or silk (Fig. 281). Though either can be used, I prefer the 
soft cuff because it is pliable, and can be more readily and quickly placed in 
position. 
Blood pressure estimations of the brachial artery should be taken at the 
level of the heart. For this purpose, the elbow of the patient iff placed com- 
foitably upon a desk or table. The cuff is then snugly applied to the bare 
arm. The arm should be relaxed, otherwise muscular tonicity tends to pro- 
duce an incorrectly high blood pressure reading. Edema also causes abnor- 
mally high blood pressure, because much of the pressure within the cuff is used 
up in displacing the oedema. 
The introduction and use of the sphygmomanometer have shown that the 
estimation of blood pressure by radial palpation alone is erroneous and 
untrustworthy. There are various methods of determining the systolic 
blood pressure by manometric readings; these are (1) the palpatory, (2) the 
visual, (3) the graphic, (4) the auscultatory. 
According to (1) the palpatory method, the systolic blood pressure is that 
degree of cuff pressure exerted on the brachial at which the radial pulse 
becomes no longer palpable. (2) The visual method consists in compressing 
the brachial beyond the point of obliteration, and then gradually lowering 
the pressure by cuff deflation until the first mercurial oscillation becomes 
visible; this point marks the systolic blood pressure. In the (3) graphic' 
method, the mercurial manometer has an additional connection with a rubber 1 BLOOD PRESSURE 
431 
bulb inclosed in a hermetically sealed small glass globe; the latter is attached 
to a recording tambour, so that differences in the mercurial oscillations are 
transmitted to the tambour and recorded on a revolving drum. 
4. The auscultatory method (Fig. 281), first used by Korotkow, is the 
one usually employed because of its accuracy. The cuff is applied and 
inflated until the brachial is obliterated, that is, beyond the point at which 
mercurial oscillations are visible. The stethoscope is then placed over the 
brachial at the bend of the elbow, and the cuff is gradually deflated until 
sharp distinct taps are heard; this marks the systolic blood pressure. In 
typical instances, it is possible to separate the auscultatory phenomena into 
five distinct “phases.” The first is the one just described and, as noted, 
establishes the systolic pressure. The artery beneath the cuff being empty, 
the first pulse wave produces sudden arterial tension with resultant short, 
popping sounds. With a gradual drop in blood pressure by further defla- 
tion, the sharp tap gives way to a murmur, somewhat resembling a super- 
ficial, rough pericardial friction sound. This marks the second phase. It is 
probably caused by sufficient blood passing under the cuff to produce swirling 
currents which mask the click of the first phase. By still further deflation 
and consequent lessened pressure on the brachial, this murmur ceases and 
the third phase begins. It is marked at its beginning by short tapping 
sounds; with continued deflation of the cuff, these gradually change to muffled 
taps. This is usually regarded as the beginning of the fourth phase. It 
seems probable that, with the gradual approach of diastolic pressure, a steady 
arterial stream begins to flow beneath the cuff between the arterial pulsations; 
this acts as a kind of buffer and thus produces the muffled, dull sounds 
characteristic of the fourth phase. The dull note is finally extinguished by a 
constantly increasing column of blood in the artery, until all sounds cease. 
This marks the fifth or last auscultatory phase. The usual difference 
between the fourth and fifth phases is from 5 to 8 m.m. of mercury. 
The various phases as outlined are not always well defined nor distinguish- 
able. As measured in the mercurial column, the average millimeters of 
pressure produced by the various phases are 14, 20, 5, 6, from the first 
to the fifth phases, respectively (Goodman and Howell). There are several 
variations from the normal. If the brachial artery is small, the separate 
phases may be indistinct and inaudible. Again, the first phase may not be 
represented by a sharp click, but by a murmur. Occasionally, the second 
phase is entirely absent, especially in aortic disease with high systolic blood 
pressure. Such differences probably depend upon the varying strength 
of arterial eddies interfering with the usual sharp taps of sudden arterial 
distention. 
The maximal normal blood pressure is still a matter of dispute. I 
regard a systolic blood pressure between 115 and 135 m.m. of mercury in 
an adult as within normal limits. In a statistical table by Fisher represent- 
ing 19,339 accepted candidates for life insurance, including ages from 15 432 
BLOOD PRESSURE 
to 60, the average systolic pressure was 129 m.m. of mercury. There is a 
gradual rise in systolic and diastolic blood pressure with advancing age; 
this probably depends upon associated vascular pathological changes in the 
cardio-renal-vascular system. 
There are certain physiological variations which must be born in mind 
when making blood pressure estimations. The systolic blood pressure is 
increased by expiration; in forced expiration this may amount to 5 to 10 m.m. 
There is also a slight diurnal variation accounted for by differences in physical 
and psychical states of the individual at various times of the day. The blood 
pressure is lowest during the first part of natural sleep. The ingestion of 
meals has a varying influence upon blood pressure; this depends upon 
different degrees of vasodilation of the abdominal vessels with compensatory 
superficial vasoconstriction. 
There are certain factors which require brief comment because of their 
influence upon blood pressure. Moderate amounts of alcohol do not regu- 
larly raise the blood pressure in man. In the experimental animal, large doses 
produce a fall in blood pressure, due to a depressant effect upon the vaso- 
constrictors and upon the heart. During smoking, there is a temporary 
rise of blood pressure from stimulation of the peripheral and central vaso- 
constrictor mechanism. Excitement—pleasurable or otherwise—some- 
times produces a temporary rise of blood pressure. Exercise and muscular 
exertion have a similar effect; in young healthy individuals the blood pressure 
soon drops to its usual level; in the middle aged and old, the rise of blood 
pressure represents a more marked reaction and lasts longer. Cyanosis may 
in itself be a cause of abnormally high blood pressure; hence therapeutic 
measures, like venesection and digitalis (which tend to diminish cyanosis) may 
directly decrease existing hypertension. This is an important consideration in 
the treatment of decompensation and hypertension in which cyanosis forms a 
conspicuous element. Another factor in the production of hypertension in 
some cases of arterial disease is that due to hyper tonus; this possible cause 
for error, however, can be controlled and obviated by repeated compression 
of the artery with the cuff. 
In general, frequent blood pressure estimations are necessary in order to 
arrive at the correct blood pressure of the individual, and to obviate some 
of the disturbing physiological and other factors that have been mentioned. 
I shall not enter into the still much debated question of the basic cause of 
clinical hypertension. That it is fundamentally due to constriction and 
spasm of the arterioles—the vascular peripheral bed—seems highly probable. 
There are, however, many factors which undoubtedly cause vaso-constric- 
tion of the arterioles. Some of these are psychic,—for example, emotional 
disturbances and mental strain. Some are probably of endocrine origin, for 
example, the hypertension at the menopause. Others again are organic; 
this applies especially to chronic glomerular disease of the kidneys and to 
aortitis with associated general vascular disease. While the statement may BLOOD PRESSURE 
433 
be true that vascular disease can produce hypertension, and hypertension, 
vascular disease, in the majority of instances we possess no knowledge as to 
which is the primary factor nor do we definitely know how arteriolar disease 
acts to bring about hypertension. 
For the purpose of studying abnormal blood pressure in organic cardio- 
vascular disease, I have found the classification below, embracing the vast 
majority of cases, of clinical value. Despite occasional Overlapping, the 
prominent lesion or type is usually readily recognized. 
(a) Hypertensive cardio-vascular disease with myocarditis. 
I. (b) Hypertension and myocardial insufficiency with labile vaso-motor mechanism, 
(c) Uremia. 
II. Myocardial disease and insufficiency without hypertension. 
III. Valvular disease and myocardial insufficiency with and without hypertension. 
IV. Senile and premature arterio-sclerosis. 
I. (a) Hypertensive cardio-vascular disease with myocarditis includes 
some of the fairly well-defined groups of the older writers; for example, 
Huchard’s presclerosis, Gull and Sutton’s arteriocapillary fibrosis, von 
Basch’s angio-sclerosis. It is becoming increasingly evident that the patho- 
logical basis of hypertensive cardio-vascular disease lies chiefly in disease 
affecting the arterioles, especially of the heart, kidneys and brain. As con- 
comitant changes in the heart, there may be cardiac hypertrophy (mainly of 
the left ventricle), and moderate or advanced aortitis. The systolic blood 
pressure commonly varies from 180 to 230 m.m. of mercury; the average, 
190 to 200. It is important to note that there may exist no parallelism 
between the degree of hypertension and the extent of kidney involvement, 
and that hypertension alone need not necessarily be of symptomatic or prog- 
nostic importance. The average diastolic pressure of this group is about 100 
m.m.; if renal involvement predominates, diastolic pressures of 120 or over 
are found. 
I. (b) Hypertension and Myocardial Insufficiency with Labile Vaso- 
motor Mechanism.—This group consists principally of patients past middle 
life with only moderate hypertension and with normal or moderately elevated 
diastolic pressures. The chief characteristic of the blood pressure is its 
marked daily variation, which may be as much as 30 m.m. of mercury. The 
symptoms referable to myocardial insufficiency are mild. The patients are 
usually stout or obese men; the prominent physical signs in the chest are 
those of bronchitis and emphysema. The palpable arteries are not thickened, 
and nephritic symptoms not marked despite the presence of a slight amount of 
albumin and a few casts in the urine. Pretibial edema is absent or only 
very slight. 
I. (c) Uremia.—The cardinal signs ahd symptoms in patients in this 
group are headache, nausea, vomiting, varying grades of pallor, attacks of 
paroxysmal dyspnoea, precordial distress and nocturnal polyuria. There are 
retinal changes of varying degrees. The phenolsulphonephthalein test 434 
BLOOD PRESSURE 
shows diminished output in two hours, the average being between 15 and 3a 
per cent. As a result of renal test meals containing weighed amounts of water, 
salt, carbohydrate and nitrogenous constituents (Chapter XXVI), and of 
chemical examination of the blood, we find as a rule low, fixed specific 
gravity for the day and night urines, decreased elimination of salt, water 
and urea in the urine, and abnormal amounts of non-protein nitrogen and 
of uric acid and creatinin in the blood. When uremic dyspnoea is marked, 
there is evidence of diminished blood alkalinity (so-called acidosis). This 
may be roughly estimated by determining the amount of bicarbonate of 
soda, administered internally, required to render the urine alkaline. Other 
more refined and direct methods consist in determining the carbon dioxide 
content of the alveolar air by the Priestly-Haldane bag or bytesting the blood 
chemically according to the Van Slyke method. The differentation between 
the “cardiac” and “cerebral” types of hypertension can sometimes be made 
by careful observation of the diastolic pressure, which presumably serves as 
the better index of the peripheral resistance. The diastolic pressure is 
between 120 and 140 in the “cerebral” cases, i.e., in those who suffer from 
such typical uremic signs as headache, vomiting and retinal changes; it is 
considerably less in those in whom “cardiac” manifestations are especially 
prominent. 
II. Myocardial Disease and Insufficiency without Hypertension.— 
Patients in whom myocarditis is the predominant pathological condition 
show little or no hypertension. The diastolic pressure is sometimes quite 
low, so that, even with a normal systolic, there is an increase in the pulse 
pressure and hence in the cardiac load. 
III. Valvular Disease and Myocardial Insufficiency with and without 
Hypertension.—The valvular lesions, that is, those without evidence of 
general arterial disease in which the systolic blood pressure is high, are 
rheumatic affections of the aorta, especially aortic regurgitation. In these, 
the blood pressure may be between 180 and 200 m.m.; the diastolic pressure is 
abnormally low, the average being 40 to 25; it is occasionally zero. There 
thus exists a very marked cardiac overload. It has been shown that in 
this valvular lesion, the systolic blood pressure in the popliteal is often much 
higher than in the brachial. This difference I have found to be as high as 50 
m.m. of mercury in individual instances. The normal difference between 
leg and arm blood pressure is from 5 to 10 m.m.; hence the diagnostic impor- 
tance of measuring the arm and leg blood pressures in cases of suspected 
aortic regurgitation in whom such usual clinical signs as typical murmurs and 
the Corrigan pulse are absent. 
Unless arterial disease or cyanosis is present, mitral lesions are unaccom- 
panied by hypertension. With beginning heart failure, the systolic blood 
pressure may become subnormal. In combined valvular disease of the mitral 
and aortic valves, blood pressure depends upon the clinically predominant 
lesion. For example, if aortic regurgitation be the more prominent, the BLOOD PRESSURE 
435 
blood pressure will be characteristic of that lesion; if the mitral predominates 
the pressure will be normal. 
IV. Senile and Premature Arterio-sclerosis.—Under this caption are 
grouped those cases with tortuous and thickened visible arteries. The 
heart valves and aorta present various degrees of intimal thickening and 
lime deposits, the main coronaries and their branches are thickened, there 
is marked myo-fibrosis, the heart may be small or only moderately enlarged. 
Such patients often have slight hypertension or even normal blood pressure, 
unless renal involvement is a marked clinical feature. 
In addition to the foregoing classified groups of organic cardio-vascular 
disease, several other important diseases and conditions which have a direct 
bearing upon blood pressure estimations require brief description. 
Exophthalmic Goiter.—A characteristic of this disease is the variability 
of the blood pressure readings; there are marked differences from day to 
day. When the disease is of moderate severity, hypertension is the rule, the 
range being between 160 and 180 m.m. of mercury. Extreme hypertension 
without accompanying cardio-vascular or renal disease is rare. 
Lead Poisoning.—During attacks of lead colic there is usually a rise of 
the systolic blood pressure. This is attributable partly to pain present 
during the attack, but chiefly to spasm of the peripheral arterioles. Plum- 
bism which causes disease of the kidneys and arteries, and ends in nephritis 
and arterio-sclerosis naturally produces hypertension because of the presence 
of these lesions. 
Increased Intracranial Tension.—Hemorrhage, meningitis and brain 
tumors are the usual causes of this condition. As a consequence of increased 
intracranial tension, cerebral anemia results, and with it, an increase— 
sometimes marked—of the systolic blood pressure. In addition to the 
hypertension, other manifestations of this cerebral anemia may consist of 
headache, vomiting, vertigo, choked disk and true bradycardia. Apoplexy is 
usually accompanied by hypertension; hypertension, if already present, is 
sometimes increased. When the blood pressure continues to rise after a 
stroke, it is usually evidence of increased intracranial pressure from continued 
bleeding. 
Cyanosis is so frequently found in broken compensation that its effect in 
producing hypertension requires special consideration. Its action may be 
ascribed to an effect, in a milder degree, similar to that of the blood in 
asphyxia. In the latter, direct stimulation of the vasomotor center is 
assumed. Cyanosis in itself may frequently account for hypertension in 
decompensation from any cause, for, with decrease of cyanosis, the blood 
pressure often returns to the normal and remains so. Therefore, by treating 
cyanosis, diverse therapeutic measures such as digitalis medication and vene- 
section may have a direct and beneficial effect upon hypertension. 
Functional Hypertension, Functional Hyperpiesis, Essential Hyper- 
tension.—Besides hypertension due to known pathological arteriolar and 436 
BLOOD PRESSURE 
vascular changes, there remains a group of patients in whom at present 
no pathological basis for hypertension can be found. This condition has been 
termed functional hyperpiesis, or functional hypertension. In this group 
may be mentioned females approaching the menopause and a few sufferers 
from gastric disturbances of a neurotic nature. The following is a typical 
case: 
Female, age 55, menopause 8 years ago. Some years previously she had 
gastric symptoms—belching, dizziness and hunger pains. Her present com- 
plaints have lasted several months; these are dizziness, slight nausea and at 
times belching. Dyspnoea, edema and urinary changes are absent; the 
sodium chloride, water, urea excretion and phthalein output are normal; the 
Wassermann blood reaction is negative. The amount of non-protein nitro- 
gen in the blood is also normal. Physical examination reveals no evidence 
of cardio-vascular disease. Despite all these findings the systolic blood pres- 
sure is regularly about 200; the diastolic, normal. It is possible that such 
cases are due to extreme susceptibility of the vasoconstrictor center to reflex 
influences. Until more of these cases have been studied by means of chemical 
examination of the blood and by functional urinary tests, and have been 
followed to necropsy, for the present they must be provisionally regarded as 
of functional, non-organic origin. 
Hypertension at the Menopause.—In the entire absence of any physical 
or organic causes for hypertension, these patients resemble the functional 
hyperpiesis group just described. They are apt to suffer from the usual 
sweats and flushes incidental to the climacteric. Apparently vasomotor 
instability is an important factor in the hypertension. With increased 
knowledge, the fundamental etiological factor may be found in some distur- 
bance of the endocrine glands. 
Functional Hypotension.—This term applies to a group of adults pre- 
senting no evidence of organic disease and in whom the systolic blood pressure 
is about 100 in males, 90 in females. Contrary to what is generally believed, 
some of these individuals are of robust physique. They never suffer from 
decompensation. I have not found gastroptosis or constipation significantly 
frequent in them: They often run a symptomless course and are only acciden- 
tally discovered in the course of routine clinical examinations. If symptoms 
be present, they consist of rapid fatigue following moderate exertion; the 
vasomotor system is unstable and susceptible to nervous influences of various 
kinds. The patients flush or become pale readily. They are excitable, often 
become dizzy or complain of feeling faint; indeed, their symptoms overlap to 
a great extent those described under “Weak Heart” (Chapter XVIII). 
BLOOD PRESSURE IN CARDIAC ARRHYTHMIAS 
It is sometimes important to estimate blood pressure when various types 
of pulse irregularities are present. The method to be employed in the com- 
moner of these requires brief description. BLOOD PRESSURE 
437 
Sinus Arrhythmia and Heart Block.—Since the beats at the wrist are of 
equal force, only the routine methods are required for the blood pressure 
determination. 
Alternation.—There is a rhythmic sequence of stronger with weaker beats. 
The systolic blood pressure of the stronger contractions can be estimated in 
the usual manner. The diastolic pressure can also be estimated in this way 
if it be higher than the systolic of the smaller beats. This fact is readily 
determined during the course of the examination by palpating the radial; the 
number of radial beats which come through will then be just half those at the 
cardiac apex. 
Coupled Rhythm.—The tension of the initial beats of the couplets in 
auricular fibrillation with coupled rhythm is not identical, but the difference is 
usually slight, so that for our purpose the coupling of auricular fibrillation 
may be grouped with that occurring in extrasystoles. The systolic blood pres- 
sure of the initial stronger beats is calculated in the usual fashion. If the 
diastolic pressure of these be greater than the systolic pressure of the weaker 
contractions of the couplet, then again the usual routine in measuring the 
diastolic pressure of the stronger is followed. 
When extrasystoles occur frequently and at irregular intervals, it is 
necessary to use a special method similar to that for auricular fibrillation 
(see below) in order to estimate the systolic blood pressure. 
In auricular fibrillation with gross irregularity in the force of the beats, 
the ordinary routine cannot be applied, for it can only estimate the systolic 
blood pressure of the strongest, and the diastolic of the weakest beat at the 
moment that the blood pressure is taken. When all ventricular contractions 
are propagated as pulse waves, and the radial beats on palpation feel approxi- 
mately equal in force, my observations have shown that the pressure of the 
individual beats do not usually vary more than io m.m. of mercury; hence 
the ordinary method of estimating the systolic levels are sufficiently accurate 
for clinical purposes. With extreme irregularity in the strength of the radial, 
and with many frustrane and abortive beats, various methods have been 
devised to arrive at an approximation of the actual blood pressure. Accord- 
ing to one method, that of James and Hart, the cuff and stethoscope are first 
applied in the usual manner. These observers have found that, although the 
rate is irregular the number of ventricular contractions for each minute is 
approximately the same. Their procedure is as follows: The number of 
radial beats which pass under the cuff between pressures of 150 and 140 m.m. 
of mercury, for example, are counted, as well as the corresponding number of 
ventricular contractions occurring during the same time. The difference 
between these represents the number of frustrane or abortive beats (pulse 
deficit). Similar observations are then made for systolic blood pressures 
between 140 and 130, 130 and 120, etc., until the systolic blood pressure of all 
the beats which pass under the cuff have been taken. The number of pal- 
pable radial beats found at the various blood pressures is multiplied by the 438 
BLOOD PRESSURE 
highest systolic limit set for that group; these products are added and then 
divided by the corresponding heart rates at the apex. The result gives the 
“average” systolic blood pressure. One objection to the method is that the 
“average” includes many abortive beats (called by the authors pulse deficit) 
which have no effect upon the circulation since they propel no blood through 
the arteries. Another plan is to average the effective beats only, i.e., those 
that actually have some effect upon the circulation by the production of pulse 
waves. This is attempted in the “fractional” method of Kilgore, according 
to which the diastolic pressures are also calculated. The systolic and dias- 
tolic pressures are plotted on a chart, the number of beats occurring at the 
various systolic and diastolic pressures being marked by points; these are 
then connected so as to form a smooth graph. In this manner it is possible 
to make fairly exact estimations of the blood pressure in auricular fibrillation. 
General Remarks on Hypertension.—Reference is here made to the 
hypertension itself and not to accompanying cardio-vascular, uremic or 
other symptoms. 
Mental calm, avoidance of excitement, diversion are the first and perhaps 
the most useful therapeutic agents in hypertension. It requires the skill 
and phychological insight of the physician to understand best how to bring 
this about. The physician must naturally individualize. Some people 
for instance actually have added nervous symptoms if told they must take a 
prolonged rest and be absolutely quiet. Some exercise and perhaps games 
like golf may be allowed in appropriate cases. The livelihood of others 
depends upon their presence at business at least part of the day or several 
days a week. To these, week ends in the country or leaving business early 
daily may answer the purpose. To hard working people, perhaps lighter 
work can be prescribed. It is never wise to let neurotic individuals know how 
high their blood pressure is. It simply adds to their worry, subserves no 
useful purpose and tends to bring patients to unskilled hands who claim 
most wonderful panaceas for hypertension but who possess no medical 
knowledge. 
THERAPEUTICS OF HYPERTENSION 
Before remedial measures are considered, it is well to emphasize that 
hypertension is often a conservative or compensatory process. As a corollary, 
it follows that hypertension itself does not necessarily require medication, 
for it is usually but an index of the underlying cardio-vascular or cardio-renal 
mischief, or of some functional or endocrine disturbance. It is the basic 
causative factor which requires therapeutic attack. Another important 
consideration is that remedies acting upon the normal individual (or animal) 
may have an entirely different effect in organic hypertensive disease. This, 
I believe, is the main reason for disappointments in the attempt to reduce 
blood pressure by vasodilators. They have been used innumerable times to 
decrease hypertension, in most cases with no or but slight temporary results. BLOOD PRESSURE 
439 
Exceptions will be noted later. Their inefficacy may probably be ascribed 
to the type of the pathological change underlying hypertension. For example 
arterioles considerably thickened by disease or in a state of hypertonus can 
scarcely be influenced by drugs that exert their dilating power upon pliable 
arteries or under normal conditions of nerve tone. 
In some hypertensive cases, there occasionally occurs a temporary rise of 
blood pressure beyond the usual level for these individuals. This rise is 
sometimes marked by dyspnoea, precordial pain, headache and vomiting. 
It is in these that relief from abnormal hypertension is especially desirable. 
The drugs usually employed in the reduction of blood pressure are nitrate 
of soda, amyl nitrite, nitroglycerin, benzyl benzoate, spiritus aetheris nitrosi, 
erythrol tetranitrate and mannitol. In urgent cases, amyl nitrite in 5 minim 
pearls may be administered. Regarding nitroglycerin, the doses usually 
prescribed, from Yoo to 3doo of a grain three times daily, rarely result 
even in temporary blood pressure reductions. If its administration is not 
followed by dizziness, I am in the habit of prescribing much larger doses, 
as much as Yl 5 of a grain three times a day. In an experimental series of 
cases, I gave as much as Yo of a grain hypodermically. In those with 
uremia, the effects upon the blood pressure were disappointing. Even these 
large hypodermic doses had only an occasional or fleeting effect upon the 
blood pressure or symptoms. In others of this series, no constant result 
following nitroglycerin could be determined. Sodium nitrite, when efficaci- 
ous, seems to have a more lasting effect. Erythrol tetranitrate has also been 
used with indifferent results. I have observed the best results when the 
vasodilators were employed in those individuals whom I have grouped as 
“ hypertension and myocardial insufficiency with labile vasomotor mech- 
anism” (q. v.). These patients are rarely uremic; the hypertension is 
relieved not only temporarily but sometimes for a prolonged period. 
The action of the iodide of potash, a drug frequently prescribed for the 
relief of hypertension, is still in dispute. In view of our knowledge that 
syphilis is a frequent cause of cardio-vascular disease, the occasional good 
effects of the iodides are to be ascribed only to its action upon the underlying 
luetic disease. 
Venesection in all cases of hypertension with urgent symptoms is an 
excellent temporary therapeutic measure, especially in plethoric and cyanotic 
patients. From 400 to 800 c.c. of blood should be withdrawn. 
Hydrotherapy, hot packs, oxygen, carbon dioxide, or hot baths, or the 
electric light bath, has been advocated to reduce hypertension. In so far 
as they promote diuresis and perspiration, and thus rid the body of toxic 
material, warm packs and baths in those not uremic may have some direct 
therapeutic value. The incidental effect upon the vasomotor system may 
also be of benefit. Oxygen and carbon dioxide (Nauheim) baths are followed 
by varying and inconstant effects upon the blood pressure (Chapter XX). 
The indications for these gas-impregnated baths in hypertension depend 440 
BLOOD PRESSURE 
upon the degree of decompensation, and in the main, follow those indications 
already discussed for that condition. If decompensation is extreme, baths 
are contraindicated; if decompensation is mild, and observation from one 
bath shows good effects upon the blood pressure or symptoms, they may be 
continued. Even in those in whom there has been a reduction of blood pres- 
sure in or immediately following the baths, the reduction is slight and tran- 
sient, so that the beneficial effect is probably to be attributed to an action 
upon the general circulation rather than upon the blood pressure. 
The effect of electric light baths, when efficacious in the reduction of 
hypertension, may be ascribed to the heat, to favorable vasomotor change, 
to incidental rest and to enforced quiet which form part of the treatment. 
Diathermy.—A special application of the D ’Arsonval current to the 
precordium is another method employed as a therapeutic agent in hyper- 
tension. Some of the reports of its effect are exceedingly enthusiastic; claims 
are made, for example, that hypertension is permanently relieved. In some 
cases which I have observed in whom diathermy was used by other practi- 
tioners, the blood pressure remained at its usual level; there was no change 
whatever in the symptoms. 
Percussion over the seventh cervical vertebra has been used, the object 
being to exert a reflex influence upon the vasodilators and thus upon the 
blood pressure. The effect of this procedure is, to say the least, exceedingly 
problematical and hypothetical. 
Absence from business, and treatments at Spas have undoubted marked 
therapeutic value in many cases of hypertension. The reasons are obvious. 
Patients are away from their ordinary environment; their routine of life 
approaches a more normal and physiological standard; excitement and 
nervous tension become almost negligible factors. 
The amount of exercise that should be allowed depends chiefly upon the 
cardio-vascular disease and upon the symptoms, rather than upon the degree 
of hypertension. At no time, however, should violent or fatiguing exercise 
be permitted. The amount of rest is also based upon the same criteria. 
For example, an otherwise active business man still capable of some physical 
exertion, who frets and becomes irritable when absolute rest is enjoined, 
may be permitted to attend to business for a short period each day. The 
week’s work should be broken by one or two days of rest; or if the patient’s 
condition allows it, by mild exercise out of doors, especially walking. Exer- 
cises of any type should be controlled by the state and degree of cardiac 
compensation, and by careful observation of the effect of exercise upon the 
individual. 
Hypotension in itself rarely requires medication. When combined with 
the symptoms of vaso-motor instability, appropriate therapy should be 
administered (Chapter XVIII). Accompanying neurotic symptoms, when 
present, require appropriate medication. The extract of suprarenal gland 
may be used as a temporary expedient to raise the blood pressure. BLOOD PRESSURE 
441 
Venous Blood Pressure.—Various instruments for this determination 
have been devised. Glass chambers, cemented to the skin (Hooker), or small 
springs and pelottes (Oliver, Sewall) appropriately connected with manom- 
eters are placed or connected over a prominent vein in the arm. The 
pressure is then read from the manometer scale. Another method (Moritz 
and Tabora) consists in plunging a needle connected with a manometer 
scale directly into the vein at the bend of the elbow. An approximate clinical 
method of determining venous pressure is that of Gaertner. The relaxed or 
flexed left arm of the patient is slowly raised until the veins at the bend of the 
elbow collapse. The height of elevation above the level of the right auricle 
(the upper border of the left fifth costal cartilage at the sternal junction, 
according to Gaertner), measures the venous pressure in millimeters of 
blood, approximately that of water. According to the v. Recklinghausen 
method, one hand of the recumbent patient rests at the side of the bed, the 
other on his thigh. If the veins of both hands are empty the venous pressure 
is low; if full, it is high: If the veins of the hand on the thigh are empty and 
those of the hand on the bed are full, venous pressure is normal. 
N. W. Brown has devised a simple method by which the usual mercurial 
manometer may be used. Water or a somewhat heavier fluid like bromoform 
(sp. gr. 2.5) is used instead of mercury. The vein employed, usually on the 
back of the hand must be at the level of the heart. The tube is connected with 
a small saddle-shaped cup 2 c.m. in diameter covered with very thin rubber 
tissue, and loosely applied so as to allow free oscillation without tension. 
Manometer pressure is regulated with a thumb screw. Pressure in the 
manometer is raised several centimeters and the cup or capsule is placed upon 
the vein with sufficient pressure to obstruct the return flow. The pressure 
in the manometer is allowed to fall by opening the needle valve. When the 
venous pressure equals the manometer pressure, the vein above the capsule 
will rapidly fill, a reading at this time will give the approximate venous 
pressure (N. W. Brown). • 
Although the subject of venous pressure has not been exhaustively studied, 
it would appear that a venous pressure of 10 m.m. or less of water is within 
normal limits. Higher venous pressures are found in decompensated cardiac 
lesions, and roughly correspond to the degree of decompensation; a pressure 
from 10 to 20 m.m. suggests moderate cardiac failure; from 20 to 30 or over, 
indicates severe cardiac failure and venous stasis. 
Capillary Circulation.—For many years, abortive attempts have been 
made to study the capillary flow and the capillaries themselves in human 
beings. A simple method has recently been devised by which this can be 
satisfactorily accomplished. The technique consists in placing the junction 
of the cuticle and nail covered with a drop or two of transparent oil on the 
stage of the microscope under the objective. A 50 or 100 Watt electric 
bulb is so focussed as to strike the finger end at an angle of about 45 degrees. 
The objective is a 16 m.m. lens, the oculars, a number 5 or 10; the capillaries 442 
BLOOD PRESSURE 
are thus magnified 50 to 100 fold. The skin capillaries form straight or 
tortuous loops. 
The method is still too new to permit definite clinical deductions. Some 
interesting observations regarding capillary stasis in shock and in cardiac 
decompensation, the capillary flow in vasomotor instability and in hyperten- 
sion have already been made. They require further confirmation before 
their clinical value is fixed. Indeed, a recent observer (Boas) claims that 
there is no actual pulsation visible in the capillaries and that arterial pulsation 
ceases in the end arterioles. 
In this chapter it has been shown how the circulation may be followed 
through the larger arteries, capillaries and veins. Each will probably come 
to have its special value in helping the clinician assess in what system—• 
arterial, venous, or capillaries—lies the important defect in the blood flow. 
REFERENCES 
Boas, E. P.: The Nature of the so-called Capillary Pulse; Archives Internal Medicine 
1922, XXIX, 763. 
Bishop, L. F.: Hypotension. 
Brown, N. W.: A Simple Method for the Determination of Venous Pressure; John Hopkins 
Bulletin, 1918, XXIX, 93. 
Fisher, J. W.: The Diagnostic Value of the Sphygmomanometer in Examinations for Life 
Insurance; Journal of American Medical Assn., 1914, LXIII, 1752. 
Friedlander and Lenhart: Clinical Observation in the Capillary Circulation; Archives 
Internal Medicine, 1922, XXIX, 12. 
Fridericia, L. S.: Eine Klinische Methode zur Bestimmung der Kohlensaeuerspannung in 
Lungenluft; Berliner Klinische Wochenschrift, 1914, LI, 1269. 
Gaertner: Munchener Medizinische Wochenschrift, 1904, 212. 
Goodman and Howell: Further Clinical Studies in the Auscultation Method of Deter- 
mining Blood Pressure; American Journal of Medical Science, 1911, CXLII, 334. 
Gull, W. W., and Sutton, H. G.: On the Pathology of the Morbid State Commonly Called 
Bright’s Disease, etc.; Medico-Chirurgical Transactions, 1872, LV, 273. 
Hill, L., and Rowlands, R. A.: Systolic Blood Pressure; Heart, 1912, III, 219. 
James, W. B., and Hart, T. S.: Auricular Fibrillation. Clinical Observations on Pulse 
Deficit, Digitalis and Blood Pressure; American Journal of Medical Sciences, 1914,, 
CXLVII, 63. 
Janeway, T. C.: Clinical Study of Blood Pressure. 
Janeway, T. C.: Important Contribution to . . . Blood Pressure; Johns Hopkins 
Bulletin, 1915, XXVI, 296. 
Kilgore, E. S.: The Fractional Method of Blood Pressure Determination; Archives of 
Internal Medicine, 1915, XVI, 939. 
Krogh, A.: The Anatomy and Physiology of Capillaries, 1922. 
Koratkow: Vratch Gazette, 1906, 218. 
Mac William, J. A., and Kesson, J. E.: The Estimation of Systolic Blood Pressure . . . 
Influence of the Arterial Wall; Heart, 1912-1913, IV, 279. 
Mall, F.: Der Einfiuss des Systems der Vena Port®, etc.; Archives f. Anat. und Phys- 
iologic, Physiologische Abteilung, 1892, 418. 
Mosenthal, H. O.: Renal Function as Measured by the Elimination of Fluids, etc.; Archives 
of Internal Medicine, 1915, XVI, 733. 
Norris, G. W.: Blood Pressure, Its Clinical Applications. 
von Recklinghausen: Arch f. Expt. Path. v. Pharmak., 1906, LV, 468. BLOOD PRESSURE 
443 
Schlayer: Funktion kranker menschlicher Nieren: Verhandlungen des XXVII ten Kon- 
gresses fuer Innere Medizin, 1910, 744. 
Stone, W. J.: The Differentiation of Cerebral and Cardiac Types of Hyperarterial Tension, 
etc.; Archives of Internal Medicine, 1915, XVI, 775. 
Taussig, A. E., and Cook, J. E.: The Determination of the Diastolic Pressure in Aortic 
Regurgitation; Archives of Internal Medicine, 1913, XI, 547. 
Van Slyke, D. D., Cullen, G. E., and Stillman, E.: Proceedings of the Society for Experi- 
mental Biology and Medicine, 1915. CHAPTER XXVI 
THE HEART AND CIRCULATION IN SPECIAL DISEASES—THE 
HEART IN DIPHTHERIA—THE TOBACCO HEART—THE 
AVIATOR’S HEART—THE CIRCULATION IN SURGICAL SHOCK 
—SURGERY AND THE ARRHYTHMIC HEART, WITH AND 
WITHOUT DECOMPENSATION—SURGERY AND HYPERTEN- 
SION—THE “FIBROID” HEART 
The Heart in Diphtheria.—The pathological changes occurring in the 
heart in deaths from diphtheria have already been described (Chapter IV). 
In severe diphtheritic infections, marked destruction of the myocardium 
may result in death. In one instance, a girl of io with severe diphtheria and 
heart block, leucocytic infiltration in the junctional tissue and in the ventricu- 
lar musculature was found. In another instance, a child developed heart 
block during the course of diphtheria. Electrocardiographic examination 
several years later still showed the arrhythmia; however, there were no 
cardiac symptoms. I have personally observed a child 8 years old with very 
toxic diphtheria, in whom, after a few days, there were attacks of convulsions 
coincident with slow rhythm. Polygraphic tracings showed regular radial 
and ventricular activity at the rate of 40 per minute; the venous tracing was 
unsatisfactory. Heart block was diagnosed. The child died one week later. 
Necropsy was not obtainable. From the virulent course of the disease, 
heart block seemed due to toxic degenerative myocarditis. 
Milder toxic destruction of the myocardium in diphtheria is evidenced 
by the usual signs of myocardial insufficiency, especially by dyspnoea. 
Another evidence is the presence of arrhythmias—heart block, auricular and 
ventricular extrasystoles, auricular fibrillation, tachycardia. These types 
may frequently interchange. They are apparently indicative of myocardial 
degeneration. Pathologically, the muscle cells undergo fatty degeneration, 
the valves and endocardium are rarely involved. With reference to the 
arrhythmias, it must be remembered that, as in other acute febrile and infec- 
tious diseases, cardiac irregularities may occur at the onset or crises, without 
any evidence of cardiac degeneration (Chapters X, XI). Such irregularities 
at these times are probably the effect of toxins on the normal neurogenic 
cardiac control; they are harmless and rarely require medication. It is there- 
fore important to differentiate the innocuous from the dangerous arrhythmias 
in diphtheria. With our present knowledge, this is the best accomplished 
by a careful and complete examination of the entire cardio-vascular appara- 
tus, and not alone by a consideration of the types of arrhythmias. The 
444 THE HEART AND CIRCULATION IN SPECIAL DISEASES 
445 
presence of cardiac failure, slight or severe—dyspnoea, cyanosis, edema, car- 
diac dilatation—indicates that any type of irregularity, except physiological 
sinus arrhythmia, is of serious or even ominous import. 
The study of the heart in diphtheria is further complicated by the occa- 
sional occurrence of unexpected, sudden death. This is usually regarded as 
due to paralysis of the cardiac nerves. Some of these deaths can, I believe, 
be explained on the assumption of a destructive, progressive myocardial 
degeneration with slight or no symptoms during life, or with the cardiac 
symptoms masked by those due to the diphtheria itself. In other cases 
in which myocardial damage is not demonstrated at necropsy, these fatalities 
may possibly be regarded as anaphylactic phenomena affecting the cardio- 
inhibitory center or the intracardiac nerve supply. 
Treatment for the diphtheria itself should be carried out along the 
well recognized lines of antitoxin injections. Where cardiac failure is present 
or imminent, vigorous circulatory remedies (Chapter XX) should be used, 
chiefly digitalis and the caffein derivatives. The presence of arrhythmias— 
even heart block—is no contraindication to this general rule. An attempt 
should be made to relieve the block by atropine sulphate, best given subcu- 
taneously in full physiological doses. 
The Tobacco Heart.—As already stated (Chapter IV), I regard the effect 
of tobacco poisoning upon the heart as being very probably the result of 
the selective action of nicotine upon .the nerve mechanism of the heart, 
rather than upon the musculature and endocardium of the heart itself. 
In addition, evidence of organic cardio-vascular disease is lacking. The 
assumption of a neurotoxic poison satisfactorily accounts for the various 
arrhythmias—sino-auricular block, extrasystoles, auricular flutter and 
even auricular fibrillation—which can be produced by tabagism. It also 
accounts for the clinical fact that in almost all instances in which tobacco is 
withdrawn, the arrhythmias soon disappear. 
Precordial pain is one of the common as well as distressing accompani- 
ments of tabagism. It seems due to disturbance in the coronary circulation 
and to referred irritation from excitation of the sympathetic ganglia. The 
types of pain and their therapy have already been described (Chapter XXIV). 
The diagnosis, symptomatology and therapy of cases of “tobacco heart” 
are given in Cardio-vascular Clinics. Brief allusion should again be made 
to the fact that during actual smoking, there is often a slight moderate rise 
of blood pressure, probably the result of stimulation of the peripheral and 
central vaso-constrictor mechanism. 
The Aviator’s Heart.—During the Great War, many studies were made on 
the effect of aviation on the heart and circulation. These observations will 
undoubtedly have great value in peace times, as aviation becomes more 
general. 
Observations were at first disjointed because they were confined to cur- 
sory examinations during flight, and there was no method of checking up 446 
THE HEART AND CIRCULATION IN SPECIAL DISEASES 
Fig. 284.—Diagram of the Henderson re-breather—the rebreathing apparatus 
employed in all routine tests of the aviator’s ability to withstand low oxygen. It consists 
of a tank, T, of about 120 liters capacity. The volume of air is determined by the amount 
of water that is run into it. The man under examination continually rebreathes the air of 
the tank (a clip is placed on his nose) through the inspiratory and expiratory valves, 
Vi and Ve. The oxygen is thus consumed and reduced. The exhaled carbon dioxide is 
taken up by sodium hydroxid in the absorber A. The movements of respiration are 
recorded by the spirometer, S, connected to a smoked drum, K. As the oxygen is consumed 
and the air volume is thus reduced, the spirometer falls and the graphic record on the 
smoked drum rises. At the end of the test a sample of air is drawn from the tank and 
analyzed as a confirmation of the oxygen consumption and of the oxygen percentages 
(that is, altitudes) indicated by the graphic record. (From Medical Studies in Aviation, 
Journal American Medical Association, 1918, LXXI, 1382-1400.) THE HEART AND CIRCULATION IN SPECIAL DISEASES 
447 
by refined methods such necessarily hasty examinations. It was soon 
discovered, however, that the atmospheric conditions of actual flying could be 
imitated in the laboratory, for oxygen deficiency in the higher altitudes 
was found to be the underlying cause of all the circulatory disturbances. 
Tests of the candidate’s ability to fly were therefore instituted. This was 
at first accomplished by the so-called re-breathing apparatus (Fig. 284). 
Later, a large steel chamber with an air pump was devised, so that several 
candidates could be examined under any desired reduction of air 
pressure. 
As was to be expected, it was found that individuals react differently to 
different amounts of oxygen deprivation in rebreathing. In some respects 
and up to a certain degree of “altitude” in the re-breather, there was found 
to be a physiological compensation for the lack of oxygen supply; this showed 
itself in the type of breathing and in changes of pulse rate and blood pres- 
sure. Most subjects breathed not only more frequently, but also more 
deeply—reactions which began quite early in some of the oxygen depriva- 
tion experiments, and which naturally resulted in increased pulmonary 
ventilation. 
The physiological circulatory reaction in the oxygen-deprivation, re- 
breathing experiments resulted in increased cardiac and pulse rates, that is, 
in increased oxygen supply. A normal reaction constituted an increase of 
from 15 to 40 pulse beats per minute when the oxygen had been lowered 
slowly to between 7.5 and 6.5 per cent. Absence of such response denoted 
“ either inability to react to a low oxygen of high altitudes and early failure, 
or that sufficient compensation is secured by increased breathing or blood 
concentration or both” (Schneider). Failure to respond is usually asso- 
ciated with poor tolerance for high altitudes. Occasionally, there is an 
abnormally increased heart rate; such reactions usually disqualify subjects for 
higher altitudes, although they may safely fly at lower levels. 
Regarding the effects of altitude on the systolic blood pressure, the best 
type of response seemed to be that in which the systolic pressure remains 
unchanged until the amount of oxygen has been considerably reduced, after 
which point it gradually rises. Similarly, the best response in diastolic pres- 
sure is that in which it remains at the same level, or is slightly increased 
throughout the test. Occasionally, in those exhibiting poor reaction, first 
the diastolic, and then the systolic pressure fell; this is then accompanied by 
a slow pulse rate and fainting attack. 
Careful roentgenographic studies were also made regarding the size of the 
heart in rebreathing tests. These observations proved that roentgenographic 
plates taken during various phases of respiration resulted in marked differences 
in the cardiac outline, especially in the transverse diameter, differences which 
ultimately depended upon how much the diaphragm was raised or lowered 
during inspiration and expiration, respectively. I have long since emphasized 
similar observations in routine fluoroscopy (Chapter XII). Although the 448 
THE .HEART AND CIRCULATION IN SPECIAL DISEASES 
observers arrived at no definite conclusion, there was no evidence that there 
was any regular change in the cardiac diameter or contour as the result of 
oxygen deficiency during rebreathing experiments. 
There were other important experimental observations of the aviator— 
for example, his visual, auditory and psychological reactions. These however 
are beyond our field. 
From the studies that have thus far been made, one may safely conclude 
that the important primary effect of aviation upon the circulatory apparatus 
is a vaso-motor one; that circulatory failure when it occurs is primarily of 
vaso-motor origin, and is only secondarily due to the heart; and that lack of 
oxygen is the fundamental cause of the vaso-motor instability. This assump- 
tion further explains why aviators should be in prime condition, and why, 
when “stale” as the result of overwork and insufficient nerve relaxation, or 
as the result of improper “ training” conditions, the vaso-motor nerve balance 
is more readily upset; as a consequence abnormal reactions under flying 
conditions appear sooner or become exaggerated with corresponding danger to 
the flyer. 
The Circulation in Surgical Wound Shock.—I refer here not to circulatory 
failure from hemorrhage—slight or severe—but to so-called surgical wound 
shock, a condition described as “functional disturbance of the circulation 
which follows severe trauma or surgical operation and which progresses 
into a severe condition, even death. Upon post mortem examination, no 
pathological changes can be found to account for it” (Wiggers). Experiences 
during the late war have given renewed impetus to the study of this important 
subject. It is now generally recognized that surgical shock is a complex 
phenomenon and that it may arise from the most diverse causes. The most 
varied theories have been advanced to account for surgical shock, from one 
emphasizing psychic disturbances such as fear and insomnia (noci impulses 
—Crile) to those which seek the fundamental causes in the veins and peripheral 
circulation. The more widely held theories will be briefly presented 
subsequently. 
Regarding some of the surgical conditions that have an influence in the 
production of shock, it has long been known that extensive burns, rough 
handling of the intestines during abdominal operations, cerebral concussion, 
etc., are such types. On the other hand, extensive muscle, tendon and bone 
operations (except upon the cranium) are not as apt to be accompanied by the 
manifestations of shock. 
The clinical picture found in shock is the same no matter what the cause. 
The pulse is soft, rapid and often irregular. When shock is severe, the pulse 
may be slow and readily compressible. The systolic blood pressure is low. 
with a very small pulse pressure; the respirations are irregular and gasping: 
the patient is usually apathetic. These signs are quite similar to those found 
in massive hemorrhages, hence the extreme importance of correctly rec- 
ognizing the etiological factor in a given case. Among other observations THE HEART AND CIRCULATION IN SPECIAL DISEASES 
449 
systolic blood pressure studies have been made, especially for the purpose of 
determining any clinical correlation between blood pressure readings and the 
onset or threatened onset of shock. The general statement may be made 
that when blood pressure has fallen from the normal to about ioo m.m. of 
mercury, it is evidence of the imminence of shock, especially if accompanied 
by a low diastolic or small pulse pressure. It should be emphasized, however, 
that low blood pressure itself is but a part of the clinical picture, and that 
other manifestations such as rate of heart action, cold extremities, presence of 
cyanosis or pallor, or irregular breathing must be considered in order to de- 
termine not only the presence of shock but to roughly estimate its degree. 
Depending also upon the urgency and type of operation, the surgeon must 
decide upon the appropriate remedies as well as upon the advisability of 
further operative procedures. 
As the result of physiological and surgical experimentation, and from 
clinical observations the following theories regarding the causes of circulatory 
failure in shock have been envolved. 
1. Shock from loss of circulating fluid—acute oligemia (Henderson) 
occurs not only in hemorrhage with loss of blood, but also in such conditions 
as serous diarrhoeas and abdominal parecentesis. This type of shock was at 
first attributed to fatigue and failure of the vaso-motor center; later experi- 
ments, however, have shown that that center remains intact and can be 
reflexly stimulated until an extreme degree of circulatory failure sets in 
(Porter). Shock in oligemia may perhaps be directly attributable to the 
toxic effect of the deprivation of large amounts of fluid. 
2. Abnormal Production and Absorption of Poisonous Proteids—This 
theory assumes that because of venous and capillary stasis found in shock, 
split proteid products are formed and act as toxic agents. Objections to 
this theory are that one does not know whether these by-products may not be 
the “normal’’ results, so to speak, of such stasis; besides, absorption is 
practically at a standstill during shock. 
3. Fat embolism has been given as one cause of shock. It has been 
shown experimentally that when oil is injected intravenously and causes 
extensive embolism in the lungs, death immediately follows from plugging of 
the bronchi; when less extensive, there is a primary fall of arterial pressure 
which later rises (Wiggers). How often such experimental conditions are 
reproduced in the human being in the assumption of fat emboli as the cause 
of shock and death must depend upon clinical findings and autopsy studies. 
It does not appear likely, however, that fat embolism is a very frequent cause 
of shock. 
4. Venous Stasis in the Venous Reservoirs of the Chest and Abdomen. 
The view that during shock “the patient bleeds into his own veins” is based 
largely upon the experimental observations that shock induced in animals by 
manipulation of the intestines is accompanied by marked turgesence and 
stagnation of blood in the mesenteric veins and intestinal walls. Such 45° 
THE HEART AND CIRCULATION IN SPECIAL DISEASES 
venous stasis, however, was not seen by surgeons in the frequent abdominal 
operations in shocked soldiers during the recent war (Cannon). 
5. Anoci-association.-—According to Crile’s theory of nerve exhaustion, 
there is impairment of the vaso-motor mechanism and exhaustion of the brain 
cells, suprarenal gland and liver. Porter has demonstrated experimentally 
that the vaso-motor center does not lose tone in shock and that it is not 
primarily exhausted. Furthermore, regarding the histological changes in the 
brain cells found by Crile, these may well be the result, not the cause of the 
circulatory failure. Besides, other observers have not considered such 
changes in the brain cells as definitely pathological. With reference to the 
assumption of suprarenal exhaustion, it may be stated that there is “experi- 
mental testimony that painful stimuli and asphyxia increase both the 
secretion of epinephrin and the percentage of sugar in the blood” (Cannon). 
These data would seem to controvert Crile’s theory in a large proportion of 
cases. It should be added that when circulatory failure in shock is extreme 
and long-continued, one will naturally find exhaustion of all glandular 
and nerve structures. 
6. “Acidosis” (Henderson) has been found in experimentally shocked 
animals; it has also been found in the human being in shock (Cannon). In 
“acidosis” there is a low carbon dioxide content in the blood. It does not 
seem likely that this condition is primary: It is probably the result of more 
fundamental disturbances found in shock, especially decrease in the amount 
of circulating blood. 
7. Stasis in the Capillaries.—This assumption is based partly upon the 
clinical observation that in shock there is concentration of the blood, and stag- 
nation of the corpuscles in the capillaries as compared with the veins (Can- 
non). The assumption is further based on the exclusion of other factors. 
The arterial system being comparatively empty and the veins not always 
overfilled, it is assumed that the blood must necessarily stagnate in the capil- 
laries. Physiological data seem to show that the capillary bed is sufficiently 
expansile to act as a reservoir for the blood lost to the circulation in shock 
and that concentrated blood has a tendency to enhance this capacity. 
8. Blood Viscosity.—Cold increases the H-ions in the blood (“acidosis”) 
in shock; it may therefore increase blood viscosity and thus have a certain 
influence in enhancing capillary stagnation. 
The following conditions—tachycardia and dilated heart—are included 
here not because they constitute shock in the true sense, but because 
they can readily develop into a condition closely resembling the shocked 
state. 
Tachycardia, especially the paroxysmal variety (Chapter XI) may have 
a decided influence in producing a clinical complex in every way resembling 
shock. In those cases that I observed, this was especially true when abdom- 
inal operations were performed upon women who feared operation and who 
had slight tachycardia before anesthesia was begun. The correlation THE HEART AND CIRCULATION IN SPECIAL DISEASES 
45i 
between tachycardia and the symptom complex of shock is described in con- 
junction with Cardio-vascular Clinics. 
Dilated Heart.—This assumption, often loosely used by surgeons and 
physicians as the cause of shock, has been described in another connection 
(Chapter VI). 
From this multiplicity of theories regarding shock it is evident that many 
causes operate to produce it. Long exposure on the battle field and a chilled 
body may be one etiological type, surgical procedure in a frightened woman 
another. Weighing all data, it seems probable that capillary stasis and a 
decrease in the amount of circulating fluid are two of the most important 
dynamic factors, and that abnormal nerve influences play an important 
role in initiating and bringing about the circulatory failure found in shock. 
It should be strongly emphasized that, no matter what the cause, the heart 
is not the organ primarily at fault. As shown experimentally, “ the effective 
right auricular pressure is low, the ventricular filling is diminished, the 
ventricular relaxation incomplete, and the output per beat consequently 
small. The heart rate is rapid but the minute volume is diminished. The 
arterial blood pressure is low and the peripheral flow is slowed” (Wiggers). 
Treatment of Circulatory Failure in Wound Shock.—The most effective 
measure is the application of warmth. This may be accomplished by the use 
of hot water bags or bottles (care being taken not to burn the patient); by 
rolling the patient in warmed blankets; or where available, by an improvised 
covered cage furnished with electric lights. The foot of the bed or table 
should be elevated. Some surgeons find bandaging of the extremities of 
added value. Blood transfusion has been frequently used but does not 
possess any special advantage. Because the fall of venous pressure and of 
peripheral resistance are the two out standing circulatory features of shock, 
epinephrin, adrenalin and pituitrin—powerful vaso-constrictors—are apt to 
have a strong although temporary effect in overcoming vasodilatation. 
Epinephrin may be given intravenously. In order to make up for loss of 
circulatory fluid, saline solutions by means of the rectal Murphy drip, or 
physiological salt solution given intramuscularly or intravenously are of 
value. The rectal drip or intramuscular injections are preferable; the fluid, 
although more slowly absorbed, is more apt to remain in the circulation. 
When injected intravenously, it passes through the kidneys very quickly and 
hence does not increase the volume of the circulating fluid for any length of 
time. Besides, some surgeons believe that by thus quickly throwing so 
much added fluid into the circulation, the heart becomes distended and 
dilated, and circulation even more embarrassed. In order to have fluid remain 
in the circulation, heavier solutions such as glucose and gum acacia mixtures 
have been tried, especially in hospitals in the war zone during the recent 
war. Such solutions, however, have not been found of more value than the 
older routine methods; some of the injections, indeed, were followed by seri- 
ous results, even death. To combat tissue “acidosis,” bicarbonate of soda 452 
THE HEART AND CIRCULATION IN SPECIAL DISEASES 
solutions may be given intravenously or by the Murphy drip. Drugs acting 
directly upon the heart such as digitalis and strophanthin possess but 
little if any value. Caffein sometimes helps temporarily. Strychnine and 
camphor are of questionable utility. 
Surgery and the Arrhythmic Heart. Surgery in Hypertensive Cases.— 
It is of course axiomatic that surgery should be practiced only for definite 
indications when heart disease is present or is suspected, that the operation 
should be as brief as possible, and that surgical intervention even in extreme 
cardiac failure is justifiable if it offers the one chance for life. 
Whenever possible, operations on those with heart disease should be done 
under local anesthesia. Where general anesthesia is indicated the best 
anesthetic is ether alone. A mixture of gas and ether may be used occasion- 
ally. Chloroform is to be avoided. 
It may be stated as a general rule that patients with decompensation from 
any cause withstand operations, even slight ones, poorly if they are nervously 
upset by fear or dread of the operative procedure (Chapter XIV). In such 
instances, nervous influences undoubtedly play an important part in further 
deranging circulation, usually by producing tachycardia and by increasing 
dyspnoea. Bromides or morphine, or both are the remedies to be given to 
these individuals before operation. In addition, all dread and fear must be 
removed by the tactful, sympathetic physician or surgeon. 
Functional arrhythmias (Chapter XI)—that is, those not produced by 
organic cardio-vascular disease, require no other care than that usually given 
to the heart and circulation during routine anesthesias and operation. This 
statement applies even to heart block if of functional origin. Thus, I observed 
a case of complete heart block with rapid ventricular activity (see Cardio- 
vascular Clinics) operated upon for tuberculous peritonitis; he stood both 
anesthesia and operation very well; polygraphic tracings that I took during the 
operation showed that it had no effect upon the block. An important excep- 
tion to the rule disregarding functional arrhythmias is to be made in cases 
of functional tachycardia due to fright. Unless the patient is sufficiently 
calmed so that fear is dispelled, serious post-operative circulatory conse- 
quences may occur (Cardio-vascular Clinics). 
Unless the surgical condition is assumed to be the cause of the cardio- 
vascular disease, as for example in local infections, decompensation calls for 
postponement of any but imperative operative procedures until attempts 
have been made to restore compensation. It naturally requires the close 
and balanced co-operation of physician and surgeon to decide how long 
one may wait for restoration of compensation in surgical conditions which, 
by waiting, may at any time become dangerous to life; acute appendicitis 
with fever and signs of peritonitis is a case in point. The presence of various 
types of arrhythmias does not of itself change the operative indication unless 
indeed the cardiac irregularity is considered special evidence of decompensa- 
tion. For example one need not necessarily postulate that heart block be s< THE HEART AND CIRCULATION IN SPECIAL DISEASES 
453 
regarded, for if such a patient has but little dyspnoea, no bronchial rales, no 
cyanosis and slight pretibial edema at the time of operation, he may stand 
even a serious operation very well. So also patients with auricular fibrillation 
and mitral stenosis if otherwise in a fair state of compensation and with no 
extreme tachycardia usually tolerate operations well. 
Decompensated patients who are cyanotic are poor operative risks. 
Patients with hypertensive cardio-renal disease with but slight dyspnoea are 
comparatively good operative risks. 
Up to the present time electrocardiographic observations have not helped 
in distinguishing the poor from good operative risks in those with cardiac 
disease. Electrocardiograms give invaluable information regarding arrhyth- 
mias and occasionally of myocarditis; but as so frequently emphasized in 
various connections, this is but one part of a cardio-vascular examination; 
we require other data in order to determine whether a heart is or is not com- 
pensating (Chapter XIV), that is to say, whether the circulation is being 
carried on efficiently or not. 
The “Fibroid” Heart.—Brief mention should be made of the assumed 
connection between the fibroid uterus and the “fibroid heart.” It had for 
a time been believed that cardio-sclerosis was a frequent accompaniment of 
this type of uterine tumor, especially when extrasystoles were also present. 
Careful post-mortem studies of women with myomata have disproved this 
theory; cardio-sclerosis was not found more frequently than in those of similar 
age without myomata. Those with fibroid uteri stand operative interference 
as well as women with other comparable operative conditions. Arrhythmias 
when present and of functional origin should not interfere with the usual 
operative indications. 
REFERENCES 
Cannon, W. B., Fraser, J., and Cawell, E. M.: The Preventive Treatment of Wound Shock; 
Journal of American Medical Assn., 1918, LXX, 618. 
Cannon, W. B.: A Consideration of the Nature of Wound Shock; American Journal of 
Medical Sciences, 1918, LXX, 6x1. 
Crile, G. W.: Surgical Shock. 
Crile, G. W.: Blood Pressure in Surgery. 
Crile, G. W.: Kinetic Drive. 
Henderson: Acapina and Shock. Failure of the Circulation; American Journal of Physi- 
ology, 1910, XXVII, 152. 
Henderson, Schneider, Whitney, Dunlap, Wilmer, Berens, Lewis, and Patton: Medical 
Studies in Aviation; Journal of American Medical Assn., 1918, LXXI, 1382-1400. 
Kochers, R. A.: The Effect of Activity on the Histologic Structure of Nerve Cells; Journal 
of American Medical Assn., 1916, LXXVII, 278. 
Levine, S. A.: Acute Cardiac Upset During or Following Operations; American Journal of 
Medical Assn., 1920, LXXV, 795. 
LeWald, F. T., and Turrell, G. H.: The Aviator’s Heart. Roentgen Ray Studies under 
Conditions Simulating High Altitudes; American Journal of Roentgenology, 1920, 
VII, 67, 86. 
Meltzer, S. J.: The Nature of Shock; Archives of Internal Medicine, 1908, I, 571. 454 
THE HEART AND CIRCULATION IN SPECIAL DISEASES 
McGlinn: The Heart in Fibroid Tumors of the Uterus; Surgery, Gynecology and Obstet- 
rics, 1914, XVIII, 180. 
Porter: Shock at the Front; Boston Medical and Surgical, 1916, CLXXV, 854. 
Porter, Marks and Swift: The Reaction of Afferent Impulses in Fatigue of the Vasomotor 
Center; American Journal of Physiology, 1907, XX, 444. 
Wiggers, C. J.: Circulatory Failure; Journal of American Medical Association, 1918, 
LXX, 508, CHAPTER XXVII 
THE HEART IN PNEUMONIA—THERAPY FROM THE 
CIRCULATORY STANDPOINT 
Because of the frequency with which cardiac drugs are employed in 
pneumonia, I wish to review my impressions gained in the drug treatment of 
many cases of that disease. I shall not touch upon the bacteriological or 
chemotherapeutical aspects of pneumonia. Statistical study of various epi- 
demics or methods of treatment have likewise not been dwelt upon. Indeed, 
it is because I feel that none of the methods of medicinal treatment has been 
followed by any demonstrable correlation of cause and effect, of therapy and 
cure, that I have discarded statistics as bringing us no nearer to the thera- 
peutic and circulatory problems of pneumonia. A study of these therapeutic 
methods, some of them directly antagonistic in theory and practice, arouses 
doubt as to their possible efficacy. Mere mention of some of the types of 
treatment, many long since discarded, may therefore not be amiss. Creosote, 
alcohol, no treatment until the crisis, no treatment for hyperpyrexia, cold 
sponges or even tubs for the fever, no stimulation, stimulation at the crisis 
only, stimulation to prevent the dangers of the crisis, camphor in oil, caffein, 
digitalis, adrenalin, venesection, fresh air, cold air—all these are or have been 
popular. 
“Stimulation” has been the usual therapeutic keynote, for the danger 
was always correctly conceived as circulatory failure. I have used all of the 
recognized cardio-tonics—digitalis, strophanthus, caffein, adrenalin, as well 
as those whose effect upon the circulation may well be questioned—alcohol, 
strychnine, camphor. Camphor I have used in smaller, repeated, as well as 
in single large hypodermic injections, though experiments have shown that 
camphor in oil had no effect in delaying or preventing death in artificially 
induced pneumonia. I have employed the other drugs mentioned in all 
possible forms and combinations; in heroic, in small and moderate doses, 
subcutaneously, intravenously, and internally, before, during and after the 
crisis. With possible isolated exceptions, I have yet to see any of the effects 
upon the circulation which follows the use of some of these drugs in the 
experimental animal, or in cardiac failure from cardio-vascular disease. 
I believe the chief reasons for disappointment in pneumonia therapy are 
that we are dealing with an infection of varying virulence, and involving 
varying amounts of lung tissue. Therefore I have attempted, for clinical 
and therapeutic purposes, to roughly group and to treat pneumonia according 
to degrees of toxicity and extent of lung involvement. I consider the crisis a 
separate problem for therapy. 
455 456 
THE HEART IN PNEUMONIA 
I. Toxic Cases.—In the extremely toxic group, typically exemplified 
by sharp onset, early delirium, subsultus, dry tongue, no pain, rapid pulse 
and breathing, my experience has been that attempts at “stimulation,” 
a term which we shall apply to drug therapy used to combat and treat cir- 
culatory failure, are almost always without efficacy. These patients appar- 
ently defy all drug therapy, and sometimes die before the area of pneumonic 
involvement becomes ‘ clinically recognizable. Death ensues from acute 
toxemia. Stimulation, even if heroic, has not in my hands delayed or pre- 
vented the fatal outcome in any visible manner. The reason is presumably 
that the drugs do not and cannot combat the infective factor. Experiments 
throw an interesting sidelight upon this problem. It has been found that 
hearts perfused with pneumonic blood lose their efficiency, which is later 
restored by the use of normal blood. Whether in the human being the 
changes in the cardiac musculature are, or later become myocarditis are 
questions into which we shall enter later. 
It is usually believed that in toxic pneumonia there is marked vasomotor 
failure, though others, as the result of animal experimentation, have held 
otherwise. I have only very rarely seen any therapeutic result from single 
or repeated injections of adrenalin given subcutaneously or intravenously. 
A like negative result has almost regularly followed the use of strophanthin 
and other digitalis bodies when the pulse was regular. That digitalis does 
localize itself and affect the heart muscle in pneumonia as in purely cardiac 
disease has already been shown by the usual electrocardiographic evidence of 
digitalization—a negative T wave in head I and III (Chapter IX). Despite 
this change in the electrocardiogram, I have found in rhythmic cases no 
evidence of any help to the circulation from digitalis—cyanosis was not 
decreased, dangers from edema of the lungs not reduced. 
As a favorable prognostic sign, Gibson has emphasized a certain parallelism 
between pulse rate and systolic blood pressure; but others as well as myself 
have found his so-called law of no significance. The removal of 500 to 700 c.c. 
of blood by venesection gives occasional temporary relief in toxic cases; the 
benefit seems attributable to ridding the body of toxic material rather than 
from any primary circulatory relief. 
2. Area of Pneumonic Involvement.—With no evidence of severe toxemia, 
slowly progressing consolidation confined to one lobe is usually not dangerous 
during the acute febrile period. Such are probably the cases in which no 
treatment or any treatment has its measure of success. If, however, there is 
sudden massive involvement of one entire lobe and part of or all of another, 
the inflamed area in itself offers a problem for therapeusis, aside from the 
question of toxicity or crisis; for the pulmonary circulation and pulmonary 
ventilation may be sufficiently interfered with to produce cyanosis and 
beginning circulatory failure. Here venesection in plethoric individuals may 
be indicated for the relief of venous stasis; “stimulation” has a better chance 
for success, for the problem approaches more nearly a purely circulatory THE HEART IN PNEUMONIA 
457 
one. Cardiac tonics should be given in large doses from the very outset to 
combat, if possible, ever impending circulatory failure. 
3. The crisis apparently marks that point at which there is more or less 
complete sudden destruction of the pneumococci in the lung, while lysis 
marks their more gradual destruction. I distinguish clinically two types of 
crises—the febrile, and that of sudden pulmonary resolution. These are 
not necessarily simultaneous. A febrile crisis alone is not dangerous, but 
sudden resolution of a consolidated area has always been regarded, and rightly 
so, as the most critical and dangerous state of the disease. At such times 
there is apparently a rapid flooding of the blood and lymph channels with 
the liberated toxic, pneumonic products. Absorption probably occurs quite 
readily because of the general liquefying process and because the lymph and 
venous radicals are released from the pressure of the solidified lung. In other 
words, chemical and mechanical factors come into play at a time when the 
toxic products are greatest in amount. The heart muscle is thus bathed 
liberally and continually with pneumonic poisons. Interference with pul- 
monary circulation, caused by the onset of resolution is doubtless an added 
burden to the right heart. The main dangers arising during the crisis are 
general, from sudden systemic toxic invasion; and local, from edema of the 
lungs. The local danger, from the circulatory standpoint, depends upon the 
amount and rapidity of resolution, and the consequent pulmonary edema. 
An extremely important factor, scarcely mentioned in the literature, is the 
presence or absence of expectoration at the crisis. Pulmonary edema com- 
plicates and accompanies resolution more frequently if expectoration is ab- 
sent; while if expectoration is profuse, there is increasing opportunity for 
pulmonary aeration, and less for edema. I insistently try to make the 
patients cough in the hope of loosening and expectorating the pneumonic 
products. When, despite this, edema of the lungs supervenes, as shown by 
the loud mucous bubbling rales over the pneumonic and other areas of the 
chest, the chances for success become less, but even then I have the attendant 
regularly rouse the patient to coughing efforts as long as consciousnes is 
retained. As far as one may judge, stimulation in acute pulmonary edema 
occasionally keeps the patient alive for some hours or even a day, and may 
exceedingly rarely seem to pull a patient from death. 
With lytic or gradual resolution, even with very sharp critical drops of 
temperature, the battle is usually won, for edema of the lungs rarely occurs, 
and stimulation may be efficacious. However, even in cases of non-massive 
pneumonic involvement in young, vigorous individuals, with no evidence 
of toxicity during the attack, sudden, almost tragic intrusion of critical resolu- 
tion, edema of the lungs, and death—all within a few hours—may supervene. 
One instance especially impressed me—that of a young, healthy individual 
to whom the pneumonia was literally a laughing matter. From the presence 
of sudden perspiration and from the physical signs in the lungs, I was able to 
foretell the onset of critical resolution some hours before the typical drop in 458 
THE HEART IN PNEUMONIA 
temperature. Heart and pulse were then perfectly satisfactory. Herculean 
efforts were made by stimulation and otherwise to ward off the dangers of 
edema of the lungs. Within six hours, however, the patient died from 
pulmonary edema; while in an adjoining ward, an old woman, severely 
poisoned by her pneumonia and very sick for over one week, had reached the 
crisis with slow, gradual resolution of the pneumonia, and slowly but surely 
convalesced. 
Where digitalis has been given, its effect in causing arrhythmia must 
naturally be considered. Aside from this, a study of cardiac irregularities 
occurring during the course and at the crisis of pneumonia offers interesting 
and important therapeutic problems. The usual types are moderate brady- 
cardia, sinus arrhythmia, extrasystoles, auricular fibrillation and heart block. 
It is sometimes assumed that the presence of such arrhythmias in pneumonia 
is indicative of some organic affection of the cardiac valves or musculature. 
But, as in the non-pneumonic individual, irregular heart action does not in 
itself necessarily mean heart disease. Indeed, some of the arrhythmias— 
especially sinus arrhythmia, moderate bradycardia and extrasystoles—when 
found with an unembarrassed circulation at or immediately after the crisis 
usually offer good clinical evidence that the disease has definitely run its 
course. The irregular cardiac action is apparently due to a neurotropic 
effect of pneumonic toxins. Whether the latter act upon the medullary cen- 
ter or upon the heart itself it is impossible to state. Because of the occur- 
rence of these cardiac irregularities at the time of crisis, and because some 
drugs (for example, morphine) produce arrhythmias by affecting the cardio- 
inhibitory center, I am inclined to the view that these arrhythmias are due 
to an effect on the cardio-inhibitory center rather than on the heart itself. 
These arrhythmias usually last a few hours or days. I have followed some 
of these cases for years and have never observed any correlation between the 
arrhythmias and the possible later development of organic cardio-vascular 
disease. 
I have observed auricular fibrillation—complete irregularity of the pulse— 
several times at the crisis. In three such patients, each of whom had several 
crises from successive involvement and resolution of various pulmonary areas, 
there were attacks of fibrillation lasting several hours with each crisis. Two 
of the patients were elderly; the third, a vigorous adult. None showed cir- 
culatory embarrassment or heart failure during the course of the fibrillation; 
on the contrary, there was the usual picture seen in favorable crises with 
normal rhythm. On the other hand, I have observed other cases of auricular 
fibrillation occurring during the course of toxic pneumonia, all of whom died. 
In these it was impossible to estimate how much the arrhythmia itself con- 
tributed to the dangers of the pneumonia. 
Complete heart block with slow ventricular rhythm is rarely found in 
pneumonia. That it may be functional in origin and probably due to 
abnormal action upon the cardio-inhibitory center seems indicated by two of THE HEART IN PNEUMONIA 
459 
my cases, one of which came to necropsy. The patient had been ill for some 
time, there was no history of digitalis medication. Microscopically and 
grossly, the cardiac musculature and the bundle of His were found normal. 
The therapeusis of arrhythmias developing in pneumonia is similar to 
that in non-pneumonic individuals. If accompanied by heart failure, the 
arrhythmias are of serious, possibly ominous, import. Except in heart block 
with slow ventricular activity, when atropine should be tried, the treatment 
of these arrhythmias is no different from that of the other phases of pneumo- 
nia already discussed. If arrhythmias are unaccompanied by failing circula- 
tion, though they perhaps should not be entirely disregarded, their import is 
slight and they rarely require separate medication. 
It may perhaps emphasize my standpoint on cardiac stimulation in pneu- 
monia to summarize my procedure in the circulatory treatment of pneumonia 
in the influenza pandemic of 1918-19, when pneumonias were seen early and 
the therapeutic course could be followed from the very inception of the 
disease. As stated, the important therapeutic effort lies in cardiac stimula- 
tion. I shall merely allude to the fact that numerous plans were then in vogue, 
regarding the dosage, time of administration and kind of stimulation to be 
employed. My practice has been in this and other epidemics to begin 
stimulation early in severe cases, or in those likely to become severe. I 
digitalize early because the fight is usually a short one—the patient recovers or 
dies within a few days. I have never found any untoward effects upon the 
heart, kidneys, pulse rapidity or blood pressure from this plan, nor have I 
found that the use of any special digitalis preparation had produced any demon- 
strable difference. When available, and the patient is able to swallow, I pre- 
fer the standardized digitan tablets. When not available, I have used the 
tincture of digitalis. When I wished a quick effect, I administered the latter 
in 60-minim doses every few hours; when not so urgently indicated, I gave it 
in 15-minim doses every four hours. I believe that the criticism of the vari- 
able strength of the tincture is valid; but when the drug is employed in large 
doses and frequently, I feel that, gauged by the usual amounts required to 
digitalize in cardiac disease—(from one to one and one half ounces) the pneu- 
monic patient soon receives enough to properly digitalize him. In exception- 
ally severe cases I added a hypodermic of strophanthin in the ampule of ;Kooo 
strength, even after the patient had already received much digitalis. I have 
seen neither bad nor good results from this procedure, although I believe the 
procedure hazardous in ordinary cardiac disease. I used caffein benzoate of 
soda liberally, usually in hypodermic form. The average dose was 5 grains of 
the double salt in solution, given every two to four hours, depending on the 
severity of the case. I observed the use of camphorated oil in cases in which I 
was consulted. I do not believe this drug possesses any chemotherapeutic or 
stimulatory power, despite its immense popularity in previous years. Phle- 
botomy I also employed in a few cases. I believe its chief value lies in getting 
rid of toxic material. I saw no beneficial results follow its use in the epidemic. 460 
THE HEART IN PNEUMONIA 
I employed adrenalin often, but with no effect. In edema of the lungs, I 
used atropin and dry cupping of the chest, and crowded stimulation. These 
procedures had no demonstrable effect in preventing or even retarding a 
fatal termination. Where indicated I used the usual expectorants—ammo- 
nium chloride and carbonate, the iodides—without demonstrable effect. 
I have sketched my “plan” of therapy and stimulation in some detail 
because I wished to demonstrate that I have followed the usual well-known 
and well-worn methods. I confess, however, that I could observe no benefi- 
cial result from the use of stimulation in the pneumonia pandemic. I may 
also add that for many years it has been my contention that the almost 
innumerable and varied therapeutic “plans,” many of which have already 
been discarded, have not met with any demonstrable success in my hands, for 
I was never able to correlate the therapy with any effect upon the circulation. 
The milder cases require no stimulation. Some of the severe lobar pneumo- 
nia cases did get well, it is true, when stimulation of various kinds was used, 
but I am not convinced that it was the stimulation, and not the specific types 
of virulence present, that saved these cases. 
In personal conversations with many practitioners and consultants, the 
great majority acknowledged that they were therapeutically helpless in the 
pandemic. And, may I not add, has stimulation helped the circulation in 
other types of pneumonia? May we not be compelled to radically revise our 
views on what stimulation can actually accomplish? 
Bearing in mind the clinical, experimental and pathological data, may we 
not find therein sufficient cause for heart failure and death, and the compara- 
tive futility of cardiac stimulation in pneumonia? Can cardiac stimulation of 
any kind, no matter when begun or how continued, counteract pneumonic 
chemical poisons which are being continually elaborated throughout the 
disease, and which at certain times—the crises—are elaborated rapidly and 
in great amounts? This appears to me the fundamental problem of cardiac 
stimulation in pneumonia. I believe we must possess, in addition to stimula- 
tion, serological or chemotherapeutic methods for counteracting or nullifying 
the pneumonic toxins, or some method of changing a rapid into a slow 
resolution. Perhaps even a mechanical method for literally aspirating pneu- 
monic products, by suction or otherwise, is not impossible in these days of 
advance in tracheal insufflation. The heart can apparently withstand a 
certain amount of toxins, moderate in quantity, which are slowly, not sud- 
denly, thrown into the circulation. Elimination and antibodies can then 
perhaps keep pace with production of toxin. Otherwise cardiac power is 
slowly or quickly weakened, and cardiac stimulation is unfortunately usually 
futile. 
Having described in detail circulatory disturbances and the circulatory 
treatment of pneumonia, it remains to emphasize that the functional power 
of the heart is not only seriously interfered with during pneumonia, but that 
actual myocardial degeneration, more serious than the common cloudy THE HEART IN PNEUMONIA 
461 
swelling (Chapter V) can occur. Finally I wish to give a few illustrative 
cases, demonstrating severe cardio-sclerosis as a late sequel of pneumonia. 
The manner in which the myocardium is damaged in pneumonia is still in 
dispute. I am of the opinion that the myocardial damage is usually the 
result of the toxemia. This is to some extent based upon the observation of 
two cases of heart block that occurred during pneumonia. From the first, a 
man of 70, I obtained typical polygraphic tracings of heart block. The 
arrhythmia was not accompanied by special signs of circulatory failure. 
An autopsy was obtained. Macroscopic examination of the brain and spinal 
cord, and microscopic examination of the heart, including the junctional 
tissues, showed that all these structures were normal. The second case, a 
man of 50, entered the hospital in collapse and semi-stupor. The temperature 
was 104°. There was pneumonic consolidation of the left upper lobe. The 
temperature ranged between ioo° and 104° for one week. The heart sounds 
were scarcely audible, the radial pulse was regular, its rate between 100 and 
120 per minute. At the end of one week there was critical defervescence, 
the temperature fell to 97.40 per rectum, there was extreme collapse. The 
ventricular rate suddenly drppped to 44, and remained between 30 and 44 
for four days. Although satisfactory polygraphic records could not be ob- 
tained, heart block was diagnosed by the clinical phenomena and pulse rate. 
The pneumonic area underwent gradual resolution. There were no general 
convulsions, but frequent convulsive tremors of the musculature of the upper 
and lower extremities. The stupor slowly deepened into coma. Suddenly, 
one week after the inception of the slow rhythm, the patient sat up in bed 
fully oriented, with good color, warm extremities, and a pulse and ventricu- 
lar rate of 76 per minute. The heart sounds, though still faint, were readily 
heard. Except for two occasions a few days later, the pulse continued regu- 
lar. The patient returned some weeks later with edema of the lower extrem- 
ities, apparently due to myocardial changes. 
The heart block in the first case may have been due to an effect of the 
pneumonic toxins upon the cardio-inhibitory center. At any rate, since the 
autopsy revealed a perfectly normal heart, it demonstrated that toxins may 
have only a temporary effect upon the cardiac musculature, and that the 
latter may then again return to normal. In the second case, the inception of 
the heart block was accompanied by circulatory collapse; the latter disap- 
peared with return of normal rhythm. Several weeks later there was again 
mild heart failure. The pathological sequence would seem to have been heart 
block and collapse at the crisis, partly from a toxic inhibitory effect and 
partly from severe acute poisoning of the myocardium. From this attack 
the patient recovered; this was followed later by sufficient myocarditis to 
cause mild decompensation. 
Cardio-sclerosis as a Late Sequel of Pneumonia.—Damage to the cardio- 
vascular apparatus as a late sequel of pneumonic infections has been 
insufficiently emphasized. Such sequelae produce symptoms only some 462 
THE HEART IN PNEUMONIA 
months or years after the pneumonia has run its course, so that the connection 
between the two diseases is usually entirely overlooked. In some instances 
the pneumonic poison seems to light up a dormant cardio-vascular process; 
in others, it primarily produces this condition. Brief case reports of both 
types follow: 
Male, age 50, entered the hospital with a mild pneumonia. He recovered 
within one week. The only point of interest in a careful examination of the 
cardio-vascular system was a slightly accentuated second sound over the right 
base suggestive of aortitis. The Wassermann blood reaction was negative. 
The urine and blood pressure were normal. Two months later the patient 
re-entered the hospital with the history of a pneumonic attack three weeks 
previously. He presented all the typical evidence of cardio-sclerosis with 
decompensation—anasarca, urine containing albumen and casts, high blood 
pressure, markedly accentuated second aortic sound. Evidences of the 
recent pneumonia were still present. 
A physician, age 50, had for several years remarked occasional dyspnoea 
upon walking but never considered himself ill. Two years before coming 
under observation, he developed a severe pneumonia which ran a toxic course 
and lasted several weeks. A few months thereafter, cardiac symptoms began. 
He became dyspnoic and edematous. Hypertension developed. The urine 
contained albumen and casts. Orthodiascopic examination one year later 
showed marked enlargement of the aortic arch and of the left ventricle. 
With some remissions, the cardiac symptoms lasted until the time of his 
death, one year and a half later. 
Both these cases illustrate the effect of pneumonia upon what seemed 
otherwise quiescent cardio-vascular disease. 
Male, aged 32, never drank or smoked. He had a grippe infection with 
fever six years previously; this lasted several months; pulmonary tubercu- 
losis was suspected but bacilli were never found. Cardio-nephritic symp- 
toms began three years later. They were at first mild and consisted of 
occasional dyspnoea when climbing stairs. The signs of cardio-sclerosis grad- 
ually progressed so that at the time of examination, although the patient 
complained of but slight dyspnoea and precordial pain, the left half of the 
chest was practically filled by a hugely hypertrophied heart. The systolic 
blood pressure ranged between 200 and 300 m.m. of mercury, the first sounds 
at the right base and at the apex were exceedingly harsh, rough and vibrant, 
indicative of probable calcification of the mitral valves and aorta. The sec- 
ond sound at the right base was markedly accentuated; the urine contained 
albumen and casts. The Wassermann blood reaction was negative. The 
clinical picture was that of extremely advanced cardio-sclerosis and nephritis. 
From the history and from the absence of other etiological factors, it is 
fair to conclude that the prior pulmonary infection six years ago was the 
direct and only cause of the extreme cardio-vascular disease. CHAPTER XXVIII 
CARDIAC DISEASE IN MARRIAGE AND PREGNANCY 
The question of marriage in women with cardiac disease is one which 
evidently requires careful consideration. The chief dangers arising from 
marriage in such cases are twofold; The strain and excitement incidental 
to coitus, and the dangers arising from pregnancy. Regarding the former, 
I know of several instances of hemoptyses immediately following coitus in 
patients with mitral stenosis and auricular fibrillation (complete irregularity 
of the pulse), and in one with cardio-sclerosis and hypertension. I also 
know of one case of death from cerebral apoplexy following intercourse; the 
patient was a man with cardio-sclerosis and hypertension. I have observed 
cases of violent tachycardia caused by intercourse. With two exceptions, the 
cardiac condition of all of these patients would have been considered fairly 
satisfactory under ordinary conditions. 
Views regarding the advisability of permitting marriage in women with 
cardiac disease are quite at variance. For example, some maintain that 
patients with heart disease should never marry, no matter what type of lesion 
be present. I believe this view to be extreme. One frequently encounters 
mothers of large families who doubtless have had valvular disease for many 
years and who have gone safely and normally through pregnancy and parturi- 
tion. Many of these patients were never aware of their disease; in some the 
lesion was discovered only in the course of a routine examination. 
The statistical tables of the lying-in institutions that I have studied have, 
in my opinion, very little value in clarifying the problem. The statistics 
are based chiefly upon patients that entered the hospitals severely decompen- 
sated; a cardiac history prior to pregnancy or to decompensation is entirely 
disregarded or only cursorily mentioned. To be of value, cases must be 
carefully studied from the cardiac as well as from the obstetrical standpoint; 
this requires the cooperation of internist and obstetrician, or the skilled 
observation of that rare combination, a clinician who has had a large, active 
obstetrical experience. 
Marriage naturally should not be advised, if at the time the patient shows 
the slightest degree of decompensation. Briefly, decompensation is evidenced 
by the presence of dyspnoea, especially on exertion; by edema of the extremi- 
ties; an enlarged liver; bronchitis; cyanosis, and by arrhythmias. The latter 
are chiefly extrasystoles (pulsus bigeminus), auricular fibrillation (complete 
irregularity of the pulse) and tachycardia. I wish to emphasize, however, 
that arrhythmias in themselves, except possibly auricular fibrillation, do not 
463 464 
CARDIAC DISEASE IN MARRIAGE AND PREGNANCY 
necessarily indicate either heart disease or decompensation (Chapter XI). 
In those who have only recently recovered from heart failure, it is a safe rule 
to interdict marriage until at least two years have passed without subsequent 
break in compensation. An exception is noted later with reference to aortic 
lesions and extreme cardiac hypertrophy. The interval mentioned—two 
years—is, of course, purely arbitrary, but seems to agree best with clinical 
experience. In valvular lesions the same time should be set as a safe interval 
in which no inflammatory symptoms have occurred. If, for example, there 
have been rheumatic endocarditic recrudescences and recurrences, as evidenced 
by louder murmurs, slight febrile attacks, pericarditis, tachycardia, arrhyth- 
mias, or other clinical manifestations, marriage should not be advised, for 
the chances are in favor of another attack within one year. In short, mar- 
riage (and pregnancy) may be considered safe if excellent compensation and 
freedom from endocardial exacerbations persist during the two-year period. 
The physician who has not had the opportunity to observe the patient within 
the prescribed antenuptial period must necessarily be guided by the history 
and physical signs. 
Of the two factors, decompensation and quiescence of the lesion, I believe 
that the latter is the more important. In my experience, more danger and 
more fatalities have resulted in pregnancies from marriage occurring when 
lesions were active than from mild decompensation. Gestation seems to 
light up dormant or only partially active cardiac processes. 
Cardiac symptoms frequently begin early in pregnancy, sometimes even 
in the third month. At the beginning, simple pulse acceleration occurring 
in attacks (paroxysmal tachycardia) may be present. Slight fever may 
appear; when due to endocardial exacerbations, it is of serious import. The 
occurrence of new or louder valvular murmurs, or of fresh pericarditis, may 
furnish clues of such recrudescences. Hemoptysis is not infrequent. As 
pregnancy advances, unless the above or similar manifestations recede or are 
checked, dyspnoea and cyanosis gradually supervene, and with them the usual 
symptomatology of frank cardiac decompensation; edema, orthopnoea, 
enlarged liver, pulmonary congestion, arrhythmias (especially extrasystoles), 
etc. The greater circulatory demands made by the growing placental and 
fetal circulation very probably also play a role in causing this heart failure. 
Labor, induced or spontaneous, does not always terminate the circulatory 
embarrassment, for insidious endocarditis may continue and death result 
from some complication or from circulatory failure. 
The above considerations refer to marriage in women with all types of 
valvular lesions. It remains to differentiate between these on the basis 
of clinical experience. I have found that rheumatic mitral stenotic lesions 
are the most dangerous during pregnancy. The patients readily develop 
paroxysmal or, more often, simple tachycardia, which may last during the 
greater part of pregnancy. The rapid heart action itself may produce such 
dyspnoea or discomfort that the induction of premature labor is indicated. CARDIAC DISEASE IN MARRIAGE AND PREGNANCY 
465 
Hemoptyses are common. Bronchitis with sibilant breathing and mucous 
rales over the entire chest is not unusual. As occasional complications during 
the puerperium, one may mention embolic infarcts in the lower extremities 
or in the lungs. 
The history of pregnant women with mitral stenosis and auricular fibrilla- 
tion presents a varied clinical picture. Some of these patients date their first 
break in compensation at a first or second pregnancy which had been carried 
to full term. On the other hand, I have observed patients who went through 
successive pregnancies with mitral stenosis and auricular fibrillation, with no 
cardiac complications or symptoms. One of these deserves brief mention; 
when first examined, she was fifty years old, with general anasarca, orthopnea, 
auricular fibrillation, a double mitral lesion and an old rheumatic history. 
She had had eighteen children without cardiac symptoms. The latter began 
only three years after her menopause, which commenced when the patient was 
forty-five years old. From her history, it seemed probable that fibrillation 
had been present at least during her later pregnancies. Another patient, 53 
years of age, was the mother of five children. She had a rheumatic history 
and double mitral lesion with auricular fibrillation for many years. During 
her pregnancies, the cardiac symptoms were very slight and of the same 
nature as those occurring when she was not pregnant; these consisted in 
occasional dyspnoea and tachycardia. 
Except by means of the general considerations above outlined, there 
seems no way of determining in advance the favorable or unfavorable sub- 
jects for pregnancy, in those with auricular fibrillation. Extreme caution in 
advising marriage or pregnancy is, of course, necessary because of the 
known tendency of patients with this arrhythmia to decompensate. 
Patients with simple mitral regurgitant lesions are the most favorable 
subjects for pregnancy and the most apt to go through gestation without 
untoward cardiac complications. When the latter do occur, they are more 
often of the mild decompensatory type from recurrence of the endocarditis. 
Pregnant women with aortic lesions suffer chiefly from tachycardia. This 
is true of those with, as well as those without, marked ventricular hyper- 
trophy. In the former, however, tachycardial attacks occur more frequently, 
are more readily evoked and are of longer duration. Decompensation is 
comparatively rare in those with but moderate or slight hypertrophy. 
When extreme ventricular hypertrophy exists, cardiac failure is apt to occur 
early in pregnancy, a tendency increased by the rapid heart action. Such 
patients should be advised against marriage or, if already married, should 
not be permitted to become pregnant even if the lesion is quiescent, and com- 
pensation in the nonpregnant state is good. 
In all types of decompensated endocardial lesions occurring during preg- 
nancy, the question of the induction of abortion or of premature labor arises. 
Severe cardiac failure in early pregnancy (before the fourth month) or slight 
decompensation which does not yield to treatment is, I believe, an indication 466 
CARDIAC DISEASE IN MARRIAGE AND PREGNANCY 
for immediate emptying of the uterus. This indication is not vitiated by the 
fact that some of these mothers may, by protracted rest and medication, carry 
the child to viability or even to full term without further complications. The 
life of the mother is the prime consideration and should not be jeopardized, 
as it would be, in an attempt to continue the pregnancy when cardiac decom- 
pensation is present in early gestation. My observation has been that an 
abortion, surgically clean and skillfully performed, is only slightly, if at all, 
more dangerous in cardiac patients than if performed for other reasons on 
those with normal hearts. I am also strongly in favor of terminating an 
early pregnancy if it is evident that there exists recurring endocarditis. As 
already stated, this may consist in the presence of fever, in the onset of parox- 
ysmal or constant tachycardia, of extrasystoles or other arrhythmias, of fre- 
quent hemoptyses, and of changes in the physical signs. 
If the signs of decompensation or of fresh endocarditis appear between the 
end of the fourth month and the time of viability, in view of the somewhat 
more serious operative procedure required to induce miscarriage, the decision 
regarding interruption of gestation hinges chiefly upon the severity of the 
cardiac complications. If decompensation is mild, or if the evidence of fresh 
endocarditis is not severe, appropriate therapy should at first be attempted 
for about a week or ten days. Should the symptoms then disappear and the 
patient improve, pregnancy may be allowed to proceed until the period of 
viability, possibly until normal labor. If decompensation or endocarditis 
does not react well to therapy or becomes suddenly severe or threatening, it 
is much safer to induce miscarriage. 
In the interim between the seventh and one half and the ninth months of 
gestation—the period of viability—the decision regarding the interruption 
of pregnancy in decompensated cases or in those with recrudescent endocardial 
lesions is of less vital importance because the premature induction of labor in 
proper hands adds scarcely any risks. The question of waiting a month or 
more until the more natural process of normal labor occurs must depend 
upon the cardiac condition; that is, if there is any reason to fear the slightest 
increase of cardiac complications, it is both wiser and safer to have pregnancy 
terminated soon than to wait until full term. 
There are two gynecological methods employed to end labor when the child 
is viable: One, the introduction of bags into the uterus; two, Caeserian section. 
The first method usually produces a tedious and often an abnormal labor, 
so that the patient’s already diminished cardiac reserve may become consider- 
ably decreased by long continued pains and the length of time required for 
the process of parturition. 
Regarding the general question of cardiac strain incident to pregnancy and 
labor, much has been written, but on the whole we possess no accurate 
information or knowledge of many factors here involved. Undoubtedly the 
demands made by the growing fetal circulation; interference with venous 
return in the splanchnic area by the growing uterus; gradual invasion of free CARDIAC DISEASE IN MARRIAGE AND PREGNANCY 
467 
diaphragmatic mobility by the uterus and by displaced abdominal contents 
are physical factors of importance during pregnancy in those with diseased 
hearts. Added to these is the cardiac strain incidental to labor itself. 
Bearing down expulsion pains unquestionably call for more cardiac energy 
and hence cause cardiac strain both by producing venous congestion and by 
holding the breath during the labor pains. Such efforts may finally result in 
more or less continuous dyspnoea. Prolonged labor—dry labor, for example 
—by interfering with sleep and by keeping the patient’s nervous condition 
keyed up and on edge, may gradually interfere with and decrease an already 
diminished cardiac reserve, so that more or less obvious signs of mild heart 
failure, especially dyspnoea and tachycardia may finally eventuate. In 
addition, the obstetrician can rarely give definite information, especially in 
primiparae, as to whether the labor is going to be difficult or easy, quick or 
slow. All these questions, some answerable, others not—are intimately 
bound up with the method of procedure to be followed during labor, and more 
particularly, at the stage of viability. At full term, labor should naturally 
be shortened and made as easy as possible for the patient. Pituitrin, when 
indicated in those with normal hearts is also indicated in those with heart 
lesions. Forceps should be applied as soon as the procedure is considered 
safe. 
With reference to induction of labor at the stage of viability, the choice 
between divulsion with bags and Caeserian section arises. The former is 
very apt to give rise to a tedious labor with all the disadvantages from the 
cardiac standpoint just alluded to. Regarding Caeserian section it is perhaps 
surprising to observe how well women with heart disease withstand the opera- 
tion. My personal experience has been limited to two cases, both with mitral 
regurgitant lesions. One had moderate dyspnoea during the last two months; 
the other had dyspnoea during the last month of pregnancy. In the latter 
the dyspnoea responded quickly to rapid digitalization, so that at the time 
of operation, compensation was fully restored. After Caeserian section in the 
two cases, the cardiac condition was satisfactory during and immediately 
after the operation. There was no untoward rise of the pulse rate. Dysp- 
noea, the main symptom, disappeared within 24 hours. The succeeding 
days showed a steady improvement; indeed, the heart reacted no differently 
than after any skillfully performed Caeserian section in those with normal 
hearts. Of interest is the previous cardiac history of one of these cases. 
This Caeserian section was her third pregnancy. Her second labor lasted one 
week. She stated that it took months for her heart to finally recuperate so 
that she could walk comfortably and go about her household duties. The 
last time I saw the patient was two weeks after the Caeserian section. The 
cardiac rate was normal. She felt perfectly well with the single exception 
that she could not yet lie comfortably on her left side. From all indications 
she will very probably recuperate perfectly from the cardiac standpoint by 
the time she is allowed out of bed, for it is the laparotomy, not the heart, 468 
CARDIAC DISEASE IN MARRIAGE AND PREGNANCY 
which keeps her in bed at present. This is an instance where the operation 
not only saved her the cardiac strain of labor but also its annoying, long 
continued, after effects. 
One word of caution is necessary regarding Caeserian section and that is 
that compensation should be restored as much and as quickly as possible by 
thorough digitalization before operation. 
An addition to the causes already given which may interfere with and 
complicate pregnancy in women with cardiac disease is superadded cardiac 
neurosis. 
Patients with various type of perfectly compensated valvular diseases 
and with no new outbreaks of endocarditis for years, may, because of their 
knowledge of the cardiac disease and because of their dread of childbirth, 
present cardiac symptoms of a neurotic type which in themselves may call 
for interruption of pregnancy. Two such cases are epitomized: 
Mrs. K., aged 21, married one year and now pregnant three months, has 
had a rheumatic double aortic lesion for years. In the past ten years her only 
complaint has been occasional palpitation due to moderate tachycardia. 
Since her pregnancy, she has had frequent crying spells because obsessed with 
the idea that she would die during childbirth. She complained almost 
continuously of palpitation. Examination revealed, besides the valvular 
lesion, moderate left ventricular hypertrophy, and a cardiac rate of over 100 
per minute. Compensation was perfect. Because of her nervous condition, 
the induction of miscarriage was advised. She was told, however, that if, 
at a subsequent pregnancy, she were less nervous, she might carry the child 
to full term with no danger to her heart. Curettage was performed under 
gas and ether without untoward symptoms. Within one year of the opera- 
tion she again became pregnant. There were no neurotic or cardiac symptoms, 
no tachycardia or palpitation. She carried the pregnancy to full term, the 
delivery and puerperium were normal. 
Mrs. L., married two years, is now pregnant six weeks. She has a typical 
double mitral lesion. Despite the valvular disease, she was always active as a 
child and has never suffered from decompensation. She is of a very neurotic 
temperament and is easily frightened. Under such circumstances she 
suffers from palpitation which, on examination, is found to be due to rapid 
heart action, usually at the rate of no per minute. When first examined, 
I advised her that the continuation of the pregnancy would depend more 
upon her general nervous condition than upon her heart, that the former 
affected the latter, and that if she were not nervous and frightened, there 
would be no reason to worry about the condition of her heart; her heart was in 
as good condition as it was ever likely to be. Mixed bromides were given. 
Ten days later she again consulted me. She feared she would lose her life if 
pregnancy continued. She had been having sleepless nights and crying 
spells. Palpitation had been frequent, almost constant. I therefore 
advised immediate termination of pregnancy, though compensation was CARDIAC DISEASE IN MARRIAGE AND PREGNANCY 
469 
perfect. In this case I also felt that a future pregnancy might be carried to 
full term without mishap if the patient did not become frightened and 
nervous. Two years later she again became pregnant. She was delivered of 
a healthy child by Caeserian section. Convalescence was normal. I again 
saw her one year after delivery. Her cardiac condition was satisfactory, 
compensation good. 
The medical treatment of the various cardiac symptoms occurring during 
pregnancy may now be briefly sketched. Decompensation, no matter 
whether evidenced by circulatory congestion (enlarged liver, edema, bronchi- 
tis, dyspnoea, cyanosis) or by arrhythmia calls chiefly for digitalis and rest. 
I believe that patients should be brought under the influence of the drug as 
quickly as possible. Where cardiac failure is extreme, the case urgent and 
digitalis has not previously been given, it is best to begin with the intravenous 
or intramuscular injection of strophanthin (dispensed in ampules in a 
solution); the dose is 10-15 minims. When given intravenously, it should 
be injected slowly. After twelve to twenty-four hours, digitalis in the usual 
doses can be given. I am in the habit of prescribing the tincture in 15-minim 
doses three or four times daily, given undiluted. The average amount for a 
full effect is one ounce, distributed over a period of about one week. When 
dyspnoea or restlessness is marked or pulmonary edema is present, luminal 
tablets, one and one-half grains each once or twice daily, or occasional doses 
of morphine are indicated. Special diet is sometimes of value in getting rid 
of edema. Where the urine output is normal in amount, I have found 
restriction of fluid intake in twenty-four hours to 1000 c.m. of milk (Karrell 
diet), or of that amount or even considerably less of other fluids (e.g., water, 
lemonade, weak tea) for two or three days in succession, combined with the 
administration of theobromine-sodium salicylate in doses three or 
four times daily of decided advantage. To appease the hunger pangs, when 
present, dry toast or baked apples may be added. 
• For the treatment of endocarditic recrudescences the salicylates are 
required; they should be administered up to their physiological limit. I 
usually give the salicylate of soda in one gram doses until eight doses have 
been given or until tinnitus occurs. The dose is then decreased or medication 
temporarily discontinued. I have found no beneficial results from serums, 
vaccines or from preparations of silver salts. Unfortunately, salicylates are 
sometimes of little or no value. Ice bags occasionally control rapid heart 
action. They are to be discontinued if no effect follows their use or if they 
make the patient uncomfortable. 
The chief types of irregularities have been mentioned. If arrhythmia is 
the result of decompensation, digitalis should be given in the usual manner. 
If due to fresh endocarditis, besides the salicylates, bromides in large doses 
or luminal may be of value, especially in the presence of tachycardia. Arrhy- 
thmias (usually extrasystoles), which are occasionally caused by digitalis 
soon after its administration has been begun, do not contraindicate its further 470 
CARDIAC DISEASE IN MARRIAGE AND PREGNANCY 
use if the object of the medication—the restoration of compensation—has not 
been accomplished. 
Summary.—We possess at present no instrumental guide or tolerance 
test which can adequately measure the cardiac reserve of the diseased heart 
of the pregnant woman. Each case must be individualized and the presence 
or absence of heart failure noted. The best clinical guide for heart failure is 
a detailed study of the patient’s symptoms together with a detailed study of 
the physical signs. Cardiac neurosis, decompensation and endocarditic re- 
currences seem the best inclusive groupings of all types of cardiac symptoms 
that occur in pregnancy with heart disease. The degree of decompensation 
and the month of pregnancy together determine the type of procedure. 
Decompensation that does not react to medication quickly or permanently, 
requires interruption of pregnancy at any stage. When viability has 
been reached and decompensation is moderate or absent, Caeserian sec- 
tion, skillfully and rapidly performed, seems to be well withstood by the 
diseased hearts of pregnant women.. It prevents the cardiac strain incidental 
to labor; it may likewise prevent a lingering, cardiac recuperation following 
labor. Should the woman come to term the labor should be shortened as 
much as possible. Ether is the anesthetic of choice. 
REFERENCES TO CHAPTER XXVII, P. 462 
Cohn, A. E.: Clinical and Electrocardiographic Studies on the Action of Digitalis; Journal 
of the American Medical Association, 1915, LXV, 1527. 
Hektoen, L.: The Mechanism of Recovery in Pneumonia; Journal of the American Medical 
Association, 1914, LXII, 254. 
Hirschfelder, A. D., and Winternitz, M. C.: Studies upon Experimental Pneumonia in 
Rabbits, Journal of Experimental Medicine, 1913, XVII, 667. 
Neuhof, S.: Functional Heart Block in Pneumonia; Journal of the American Medical 
Association, 1914, LXIII, 577. 
Neuhof, S.: Clinical Aspects of the Influenza Pneumonia Pandemic; Interstate Medical 
Journal, 1919, XXVI, 14. 
Neuhof and Davidson: Clinical Survey of Acute Pulmonary Affections of 1916; New York 
Medical Journal, June 2, 1917. 
Newburgh, L. H.: The Use of Strychnine and Caffein as Cardiovascular Stimulants in the 
Acute Infectious Diseases; Archives of Internal Medicine, 1915, XV, 458. 
Newburgh, L. H., and Porter, W. T.: The Heart Muscle in Pneumonia; Journal of Experi- 
mental Medicine, 1915, XXII, 123. 
Porter, W. T., and Newburgh, I.: Vasomotor Apparatus in Pneumonia; American Journal 
of Physiology, 1914, XXV, 1. CHAPTER XXIX 
CARDIO-VASCULAR EXAMINATIONS OF WAR RECRUITS 
This subject is of importance because it indicates the types of young men 
seen in routine clinical work. 
Men of the draft age, that is those between twenty-one and thirty years of 
age, who present themselves for examination before the local draft boards 
may be divided into two groups, in regard to cardio-vascular conditions, 
(i) Those with frank, unmistakable cardio-vascular disease; (2) those with 
cardiac abnormalities, that is, with physical or clinical signs which resemble 
and may be mistaken for real cardio-vascular disease. 
1. Evident Cardio-vascular Disease.—By far the larger percentage of 
candidates in this category have valvular lesions; a much smaller group com- 
prises those with hypertensive cardio-vascular or cardio-renal disease. Myo- 
carditis as an entity in the adult of the draft age need scarcely be considered 
because its incidence is negligible, and its discovery and diagnosis as a single 
pure lesion are surrounded by pitfalls and mistakes (Chapter VII). It is 
self-evident that men having valvular disease with signs of advanced or even 
beginning decompensation are not fit to become soldiers and hence should be 
rejected. It may become a part of the medicomilitary problem properly to 
sort the valvular cases which are perfectly compensated and present no symp- 
toms and who even if non-combatants can be of some military service. I 
have met men, for example, who knew of their lesions and yet were suffi- 
ciently patriotic to wish to enter the army in any capacity. One such case 
was that of a young lawyer, twenty-three years of age, who had mitral 
regurgitation for ten years and who in order to prove to himself his capacity 
for marching and for exertion, had taken a fifteen mile hike. Examination by 
me the next day revealed no ill effects from the walk. I also recently had the 
opportunity to examine two infantry recruits in one of the cantonments, 
both of whom had been in camp several weeks, and whose lesions were dis- 
covered only while making a routine chest examination. It then appeared 
that both of the men had known of their valvular disease; both had succeeded 
in convincing the examining physicians of the local draft boards that they 
had only heart murmurs and not heart disease; both stood the preliminary 
training without mishap or symptoms; both were exceedingly anxious to stay 
in the service. While no special provision had been made for perfectly com- 
pensated cases of this type, it would seem unwise to put them, even if willing, 
in such laborious service as is entailed in the infantry or engineering. The 
probabilities seem more in favor in their decompensating or of their developing 
the irritable soldier’s heart (Chapter XVIII), with its tachycardia and other 
47i 472 
CARDIO-VASCULAR EXAMINATIONS OF WAR RECRUITS 
symptoms than will those with perfectly normal hearts. Of perhaps equal 
importance is the possibility that trench and other disesaes—trench fever, 
trench nephritis, catarrhal fevers, pyrexias of unknown origin, or pneumonias 
—may light up dormant and quiescent endocarditic lesions with resultant 
syndromes similar to, or as serious as, the usual recrudescences of valvular dis- 
ease. With cooperation between the medical and the military branches, 
there appears no harm in admitting these perfectly compensated and quies- 
cent valvular cases into the less laborious work of the quartermaster’s or 
similar departments. 
Hypertension for the purposes of draft examination I would define roughly 
as a systolic blood pressure of 150 m.m. or over. Blood pressure estima- 
tions have thus far not been done as routine procedures in the local boards. 
Associated with the presence of albumin and casts in the urine, men with 
hypertension, even if moderate, should be regarded as unfit for combatant 
military service. Another group with hypertension is that found in recruits 
with tachycardia. The desirability of accepting these recruits depends not 
upon the hypertension, even if considerable, but upon the tachycardia, a sub- 
ject which will be discussed later. Still another group, though small, con- 
sists of those with moderate hypertension but with no evidence of renal or 
cardiac disease, cases of functional hypertension (Chapter XXV). These 
comprise the cases which in civil practice are usually rejected for life insur- 
ance. Repeated examination of the urine and of the heart shows no renal or 
cardiac disease. I feel that these individuals represent hypertension, tem- 
porary or permanent, due to emotional excitement incidental to the examina- 
tion, or to heightened vasomotor tone from obscure though unimportant 
reflex causes. I believe that when careful and repeated examination of the 
urine and heart shows no abnormality, and the usual symptoms accompanying 
hypertensive cardiac disease are absent, the applicants should be accepted in 
the ordinary routine fashion. In civil practice, where I have been able to 
follow similar cases for some time, the young men have been athletic and have 
followed their vocations without hindrance or untoward symptoms. 
Another temporary cause of hypertension which is usually overlooked is 
that due to abnormal resistance of the arterial wall, known as arterial tonus 
(Chapter XXV). This cause can be readily determined by keeping up the 
cuff pressure on the brachial for a few minutes before a second systolic reading 
is taken. When the hypertension is due to hypertonus, the second reading 
will be within normal limits and will represent the actual blood pressure of 
the individual. The second systolic reading is sometimes 15 to 30 m.m. 
lower than the first. 
2. Signs Simulating Cardio-vascular Disease.—We now come to a larger 
and more important group of applicants, viz., those with physical or clinical 
signs simulating actual cardio-vascular disease. All these may be regarded as 
non-organic (functional) in nature; hence, with the limitations to be men- 
tioned, such recruits may be drafted in the service. For purposes of classifi- CARDIOVASCULAR EXAMINATION OF WAR RECRUITS 
473 
cation, this subject may be studied from the standpoints of: (i), size of the 
heart; (2), abnormal cardiac rhythm; (3), abnormal cardiac sounds, and, (4), 
dyspnoea. 
1. Size of Heart.—In another chapter (Chapter XII), I have indicated 
the common sources of error inherent in percussion methods which attempt 
to delimit the cardiac area with any exactness. Frank and gross enlarge- 
ments can be readily diagnosed, but their importance lies in the category of 
those with definite lesions. I consider it of minor importance in those with 
equivocal physical signs of cardiac disease to be able to map out the exact size 
of the heart, for there are many factors which produce considerable variations 
even within normal limits. The broad and deep chested are apt to have larger 
hearts than the small and narrow chested (Chapter XII). The tall and gaunt 
have as a rule, narrow, graceful and pendulous hearts. The fat and stocky 
are apt to have hearts which tend to occupy horizontal positions in the chest. 
There are, however, numerous exceptions. For example I have often been 
surprised to find upon fluoroscopic examination that thin and narrow chested 
individuals possessed large, though normal, hearts. Fluoroscopy will also 
confirm the fact that the actual apex is often several centimeters below the 
point of the maximal apical impulse. To those variations as found in quiet, 
normally beating hearts, I may further state that hearts beating vigorously 
and rapidly usually give the impression of enlargement, although X-ray 
examination often reveals them to be of normal contour and size. These 
brief considerations show the difficulty of standardizing the size of the heart 
and of mapping out its size and contour by percussion. However, while for 
other purposes such exact knowledge may be of interest and importance, it 
possesses but slight and subsidiary value in the examination of recruits with 
hearts simulating actual disease. 
2. Abnormal Cardiac Rhythm.—The great majority of cases in this group 
are those'with simple pulse acceleration, usually due to the incidental, emo- 
tional excitement of the examination. The usual rates are in the neighbor- 
hood of 100 a minute. Sinus arrhythmia, i.e., an alternate slowing and 
acceleration of the cardiac and pulse rate in consonance with inspiration and 
expiration, respectively, is less frequent than simple tachycardia. A combi- 
nation of slow and then rather rapid heart action, with sudden transition from 
one to the other, each phase lasting approximately four to eight beats, is not 
unusual. Occasionally premature contractions (extrasystoles) are encoun- 
tered. Tachycardias of paroxysmal nature, that is, sudden attacks of 
extremely rapid cardiac acceleration with ventricular rates between 150 and 
200, lasting several seconds or minutes, are occasionally found in the draft 
candidates. All of these cardiac irregularities are readily diagnosable by 
ordinary clinical methods. Of even more importance than their diagnosis 
is the fact that none of these irregularities are in themselves indicative of, nor 
do they form any basis for, the diagnosis of heart disease (Chapter XI). 
They are usually of purely functional origin. Other concomitant signs and 474 
CARDIO-VASCULAR EXAMINATIONS OF WAR RECRUITS 
symptoms in addition to cardiac irregularity are necessary before the candi- 
date can be classified as having cardiac disease. A persistent tachycardia, 
however, may produce sufficient subjective annoyance and objective dyspnea 
upon exertion to unfit the candidate for the duties of the soldier. Such 
men, to be finally rejected, should present this symptom while under observa- 
tion for at least one-half hour, the rates should be 120 or over, the tachycardia 
should be accompanied by unmistakable evidences of dyspnea, and the same 
pulse acceleration should again be present at some future examination. 
3. Abnormal Cardiac Sounds.—I refer here to those murmurs, reduplicated 
(so-called gallop and double rhythms) and other adventitious sounds heard 
over the normal heart. All these may be conveniently grouped as occurring 
over the right base, over the left base, or over the apical region. Over the 
right base are heard soft, whiff-like systolic murmurs usually accompanying, 
not replacing the normal first sound. They commonly occupy the whole 
systolic period. They are rarely transmitted to the carotids, although undue 
pressure with the stethoscope upon these vessels may give that mistaken 
impression. Unless the definite signs of an aortic stenotic lesion are present, 
the murmur just described is not significant of actual disease. 
Over the left base are found chiefly the so-called cardro-respiratory mur- 
murs. These have a superficial character, may be quite loud, and are usually 
systolic, though very rarely both systolic and diastolic in time. The murmur 
is sometimes transmitted to the midprecordium or even lower. Its intensity 
usually varies with the position of the patient" and with the phase of respira- 
tion. It is ordinarily least intense and indeed may be found to disappear 
entirely if auscultation is practiced at the end of deep inspiration. Even if 
loud, these left basal murmurs are not indicative of heart disease. They are to 
be differentiated particularly from the friction sounds of localized pleuroperi- 
carditis in this area, as well as from patent ductus arteriosus and pulmonary 
stenosis. In the latter cardiac lesions, there are definite physical signs and 
symptoms (Chapter XIX). 
Different from murmurs over the left base, are the reduplicated sounds, 
usually called gallop or double rhythm (Chapter XIII); they are characterized 
by a sharp double valvular click, as if there were a double closure of the 
pulmonary valves. These sounds are of functional origin and may be dis- 
regarded as evidence of actual cardiac disease. 
A study of apical adventitious sounds is of great practical importance 
because these are most apt to be confused with actual mitral disease. Most 
of the adventitious sounds in this area consist of soft blowing murmurs, 
accompanying, but not replacing, the first sound, and only slightly transmitted 
to the right and left of the apex. It has been asserted that these functional 
murmurs may even be transmitted posteriorly. I have not been able to 
corroborate this statement. These murmurs are occasionally loud; indeed, 
they may be as loud as some organic mitral murmurs. They usually vary 
with the position of the patient, and are sometimes capricious in that they are CARDIOVASCULAR EXAMINATIONS OF WAR RECRUITS 
475 
present at some examinations and not at others. In addition to these 
adventitious apical murmurs are other abnormal sounds, scarcely mentioned 
in the literature, which I consider of great importance. I can best describe 
them as thrill-like or split first sounds. (See also Cardiac Neurosis, Chapter 
XVIII.) They are systolic in time and are usually confined to the apex. 
They are commonly found in tachycardias, or even with normal rates if the 
cardiac impulse is exceptionally vigorous. If the tachycardia disappears 
spontaneously, or if the heart rate or overaction can be quieted by having the 
applicant take and hold a deep breath, this thrill-like split first sound often 
disappears. Besides other characteristics distinguishing it from the typical 
presystolic rumble of true mitral stenosis (Chapter XIII), the adventitious 
sound described is not accompanied by the double click valvular sound so 
common in stenosis. * 
4. Dyspnoea.—The dyspnoea accompanying actual decompensation re- 
quires no comment here. I wish but to refer to the two types occasionally 
seen among the draft candidates. First, when found in tachycardia, the rapid 
heart action is the cause of the dyspnoea. The possible rejection of candi- 
dates should then be based upon the observation of the tachycardia along the 
lines already discussed, and not upon the dyspnoea. The second type of 
dyspnoea-is that accompanying the subjective feeling of palpitation, with a 
perfectly normal, or even somewhat slow, heart rate. It is found more often 
in civil practice among neurotic individuals (Chapter XVIII) than among 
draft candidates, but is sufficiently frequent to deserve mention. It is not 
accompanied by any evidence of decompensation and is not appreciably 
increased even by sustained effort. It is a symptom which may, of course, 
be simulated by the candidate, but it is not a sign of cardiac disease and 
hence does not excuse the candidate from service. CHAPTER XXX 
THE ROLE OF THE HEART IN LIFE INSURANCE EXAMINATIONS 
I believe that examination for life insurance is basically nothing more 
than the application of objective clinical medicine, for one cannot depend 
upon the history of the life insurance applicant. 
The fact is fundamental and axiomatic, but will still bear repetition, that 
a person giving no history of infection, with a heart that presents perfectly 
normal sounds, with no murmurs, no enlargement, no overaction, no arrhyth- 
mia, no undue tachycardia, and associated with no dependent edema, no 
distress or dyspnoea after moderate exertion and no abnormal blood pressure 
reading, possesses a normal organ. In fact, it is more than normal; its an ideal 
heart, and from the standpoint of physical diagnosis and actual experience 
such an organ is indeed rare. This rarity alone forces us to consider as 
normal or satisfactory, from the clinical and insurance standpoints, hearts 
that are less than ideal, and to sift out a “standard” heart,despite murmurs 
and other apparent anomalies—I stress the word “apparent.” Indeed, our 
increasing clinical experience, as the result especially of what was learned 
about the heart in the World War, has gradually, yet surely, weaned us away 
from the notion that the ideal is the only expression of an organically sound 
heart. And it behooves those who wish to advance and keep in touch with 
real progress in medicine—and this surely applies to the life insurance 
examiner—to take full cognizance and heed of facts as they are gleaned from 
actual clinical experience. 
Since we rarely find an ideal heart such as outlined, let us see to what 
extent and in what direction deviations may occur, and yet have a heart 
that can be pronounced sound from the life insurance viewpoint. 
During the routine study and examination by the life insurance examiner, 
certain outstanding queries should be constantly in his mind. First and 
foremost he must ever be on the lookout for any evidence of actual heart 
failure. With this presumably ruled out, he should be able to decipher, so to 
speak, cardiac abnormalities which may present themselves. He must ask 
himself whether such abnormalities, if present, are of functional or organic 
origin. Do they now or may they in the future interfere with the efficiency 
of the heart? Are murmurs present? If so, what is their time relationship 
to the cardiac cycle? Are they transmitted or not? Where are they best 
heard? Are cardiac irregularities present? If so, are they of functional or 
organic origin? It is, of course, understood that in one form or another, 
either in the medical blank or otherwise, many or all of these questions 
demand an answer from the examiner. Unless, however, there is a clear 
476 THE ROLE OF THE HEART IN LIFE INSURANCE EXAMINATIONS 
477 
mental background as to the bearing of these questions upon the efficiency 
of the heart and upon the probability of circulatory failure and, later, death 
from heart disease, they lack point and directness. Indeed, I have often 
thought it would be a wiser plan to give the examiner more scope, to perhaps 
discard or simplify the questionnaire, and to have the examiner briefly note 
abnormalities if present, and their bearing upon the soundness of the heart. 
It may be here remarked that companies that do only a “standard 
business” should be more vitally interested in these questions than those who 
do also a “substandard business,” for if some assumed “circulatory defects” 
have but an academic or scientific significance and are not indicative of heart 
disease or of a shortened span of life, such individuals should surely be accepted 
at normal rates, possibly after re-examination. 
What constitutes heart failure from the life insurance standpoint and how 
can it be detected? The obvious signs are edema, dyspnoea, enlarged liver, 
pulmonary congestion; these are comparatively late developments. The 
only early sign, easily detected, is an unnatural, abnormal shortness of breath 
after comparatively brief exertion; this is the best, easily ascertainable and 
most tangible evidence, we possess of decrease of the normal cardiac reserve 
power. In availability, simplicity and accuracy it surpasses all other func- 
tional tests. Abnormal breathlessness can be elicited by having the patient 
go through some simple exercises, such as rapid walking, hopping, bending, 
etc. Mere tachycardia after exercise, especially in younger individuals, even 
when lasting an abnormally long time, is not a sufficiently accurate index of 
loss of cardiac reserve, for tachycardia is sometimes long continued in per- 
fectly normal hearts after exercise. 
When individuals are secretive and do not wish to cooperate with the 
examiner, a fair index of the average daily cardiac power can be gauged by 
guarded questions as to the amount of usual exercises indulged in either at 
work or play. 
What is a circulatory defect or abnormality? Cardiac failure, just de- 
scribed, is naturally the prime one. Insurance companies, however, usually 
emphasize cardiac irregularities and murmurs as other important ones. With 
reference to cardiac irregularities, the preponderance of those encountered, 
both in life insurance and clinical work, are sinus arrhythmia and extrasys- 
toles. It is now generally held that sinus arrhythmia is a physiological 
phenomenon in the majority of cases. Its detection is easy without instru- 
mental methods; there is alternate slowing and quickening of the heart, with 
the respective inspiratory and expiratory phases of respiration. When sinus 
arrhythmia accompanies organic disease, as it occasionally does, the evidence 
of the latter is unmistakable. With this exception applicants with sinus 
arrhythmia should be regarded as normal risks. 
Extrasystoles (premature contractions, or dropped beats, as they are 
popularly called) are also easily detected in most instances. Since, in insur- 
ance examinations, the applicant may purposely withhold facts, his sensa- 478 
THE ROLE OF THE HEART IN LIFE INSURANCE EXAMINATIONS 
tions are not dependable, and hence cannot be used as guides. The diagnosis 
is readily made by the fact that there is a weaker premature beat at the heart, 
accompanied or not by a weaker pulse beat, and usually followed by a some- 
what long compensatory pause (Chapter XI). Is the extrasystole of func- 
tional or organic origin? The first part of the question—is it functional?—is 
in itself a concession toward a modern view in cardiology, only gradually 
gaining credence in life insurance work, for it was originally held that extra- 
systoles are always indicative of a muscular cardiac impairment. Those who 
have observed extrasystoles accompanying many types of extracardiac 
disturbance, for example, dyspepsia, are impressed with the view that they 
are often of functional origin, that they do not impair the efficiency of the 
circulation and that in themselves they do not indicate heart disease. Indeed, 
the insurance examination itself may produce extrasystoles in a nervous indi- 
vidual. Extrasystoles can, of course, also accompany organic cardio-vascular 
disease, hypertensive or otherwise. But here again the signs of disease 
are usually outspoken. Here, then a simple rule can be supplied for the 
examiners, namely: When extrasystoles (dropped beats) occur infrequently 
and are not accompanied by obvious cardiac disease, they should not be 
considered as evidence of impairment of the risk. 
Constant rapid heart action, not truly an arrhythmia, requires brief 
mention. It is not always a sign of heart disease and is often and easily 
caused by nervousness incidental to the examination. The manner of the 
examiner frequently influences this. The following expedient to slow the 
heart is worth trying: The patient is asked to breathe deeply and to hold his 
breath a moment at the end of inspiration; this usually slows the nervous type 
of tachycardia. It should also be emphasized that rapid heart action, per se, 
can cause functional thrills and murmurs, to be mentioned later; these are 
usually systolic and are found at the apex. Hence, the importance of slowing 
the heart to exclude such functional adventitious murmurs and thrills. If 
it be impossible to slow the heart rate, a re-examination should be arranged 
for. 
We may now consider murmurs and thrills. At the outset, I wish to 
emphasize this statement: That heart disease may be present without mur- 
murs, and murmurs without heart disease. The importance and truth of this 
should be recognized. It comports well with what we know of the frequency 
and innocence of adventitious cardiac sounds—so-called functional murmurs. 
When these are definitely diagnosed as functional, it is proper to regard the 
applicants as standard risks. Up to the present, however, I believe many 
companies do not accept such a view in spite of the fact that re-examination 
often shows disappearance of these murmurs, and disappearance is almost 
positive evidence of their innocuousness. Although subject to many excep- 
tions, functional murmurs are usually softer, less intense and are not trans- 
mitted to the same extent as organic murmurs. They are systolic in time in 
the great majority of instances. Rather than enter into the etiology of THE ROLE OF THE HEART IN LIFE INSURANCE EXAMINATIONS 
479 
functional murmurs, or into the characteristics of organic ones, it were better 
to briefly indicate simple methods of differentiation. 
For insurance purposes, functional murmurs may be divided into those at 
the right base, at the left base and at the apex. They vary in intensity from 
faint to the rather harsh. Functional right base murmurs are systolic 
in time. They are differentiated from the organic aortic, stenotic or arterio- 
sclerotic ones in this region by the fact that the latter produce a loud, harsh, 
vibrant systolic murmur, often transmitted to the carotids; there is some- 
times in addition a rough palpable thrill. 
Functional left base murmurs are, with very rare exceptions, systolic in 
time. They constitute the so-called cardio-respiratory murmurs. They are 
usually whiff-like and are confined to the left interspace. Occasionally they 
are blowing in character and are heard over the third interspace, and even 
further downward. They are ordinarily affected by respiration; during 
inspiration they become fainter. The cardio-respiratory murmur can readily 
be distinguished from the organic lesions (pulmonary stenosis and patent 
ductus arteriosis) at the left base, for these produce rough murmurs and 
thrills. 
Murmurs at the apex, that is, over the mitral area, are more puzzling 
to differentiate as regards organic and functional. The history of rheuma- 
tism—an important guide in private practice—it may be impossible to learn 
from the applicant. Functional murmurs at the apex are occasionally as 
loud as the softer systolic ones sometimes heard in true mitral regurgitation. 
When evidence of heart failure accompanies the murmur the decision natu- 
rally is easy. But quiescent mitral regurgitant lesions often show no loss 
of cardiac reserve; there is no decompensation, the only physical sign is the 
murmur. Soft apical murmurs accompanying (not replacing) the first 
sound and but slightly transmitted are functional in the majority of instances. 
They are more apt to disappear with change of position of the individual, 
although I have not found that either this or increase of intensity of the 
murmur after exercise constitute sufficiently sharp diagnostic criteria between 
border-line functional and organic mitral murmurs. If, at another examina- 
tion, the murmur is not heard at all, it argues very strongly in favor of an 
inorganic, functional murmur. Apical murmurs open to question shouid 
be re-examined. If finally regarded as probably functional, it seems to me 
they should be accepted on some plan. 
Thrills over the base—right or left—are evidence of organic disease and are 
accompanied by auscultatory evidence of valvular damage. 
In addition to these adventitious apical murmurs there are other abnor- 
mal sounds, scarcely mentioned in the literature, which I consider of great 
importance. I can best describe them as split, thrill-like first sounds, or even 
actual thrills (Chapters XVIII, XXIX). They are systolic in time and are 
usually confined to the apex. They are commonly found in tachycardia, or 
even with normal rates, if the cardiac impulse be exceptionally vigorous. If 480 
THE ROLE OF THE HEART IN LIFE INSURANCE EXAMINATIONS 
the tachycardia disappears spontaneously, or if the heart rate or overaction 
can be quieted by having the applicant take and hold a deep breath, or by 
having him lay on his back, this thrill-like split first sound often disappears, 
a definite evidence of its innocent nature. Besides other characteristics 
distinguishing it from the typical presystolic rumble of true mitral stenosis, 
this adventitious sound is only exceptionally followed by the double-click 
valvular sound so common in stenosis. A further differentiation from mitral 
stenosis is the time relationship of the latter murmur. To repeat, the apical 
murmur is systolic in the functional cases and presystolic in the organic. 
Functional cases of the type I have described may be safely accepted as 
unimpaired risks. 
The size of the heart as delimited by percussion is made much of in 
insurance examinations, but hypertrophy and enlargement are not as readily 
diagnosed as is popularly believed. Indeed, in the hearts just described, vig- 
orous overaction alone frequently gives the impression of enlargement, an 
assumption which the X-ray often shows as fallacious. It may perhaps 
surprise life insurance examiners, when I state that I believe as time-honored 
a method as percussion has but a very limited sphere in the cardiac examina- 
tion of the normal or of the assumed hypertrophied heart. Indeed, I believe 
inspection and palpation more valuable than percussion. The detailed 
reasons and an excellent clinical method for outlining the heart are given in a 
previous chapter (Chapter XIII). 
There is much variability in the size and diameter of normal hearts (Chap- 
ter XII), they vary so much with the contour of the chest and the muscular 
makeup of the individual that wide differences in size may exist and yet the 
heart be normal. A heart with hypertrophy sufficiently pathological to 
exclude a risk will usually present other evidences of cardiac disease—hyper- 
tension, valvular murmurs, loss of cardiac reserve. All of this leads me to 
the important life insurance deduction I wish to make, namely, hearts pre- 
sumably enlarged, but in other respects normal, might safely be accepted as 
normal risks. 
I shall not enter here into the question of blood pressure (Chapter XXV). 
It is, however, of interest to note, since it has a bearing upon the subject of a 
“standard” circulation, that I do not consider low blood pressure (hypo- 
tension)—no matter how low—of any important significance from the stand- 
point of an organically sound heart. Such individuals often have many 
symptoms, chiefly giddiness, fatigue and a tendency to faint; in fact, they some- 
times do faint. But the point I wish to emphasize is that the normal span of 
life does not seem to be interfered with, except possibly that a person falling 
in such a faint may become injured and even be killed. My own experience 
has been that low blood pressure is perfectly compatible with an organically 
sound, normal heart. I naturally leave out of account that type of low blood 
pressure which occasionally accompanies obvious severe cardiac decompen- 
sation. I also make an exception of those rare cases of coronary disease THE ROLE OE THE HEART IN LIFE INSURANCE EXAMINATIONS 
481 
occasionally found in middle life, in which hypotension may be the only 
objective evidence of myocarditis. 
. I have not entered into the advisability of accepting applicants with 
definite organic lesions. As a rule, this would apply to those with mitral regur- 
gitant lesions quiescent and stabilized for several years, and without hyper- 
trophy. Tangible evidence of a quiescent state may be gained from the fact 
that the applicant has regularly followed his usual occupation. The question 
of accepting such risks must rest upon the willingness and general policy of 
companies to insure, under sub-standard rating, individuals with stabilized 
lesions in whom the disease in no way affects the circulatory function. 
I have attempted to portray some of the modern cardiological conceptions 
as applied to life insurance examinations in order to simplify the interpreta- 
tion of some of the commoner circulatory abnormalities, and to indicate how 
decisions based upon modern clinical methods of examination may be arrived 
at by the usual clinical examination. All this, of course, presupposes good 
knowledge of cardiac physiology, as well as clinical experience. Some of my 
statements may perhaps seem questionable and not in accord with the 
insurance viewpoint. But general clinical knowledge should be in a sense a 
practical laboratory and have an influence on insurance statistics. Indeed, 
clinical experience in its broader aspects might well be a guide. The life 
insurance examiner should avail himself of newer cardiological viewpoints. 
Lessons taught by the X-ray, electrocardiograph and polygraph should be 
made practical and pertinent, and be intimately intertwined with the 
every-day work of the examiner. CHAPTER XXXI 
GRAPHIC METHODS—HEART SOUND REGISTRATION—PHONO - 
CARDIOGRAMS 
Perhaps the crudest beginnings of the graphic representations and regis- 
tration of heart sounds were the manometric flames of Koenig. The appa- 
ratus used was a thin-walled box one of whose sides consisted of thin 
membrane. The box was placed in circuit with illuminating gas by means of a 
tube connected with the gas main. The tube of exit was connected with the 
gas burner. The sound waves—for example, the human voice—were made to 
impinge upon the membrane. These compressed or rarified the gas contained 
in the box. The volumetric variations were transmitted to the burning flame 
with consequent variations in its height, cor- 
responding to the voice sounds. By means of 
a mirror the image of these variations was 
reflected upon a photographic plate and thus 
registered. Another old instrument for register- 
ing sounds was Scott’s phonautograph, invented 
in 1856, the forerunner of the modern phono- 
graph. The phonograph itself has also been 
used for the study of heart sounds. 
Various other appliances, non-electrical in 
nature, have been devised for heart sound 
graphs. A few will be briefly described. 
Ohm’s Gelatine Membrane Apparatus (Fig. 
285) consists of a tiny mirror glued to a gelatine 
membrane by means of a few fibers of absorbent 
cotton. This vibrating mirror system is in 
circuit with the source of the sound (the chest 
wall) by means of two cylinders: The one to be 
applied to the chest wall is closed off with a 
thin wooden membrane at its “chest” side, and 
a rubber membrane at the other. Upon this 
cylinder rests another closed by a rubber dam. 
The second cylinder contains a tube leading to the registration apparatus. 
The reason for two cylinders is dampening of the coarse sounds derived from 
the chest wall itself. The reflections of the tiny mirror resting upon the 
gelatine membrane are registered upon a photographic film. 
In Gerhartz’s apparatus (Fig. 286) a small reflector is kept steady by a 
magnet placed near it. The mirror is backed by a small thin iron sheet; on 
Fig. 285.—Ohm’s gelatine 
membrane apparatus. 
M, Gelatine membrane; A, 
lever; CC, carrier for the lever; 
S, small mirror; V, stop cock to 
have the system communicate 
with the open air. (After H. 
Gerhartz.) 
482 GRAPHIC METHODS 
483 
either end of the mirror are two small perforations which carry fine needles 
that are connected respectively with the north and south poles of a magnet. 
The mirror is fastened to a membrane with a fine bamboo splinter glued to 
its center. The membrane itself consists of a collodion film 20 m.m. in diam- 
Fig. 286.—Schematic view of Gerhartz’s heart sound registration apparatus. (After 
Gerhartz.) 
A, Membrane; B, mirror support; C, mirror; D, light ray; E, lamp; F, film; G, sound 
funnel and tube. 
eter. The phonendoscopic tube which carries the sound is only 6 m.m. in 
diameter, and so placed that the sound is conveyed to the center of the 
collodion film. 
Several methods for the registration of heart sounds have been devised 
upon the basic principle of the interference rings of Sir Isaac Newton. They 
depend upon the following optical principles: If a sharply curved plano-convex 
lens is placed with its curved surface upon a flat glass plate, and a homogenous 
light is focussed upon the plate, optical interference rings will be produced 
which change with the change in distance between the two opposed glass 
Fig. 287.—Photographic records of normal heart sounds (one cycle) based upon the prin- 
cipal of Newton’s interference rings. (After Austin.) 
A, normal heart sounds; B, apex tracing; C, time curve. 
surfaces. Holowinski was the first to apply this principle to heart sounds. 
He used a specially constructed microphone to collect and magnify the sounds 
from the chest wall. The heart sounds then excited a telephone upon whose 
diaphragm there was adjusted an interference optical system such as just 
described. A modern adaptation of the Newtonian principle is found in the 484 
GRAPHIC METHODS 
micrograph of Crehore. The optical interference instrument here consists of 
a metal tambour, the upper surface of which is a thin brass diaphragm. To 
the center of the latter a small mirror is attached; immediately above the 
mirror is a stationary glass lens. When used for transcribing cardiac pul- 
sations, a cup connected by rubber tubing to the interference instrument is 
placed over the cardiac apex. The movements in the enclosed column of air 
cause the telephone diaphragm, and with it, the mirror, to vibrate. When 
the rays of a mercury vapor lamp are thrown upon the optical system, the 
change in distance between the glass surfaces causes movements of the light 
interference rings. The rings are then photographed by a kymophotographic 
apparatus. In order to adapt the Crehore instrument to the registration of 
ABCD, Box; S, slide; T, tube; T, plate; Z, opening, i c.m. in diameter, over which the 
soap film is spread. (After Gerhartz.) 
Pig. 288.—Weiss phonoscope. 
sound records and to make it more sensitive, a rubber diaphragm was sub- 
stituted for the metal one. Figure 287 shows the registration of a complete 
cardiac cycle. In addition to the sound records, a simultaneous apex trac- 
ing had been taken with another interference micrograph. 
The Weiss soap-film phonoscope (Fig. 288) consists of a metal box with a 
side opening into which fits a centrally fenestrated plate. The latter is 
covered by a thin soap film. On the top of the box rests a fine silvered rec- 
tangular glass lever connected with the soap film by means of an adjustment 
screw. The sound is transmitted from the chest wall to the soap film 
through the medium of a suspended funnel; the resultant vibration produces 
movements in the glass lever. These movements are illuminated and magni- 
fied by means of a microscope and a light projection system focussed upon 
the lever; a second lens projects the image upon the photokymograph. 
The Frank segment capsule (Chapter VII) has also been employed in the 
registration of heart sounds. The sound transmitting apparatus consists of a 
stethescope bell or phonendoscope which is connected to the recording capsule GEAPHIC METHODS 
4§5 
by means of a rubber tube having an adjustable lateral opening. When the 
lateral opening is closed, heart sound vibrations are obtained, some of which are 
superimposed upon the apex tracing (Fig. 289). In order to exclude the 
coarser apical vibrations, the lateral opening should communicate with the 
outer air. 
Fig. 289.—Heart sounds, apex tracing (above) and supraclavicular venous pulse (below), 
taken with the Frank segment capsule. (After Wiggers.) 
acv. Venous pulsations; Apex (upper) tracing; C, initial vibration; C1, valve vibrations; 
S2, vibration due to second sound (transmitted to apex and jugular tracings). 
Resistance 
Microphone 
Secondary 
Primary 
.Adjustable 
/, Opening 
Qalvar ometer 
Key 
Cell 
Receiving 
Bell 
Fig. 290,—Scheme of microphone apparatus and connections with the electrocardiographic 
apparatus for the taking of phonocardiograms. (After Wiggers.) 
The Phono cardiogram.—Of all methods of taking graphic sound records, 
that in which the electrocardiographic apparatus is employed is the most 
accurate. While there are some differences in the type of the sound-receiving 
apparatus, they all consist essentially of a receiving bell to be applied to the 
chest wall. The bell is connected to a microphone by means of a rubber tube; 
the rubber tube has an adjustable opening through which it may be made 486 
GRAPHIC METHODS 
to communicate with the outer air. The microphone is placed in circuit 
with the string galvanometer by means of a coil and rheostat. Figure 290 
shows a compact apparatus for the taking of phonocardiograms. 
For the actual registration of the sounds, it is necessary to have the string 
at about four times the tension employed in taking an electrocardiogram; 
Fig. 291.—Normal phonocardiogram with simultaneous electrocardiogram (upper tracing); 
phonocardiogram (lower tracing). (After H. B. Williams.) 
1. First sound; 2, second sound. 
in other words, instead of one centimeter deflection for 1 millivolt of current 
(Chapter VIII), the string deflection should be 1 centimeter for 4 millivolts 
of current when phonocardiograms are to be taken. The heights and other 
characteristics of phonocardiograms cannot be standardized because it may 
Fig. 292.—Phono- and electrocardiogram taken simultaneously with one string. (After 
Fahr.) 
be necessary to change the string tension in order to record various abnormal 
sounds and murmurs. 
A normal phonocardiogram is shown in Fig. 291. Two strings have been 
used, one for the electrocardiogram, the other for the sound record. In this 
manner, it becomes easy to measure not only the duration of the sounds, 
but also to see and measure their incidence and relation to the events in the 
cardiac cycle (Fig. 57), for, with our knowledge of the electrocardiogram, 
we are enabled to fix the relation of cardiac sounds and murmurs in systole 
and diastole, as well as in the cardiac pressure curve (Fig. 57). GRAPHIC METHODS 
487 
Although it is necessary to employ two strings for purposes of accurate 
study of the time relationships of the sounds with cardiac events, one string 
alone may also be used. The patient is then connected with the galvanometer 
as for an ordinary electrocardiogram, the phonocardiographic apparatus 
is put into circuit at the same time. In this manner the heart sound records 
Fig. 293.—Phonocardiogram of third heart sound. (After Bridgman.) 
will produce vibrations which will break the symmetry of the electrocardio- 
gram, but enough of the landmarks of the latter are usually visible to fix the 
auricular and ventricular events, and thus to fix the time relationship of the 
phonocardiographic events as well (Fig. 292). 
Fig. 294.—Phonocardiogram taken from apex. The systolic murmur (1) occupies the 
entire systolic period. (After Battaerd.) 
In their appropriate connections (Chapter XIII), the causes of the normal 
sounds, and the etiological, diagnostic and clinical significance of abnormal 
sounds and murmurs are fully dealt with. Here it is sufficient to reproduce 
the more important types of normal and abnormal phonocardiograms, and 
to indicate how this method of sound registration is an aid to auscultation. 488 
GRAPHIC METHODS 
Reference to the simultaneous phono- and electrocardiogram (Fig. 291, 
292) shows that the beginning of the first sound takes place very shortly after 
the onset of the R wave. Since it is practically certain that the R wave 
occurs almost simultaneously with ventricular contraction, it seems probable 
that at least the onset of ventricular contraction causes no sound. This 
has an important clinical application in the assumption that weak heart 
sounds are indicative of weakened or diseased heart muscle (Chapter XIII). 
Fig. 295.—Phonocardiogram showing a diastolic (f i) and a systolic (f 2) murmur. 
The photographic plate is traveling at a fast rate (100 m.m. per s.) in order to get a detailed 
curve. (After Battaerd.) 
Fig. 296.—Phonocardiogram showing an accentuated second pulmonic sound. The 
microphone was placed over the pulmonary valve. (After Battaerd.) 
In addition to the phonocardiograms of the first and second sounds, occa- 
sionally a phonocardiogram of a third heart sound may be obtained 
(Fig. 293). Types of systolic and diastolic murmurs are shown in Figs. 294, 
295. The phonocardiogram of an accentuated second sound is shown in Fig. 
296. The figures and accompanying legends sufficiently describe the time 
relationships and types of the murmurs. 
Phonocardiograms are undoubtedly of great aid in helping to solve some 
of the physiological factors connected with sound production. This is accom- GRAPHIC METHODS 
489 
plished by a comparative study of their time relationship with the electro- 
cardiogram, with intraventricular pressure curves and with the time of 
valve closure (Fig. 57). In this manner, graphic sound records are of value, 
particularly in determining the question of the muscular element in the pro- 
duction of heart sounds. 
The special clinical value of phonocardiograms rests in the graphic 
representation of murmurs, for phonocardiograms may give added informa- 
tion regarding the time-relationship and intensity of adventitious sounds. 
It should be stated that the phonocardiogram gives no information regarding 
the source of a murmur; it simply gives, as stated, its time relationship and 
relative intensity. And while it will always transcribe the murmurs, it has 
this disadvantage as compared with auscultation in that the trained ear 
invariably selects the sound or murmur which seems of greatest importance 
clinically, and follows it through the heart cycle (Chapter XIII). Besides, 
faint murmurs do not always register in the phonocardiogram. 
I believe the great clinical advantage of the phonocardiogram is its ability 
to transcribe the time relationship of a given murmur, which upon ausculta- 
tion may be open to question as to whether it is systolic or diastolic. To clear 
up such a problem is naturally of great diagnostic importance, especially 
when dealing with the probability of the two valvular lesions: Aortic regurgi- 
tation and mitral stenosis. As an instance, I recall a case of aortic aneurism, 
visibly pulsating in the jugulum, that required a phonocardiogram in order to 
determine whether a murmur which was quite loud on auscultation was 
systolic or diastolic in time. The phonocardiogram showed it to be diastolic. 
Even here, however, careful palpation over the aneurism at the time of aus- 
cultation would have given the desired information; for if the murmur were 
not synchronous with the pulsation of the aneurism (and therefore with cardiac 
systole), it must of necessity be diastolic. 
REFERENCES 
Austin: Application of the Crehore Micrograph ... to Recording Heart Sounds; 
American Journal of Medical Science, 1912, CXLIII, 193. 
Battaerd: Heart Sound Records; Heart, 1915-17, VI, 121. 
Bridgman: Observation on the Third Heart Sound; Heart, 1915-17, VI, 41. 
Einthoven: Registrirung d. Herztone mittels Saitengalvanometer; Archives, f. d. ges. 
Physiologie, 1907, CXVII, 461. 
Fahr: On Simultaneous Records of the Heart Sounds and Electrocardiogram; Heart, 
1912-13, IV, 147. 
Holowinski: Physikalische Untersuchung der Herztoene, Zeitschrift f. Klinische Medezin, 
1901, XLII, 186. 
Huerthle: Mechanische Registrirung der Herztoene; Archives, f. d. ges Physiologie, 1895, 
LX, 263. 
Lewis: Heart Sounds in Mitral Stenosis; Heart, 1912-13, IV, 241. 
Lewis: Illustrations of Heart Sound Records; Quarterly Journal of Medicine, 1912-13, VI, 
44i. 
McKendrick: Experimental Phonetics, Report of Smithsonian Institute, 1902. 49© 
GRAPHIC METHODS 
Ohm: Photogophische Herzregistrirung; Deutsche Med. Wochenschrift, 1911, XXXVII, 
1432. 
Sommerfeld und Frank: Deformationen der Segment Membrane, 
Weiss: Erwiderung zu O. Frank: Archives, f. ges. Physiologie, 1910, CXXXII, 544. 
Wiggers: Circulation in Health and Disease. 
v. Wyss, Aufzeichungen von Herztone . . . Galopprythmus-Deutsches Arch. f. Klinisches 
Medezin, 1910, Cl, 1. CHAPTER XXXII 
CLINICAL SIGNIFICANCE OF THE ABNORMALLY WIDE VENTRICU- 
LAR DEVIATION IN THE ELECTROCARDIOGRAM 
Because of the importance and clinical significance of myocardial disease, 
attempts are constantly being made to interpret the condition of the myocar- 
dium from the electrocardiogram. 
In an electrocardiographic study of a series of patients with valvular and 
myocardial disease, reference to which has already been made (Chapter IX), 
I observed a characteristic which seems of importance in the diagnosis of 
myocarditis, namely, the abnormal width of the main deviation of the ven- 
tricular complex, commonly called the R-wave or the first ventricular spike. 
The width of the normal R-wave has been variously estimated. Hirshfelder 
estimates it as 0.02 of a second; Lewis as from 0.03 to 0.04 of a second. 
Though not directly mentioned by Einthoven or Nicolai, measurements of a 
number of their normal ventricular complexes give an average width of less 
than 0.05 second. All the measurements have reference to R waves of 
normal form, that is, to those that are neither split or splintered, and whose 
sides form rectilinder lines which meet at a sharp angle and form a sharp 
apex. In the measurements of my cases I have included only clean-cut 
deviations of normal form. As an arbitrary standard in my series I have 
adopted a base line width of 0.07 or over as representing abnormally wide 
deviations. From my own measurements of many ventricular deviations 
of patients with normal hearts, and from the normal standards of others, I 
believe that 0.07 of a second (or over) probably represents a deviation which 
has taken an abnormally long time for its completion. Indeed, in only one 
instance (M.G., Case 13) have I found the R wave of a normal heart wider 
than 0.07 of a second. 
Robinson pointed out the clinical importance of abnormally wide and 
splintered ventricular complexes as evidence of marked functional changes in 
the heart (Chapter IX). Oppenheimer and Rothschild have shown that 
some cases of myocardial disease involving the subendocardial myocardium 
(intraventricular block) present an R complex of low voltage, wide base and 
irregular sides (Chapter IX). They believe this occurs because myocarditis 
in this location interferes with the rapidity and uniformity of the spread of the 
electrical impulse through the heart by involving the superficial end branches 
of the conduction system. These observers have confirmed the deductions 
drawn from the electrocardiograms by the pathologic study of a number of 
necropsies. Eppinger and Rothberger induced experimental destruction of 
various parts of the cardiac musculature by freezing with ethyl chlorid, or 
49i 49 2 
CLINICAL SIGNIFICANCE OF THE WIDE R 
by the injection of destructive substances. Electrocardiograms were taken 
before and after the injections. When, for example, a strong nitrate of silver 
solution was injected in the deeper layers of the left ventricle either at the 
base or apex, there was a marked change in the ventricular deviation. Within 
five minutes after the injection the descending limb became shorter so that it 
no longer touched the base line; this shortening became progressive so that in 
about twenty minutes the R and T deviations formed practically a mono- 
phasic curve. Injections of nitrate of silver in the superficial layers, or in the 
anterior and posterior papillary muscles were not followed by the foregoing 
changes in the electrocardiogram. Injections in the right ventricle were not 
regularly followed by electrocardiographic changes; the most typical consisted 
in a widening and prominence of the S and T deviations. I mention these 
experiments in some detail because they have an important bearing on the 
present clinical study. We must assume that we clinically meet with focal 
myocardial changes probably at times similar in location and destructiveness 
to the experimental lesions quoted; yet in only a single instance in a study of 
very many cases of marked cardio-sclerosis did I observe an electrocardiogram 
which resembled that derived from Eppinger and Rothberger’s experimental 
injection in the deeper layers of the left ventricle. It therefore seems unwar- 
ranted to draw deductions of the state of the pathologic process in the human 
heart from the type of experimental damage already quoted. This discrep- 
ancy may rest on the fact that rapid experimental destruction of the myo- 
cardium produces some special change of the electrocardiogram, or that in 
almost every instance in the human heart where there are marked localized 
changes, there is also damage in other portions of the myocardium; that is, 
the local damage is only part of general myocardial disease. 
In a description of cases assuming defective conduction in one of the main 
branches of the auriculo-ventricular bundle (Chapters IX, X), Carter describes 
as characteristics of these lesions, a Q-R-S time exceeding o.io second, 
increased amplitude of the R deflections, and T waves, often exaggerated and 
usually in a direction opposite to that of the prominent initial deflection. The 
initial deflections themselves are very frequently atypical in form in at least 
one lead; bizarre forms are common. The assumption of branch bundle 
lesions in these cases has recently been questioned (Oppenheimer and 
Rothschild). 
In the cases that I report there has been no reason to assume an abnormal 
path for the impulse, for the electrocardiograms possess none of the charac- 
teristics of the aforementioned groups. Except for the abnormally wide base 
line, the electrocardiograms are of the usual normal types in form and size. 
Some of the deviations are tall. That amplitude in itself, however, need not 
necessarily imply an abnormally wide base is shown in cases in which R I is 
quite tall though of normal width (Chapter IX). 
A glance at the summary in the accompanying table of cases shows that, 
grouping them by their clinical characteristics, in all instances but two CLINICAL SIGNIFICANCE OF THE WIDE R 
493 
(Cases 3 and 5), there was grave disease of the myocardium; that is, myo- 
carditis represented an important part of the clinical entity. The two 
exceptions were cases of rheumatic aortic disease in both of which ventricular 
hypertrophy was extreme. That abnormal prolongation of the time of the 
electrical impulse is not due to decompensation itself is evidenced by the fact, 
as noted in the clinical histories, that many of the electrocardiograms were 
taken when the patients were perfectly compensated. Ventricular dilata- 
tion per se as a cause for the abnormally wide R could be excluded. First, 
there was no evidence of any extreme dilatation, certainly not in the 
compensated cases. Secondly, in a study of a large series of cases of decom- 
pensated valvular lesions, in which cardiac dilatation was presumably a 
prominent feature, I found no abnormally wide R. Nor had I there found 
any correlation between hypertrophies—even extreme—and the width of the 
R deviation. Whether in the present study Cases 3 and 4 may be regarded 
as evidence of myocarditis in addition to hypertrophy, it is impossible to say. 
Width of R in 
Case 
No. 
Clinical diagnosis 
Rhythm 
hundredths of 
Remarks 
second 
i 
Myocarditis; coro- 
nary disease 
Normal 
R II =0.07 
R III = 0.08 
Arrhythmia and death 
2 
Luetic aortitis; 
myocarditis 
Interpolated ex- 
trasystole 
RI =0.12 
R II =0.07 
R 111= 0.13 
3 
Rheumatic aortitis 
Auricular fibril- 
R II =0.07 
Massive ventricular hyper- 
lation 
trophy; death in one year 
4 
Cardio-nephritis 
Normal 
RI =0.08 
R II =0.08 
Precordial pains 
Massive ventricular hyper- 
5 
Rheumatic aortitis 
Normal 
R II =0.09 
R III =0.08 
trophy 
6 
Cardio-sclerosis 
Normal 
• 
RI =0.10 
R III = 0.07 
Cardio-nephritis 
Auricular fibril- 
RI =0.08 
7 
lation 
Died in uremic coma 
8 
Myocarditis; arte- 
Sinus arrhyth- 
RI = 0.08 
riosclerosis 
mia 
R III = 0.08 
9 
Aortic aneurism 
Normal 
R II =0.07 
Moderate amount of myo- 
Cardio-sclerosis 
Auricular fibril- 
carditis at necropsy 
R II =0.08 
IO 
lation 
Normal 
1 R 111= 0.09 
RI =0.12 
Aneurismal dilatation of 
ii 
Cardio-sclerosis 
R II =0.08 
the aortic arch 
Summary of Cases 
It will be noted from the table that the electrocardiograms showed an 
abnormally wide R in one or two leads, rarely in three. In view of the fact 494 
CLINICAL SIGNIFICANCE OF THE WIDE R 
that the leads draw off the current from various cardiac areas—breadthwise 
in Lead I, diagonally in Lead II, and lengthwise in Lead III—one may possi- 
bly assume that the diseased myocardium lay more in one plane of the current 
than the other, thus interfering with the quick distribution and spread of 
the electrical current in that particular plane. 
It remains to indicate this important fact that while the cases mentioned 
show abnormally wide ventricular deviations and are apparently indicative 
of severe myocardial disease, I have observed cases clinically similar to the 
above with perfectly normal electrocardiograms. The reason for this is not 
at present apparent. 
The conclusions are given in another chapter (Chapter IX). 
REPORT OF CASES 
Case i.—A. G., man, aged 54, had complained for two years of indefinite 
precordial pains radiating to the left hand, and of attacks of dizziness. He 
had been unable to work for several months because of these attacks. On 
examination, the systolic blood pressure was 166, the diastolic, 88. The first 
aortic sound was blurred, the second somewhat accentuated. The other 
heart sounds were normal. There was slight edema of the legs. The urine 
contained no albumin or casts. Fluoroscopic examination showed a normal 
sized aorta; the ventricular outline was somewhat enlarged to the left. 
The electrocardiogram at that time showed normal rhythm; R II and R III 
were respectively 0.07 second and 0.08 second in width. The subsequent 
history of the patient was of interest. Following the use of digitalis and of 
theobromin sodium salicylate, there was gradual improvement in the symp- 
toms for about one year. The patient then developed sudden attacks of 
tachycardia, each of which lasted several days. The symptoms during these 
attacks were mainly subjective and consisted in the uncomfortable recogni- 
tion of the rapid heart action; dyspnoea was slight. About one week after 
the last attack he suddenly complained of precordial distress, followed by 
faintness. The patient was moderately dyspnoeic. Auricular fibrillation 
with rapid ventricular activity was present. A diagnosis of coronary throm- 
bosis was made. Five days after the onset of fibrillation, while sitting 
quietly on a chair and apparently quite comfortable, he suddenly gasped and 
died within a few minutes. The clinical diagnosis was myocarditis and 
coronary sclerosis. 
Case 2.—W. Z., man, aged 57, entered the hospital with general anasarca 
and the usual symptoms of cardiac decompensation. This had been the 
third break of compensation within recent years. The physical signs revealed 
the presence of an aortitis and of left ventricular hypertrophy. This was 
corroborated by roentgenography, which showed in addition, aneurismal 
dilatation of the entire thoracic aorta, and ventricular enlargement which 
practically filled the lower left half of the chest. The Wassermann blood clinical significance of the wide r 
495 
examination was 4 plus. On antisyphilitic treatment, Karrell diet, digitalis 
and theobromin sodium salicylate, the patient quickly improved. The electro- 
cardiogram taken when the patient was compensated, showed abnormally wide 
ventricular deviations in all leads, especially in the first and third. The R 
widths were respectively 0.12 and 0.13 second; R II was 0.07. The clinical 
diagnosis was syphilitic aortitis, myocarditis and left ventricular hypertrophy. 
Case 3.—H. Y., male, aged 31, had acute articular rheumatism six years 
prior to admission. Six weeks ago he suffered from what at first appeared to 
be grippe; this was soon followed by fever and joint pains. He had never 
had any cardiac symptoms until recently. Examination revealed markedly 
throbbing carotid, subclavian, brachial and radial arteries. A rough systolic 
thrill was heard over the carotid and over the aorta in the jugulum. There 
was a loud, rough, double murmur over the right base. The liver was some- 
what enlarged. The urine contained a trace of albumin and a few granular 
casts. The Wassermann blood examination was negative. The orthodia- 
scope revealed an enlarged and hyperacting aorta, the left ventricle was 
moderately enlarged. The electrocardiogram showed auricular fibrillation; 
the width of R II was 0.07. The patient developed hemorrhagic erythema of 
the legs, and later, rheumatic joint manifestations. He died within three 
months. The clinical diagnosis was a double aortic lesion and moderate 
left ventricular hypertrophy. 
Case 4.—I. K., woman, aged 57, complained for several years of a feeling 
of oppression in the chest and of numbness in the fingers of both hands. 
There were also occasional attacks of nocturnal dyspnea accompanied by 
precordial pains. The systolic blood pressure ranged between 180 and 220, 
the diastolic between 90 and no. There was a metallic second sound over 
the aorta, and a systolic murmur at the apex. With the fluoroscope the aor- 
tic arch was found enlarged, the left ventricle moderately hypertrophied. The 
urine showed a trace of albumin and a few casts. R I and R III were each 
0.08 second in width. The clinical diagnosis was cardio-nephritis. 
Case 5.— E. O., woman, aged 21, had “growing pains” as a child. Her 
“heart trouble” began at the age of 10. The chief complaint was palpitation, 
especially after undue excitement. The systolic blood pressure was 180, 
the diastolic 30 m.m. The classical signs of a double aortic lesion and left 
ventricular hypertrophy were present. The orthodiascope revealed a 
violently pulsating aorta and massive ventricular hypertrophy, as well 
as enlargement of the cardiac shadow to the right. The electrocardiogram 
showed the widths of the R deviations as follows: R I = 0.09 and R II = 0.08. 
Case 6.—A. K., physician, aged 53, had scarlet fever at the age of 15. 
Since then he had had occasional traces of albumin and a few casts in his 
urine. Of late, he has become somewhat dyspneic. The systolic blood pres- 
sure ranged between 175 and 190, the diastolic between no and 85. The 
second aortic sound was somewhat accentuated; there was a systolic mur- 
mur at the apex. The liver was somewhat enlarged. The urine contained 496 
CLINICAL SIGNIFICANCE OF THE WIDE R 
a trace of albumin, and granular and hyaline casts. There was slight edema 
of the legs. The blood Wassermann was negative. The orthodiascopic 
examination revealed a somewhat enlarged aorta and cardiac shadow. In 
the electrocardiogram, R I and R III were each 0.07 second wide. The 
clinical diagnosis was cardio-nephritis. 
Case 7.—I. W., woman, aged 45, was brought to the hospital in a coma- 
tose condition. The only history obtainable referable to her present condi- 
tion was that six years previously, when pregnant, she lost her eyesight 
(uremia?); labor was induced and her eyesight returned. At the present 
examination, her heart was found hypertrophied, there was marked accentua- 
tion of the second sound at the apex and base. The systolic blood pressure 
was 270 m.m. A blood culture was sterile. The electrocardiogram showed 
that R I was 0.08. Two days after admission the patient died in uremic 
coma. The clinical diagnosis was cardio-nephritis. 
Case 8.—S. M., male, aged 53. He complained for several years of dysp- 
nea and precordial pains, particularly on slight exertion. He had had 
transient attacks of Cheyne-Stokes breathing; at such times his pulse was 
arrhythmic, electrocardiographic curves showed that the arrhythmia was of 
sinus origin. The apex was in the sixth left interspace, 14 c.m. from the mid- 
sternal line. The heart sounds were faint, there was a soft systolic murmur 
at the apex and a slightly accentuated second sound at the base. The radial 
arteries were thickened and tortuous. The systolic blood pressure was 190 
m.m., the diastolic, no m.m. The electrocardiogram showed that R I and 
R III were each 0.07 second wide. The clinical diagnosis was myocarditis 
and cardio-sclerosis. 
Case 9.—J. J., aged 53, man, had a protuberant aneurismal tumor the 
size of a large orange, situated in the upper right side of the chest. There 
were loud systolic and diastolic thrills and pulsations over the aneurism, there 
was also a systolic murmur and a systolic thrust at the cardiac apex. The 
apex was in the sixth interspace, one inch outside the nipple. Though the 
patient was somewhat dyspneic at first, there was no marked decompensation. 
R I and R III were each 0.07. The aneurism was wired. After some weeks, 
there were frequent external hemorrhages from the aneurismal sac; the 
patient gradually succumbed. At necropsy, besides the aneurism, the ventri- 
cles were moderately hypertrophied and showed a moderate amount of 
myocarditis. 
Case 10.—J. C., man, aged 60, was addicted to alcohol. During the pre- 
vious two years, he had had several mild attacks of dyspnea and of edema of the 
legs; the last attack occurred one week prior to admission. The cardiac apex 
was in the fifth interspace, 12 c.m. from the midsternal line. There was a 
blowing systolic murmur at the apex, the second sound at the base was impure 
and slightly accentuated. The arteries were thickened. The electrocardio- 
gram showed auricular fibrillation. R II was 0.08 second, R III 0.09 second 
wide. The clinical diagnosis was cardio-sclerosis. CLINICAL SIGNIFICANCE OF THE WIDE R 
497 
Case ii.—M. M., aged 65, had rheumatism several years prior to admis- 
sion. She had been somewhat dyspneic for several years; of late this symp- 
tom has become more marked. The first examination revealed mucous rales 
over the entire chest. There was a loud systolic murmur heard over the 
upper right chest, transmitted into the carotids and to the left of the scapula 
posteriorly. There was also a loud systolic murmur over the mitral area. 
The blood pressure was normal. There was slight edema of the legs. The 
urine showed a slight trace of albumin and a few casts. In the fluoroscope, 
there was found aneurismal dilatation of the first portion and arch of 
the aorta; the heart was moderately enlarged. R I was 0.12 and R III 0.08 
in width. The clinical diagnosis was cardio-sclerosis. CHAPTER XXXIII 
MATHEMATICAL CONSIDERATIONS UNDERLYING THE 
ELECTROCARDIOGRAM 
To those interested in understanding some of the mathematical prin- 
ciples upon which the electrocardiogram is based, this chapter wdiile some- 
what obstruse, may be of importance. 
In previous chapters (Chapters VIII, IX) the fact was emphasized that 
the electrocardiographic deviation represented the resultant of the differ- 
ences of electrical potential existing at any given moment. In the case of the 
ventricles, it is in fact the resultant of separate activities of the ventricular 
chambers. The diagnostic significance of the direction of the R wave was 
also discussed. The elementary mathematical principles upon which dif- 
ferences in the R deviations depend now require brief comment. 
Stress has been laid upon the fact that the size of the R peaks depends 
upon the angle formed by the line across the heart (represented by the 
“leads,” Chapter VIII) and the “electrical axes;” the nearer the electrical 
axes approach parallelism to the leads, the taller the corresponding peaks; the 
nearer these approach the right angle, the smaller the peaks. The size 
of the deviation thus varies with the angle made by the lead and the electrical 
axes. In other words, the electrocardiogram is modified in each lead by the 
relation of the direction of the active current in the heart to that of the leads 
placed upon the extremities. Conversely, the angle made by these two lines 
may be computed from the differences in size of the deviation in the three 
leads. 
Manifest Size.—Einthoven has differentiated the “actual” size of the 
deviations, as reproduced in the electrocardiogram, from their “manifest” 
size or the “manifest” difference of the electric potential. He defined the 
latter as that dimension in millivolts which is derived when the electrical axis 
and leads coincide: It is the maximal size of the electrical potential of the 
heart in the lead. The manifest size of any deviation is computed from the 
registered actual electrocardiogram. Einthoven and his pupils, Fahr and 
de Waart, have laid down mathematical principles by which it is possible to 
estimate the angles formed by the electrical axes with the leads. If, for 
purposes of simplification, the lines of the three leads be conceived as forming 
the sides of an equilateral triangle (Fig. 297 R. L. F.), and its middle point, H, 
represent the heart, the size of the R deviations in the three leads is obtained 
by the right angled projection of the deviations upon the electrical axis pass- 
498 MATHEMATICAL CONSIDERATIONS 
499 
ing through the point H. From these, data are derived for the determination 
of the angle formed by the electrical axis and the leads.1 
Measurements of the Angles Made by the Leads and the Electrical Axis. 
If smaller angles be discarded, and for purposes of clinical approximation, 
only those be considered which are multiples of 30 deg., the computation 
of Ei:E2: (Fig. 297) is much simplified; for example, 
When 
a = 0°, then Ei: E2: E3 = 1: + .5: — .5 
a = 30°, then Ei: E2: E3 = 1:1:0 
a = 6o°, then Ei: E2: E3 = +.5:1: — .5 
a = 90°, then Ei: E2: E3 =0:1:1 
etc. 
From these numerical proportions, the angle a can be approximated within 
30 deg. The “manifest” equals the actual size of Ri (Ei, Fig. 297) when a 
equals o deg.; of R2 (E2) when a equals 60 deg., and of R3 (E3) when it equals 
120 deg. For the exact determination of this angle, tables are required. In the 
Appendix to this chapter (q. v.) there is a table for approximation within 10 
deg.; by the use of the second table (Interpolation Table) the exact angle may be 
computed. For example, if Ri equals 3.2, R2 equals 12.5, and R3 equals 9.3, 
thenEi (Ri): E2 (R2): E3 (R3) =3.2:12.5:9.3. To derive an approximation 
within 10 deg. (Table 1), 12.5, the tallest deviation, becomes the denominator, 
10 
thus: 12.5. Substituting this fraction for 12.5 in the equation, we find Ei: 
I2-5 
E2:E3 = 2.6:10:7.4. Furthermore, from the same table we note these figures 
determine that the angle a falls between 70 and 80 deg.; and that Ei between 
70 and 80 deg. has a value between 3.5 and 1.8, a difference of 2.7. In Table II 
(Interpolation Table, Third Column) the nearest approximation to this dif- 
ference is 2.6, which is equivalent to 6 deg.; hence, a = 70 deg. + 6 deg. = 
76 deg. 
As another example, suppose Ti = 4, T2 = 1.5, and T3 = 3.5, we then 
have the proportion Ei: E2:E3 = 4:1.5: — 2.5. To derive approximation 
within 10 deg. we multiply by the fraction 4 being the tallest deviation. 
Then Ei: E2: E3 = 10: 3.75: — 6.25. From Table I, this proportion shows 
that the angle a is between o deg. and — 10 deg., and also that E2 varies from 
5 to 3.5. In Table II, its nearest approximation is 3.8, an angle of 8 deg. 
Hence a = o deg. —8 deg. = — 8 deg. 
1 To insure mathematical accuracy it is necessary to measure the R deviations at iden- 
tical phases of the heart cycle. With this in view, two galvanometers may be 
simultaneously employed; one to record sound records, the other to record the electrocar- 
diograms. Although this method is necessary for absolute accuracy, measurements derived 
from the ordinary electrocardiogram are sufficiently exact for clinical purposes unless 
phasic differences of the heart cycle produce marked changes in the electrocardiogram. 5 00 
MATHEMATICAL CONSIDERATIONS 
Since the value of the angle alpha can be computed, it is possible by trigo- 
nometry1 to determine the manifest size (Fig. 297) of the various deviations. 
In a schematic diagram by Pardee (Fig. 298), based upon the Einthoven 
conception of the leads forming a triangle with the heart in the center, 
the angle a can be roughly measured by conceiving the direction of the electro- 
Fig. 297.—The right and left arms and left foot (designated R, L, F, respectively) 
form the angles of an equilateral triangle. The point H is in the center and represents the 
heart. If the arrow EA represent any given electrical axis, the angle it forms with the first 
lead (RL) be represented by X, and any given length PQ be called E, the right angled 
projection of its length will give its corresponding value in the various leads; that is, in L I 
it will equal E I; and L II, E2 and inL III, E3. The distance Ei, E2, E3 are proportional, 
that is, Ei : E2 : E3. Since any angle of an equilateral triangle is equal to 60 deg., the follow- 
ing trigonometrical formulae are derived: 
El = E cos a; 
E2 = E cos (a — 60°); 
E3 = E cos (120 — a); 
E3 = E2 - El. 
The formula E3 = E2 — Ei is of special importance, for, given the heights in deviations 
in any two leads, the height of the remaining peak may be derived. (After Einthoven, 
Fahr and De Waart.) 
cardiographic current as lying in one of six sectors of 60 deg. each. Thus, cur- 
rents or electrical axes between + 30 deg. and + 90 deg. (the normal segment) 
give + Ri + R2 + R3. 
Axes between + 90 deg. and +150 deg. give — Ri + R2 + R3 
Axes between + 150 deg. and — 150 deg. give — Ri — R2 + R3 
Axes between — 150 deg. and — 90 deg. give — Ri — R2 — R3 
Axes between — 90 deg. and — 30 deg. give + Ri—R2 — R3 
Axes between — 30 deg. and + 30 deg. give+Ri + R2 — R3 
These results are diagrammatically shown in Fig. 299. 
1The formulae by which the value of E (the manifest size) may be derived are: 
Ei 
E = 
cos a 
F = E2 
cos (a — 6o° 
E = 
/ o 
cos (i 20 — a MATHEMATICAL CONSIDERATIONS 
f? t G HT 
1_EFt 
Fig. 298.—a, b, c, represent the numerical value of the deflection caused by an action 
current in leads I, II, III, respectively, b = a + c and will be directed upwards or 
downwards according as a and c are directed; + before the letter signifies an upward deflec- 
tion; — signifies a downward deflection. (After H. E. Pardee.) 
Fig. 299.—Diagram showing the direction of the leads with current (electrical axes) at 
various angles. The circle is divided into six sectors at 60 deg. each. The direction of the 
currents is marked by the arrow heads, the ventricular deviations for the respective leads 
by Ri, R2, R3. 502 
MATHEMATICAL CONSIDERATIONS 
By these computations and methods, accurate knowledge of the direction 
and size of the electrical axis and of the electrical balance of the heart is 
obtained, but definite information regarding the origin of the excitation wave 
is not thus derived. A knowledge of the manifest size in conjunction with 
the electrical axis helps to diagnose the most likely point or points of origin of 
the excitation wave. By further amplification and applications of the 
Einthoven formulae, Fahr and Weber have concluded as follows: The 
deviation Q results from excitation in the neighborhood of the middle zone of 
the heart; the papillary muscles and their environment. The apex of R is the 
resultant of excitation in the base of the heart, usually over its middle portion. 
The area is ordinarily to the left, but sometimes to the right of the middle line. 
The deviation S in general denotes apical negativity; the electrical center is 
usually to the left, but may be to the right of the median line. The deviation 
T is the end of the excitation wave. As a rule, it results from excitation of 
the ventricular base, to the right or left of the median line. 503 
Table I 
Appendix1 
Table II 
«» 
degrees 
Registered potential differences, 
e 
Manifest 
potential 
differ- 
ences 
e1 
e2 
e3 
E 
0 
10 
S. 0 
- 5.0 
10, 0 
10 
10 
6, S 
- 3, s 
10, 2 
20 
10 
8, 2 
- 1, 8 
10, 7 
30 
10 
10 
0 
n> 5 
40 
8, 2 
10 
1, 8 
10, 7 
so 
6, S 
10 
3. S 
10, 2 
6o 
5, 0 
10 
5. 0 
10, 0 
70 
3, S 
10 
6, 5 
10, 2 
8o 
1, 8 
10 
8, 2 
10, 7 
90 
0 
10 
10 
11. s 
100 
- 1, 8 
8, 2 
10 
10, 7 
no 
- 3. S 
6, S 
10 
10, 2 
120 
- 5, 0 
S. 0 
10 
10, 0 
130 
- 6, s 
3. s 
10 
10, 2 
140 
- 8, 2 
1, 8 
10 
10, 7 
ISO 
—10 
0 
10 
11.5 
160 
—10 
- 1, 8 
8, 2 
10, 7 
170 
—10 
- 3. S 
6, 5 
10, 2 
+180 
—10 
- 5. 0 
5. 0 
10, 0 
— 170 
—10 
- 6, s 
3, S 
10, 2 
—160 
—10 
— 8, 2 
1, 8 
10, 7 
- iso 
—10 
—10 
0 
11.5 
—140 
- 8, 2 
— 10 
- I, 8 
10, 7 
-130 
- 6, s 
— IO 
- 3, S 
10, 2 
— 120 
- 5. 0 
— 10 
- S, 0 
10, 0 
— no 
- 3. S 
— 10 
- 6, S 
10, 2 
—100 
- 1, 8 
— 10 
— 8, 2 
10, 7 
- 90 
0 
— 10 
—10 
II. s 
— 80 
1, 8 
— 8, 2 
— 10 
10, 7 
- 70 
3. 5 
— 6, S 
— 10 
10, 2 
— 60 
5. 0 
- 5. 0 
— 10 
10, 0 
- 50 
6, S 
- 3. S 
— 10 
10, 2 
- 40 
8, 2 
- 1, 8 
— 10 
10, 7 
- 30 
10 
0 
—10 
11.5 
— 20 
10 
1, 8 
— 8, 2 
10, 7 
— 10 
10 
3. 5 
- 6, 5 
10, 2 
0 
10 
5. 0 
- 5, 0 
10, 0 
Interpolation table 
Differ- 
Potential 
Differ- 
ences in 
differences 
ences in 
E 
degrees 
+e 
degrees 
0 
0 
10 
11. S 
Leads f 2 
0, 4 
8 
II. 3 
0, 8 
6 
II, I 
I, 2 
4 
II, 0 
u 
1. s 
2 
io, 8 
10 
I, 8 
0 
10, 7 
(2 
2, 2 
8 
10, S 
II 4 
2,5 
6 
10, 4 
1 6 
2, 9 
4 
10, 3 
18 
3,2 
2 
10, 2 
10 
3. 5 
0 
10, 2 
(2 
3, 8 
8 
10, I 
III 4 
4. 1 
6 
10, I 
] 6 
4. 4 
4 
10, 0 
[8 
4. 7 
2 
IO, 0 
.0 
S, 0 
0 
10, 0 
* These tables and the examples in the 
text were taken from Einthoven, Fahr 
and de Waart “Ueber die Richtungen 
und die Manifest Grosse der Potential- 
schwankungen, . . . des Elektrokardio- 
gramms.” (Arch. f. d. ges. Physiologie, 
1913, CL, p. 308.) 
Carter: Archives Internal Medicine, 1914, XIII, 805. 
Einthoven: Pfluger’s Arch. f. d. ges Physiol., 1912, LXIII, 152. 
Eppinger and Rothberger: Wien. Klin. Wchnschr., 1909, XXII, 1091. 
Hirshfelder: Diseases of the Heart, Ed. 2, p. 89. 
Nicolai: Handb. d. Allg. Path. u. Krankh. d. Herz. u. Gefaesse., 3, Part I, 137. 
Oppenheimer and Rothschild: Proc. Soc. for Exper. Biol, and Med., 1916, XIV, 57. 
Oppenheimer and Rothschild: Jour. Am. Med. Assn., 1917, LXIX, 429. 
Robinson: Archives Int. Med., 1916, XVIII, 830. 
REFERENCES PART II 
CARD10-VASCULAR CLINICS - CONTENTS 
Case No. Page 
1. Typical Mitral Regurgitation with Pericarditis. 507 
2. Typical Mitral Regurgitation and Pericarditis; Re-exami- 
nation six Months Later: Remarks on Tonsillectomy 
and Extraction of Teeth 508 
3. Compensated Mitral Regurgitant Lesion with Variable 
Auscultatory Signs 511 
4. Mitral Stenosis—Typical Physical Signs—Rheumatic 
Recrudescence 512 
5. Acute Rheumatic Endocarditis—Hemiplegia—Death... 513 
6. Mitral Stenosis—Sudden Onset of Vaso-motor Symp- 
toms 515 
7. Mitral Stenosis—Pulmonary Infarct—Gastric and 
Vaso-motor Symptoms 516 
8. Mitral Stenosis—Atypical History and Symptoms 518 
9. Mitral Stenosis—Hypertension—Neurasthenia 520 
10. Rheumatic Endocarditis in a Syphilitic 521 
11. Double Mitral Lesion—Acute Pericarditis—Classical 
Signs and Symptoms 523 
12. Double Mitral Lesion—Decompensation—Streptococ- 
cemia 524 
13. Mitral Regurgitation—Coronary (?) Involvement of 
Undetermined Origin 525 
Mitral Valvular Le- 
sions. 
14. Aortic Regurgitation—Typical Physical Signs 528 
15. Aortic Regurgitation—Mitral Regurgitation—Acute 
Pericarditis 529 
16-18. Rheumatic Aortic Stenosis and Regurgitation—Bovine 
Hearts—Remarks upon Gastro-intestinal Symptoms 
in Patients with Aortic Lesions 331 
19. Beginning Rheumatic Double Aortic Lesion—Contin- 
uance of the Lesion Despite Tonsillectomy 534 
Aortic Valvular Le- 
sions. 
20. Typical Luetic Aortitis 536 
21. Syphilitic Myocarditis—Caries of Teeth—Gingivitis— 
Pyorrhoea—Remarks upon the Connection between 
Heart Disease and Pyorrhoea 537 
22. Aortic Aneurism and Auricular Fibrillation 539 
23. Luetic Aortitis—Constant Precordial Pain 541 
Cardiac Syphilis. 
5°5 5°6 
CARDIOVASCULAR CLINICS—CONTENTS 
Case No. Page 
24-26. Senile Cardio-sclerosis—Loud Systolic Murmur over 
the Entire Anterior Surface of the Chest. General 
Comment 542 
27, 28. Cardio-sclerosis in the Middle-aged. Loud Systolic 
Murmur over the Entire Surface of the Chest 544 
29. Cardio-sclerosis—Remarks on the Cause of Symptoms 
in Senile Cardio-sclerosis 545 
30. Cardio-sclerosis—Cholecystitis 547 
31. Alcoholic Cardio-sclerosis.... 548 
32, 33. Myocarditis without Hypertension or Physical Signs.. 550 
Cardio-sclerosis. 
Pregnancy and Heart 
Disease. 
34. Pregnancy with Cardiac Disease and Endocarditic 
Recrudescence 552 
35, 36. Pregnancy with Cardiac Disease and Neurotic Symp- 
toms 553 
37. Overacting Heart—Abnormal Physical Signs—Remarks 
upon a Rational Method of Outlining the Heart 554 
38-43. Irritable Heart without Organic Heart Disease. 
Remarks Comparing the Irritable Heart in Civil 
Practice with the Irritable Heart of Soldiers 557 
44-46. Vaso-motor Instability and Fainting Attacks from 
So-called Weak Heart—Remarks on “Weak” Heart... 562 
47, 48. Irritable Heart from Physical Overstrain 565 
49-54. Cardiac Neurosis (especially Tachycardia) following 
Febrile Crises. General Comment 568 
55. Irritable Heart in a Patient with Previous Paroxysmal 
Tachycardia 574 
56, 57. Cardiac Neurosis Following Gastro-intestinal Distur- 
bance 575 
58. Cardiac Neurosis—Subjective Dyspnoea 577 
59. Cardiac Neurosis and Pregnancy 578 
Cardiac Neuroses. 
Irritable Heart 
without Organic 
Heart Disease. 
“Weak” Heart. 
Irritable Heart 
from Physical 
Overstrain. Car- 
diac Neurosis from 
Febrile Causes. 
“Irritable Heart.” 
Cardiac Neurosis 
and Pregnancy. 
Exophthalmic Goitre. 
60. Recurrence of Symptoms of Exophthalmic Goitre at the 
Menopause 578 
61. Exophthalmic Goitre with Hypertension 580 
Tobacco Heart 
Irritable Heart with 
Organic Heart Dis- 
ease. 
62-64. Tobacco Heart—General Comment 581 
65-67. "Irritable Hearts” in Patients with Organic Valvular 
Disease. General Comment 586 
Congenital Cardiac 
Lesions. 
68. Congenital Patent Ductus Arteriosus with very Slight 
Cardiac Symptoms 591 
69, 70. Congenital Cardiac Lesion, Probably Patent Inter- 
ventricular Septum 592 
Tachycardia and Col- 
lapse at Parturi- 
tion. 
71. Tachycardia and Collapse at Parturition 595 
Transient Hyperten- 
sion without Or- 
ganic Heart Dis- 
ease or Cardiac 
Symptoms. Hy- 
pertension— D i a - 
b e t e s—V aso -mo tor 
Symptoms. 
72, 73* Transient Hypertension without Organic Cardio- 
vascular Disease or Cardiac Symptoms 596 
74. Hypertension—Diabetes—Vaso-motor Symptoms.... 598 CARDIO-VASCULAR CLINICS—CONTENTS 
507 
Case No. Page 
Climacteric Hyper- 
tension without 
Cardio-v a s c u 1 a r 
Disease. 
75-78. Hypertension at the Menopause without Organic 
Cardio-vascular Disease. General Remarks upon 
Hypertension at the Menopause 599 
Hypertension with- 
out Cardio-vascular 
Disease. 
79, 80. Hypertension and Vaso-motor Instability without 
Cardio-vascular Disease 605 
Extrasystoles 
81, 82. Extrasystoles without Organic Heart Disease 609 
83. Functional Extrasystoles 611 
84. Aortitis and Hypertension—Decompensation—Extrasys- 
toles—Neurosis 612 
Paroxysmal Tachy- 
cardia. 
85-87. Paroxysmal Tachycardia without Organic Disease— 
Report and Remarks upon Two Other Fatal Cases. . . 614 
88. Paroxysmal Tachycardia Due to Gastric Neurosis at the 
Menopause 619 
89. Discussion of Auricular Fibrillation with an Illustrative 
Case 620 
90-92. Discussion, Description and Tabulation of Various 
Types of Auricular Fibrillation with Illustrative 
Cases 625 
93. Aortitis with Attacks of Auricular Fibrillation 633 
94. Myocarditis—Auricular Fibrillation—Decompensation 
—Therapeutic Results 635 
Auricular Fibrilla- 
tion. 
Transient Auricular 
Fibrillation. 
95. Transient Auricular Fibrillation Due to Coffee 636 
96. Auricular Fibrillation from Fright 637 
97. Transient Auricular Fibrillation. Permanent Hyper- 
tension 639 
Cases of Auricular 
Fibrillation Illus- 
trating the Use of 
Quinidin. 
98-104. Cases of Auricular Fibrillation Illustrating the Use 
of Quinidin 641 
Heart Block. 
105. Heart Block 652 
106. Complete Heart Block 656 
107. Complete Heart Block 659 
Heart Block and Au- 
ricular Fibrillation. 
Postmortem Spec- 
i m e n . Remarks 
on the Etiology of 
the Fibrillation. 
108. Heart Block and Auricular Fibrillation. Postmortem 
Specimen. Remarks on the Etiology of the Fibrilla- 
tion 663 
H. R., female, aged eight, has never had scarlet fever, rheumatism or 
growing pains. There is no definite history of tonsillitis or of colds. Seven 
months ago she was supposed to have had “stomach trouble.” She has had 
occasional nose-bleeds. Of late she has been short of breath. 
CASE i—TYPICAL MITRAL REGURGITATION WITH DRY PERICARDITIS 508 
CARDIOVASCULAR CLINICS—CONTENTS 
Examination.—You see, gentlemen, that the child is well developed but 
is somewhat anemic. The systolic blood pressure is 90; the diastolic, 60. 
Inspection of the neck reveals nothing abnormal. Upon observing the chest 
you immediately notice the diffuse, precordial heave caused by ventricular 
systole. In addition to diffuse ventricular activity, palpation also reveals a 
distinct systolic thrill. There is no pain on pressure over the precordium. On 
auscultation you hear a loud, rough systolic murmur over the mitral area; 
this is transmitted to the axilla and over the entire back posteriorly. There is 
also a superficial musical murmur heard over the lower precordium and axilla. 
There is a soft systolic murmur over the aorta. The liver is not palpable. 
There are a few decayed teeth. The tonsils are enlarged. The urine is 
normal. 
In this orthodiascopic tracing, you see an enlarged aorta; the heart is 
enlarged in a downward direction. The fluoroscopic examination does not 
reveal any fluid in the pericardial sac. 
I present this case because the physical signs are so characteristic of a 
mitral regurgitant lesion with dry pericarditis. This combination is particu- 
larly frequent in children. In them pericarditis is often an accompaniment 
of a rheumatic exacerbation; it is apt to disappear with improvement or reces- 
sion of the latter. 
In spite of the absence of any definite history of tonsillitis or rheumatism, 
the great probability is that the child is suffering from the usual type of rheu- 
matic endocarditis. Still, the original infection may have been a slight for- 
gotten tonsillitis or even a catarrhal pharyngitis—the latter can occasionally 
(although rarely) be the starting point of endocarditis. 
Therapy.—For the present, the child should be kept from school but she 
need not be confined to her room. She should have as much fresh air and 
sunlight as possible. She should be given substantial, fattening diet, includ- 
ing a fair proportion of meat. This is also a good time to have her tonsils 
and decayed teeth removed because the lesion is in a quiescent state. The 
final prognosis depends upon the frequency and the severity of future rheu- 
matic or tonsillar attacks. If these be entirely absent or very infrequent 
within the next two or three years, the chances are that the endocardial lesion 
will remain quiescent. Under such favorable circumstances, one may prom- 
ise this child a fairly active and useful life, as far as her cardiac condition is 
concerned. 
CASE 2.—TYPICAL MITRAL REGURGITATION AND PERICARDITIS; RE-EXAMI- 
NATION SIX MONTHS LATER; REMARKS ON TONSILLECTOMY AND EX- 
TRACTION OF TEETH 
H. F., female, aged eight, has had frequent attacks of tonsillitis, “growing 
pains,” and articular rheumatism. She has also had nosebleeds occasionally. 
The family physician informed me that she has had a loud endocardial mur- 
mur for at least eight months. Three days before I saw her she had slight CARDIOVASCULAR CLINICS 
509 
fever, and painful and swollen knees. She now has shortness of breath and 
rapid, heart action. The last attack similar to this one occurred several 
months ago. The child’s weight has been stationary for one year. She 
has been kept on a strict meat-free diet. 
Examination.—The child you see is thin and anemic. Upon inspection, 
rapid heaving and regular ventricular action is plainly discernible. There is 
no pain upon palpation over the cardiac area. The apical impulse is redu- 
plicated, and is felt most prominently in the fifth interspace, three inches 
from the mid-sternal line. On auscultation, the second pulmonic sound is 
accentuated. Over the mitral area you hear a loud, rough systolic murmur, 
which becomes more superficial and more musical toward the apex. The 
systolic murmur is also heard posteriorly. The aortic sounds are normal. 
The border of the liver is felt one and one-half inches below the free border of 
the ribs. There is no edema of the legs. The urine is normal. The tonsils 
are enlarged and look fleshy. Some of the teeth are bad. 
The endocardial lesion is doubtless mitral regurgitation. The localized 
superficial musical murmur in the apical region can probably be regarded 
as indicative of dry pericarditis. Remember that typical to-and-fro friction 
sounds and pleuro-pericardial friction rubs are often absent in pericarditis. 
The only indication may be the superficial murmur, such as you hear so 
markedly in this case. The child is evidently suffering from an exacerbation 
of endocarditis due to the last attack of rheumatism. The pericarditis seems 
also due to rheumatism, for this lesion is often a superadded though temporary 
one. 
The treatment I should suggest is rest in bed for about two weeks, and 
icebags to the heart when the action is rapid and violent. Salicylates are 
also indicated. The question of tonsillectomy and extraction of teeth I 
should hold in abeyance until the lesion has reached a quiescent stage. I 
consider it of prime importance to fatten the child. Starchy and fatty foods 
should be given, as well as some meat. If we succeed in fattening and strength- 
ening the child, the chances are that she will be more resistant to future infec- 
tions. I do not believe that meat should be excluded from the dietary 
for I have never been able to discover any connection between a diet contain- 
ing meat proteins and rheumatic manifestations. As a matter of fact, this 
child has not had meat for months, yet she is now suffering from a fresh rheu- 
matic endo-pericardial process. I believe that over-eating of meat can 
produce faulty metabolism, and can cause various so-called rheumatic 
manifestations, but I see no comparison between such cases (so-called rheuma- 
tism of metabolic origin) and actual bacterial infection, for that is probably the 
nature of rheumatic endocarditis. 
Examination Six Months Later.—The history since the last examination 
states that there has been no epitaxis or rheumatism. The child’s appetite 
has improved. She is now able to play with other children, and to go to 
school. The mother says that there has been no shortness of breath or rapid 5io 
CARDIO-VASCULAR CLINICS 
heart action. The child’s color is now good. There has been a decided gain 
in weight. 
In this present examination you observe that the heart action is of normal 
rapidity when the child is at rest; there is a slight but normal temporary 
increase of cardiac rate after walking. Upon palpation, the reduplicated 
apical impulse (so-called gallop rhythm) felt six months ago has disappeared. 
On auscultation, you hear the same loud mitral systolic murmur as formerly, 
but the evidence of pericarditis—the superficial musical murmur at the 
apex—has disappeared. The orthodiascopic tracing now being passed 
around reveals an enlarged, somewhat ball-shaped heart. This contour is 
caused by an exaggeration and rounding out of the pulmonary, left ventricular, 
and right auricular curves. 
It is evident that the cardiac and general condition is much better than 
when we first examined the patient. Her general appearance is better; there 
is no dyspnoea or tachycardia. The chief difference in the auscultatory 
signs is the absence of pericarditis. This is important not only because of the 
possibility that a localized pericarditis may interfere with proper cardiac 
activity, but principally because it is definite evidence that pericardial infection 
has receded. Quiescence of the endocardial lesion may also be assumed, for, 
although the mitral regurgitant murmur is as loud as formerly, still the gain in 
weight, and attendance at school without symptoms show unmistakably that 
no new endocardial damage has occurred. This is of the utmost prognostic 
importance, for it means that despite the present permanent changes in the 
valves and musculature, there is good ground for hope that the lesion will not 
progress any further, and that rheumatic manifestations will become less 
virulent and frequent. 
The child’s tonsils are enlarged. They look fleshy. I believe that this is 
the appropriate time for their excision. 
What should be our attitude towards tonsillectomy in patients with rheu- 
matic endocarditis? I think the present popular attitude of removing every 
tonsil that looks diseased is far too radical. It does not sufficiently consider 
the fact that tonsils are rarely normal, for they are the lymphatic portals 
through which, because of their position, bacteria of the most diverse kind 
must filter. We should, therefore, use discrimination in our advice regarding 
tonsillectomy. Tonsils that are palpably diseased, as shown by their gross 
appearance, and are, or have been the site of frequent inflammation, require 
thorough removal at the earliest favorable moment. The most propitious 
time is not during an attack of acute or subacute endocarditis, but when that 
process has become quiescent. 
I hold similar conservative views with regard to the extraction of teeth. 
Decayed teeth have been almost indiscriminately accused of being the medium 
for rheumatic and endocarditic infections. Bad teeth, of course, require 
proper dental attention, usually extraction. I do not believe, however, that 
extraction should be practiced more radically because a patient happens to CARDIO-VASCULAR CLINICS 
5ii 
have heart disease. In my own experience, I have not yet discovered that 
people with diseased teeth are especially prone to heart disease. I have, for 
example, found endocarditis in children with sound teeth and gums, as well 
as in those with diseased ones. 
CASE 3.—COMPENSATED MITRAL REGURGITANT LESION WITH VARIABLE 
AUSCULTATORY SIGNS 
J. R., female, aged 25, unmarried, was examined by me for the first time 
two years ago. The history was one of frequent attacks of tonsillitis, for 
which the tonsils had already been removed. She has had nc cardiac com- 
plaints, and no cardiac disease was suspected until two days prior to my 
first examination. She then had a sudden attack of “palpitation” with dizzi- 
ness and vomiting. She had been swimming and roller skating the previous 
day. 
Examination at that time showed a systolic blood pressure of 140; the 
diastolic, 90. Inspection of the chest revealed nothing abnormal. On pal- 
pation, there was a thrill-like systolic impact at the apex; there was no pain 
on pressure. Upon auscultation, there was a blowing, systolic murmur over 
the lower precordium, increased with exercise. There was also a soft systolic 
murmur at the right base. Abdominal examination presented nothing abnor- 
mal. The urine and the knee reflexes were normal; the pulse was regular, 
the rate, 76 per minute. Roentgenological examination showed slight 
enlargement of the aortic and ventricular shadows. 
I regarded the case as one of simple mitral regurgitation. Because of her 
nervous temperament, I advised her to leave the city and to rest for a few 
weeks. Upon her return, the mitral murmur was scarcely audible. 
I have had occasion to examine her two or three times since then for tachy- 
cardial attacks following acute indigestion. The cardiac rate would reach 
120, the heart action, regular. Within twenty-four hours after a good 
purge and an ant-acid powder, the attacks passed off. 
With these previous physical findings and history in mind let us consider 
her latest complaint. Yesterday, she had her usual sick headache from 
indigestion. She felt cold and weak and had occasional palpitation. The 
heart beat fast and regularly for about half a dozen beats. This was succeeded 
by a phase of several slow and irregular beats due to sinus arrhythmia. The 
composite effect on the rhythm may be compared to a horse galloping for a 
few seconds, and then suddenly checked and slowed. Now let us listen to the 
heart. We hear a very loud, blowing systolic murmur not only over the mitral 
area but over the entire anterior surface of the chest; I wish to emphasize the 
fact that the patient has no fever, nor any signs of decompensation. In 
view of my past physical findings—a soft mitral, and faint aortic systolic 
murmur—it will be of interest to re-examine this patient in a few days. For 
the present, without further attempts at diagnosis or of the import of the 512 
CARDIOVASCULAR CLINICS 
murmur we shall give her an ant-acid powder, and small doses of codeine 
for her headache. 
Examination Two Days Later.—The patient says she feels better. She 
has no headache nor “palpitation.” Upon examination the extremities 
are no longer cold. Instead of the loud systolic murmur over the entire 
heart, there is again the soft, faint systolic murmur over the right base, and a 
somewhat louder one over the mitral area. In fact, the murmurs are of the 
same intensity as those I found at previous examinations. The cardiac 
activity is again normal in rate and rhythm. 
How shall we interpret these differences in the auscultatory findings? 
In the absence of fever, and because of the temporary nature of the attack, I 
believe we can exclude recrudescent or recurring endocarditis as their cause. 
We know that mitral systolic murmurs may be not only of organic, but also 
of non-organic (so-called “functional”) origin. In the latter instance, we 
assume that they can be caused by abnormal degrees of dilatibility of the 
mitral ring. In our patient, such a dilatation seemed to have been produced 
by the rapid heart action; this presumably allowed more regurgitation 
through an already damaged valve, and thus increased the loudness and 
propagation of the mitral murmur. Regarding the loud aortic murmur 
present two days ago, unless we believe this to have been due to upward 
transmission of the loud mitral murmur, its cause is difficult to explain. Even 
assuming a dilated aortic ring, this could scarcely be productive of an aortic 
systolic murmur. 
This case is another exemplification of the fact that although murmurs 
are sometimes of great interest, they may after all have but little bearing on 
prognosis and therapy. 
CASE 4.—MITRAL STENOSIS—TYPICAL PHYSICAL SIGNS—RHEUMATIC 
RECRUDESCENCE 
This man, 32 years old, had rheumatism several years ago. He was then 
told that he had “heart trouble.” Except for occasional palpitation, he had 
no symptoms and was always able to work uninterruptedly at his trade as 
clothing cutter. About three months ago he caught a “ cold,” as he expresses 
it, which later developed into severe pains in the right thigh and leg. At 
about the same time he began to complain of shortness of breath, of palpita- 
tion and of slight precordial pains. 
Examination.—You observe that the man is well-nourished, with a some- 
what suffused cyanotic facies. Inspection shows exaggerated ventricular 
action. The pulse and heart action are regular: The rate, no per minute. 
Upon auscultation and palpation, you find at the apex the typical signs of a 
mitral stenotic lesion: A diastolic thrill both audible and palpable. The 
reduplicated second sound, rather typical of mitral stenosis, is absent. The 
liver is not enlarged, there is no edema of the legs. The blood pressure is 
normal. The urine is normal. CARDIO-VASCULAR CLINICS 
5i3 
To judge from the hospital records and from the description of the 
patient’s pains in the thigh he suffered from rheumatic sciatica. What 
caused the sudden onset of cardiac symptoms after years of quiescence? 
It was doubtless the rheumatic recrudescence, of which the sciatica was evi- 
dence, that caused the old valvular lesion to flare up. 
Such recrudescences, actually re-infections, when severe, are often marked 
by irregular fever, by dry or serous pericarditis, by tachycardia, by dyspnoea, 
and by precordial distress. With continued infection and with changes in 
the cardiac musculature as well as in the endocardium, the patient begins to 
show some of the signs of decompensation: Enlargement of the liver, constant 
dyspnoea, brouchitis, edema of the legs, etc. In this stage, auricular fibrilla- 
tion (q. v.) is apt to occur in mitral stenotic lesions, and with it, the special 
physical signs characteristic of that condition. 
The remarks just made refer to severe re-infections. In milder rheumatic 
recrudescences, fever and other evidence of severe infection may be absent, 
or may be slight and fleeting, and, as in this patient, the cardiac complaints 
may be comparatively mild. Such cases are usually improved by salicylates. 
The patients should be kept quiet, although it is not necessary to confine them 
to bed for an inordinate length of time. Some physicians still believe that 
rest in bed for several months is necessary. In a mild case such as this, two 
or three weeks in bed are sufficient. The patient should then be allowed to 
walk around, and, if his occupation be not a very laborious one, he should 
then gradually retrain himself for his work. 
Question.—How long does it take for mitral stenosis to develop? 
Dr. N.*—That depends a good deal upon the severity, the frequency and 
upon the site of the infection. It is the general assumption that it requires 
more than one attack of endocarditis to produce mitral stenosis. One may 
state in a general way that it takes several years for the development of 
marked mitral stenosis. 
Question.—Is it possible to “clear up” an endocardial lesion with 
salicylates? 
Dr. N.—The effect of the salicylates on the endocardium is still in dis- 
pute. Their action, in part at least, is to counteract the toxic effect of the 
rheumatic poison on the endocardium and on the joints. Since we possess no 
other specific at present, I deem it advisable to use salicylates in all cases of 
rheumatic endocarditis during the acute or subacute stages. I am in the habit 
of prescribing salicylate of soda in one gramme doses with compound syrup of 
sarsaparilla as the vehicle, given hourly, until six doses are given or tinnitus 
occurs. I then decrease the dose. 
CASE 5—ACUTE RHEUMATIC ENDOCARDITIS—HEMIPLEGIA—DEATH 
M. L., aged 16, had always been well until several months ago. She then 
developed a typical attack of acute articular rheumatism, with involvement 
of the, larger joints and high temperature. An endocardial murmur was 514 
CARDIOVASCULAR CLINICS 
heard for the first time several weeks ago. With one remission the tem- 
perature remained around 103° for eight weeks. There were irregular chills, 
anorexia and loss of weight. The pulse rate varied between 120 and 140 
per minute. 
Examination.—The patient looks emaciated. She says she has lost 25 
pounds since her illness. The systolic blood pressure is 130; the diastolic, 80. 
Her face is flushed. You note that there is very little dyspnoea. You observe 
the rapid and regular ventricular action through the chest wall, and the 
rapidly pulsating aorta in the jugulum. Upon palpation, the ventricular 
impulse seems diffuse, although the cardiac outline is normal on percussion. 
Such impression of decided enlargement is frequently caused by a rapidly 
beating or overacting heart, although there may be no actual enlargement. 
I have often been able to demonstrate that fact fluoroscopically. Upon 
auscultation you hear a loud, rough systolic murmur over the lower left half 
of the chest; it is also transmitted posteriorly on the left side. There is a 
soft systolic murmur over the aorta. There are no signs of pericarditis. The 
lungs are normal. The heart is regular, its rate is 120 per minute. There are 
no petechiae. There are at present no rheumatic articular manifestations. 
The liver is not palpable. A blood culture and blood count have not yet 
been made. The urine and blood pressure are normal. 
There is, of course, no doubt as to the anatomical diagnosis. The patient 
is suffering from an acute endocarditis affecting the mitral valve. The im- 
portant question to decide is whether the endocarditis is of the ordinary, 
so-called rheumatic type, or of bacterial origin. By bacteria, I mean strep- 
tococci, with actual recovery of the organism from the blood. It must be re- 
membered that one, or even several negative blood cultures do not exclude 
the possibility of a streptococcemia. Since the blood culture was negative in 
our case, we shall have to arrive at a tentative diagnosis by studying the 
general clinical manifestations, and by searching for the usual characteristics 
of a streptococcus viridans bacteremia. We must search for petechiae, for 
renal involvement (especially for the presence of microscopic blood in the 
urine), for a marked leucocytosis and for the usual signs of a severe sepsis: 
Delirium, chills, gastric symptoms, etc. The signs and symptoms just 
enumerated are present only in the more severe and acute forms of a strep- 
tococcic viridans infection. Even then remissions lasting weeks, or, rarely, 
months, may occur. Indeed, in cases in which the streptococcus viridans has 
actually been recovered from the blood, remissions of many months or years 
have been encountered. It is, of course, a question of terminology as to 
whether such long quiescent periods should be called “remissions.” I have, 
for example, observed one case in which, after a violent course of several 
weeks, and with streptococci in the blood, the patient became well. The 
patient re-entered the hospital one year later, with a different complaint: He 
had been well in the interim. It has been stated that certain pathological 
characteristics of the heart and kidneys unquestionably demonstrate that 5IS 
CARDIOVASCULAR CLINICS 
such patients have had healed lesions from an actual streptococcic viridans 
infection. A little consideration of this statement will show that this is by no 
means improbable. The long-continued infection, and the re-invasions so 
frequent in streptococcus viridans, are due to the washing into the blood 
stream of infected material and bacteria from the heart valves. Should these 
valvular vegetations be so protected or so favorably situated that the bacteria 
cannot be readily washed into the blood stream, it seems reasonable to assume 
that an occasional case of an actual stieptococcic invasion will not only be 
quiescent for a long interval, but perhaps give time for actual healing of the 
infected valves. 
To return to our patient, although the onset of the disease is violent and 
this patient is suffering severely from the endocarditic infection, the absence 
of petechiae, of chills, and of delirium make me inclined to consider this case 
one of rheumatic endocarditis of a particularly virulent type. This is, of 
course, of great prognostic importance, since the chances for recovery from 
such an infection are greater than from a streptococcemia. Perhaps, also, the 
anti-rheumatic remedies—the salicylates—will be of help in controlling the 
symptoms. I believe the patient should get enough bromides, and, if neces- 
sary, opiates, to relieve her restlessness and quiet her heart action. Digitalis 
is not indicated because there is no decompensation. 
Later Report.—A few days after you saw this patient, the family physician 
was suddenly called to her at her home. She developed hemiplegia, became 
unconscious and died a few hours later. It is evident that an embolus from 
the heart valve caused her death. 
CASE 6.—MITRAL STENOSIS—SUDDEN ONSET OF VASO-MOTOR SYMPTOMS 
F. F., aged 38, married four years, has never been pregnant. She gives 
no history of rheumatism or tonsillitis. For some years she has had “heart 
burn” relieved by eructations. She has also complained of occasional palpi- 
tation and of shortness of breath when climbing stairs. She is able to walk 
well upon level ground. Three weeks ago, while walking against a strong 
wind, she developed severe mid-sternal pain. Since then, she feels as if she 
were unable to breathe freely and deeply. This, and the mid-sternal pain 
awaken her at night. 
Examination.—The systolic blood pressure is 120; the diastolic is 70. In- 
spection of the chest reveals nothing abnormal. On palpation you feel a soft 
presystolic thrill in the apical region. On auscultation, you hear the typical 
presystolic thrill of mitral stenosis, and a somewhat accentuated second pul- 
monic sound. The knee reflexes are lively. There are no signs of decompen- 
sation. The urine is normal. The orthodiascopic examination shows a heart 
practically normal in outline. 
The history is definite that the onset of the cardiac symptoms directly 
followed walking against a strong wind. Prior to that, there were very few, 516 
CARDIO-VASCULAR CLINICS 
if any, cardiac symptoms. One may of course dismiss this case as one of 
hysteria. But that diagnosis, so readily made and so often a cloak for inexact 
knowledge, will scarcely apply here. The patient states that the attacks 
occasionally awaken her from a sound sleep; that does not sound like 
hysteria. You also doubtless recall similar patients who otherwise bore their 
cardiac disease for years without pain or discomfort, in whom some inad- 
vertance as fright, excitement or unwonted physical effort initiated cardiac 
symptoms. I believe we are here dealing with a similar instance. The 
occasional breathlessness is real, not imaginary. Its explanation however, is 
difficult. I believe it is of vaso-motor origin, and probably depends upon 
transitory changes in the vaso-motor center. One of my reasons for this 
belief is the beneficial effect produced by the extract of suprarenal gland in 
such individuals; it seems to have an immediate, although only temporary 
effect in restoring vaso-motor tone. Another possible cause of the breath- 
lessness may be slight evanescent changes in ventricular dilatibility, which 
may also conceivably be accompanied by dyspnoea. With our present 
limited knowledge, this supposition is not susceptible to proof. 
Therapeutically, I would advise suprarenal gland extract, in 2 grain doses, 
to be given during the attacks. I should also administer mixed bromides in 
15 grain doses three times daily for several days. Depending on its effect, it 
may later be given in smaller doses. The patient should be reassured and told 
that she will positively improve, at first slowly, and then more rapidly. It 
will probably be several months before the symptoms disappear entirely. 
CASE 7.—MITRAL STENOSIS—PULMONARY INFARCT—GASTRIC AND VASO- 
MOTOR SYMPTOMS 
M. A., aged 30, married, has had two children. Both confinements were 
normal. There is no antecedent history of tonsillitis, scarlet fever or rheu- 
matism. Her baby is now nine months old. She had no symptoms which 
pointed directly or indirectly to her heart until three weeks ago. She then 
had an attack of hemoptysis. Since then she has frequent sudden attacks 
of an “empty” and “gone” feeling in the abdomen, and of precordial pains. 
Her pulse, the family physician tells us, has always been regular; its rate, 70 
per minute. There has been no bronchitis. The patient has not vomited; 
she has no desire for solid food. 
Examination.—You note that the patient is well nourished; that her face 
is flushed, and that she has no dyspnoea. Examination of the lungs shows 
the absence of rales and of other signs of pulmonary tuberculosis. An 
examination of the sputum one week ago showed the absence of tubercle 
bacilli. Inspection of the precordium and neck reveals nothing abnormal. 
Palpation and auscultation present typical signs of a mitral stenotic lesion: 
There is a palpable presystolic rumble and a loud presystolic murmur, both CARDIO-VASCULAR CLINICS 
5*7 
most prominent in the apical region. Percussion shows that the cardiac 
outlines are within normal limits. The liver is not palpable; there is no 
edema of the legs; the urine and blood pressure are normal. 
I present this case to you for several reasons. First, because it exempli- 
fies a typical valvular lesion without a definite history of rheumatism, sore 
throat, or scarlet. However, the patient may have had “growing pains” 
in childhood, pains so mild in nature that she has long since forgotten them; 
a mild scarlet may have entirely escaped attention, or one slight attack of 
tonsillitis may have been the original source of the endocardial infection. 
We must also remember that patients of different types give varying heed to 
pains and symptoms, and what one may regard as a serious ailment, the other 
disregards entirely. 
The second reason for presenting the case is that the patient did not know 
she had heart disease until the attack of hemoptysis, which was undoubtedly 
caused by a pulmonary embolism from the mitral stenotic lesion. The patient 
is not suffering from decompensation but since the hemoptysis, various pre- 
cordial, gastric and vaso-motor symptoms have been present. Whether the 
cause of the infarct is to be sought in renewed endocardial infection or in the 
unfortuitous breaking off of an endocardial vegetation, I am not prepared 
to state. I am inclined to the latter view, however, because there are no 
symptoms—fever, sore throat, or rheumatism—suggestive of re-invasion. I 
do not know the exact nervous mechanism involved in the production of pre- 
cordial pains in this case, but it has been my experience that any “ insult” 
or renewed damage to a quiescent cardiac lesion can give rise to precordial 
discomfort accompanied by vaso-motor, gastric and other referred symptoms. 
I shall later point out that there exists an intimate relationship between the. 
stomach and heart nerves, and that excitation of the one set often produces 
excitation in the other. I do not think that the patient is suffering from a 
primary gastritis; the sudden hunger spells, and the feeling of emptiness are 
probably reflex phenomena due to excitation of nerves of the stomach. One 
must also think of the possibility of an embolic infarct in the gastric vessels 
as a cause of the stomach symptoms. I believe, however, that it can be here 
excluded because there is no local epigastric sensitiveness nor has there been 
any hematemesis. The vaso-motor phenomena—flushes—are probably also 
of reflex origin. I recognize that these statements are not susceptible to 
proof; too many links in the chain of evidence are missing; hence I do not wish 
my theories taken too dogmatically. On the other hand my experience with 
other similar cases makes me feel that the explanation given, although hypo- 
thetical, is essentially the correct one. 
The treatment and prognosis in this case are of interest. When vaso-motor 
symptoms of reflex nature (especially when associated with precordial pains) 
are prominent, 1 have found the solid extract of the suprarenal gland in one 
or two grain doses, administered three times daily, to be of great value. 
The gastric symptoms can usually be controlled by giving half a teaspoonful 518 
CARDIOVASCULAR CLINICS 
of an alkaline powder containing equal parts of magnesium usta and bicar- 
bonate of soda after nourishment. Food should be light, should be given 
frequently and in small quantities. Acids, and heavy and greasy meals should 
be avoided. It may be necessary to follow a strict “ulcer diet” for a week or 
two. Digitalis is of no value in this case, and should not be advised. The 
patient should be kept in bed for about a week or two, until the precordial and 
gastric symptoms subside. Later, she may gradually return to her previous 
mode of life and diet. I emphasize “gradually,” because if too much is 
undertaken at first, the symptoms are apt to be aggravated, and convales- 
cence correspondingly retarded. 
CASE 8.—MITRAL STENOSIS—ATYPICAL HISTORY AND SYMPTOMS 
S. A. male, aged 58, states that about four years ago he had “rheumatic” 
pains in the shoulder; these lasted several weeks. He does not remember 
any previous attack. He does not know whether he ever had scarlet fever. 
He had no cardiac complaints until several months ago. The initial symptoms 
were pains in the left chest and some dyspnoea upon walking. He also devel- 
oped gastric symptoms; these consisted of sticking pains in the left, and 
occasionally in the right breast, one-half hour after his meals; his hands would 
then become cold. None of the usual symptoms or signs of indigestion 
were present; no nausea, anorexia, epigastric distress, distension or coated 
tongue. 
A more exact history of the onset of the very first rheumatic attack would 
have been of importance, for the patient’s valvular lesion—mitral stenosis— 
could scarcely have developed, according to his story, within four years, 
without repeated and severe rheumatic attacks and endocardial recrudes- 
cences. The assumption, therefore, seems fair that there had been other 
rheumatic manifestations, overlooked or forgotten by the patient, and ante- 
dating the distinct rheumatic attack of four years ago. 
Physical Examination.—You note that the patient is somewhat dyspnoeic 
when lying down. Upon inspection of the chest you observe the slight 
ventricular hyperaction confined to the apical region. Upon palpation you 
feel the typical diastolic thrill so characteristic of advanced mitral stenosis. 
On auscultation you hear the rumble occupying almost the entire diastole and 
apparently increasing in intensity as it approaches the systole. Following 
the systole, you hear a reduplicated second sound characterized by a sharp, 
valvular double click. In brief, all the classical signs of a mitral stenotic 
lesion are present. I would remind you, however, that you must not expect 
all the text-book signs of valvular disease in every case; if you do you will be 
doomed to frequent disappointments. 
Of great clinical interest is the advanced age of this patient, for it is very 
rare to observe a patient over 50 with mitral stenosis, especially with a normal, CARDIOVASCULAR CLINICS 
519 
rhythmical pulse. Of even greater rarity is the first appearance of any 
cardiac symptom of this lesion so late in life. 
Let us now attempt to correlate the symptoms following the ingestion of 
meals with the chest pains. You recall that there exists a ganglionic 
connection between the gastric filaments of the vagus and the nerves of the 
heart. The exact nerves forming the reflex arc are not known, but we possess 
many clinical observations which demonstrate that cardiac symptoms, e.g., 
dyspnoea and precordial pains, otherwise slight, are often aggravated during 
meals or during digestion. Such chest pains are currently attributed to 
pressure exerted by an overdistended stomach against the diaphragm and 
thus against the heart, with consequent circulatory embarrassment and 
precordial pains. I have made a fluoroscopic study of the stomach in some 
patients with cardiac disease who suffer from the symptoms I am describing. 
In no instance in which I gave opaque meals of bismuth or barium, did I find 
evidence of any undue amount of gastric distension or of pressure against the 
diaphragm. I therefore conclude that neither gastric overdistension nor 
pressure is a factor in the production of precordial pains after meals in these 
individuals. I believe that the precordial pains are caused by excitation of 
cardiac nerves or plexuses that are reflexly stimulated by the gastric filaments 
during the process of digestion. We know that the heart does not contain 
nerves of sensation, but, according to the theory of Head, we assume that 
corresponding spinal segments can be reflexly excited by peripheral irrita- 
tion from an end organ, in this instance, the heart. The spinal segment or 
segments involved then produce centripetal impulses along the spinal nerves 
supplying the skin and muscles of the precordium, which the patient feels as 
pain. To use an analogy, I have observed that, similar to the hypersuscepti- 
bility found in anaphylaxis, the cardiac nerves and spinal segments are 
frequently sensitized, so to speak, a condition which makes them hypersuscepti- 
ble to any neurogenic influence, normal or abnormal. To apply these con- 
siderations to our patient, the vaso-motor symptoms (cold hands) and the 
chest pains, both occurring during the process of digestion, are probably due 
to reflex excitation, in the former, of the vaso-motor center, and in the latter, 
of a spinal segment. 
Therapy.—There is no actual decompensation nor any evidence of 
endocarditic recrudescence. The cold hands, precordial pains, and dyspnoea 
after meals seem due, according to my assumption, to reflex disturbances in a 
“nerve-sensitized” individual with a mitral stenotic lesion. I do not believe 
digitalis is indicated. I shall advise the patient to take a cup of warm milk or 
hot coffee in bed before arising. He should rest for about one hour after 
meals. If the symptoms do not improve, I shall advise him to take one or 
two teaspoonfuls of aromatic spirits of ammonia in water at such times when 
symptoms occur. This simple remedy seems to act favorably by its effect upon 
the nerve filaments of the stomach. 520 
CARDIO-VASCULAR CLINICS 
CASE 9.—MITRAL STENOSIS—HYPERTENSION—NEURASTHENIA 
Mrs. F., aged 32, had chorea as a child. She has had “palpitation” for 
many years, especially when walking up stairs or when nervous. The palpi- 
tation is occasionally accompanied by a tight feeling across the chest. The 
patient has had frequent crying and hysterical spells. She has two children. 
There are no cardiac symptoms during sexual intercourse. She has had a 
good deal of trouble with servants of late, a matter which has upset her and 
brought on attacks of crying. She has always been stout; there has been no 
loss of weight in recent years. 
Examination.—This patient, as you notice, is plump and florid. She 
is even now having a crying spell. This has the effect of causing a pulse 
rapidity of no per minute. Immediately before crying, the rate was normal. 
It seems probable, therefore, that the “palpitation” of wdiich the patient 
complains is due to tachycardia. There is no dyspnoea when she is sitting or 
lying down. Examination of the mouth shows that many of the teeth have 
been filled. Inspection" of the chest reveals nothing abnormal. Onpalpation 
and auscultation, a typical presystolic thrill is felt and heard. There is no 
pain upon precordial or epigastric pressure. You hear a reduplicated second 
sound over the cardiac apex and over the pulmonic; it is more intense at the 
latter site. Over the aorta, there is a very soft systolic murmur which accom- 
panies the first sound; the second sound is somewhat accentuated. Exami- 
nation of the abdomen reveals nothing abnormal. The urine is normal. 
The knee reflexes are normal. There is no edema of the legs. The blood 
pressure reading is surprisingly high; the systolic is 230; the diastolic, no. 
The orthodiascopic tracing being passed around shows a somewhat enlarged 
aorta. The heart lies rather flattened upon the diaphragm; it is slightly 
enlarged to the left, as shown by the X-ray. 
There is no doubt as to the car diac lesion. The patient has a typical mitral 
stenosis. In the absence of any unwonted exertion or excitement, however, 
she has no cardiac symptoms. Indeed, I understand from her family physi- 
cian, that it is only very recently that she was thought to have heart disease. 
The lesion is undoubtedly a quiescent one, for the cardiac symptoms are due 
entirely to the strain of domestic trouble with servants in a pampered individ- 
ual. It shows again how extraneous circumstances can affect a heart lesion 
and can give rise to symptoms. This patient, for example, might have con- 
tinued for a very long time with no more than her previous symptoms of 
occasional tachycardia from stair climbing. She belongs to the type of women 
who are easily ruffled and upset when their menage does not run smoothly. 
They are not the individuals who can “pitch in” and do things themselves. 
They become restive and nervous, a condition which deleteriously reacts upon 
various mechanisms under the control of the nervous system. You recall 
the extremely high blood pressure in this patient, yet there is nothing in the 
cardio-vascular examination to suggest a pathological organic cause for this CARDIO-VASCULAR CLINICS 
521 
extreme hypertension. The arteries are not thickened; the urine is normal; 
there is no edema. A pheno-sulphophthalein test has not as yet been done, 
and it would be hazardous to diagnose this hypertension as being entirely of 
neurotic origin upon only one blood pressure reading, but I shall be much 
surprised if further observation does not show lower and even normal blood 
pressures. Indeed the crying itself may have caused the hypertension. 
Therapy consists chiefly in reassuring the patient and in getting her away 
from her home environment for a while. A short vacation of a week or two 
would be of great benefit. Bromides given in moderate doses for several 
days would also be of value in tiding the patient over the critical stage of her 
nervousness. 
CASE 10.—RHEUMATIC ENDOCARDITIS IN A SYPHILITIC 
Mrs. W., aged 38, has two children. She has had several miscarriages. 
At various times she had luetic ulcers in the mouth and luetic skin lesions. 
She has been on mixed treatment for a long time. Although frequently “nerv- 
ous” and suffering from fatigue, she never had any actual rheumatic mani- 
festations until four years ago. She then had an attack of tonsillitis followed 
by lumbago. Several months thereafter she had a stiff neck, “blood spots” 
over her body (probably purpura hemorrhagica) and two severe attacks of 
migraine. One year later she had a “cold” followed after four weeks by 
irregular chills and by pains in the lower right hypogastrium. Shortly there- 
after she suddenly developed sharp epigastric pains with chills, vomiting, 
fever and jaundice. 
When I first examined her, two days after her attack, the jaundice had 
disappeared. She was dyspnoeic; the temperature was ioi°. Pressure over 
the epigastrium caused pain which radiated to both lumbar regions. There 
was no pain over the appendix or gall bladder region. 
Cardiac Examination.—Inspection and palpation of the precordium 
revealed nothing abnormal. The cardiac area also seemed normal to per- 
cussion. Auscultation at the apex revealed a loud systolic murmur which 
was transmitted laterally to the left axilla. There was a localized pericardial 
friction rub heard over the apical region. The throat was normal. There 
were no purpuric spots on the body. There was no edema of the legs. The 
urine and blood pressure were normal. The Wassermann blood examination 
was positive. Several months later the patient developed nose bleeds and an 
attack of erythema nodosum. 
Present Examination.—Despite the stormy and typical rheumatic history 
lasting over one year, you note that the patient is at present in excellent con- 
dition. She is not dyspnoeic; she says she can again take up her household 
work; she can walk well without losing her breath. There is still a loud sys- 
tolic murmur over the mitral area. There are no signs of pericarditis or 
decompensation. 522 
CARDIOVASCULAR CLINICS 
There are two points of especial interest in the previous history: Syphilis 
and rheumatic infection. In view of the definite and typical rheumatic his- 
tory and of the present typical mitral regurgitant lesion, and because of the 
absence of any active syphilitic lesion during the course of the rheumatic 
attack, I have no doubt that the endocarditis is of rheumatic origin. Further 
evidence of this is the absence of aortic involvement, the usual cardiac affec- 
tion in syphilis. The endocarditis has reached a quiescent stage; this probably 
accounts for the excellent cardiac condition of the patient. Mitral regur- 
gitant lesions, when quiescent and not re-infected, are especially prone to 
allow the heart to carry on the circulation almost normally, despite crippling 
of the valve. Such a favorable status naturally also depends upon the con- 
dition of the musculature. For example, if there be extreme ventricular 
hypertrophy, or if upon clinical grounds, there is assumed to be infiltration of 
the myocardium with submiliary nodes (Aschoff’s bodies), cardiac power will 
suffer, cardiac reserve power will be diminished, and dyspnoea and other signs 
of heart failure will appear. Questions regarding prognosis in cardiac dis- 
eases always involve not only the amount of damage and the cardiac status, 
but also the state of activity of the lesion. The latter cannot usually be 
decided by physical signs alone. In the case before us, for example, the 
physical signs indicate simply a rheumatic affection of the mitial valves. 
The history, however, becomes a fair prognostic guide. You recall that 
endocarditis began after many months of rheumatic manifestations. There 
have been no rheumatic or cardiac symptoms since that time. There is at 
present no decompensation; the heart is apparently not enlarged. In other 
words, we must assume that the endocardial infection has been inactive for 
some time, that the damage to the musculature has been minimal, and that 
the cardiac power is practically normal. There must of course be some reser- 
vation as to what might happen to this heart in the future. From my 
experience with similar cases, I believe the main danger lies in the possibility of 
a rheumatic endocarditic recrudescence. Such a process often lights up dor- 
mant and quiescent lesions. It may then rapidly lead to death either by 
causing embolic infarcts into important organs, or more slowly, by initiating 
a progressive train of symptoms, from mild myocardial insufficiency to fatal 
heart failure. On the other hand should no infection occur, the patient may 
live comfortably and perhaps as long with, as without, the mitral lesion. I 
do not believe that a luetic infection superimposed upon the present lesion 
need be feared, in spite of the positive Wassermann reaction. The latter 
simply means that there exists an active luetic focus somewhere in the body. 
Were the heart the site of this focus, evidence of an aortitis ought to be 
present by this time. 
Regarding therapeusis, I have at no time given the patient digitalis, 
because decompensation was never present. Besides, digitalis is rarely of 
value when the heart is the seat of an active inflammatory process. Main 
therapeutic reliance was placed upon the salicylate of soda which I gave at CARDIOVASCULAR CLINICS 
523 
first in 15 grain doses hourly for 8 doses, and then in decreased quantity and 
at longer intervals. When the heart action was rapid I gave codeine, com- 
bined with the bromides alone or together with chloral. In other words I 
attempted to treat the infection with the drugs at our command. I say 
“drugs” advisedly, because I have seen no beneficial effects in similar cases 
from stock or autogenous vaccines of various kinds, nor from the use of silver 
salts intravenously, as more recently recommended. Rheumatism is very 
probably of bacterial origin, although the specific organism has not yet been 
positively identified. And if the bacterium be a streptococcus, as is gener- 
ally assumed, we have no grounds for believing in the present state of our 
experience with vaccines that they will in any way influence, control, or 
curtail the infection. 
CASE 11— DOUBLE MITRAL LESION—ACUTE PERICARDITIS WITH EFFUSION- 
CLASSICAL SIGNS AND SYMPTOMS 
R. W., male, aged 16, has had “heart trouble” for ten years. The 
only cardiac symptom during the entire time was occasional dyspnoea 
when running. He has had attacks of articular rheumatism every spring. 
One week ago he had a sore throat accompanied by pain in the legs. A day 
thereafter he had severe dyspnoea, chills, fever and pain in the right nipple 
region when breathing. 
Examination.—You note that the boy is orthopnoic; he has to sit straight 
in bed in order to breathe with any comfort. Upon inspection, you observe 
the diffuse precordial heave and the throbbing carotids. Upon palpation, 
you feel a typical presystolic thrill at the apex, indicative of mitral stenosis. 
Upon percussion, I want you especially to note, besides enlargement of the 
entire cardiac area to the right and left, the small but definite area of dullness 
in the second and third left interspaces. Upon auscultation, there are heard 
a loud systolic, and a rough and rasping presystolic murmur. In addition, 
you hear the to-and-fro friction rub over the lower sternum, the classical sign 
of pericarditis. The liver is not palpable. There is no edema of the legs. 
The pulse is regular, the rate, 120 per minute. The systolic blood pressure is 
140; the diastolic, 80. The urine is normal. The throat and teeth are 
normal. The present temperature is 103 °. 
I present this case in contrast to the last (Case 10), because of its many 
typical features. The history of regular attacks of rheumatism and tonsilli- 
tis, the typical signs of a double mitral lesion with pericarditis, the breathing, 
the sharp onset of the present invasion preceded by a sore throat, all are 
characteristic features of rheumatic endocarditis with an acute recrudes- 
cence. What is of especial interest, perhaps, is the area of dullness in the upper 
left interspaces already pointed out to you. That is most probably indicative 
of fluid in the pericardial sac. Fluid in the pericardium is by no means readily 
recognized; indeed, of all lesions, it most often evades our most painstaking 
efforts at diagnosis. It has been shown experimentally that at the beginning, 524 
CARDIOVASCULAR CLINICS 
fluid accumulates at the base of the heart around the great vessels. When 
the effusion is massive, it may produce dullness in the upper left interspaces 
as in this case. More often, however, dullness cannot be elicited, even when 
the fluid begins to fill up the lower part of the sac. This may be because 
such fluid is apt to sag posteriorly instead of anteriorly; or because dullness 
caused by it cannot be distinguished from that of the heart itself. Perhaps 
differential dullness can be more readily elicited in those instances in which 
the heart is not enlarged, and the pericardial fluid is disproportionately 
massive. Even roentgenograms often fail to demonstrate the presence of 
fluid, for a definite double shadow—roentgenographic evidence of pericardial 
effusion—is by no means always present. Clinically, we must often rely upon 
the presence of the dry pericardial friction rub, and upon the course of the 
invasion, for our diagnosis. If the former is present, the invasion febrile 
and stormy, and the patient young, the great chances are that fluid in varying 
amounts is present in the pericardial sac. This is borne out by many autopsy 
examinations. In addition, we find clinically that dyspnoea is often present 
and that convalescence is prolonged, even when the physical signs of dry peri- 
carditis have disappeared. In other words, when definite differential dull- 
ness cannot be elicited, we must be guided by the severity of the invasion, by 
the prolonged convalescence, and by the pericardial friction rub. The latter 
is rarely absent throughout the entire disease. 
I believe that the boy will weather this attack of pericarditis despite its 
stormy onset. I shall put him on large doses of salicylate of soda for the next 
few days. I shall give him sufficient bromides, and if necessary, codein, 
in order to quiet his pain and dyspnoea. The probabilities are that the signs 
of dry pericarditis and of fever will disappear in several weeks. Blood cul- 
tures will also be made, although my past experience with many similar cases 
has been that the culture is negative. Of course, when this invasion is past, 
the signs of endocarditis—the double mitral lesion—will still be present. 
CASE 12—DOUBLE MITRAL LESION—DECOMPENSATION— 
STREPTOCOCCEMIA 
H. G., aged 15, was said to have had a “heart murmur” three years ago. 
There was no definite history of rheumatism, scarlet or tonsillitis. The boy 
had always been able to run and play until three months ago, when cardiac 
symptoms appeared for the first time. The main complaint -was dyspnoea. 
The family physician told me that at that time the patient’s liver was 
enlarged and that it pulsated. He vomited, but had no fever. His pulse was 
rapid, the rate 140 per minute. Two days ago petechiae appeared upon 
the chest. He has been vomiting almost continually since then. 
Examination.—You note that the boy is emaciated and orthopnoic. He 
is somewhat drowsy. You note also the enlarged and tortuous jugulars. 
You observe the tremendous diffuse precordial systolic heave of the entire 
lower and left lateral half of the chest, indicative of extreme ventricular CARDIO-VASCULAR CLINICS 
525 
hypertrophy. The left side of the chest is much more prominent than the 
right. This in itself would indicate hypertrophy rather than dilatation. 
Upon palpation, you feel a diffuse pulsation and a distinct systolic thrill. 
Upon auscultation, you hear a loud double mitral murmur transmitted mainly 
to the left. You also hear a superficial friction sound in the second left 
interspace, indicative of dry pericarditis. The pulse rate is 70 per minute. 
The liver is enlarged, its lower right border is one inch below the umbilicus. 
You can also see the liver pulsate quite distinctly. There is slight edema of 
the legs. The urine is scanty and contains albumen and casts. The anterior 
surface of the chest is sparsely covered with little hemorrhagic spots which do 
not disappear upon pressure; these are petechiae. 
It is of course evident that the patient is suffering from extreme heart 
failure; the orthopncea alone is sufficient evidence of that. If the facts of the 
history be correct—namely, that a heart murmur, and therefore presumably 
that heart disease existed for but three years, there has been exceptionally 
vast damage to the heart muscle in that comparatively short time, especially 
in view of the absence of cardiac symptoms until three months ago. The 
present streptococcic condition is demonstrated by the petechiae, which can 
be regarded as undoubted clinical evidence of such infection. I emphasize 
clinical, for a single or even several bacteriological examinations of the blood 
may not recover the invading organism. Its recovery from the blood 
depends not only upon frequency of blood cultures but also upon the number 
of the invading organisms, and the latter can only be approximately guessed 
at by the severity of the clinical manifestations and the amount of petechias. 
Invasions with the streptococcus viridans is not unusual in severe endocarditis 
and is often a terminal event. 
The drowsiness and vomiting may be nephritic in origin, the result of renal 
congestion or bacteremia. The renal condition may be aided by the adminis- 
tration of a Murphy drip of 5 percent, glucose solution containing bicarbonate 
of soda; this would not only aid the kidney function, but would also supply 
fluid to the body and help combat a threatening acidosis. Digitalis may also 
be of some advantage. But because of the advanced heart disease with the 
added bacterial infection, I believe the case is hopeless and will probably 
end fatally in a short time.* 
CASE 13.—MITRAL REGURGITATION—CORONARY (?) INVOLVEMENT OF 
UNDETERMINED ORIGIN 
Gentlemen.—We are fortunate in having the advantage of a careful 
history and the results of several prior examinations in this interesting case. 
The history is as follows: 
R. R., male, aged 39, a dentist, is married and has two children. He had 
gonorrhea many years ago. A Wassermann blood examination taken seven 
* The patient died within a week of this examination. 526 
CARDIO-VASCULAR CLINICS 
years ago was negative. He has never suffered from rheumatism and only 
very rarely from tonsillitis. Eight years ago he was operated upon for gan- 
grenous appendicitis. Six years ago a gastro-enterestomy was done for 
duodenal ulcer. He has had no gastric complaints since the last operation. 
About two years ago he was accepted for an increase in life insurance, so that 
he very probably had no obvious signs of endocarditis at that time. 
The cardiac history begins with the statement that about a year and a 
half ago a friend of the patient, a physician, noticed that his finger nails were 
somewhat cyanotic. The patient at that time, however, had no cardiac 
complaints nor did a cardio-vascular examination then made disclose abnor- 
mal or other signs. About one year ago and again eight months ago, the 
patient suffered from sudden severe midsternal pains radiating to the back. 
These attacks lasted several hours; they were not accompanied by dyspnoea. 
Again a cardio-vascular examination revealed nothing abnormal: No mur- 
murs, no decompensation; the urine was noripal; there was no fever. The 
attacks were regarded as being probably of gastric origin. In the interim 
between attacks and until several months ago, the patient felt perfectly 
well and was able to attend to his work. He then began to suffer from 
dyspneic attacks which, with intervals, have continued up to the present 
time. Coincident with the dyspnoea an endocardial murmur was heard for 
the first time. The first dyspneic attack was accompanied by a temperature 
of ioi° which lasted several days. 
The patient states that he cannot climb stairs or walk rapidly without 
having dyspnoea and tachycardia. Two or three months ago cultures from 
tooth sockets were made and the streptococcus viridans was isolated. 
Several teeth were extracted upon the theory that these had some 
relation to his cardiac disease. No improvement followed the extraction. 
Now let us examine the patient. The man you observe is well nourished. 
When sitting quietly, dyspnoea is not noticeable. The systolic blood pressure 
is 120; the diastolic, 90. Upon inspection and palpation, you note ventricu- 
lar overaction in the mitral area. The carotid and jugular pulsations are 
normal. There is no pain on precordial pressure. Upon auscultation you 
hear a loud, somewhat musical murmur over the lower precordium; it 
is transmitted to the left and is unaffected by respiration. The other 
sounds are normal. The orthodiascopic tracing, as you see, shows a normal- 
sized aorta. The left ventricular and right auricular curves are enlarged. 
The electrocardiogram of this patient is also of some interest and importance. 
Note that the rhythm is normal; all the deflections are small and the ven- 
tricular deflection in lead III is marked by being splintered and by its abnor- 
mal width. These characteristics are strongly suggestive of myocarditis. 
Except for scars of previous operations the abdominal examination reveals 
nothing abnormal. The liver is not palpable. There is no edema of the legs. 
The knee reflexes are almost entirely absent. The pupillary reflexes are 
normal. There is no ataxia or Rhomberg symptom. CARDIOVASCULAR CLINICS 
527 
It is apparent that the patient is suffering from a mitral regurgitant lesion 
with heart failure: You observed, for example, that even when he walks slowly 
about the room dyspnoea becomes quite marked. The subjects of special 
interest are the etiology of the endocarditis and of the previous severe 
substernal attacks of pain, and the therapy to be applied. 
I believe the usual causes of endocarditis—rheumatism and tonsillitis may 
be excluded in this individual. Another Wassermann examination should 
be made to exclude syphilis, although neither the history nor the type of 
lesion point to syphilis. Nor do I regard the teeth as a possible causative 
factor despite the discovery of the streptococcus viridans in cultures from 
tooth sockets. It has been demonstrated that this organism is by no means 
an infrequent harbinger in the mouths of persons with normal hearts. I 
believe the importance and frequency of tooth infection as a source of endo- 
carditis have been tremendously overrated. And even in rare instances where 
this etiology can be definitely established, it is in my opinion still an open 
question as to how much good can be accomplished by routine extraction in 
an assumed hemotological infection which has already damaged the cardiac 
valves, although of course extraction seems indicated in such cases. 
In view of the previous abdominal operations on our patients one must 
naturally attempt to correlate a possible post-operative infection with the 
present endocarditis. But the operations have so long antedated the cardiac 
symptoms, and the abdominal and gastric condition is now so satisfactory 
that, in the light of our present knowledge such correlation can only be 
regarded as hypothetical. 
In occasional instances of marked cardio-sclerosis, the coronary arteries 
seem to be the first point of attack; and as evidence of this, the symptoms of 
such patients begin with attacks of precordial pain before other marked 
manifestations of cardiac disease present themselves. So also in this case, to 
judge from the history and subsequent course the first of the cardiac structures 
to be attacked were presumably the coronary arteries, for I believe the pre- 
vious attacks of precordial pain must be regarded as very probably of coro- 
nary origin. Even the cyanosis of the finger nails, months before the actual 
cardiac symptoms began, may have been a precursor of disturbance of the 
circulation antedating more obvious signs and symptoms. 
The prognosis must be regarded as exceedingly grave because we are 
probably dealing with a progressive, non-quiescent process; because of the 
more or less constant dyspnoea; and because of the significant evidence of 
probable hypertrophy and myocarditis revealed by the X-ray and electro- 
cardiogram. Should the endocarditis subside or yield to therapy, the 
patient may be comfortable for a number of years. 
Therapjq however, does not offer much to this individual. I would recom- 
mend a mixture containing the salicylate of soda and the mixed bromides 
with some simple syrup as a vehicle. The bromides are meant to quiet the 
heart action. The salicylates are given upon the possibility that the endo- 528 
CARDIOVASCULAR CLINICS 
carditis is of rheumatic origin. I expect no benefit from its use here but I feel 
that it is due the patient to administer remedies even empirically, so long as 
they do no harm. Digitalis is not indicated just now because the dyspnoea 
is probably caused by insidious advance of the inflammatory process in the 
endocardium and myocardium. Yet its use can do no harm. Should a 
Wassermann blood test be strongly positive, we would then naturally have 
some assurance that appropriate antiluetic treatment would be followed by 
excellent results. 
CASE 14.—AORTIC REGURGITATION—TYPICAL PHYSICAL SIGNS 
L. J., male, aged 26, married, for many years has had attacks of fever twice 
yearly, unaccompanied by catarrhal manifestations. He has had no sore 
throat nor cough. He is a moderate cigarette smoker. Aside from the fever 
spells and one attack of gonorrhea several years ago, he has always considered 
himself well. He has always been athletic and has never had any cardiac 
complaint, except occasional “pounding” of his heart when lying upon the 
left side. His work is now sedentary. 
Examination.—The systolic blood pressure is 130; the diastolic, 25. You 
note that the patient lies down and walks without dyspnoea. You observe 
the overacting carotids and the over-pulsatile rise of the tissues in the jugulum. 
You observe also the strong ventricular impulse shown by overaction in the 
mitral area. There is no pain on pressure over the precordium. There is a 
suggestion of a palpable systolic thrill in the apical region. Upon auscul- 
tation, there is a loud diastolic murmur heard especially over the left base and 
transmitted downward. At the apex, there is heard a short, presystolic 
murmur. You likewise feel the typical collapsing, so-called Corrigan pulse; 
this becomes more evident by feeling the radials when the patient’s arms are 
extended above his head. The abdomen presents nothing abnormal. The 
urine and knee reflexes are normal. There is no edema of the legs. The ton- 
sils are small; the teeth are in excellent condition. A Wassermann blood 
reaction was negative; a complement fixation test for gonorrhea was also neg- 
ative. The orthodiascopic tracing, a copy of which you see, shows that the 
aorta is slightly enlarged and that the left ventricle is enlarged to the left and 
below. It would have been interesting to have you observe the aortic over- 
pulsation in the fluoroscope, a condition which always gives the impression of 
a very much enlarged vessel. 
I show this patient because the physical signs of aortic regurgitation are 
so characteristic. The murmurs of aortic regurgitation are occasionally so 
indistinct that, if the pulse be not of the characteristic collapsing type, a 
diagnosis of aortic regurgitation may be almost impossible. One may then 
compare the arm and leg blood pressures; in aortic regurgitation, the differ- 
ence between the leg and arm systolic pressures is much more than in 
normal individuals. CARDIOVASCULAR CLINICS 
529 
The infection which produced the aortic lesion in this case is obscure. 
Clinically there is little reason to doubt that the semi-annual febrile out- 
bursts have some etiological connection with the lesion, but their exact 
nature—whether of tonsillar, rheumatic or other origin—cannot be deter- 
mined from the patient’s description. Treatment for the present must, if 
possible, be preventative. I shall allow the patient some exercise, because 
the lesion is quiescent, there is no decompensation, nor are there any cardiac 
symptoms. I shall limit his smoking, because the latter may initiate 
abnormally rapid heart action or make the patient more likely to get precordial 
pains. I shall later explain my view of the effect of tobacco upon the heart. 
I shall allow the patient to play golf occasionally and to do a moderate amount 
of walking, but I shall warn him against running and excitement because of 
their possible effect in inducing rapid heart action. Once tachycardia, no 
matter from what cause, occurs in aortic regurgitant lesions, it becomes a 
troublesome symptom and is difficult and tedious to control. 
Patients with aortic disease often do well until about their fortieth year. 
They then are apt to develop streptococcic viridans infections. I am as yet 
uncertain whether it may not be wise to vaccinate such patients with strepto- 
coccus viridans in their earlier years, in order to minimize this danger if 
possible. Stock vaccines would of course have to be used. A series of 
injections would probably have to be repeated every two to three years, the 
chances being that the immunity would not last longer than two years after 
each series of injections. 
CASE 15.—AORTIC REGURGITATION—MITRAL REGURGITATION—ACUTE DRY 
PERICARDITIS 
Gentlemen.—This little girl is nine years of age. The mother says that 
the child had a distinct attack of articular rheumatism of two weeks duration 
when she was three and one half years old. There was no evidence of car- 
diac involvement then, the mother tells us, for the physician at that time 
carefully and regularly examined the child. Later the diagnosis of heart 
disease was made. As a consequence the child has been kept quiet and rarely 
allowed to romp about. Several months ago the child complained of head- 
ache and of pains in her hands and feet for several days. The little patient 
herself never made any complaint about her heart until about one week ago. 
She then had fever and said that her left side hurt her. 
Examination.—You observe that the child is somewhat undersized and 
anemic. She is not dyspneic. You note the exaggerated ventricular action 
in the left nipple region. Because of the thin chest walls you may even 
observe the overacting pulmonary artery at the second left interspace. On 
palpation, you feel an exaggerated ventricular impact in the apical region and 
the click of pulmonary valve closure in the second left interspace. The 
sounds heard upon auscultation are confusing and require careful study 
for their proper interpretation, especially since the heart beats irregularly. 530 
CARDIOVASCULAR CLINICS 
We shall disregard the arrhythmia for the present and attempt to unravel 
the various murmurs and adventitious sounds. Let us start with the mitral 
area. There we hear a systolic murmur which accompanies but does not 
replace the first sound; the murmur is transmitted slightly toward the left 
axilla. There is also a somewhat superficial friction rub heard at the apex at 
the extreme end of inspiration. In addition, there is a short presystolic mur- 
mur heard only over the left nipple. Over the right base the first sound is 
normal and the second is continued into a soft diastolic murmur. Over the 
left base the first sound is normal and the second pulmonic is markedly accen- 
tuated; this is the sound which caused the palpable click already referred to. 
The second pulmonic is immediately followed by a diastolic murmur some- 
what louder than the one on the right side; the murmur tails away toward the 
cardiac apex. I believe we are dealing with two distinct valvular lesions; 
aortic and mitral regurgitation. The former has caused the diastolic murmur 
over the right and left base with transmission downward; the murmur is more 
distinct upon the left than upon the right side-—a not unusual occurrence. The 
aortic regurgitation is also the cause of the short presystolic murmur at the 
apex, a so-called Flint murmur. You may ask, why may not the latter be 
caused by a mitral stenotic lesion? Several facts speak against this suppo- 
sition. First, mitral stenosis is very rare in children. Second, there is 
absence of a palpable diastolic thrill at the apex. Third, there is no redu- 
plicated second sound so common in mitral stenosis. There is something to be 
said as to whether the left sided diastolic murmur may not be due to relative 
insufficiency of the pulmonary valves. This produces the so-called Graham- 
Steele murmur which is also diastolic in time and is transmitted along the 
left sternal border. I believe however, the Graham-Steele murmur can be 
excluded because we have unmistakable evidence of closure of the pulmonary 
valves in the sharply accentuated second pulmonic sound. 
Let us now study the arrhythmia. By listening at the apex and feeling 
the pulse, you note that every systole produces a corresponding pulse wave; 
that is, there are no pulse intermission or so-called “missed” beats. The 
heart pulsates at an increased rate for several seconds, then at an abnormally 
slow rate for three or four beats, to be followed by a pause comprising an 
interval of about two normal systoles. In this silent cardiac interval there 
are no jugular or carotid pulsations, a fact which you may determine by 
scrutinizing the neck. We may therefore exclude extrasystoles as 
well as the rarer arrhythmia known as blocked auricular beats. I believe 
that we are dealing with sinus arrhythmia, here sufficiently marked to 
occasionally block out an entire auriculo-ventricular sequence, i.e., a 
complete heart beat. This is known as sinus block or sino-auricular block 
and is ordinarily but an extreme degree of sinus arrhythmia.* 
* An electrocardiogram which I took some days later showed marked sinus 
arrhythmia. CARDIO-VASCULAR CLINICS 
531 
To Summarize.—A child of nine with a typical rheumatic history only 
recently complained of left-sided precordial pain. Examination revealed 
pleuro-pericarditis, aortic and mitral regurgitation, sinus arrhythmia, and 
perhaps also sinus block. There were no signs of decompensation. Perhaps 
some of the physical signs will become less marked as the acute endo-peri- 
carditis subsides, for physical signs are usually more pronounced during the 
acute stage, become less distinct and may indeed entirely disappear during 
the quiescent period. 
The prognosis for this attack is excellent because the child has no fever 
now, and despite the murmurs, there are at present no cardiac symptoms 
and no decompensation. I wish to emphasize here the important distinc- 
tion between physical signs and the actual cardiac condition of a patient. 
The former may be and indeed usually are of extreme diagnostic and prog- 
nostic importance, and of great scientific interest; yet, as in this case, they 
may furnish only an insufficient clue to the efficiency of the heart. Loud 
murmurs do not necessarily mean severe heart disease, nor do faint ones mean 
slight heart disease. In other words physical signs form only a part of the 
clinical picture and examination, and must always be correlated with other 
data, such as can be gathered from a careful history, from the patient’s 
symptoms, and from the actual state of the circulation. For instance, if a 
patient be dyspnoeic, or have edema, or an engorged liver, or cannot walk 
stairs without becoming inordinately short of breath, that patient has some 
severe cardiac lesion, whether typical murmurs be present or not. Regarding 
medication for this child, I shall advise salicylate of soda in five grain doses 
three times daily for about one week. She should be kept in bed for about 
two weeks; thereafter if there be no untoward symptoms, she may gradually 
begin to walk around, and perhaps at the end of a month, she may again go to 
school. It is necessary to give the child as much fresh air and sunlight as 
possible and to feed her up. It is of great importance to have her gain several 
pounds by proper dieting, for children thus fattened bear their disease much 
better than those of substandard weight, and the increase of weight is itself a 
good index that there has been general improvement. 
CASES 16, 17, 18.—RHEUMATIC AORTIC STENOSIS AND REGURGITATION; 
BOVINE HEARTS—REMARKS UPON GASTRO-INTESTINAL SYMPTOMS IN 
PATIENTS WITH AORTIC LESIONS 
Gentlemen.—I present these three patients together because their histo- 
ries and physical signs are similar, because their hearts are typical bovine or 
ox-hearts, and because in addition they have attacks of severe and widely 
distributed pains. 
Case 16.—J. J., male, aged 32, states that his mother told him he had 
“palpitation” when five years old. Since the age of ten, he has had fre- 
quent precordial thumpings and pounding, especially upon exertion or when 
excited. He has had articular rheumatism frequently; the last time one year CARDIOVASCULAR CLINICS 
532 
ago. He often has attacks of what he considers indigestion, with eructation 
and belching. He also has attacks of chest pains and rapid heart action, 
which wake him up from sound sleep. In addition to these attacks, he has 
occasional spells of nocturnal pains, in which he has to “shake himself” for 
hours in order to get rid of the pain. He has had several attacks of consti- 
pation so severe that his family physician says they resemble intestinal 
obstruction. 
Examination.—Upon feeling the radial, you note that the pulse is of the 
typical Corrigan type, the sudden collapse of the radial becomes more evident 
by raising the patient’s arm above his head. The blood pressure reading 
corroborates the collapsing pulse; the systolic being 105; the diastolic, o. 
You notice the tremendously throbbing carotids, the aorta in the jugulum 
and even the subclavians. You can see the immense precordial systolic heave 
which occupies the lower half of the left chest. Upon palpation, you readily 
feel the systolic thrill over the aorta in the second right interspace as well as in 
the jugulum, and the carotid thrill in the neck. You feel the jerky, diffuse 
ventricular impact almost as if the apical thrust were split up into several 
waves. Upon auscultation, you hear a very loud, rasping systolic murmur 
not only over the aorta, but also over the carotids and upper half of the right 
chest. The same murmur is transmitted posteriorly in the right and left 
interscapular regions. There is also a loud diastolic murmur, most intense 
over the right base, and transmitted with less intensity along the left border 
of the sternum. At the apex a soft systolic and a soft diastolic murmur are 
heard. There is no sensitiveness upon precordial pressure. The pulse is 
regular, the rate 80 per minute. The liver is not enlarged, there is no 
abdominal sensitiveness. There is no edema of the legs. The urine is 
normal. 
Summarizing the physicial data, we find that the patient has an old rheu- 
matic double aortic lesion, with tremendous left ventricular hypertrophy. 
The murmurs over the mitral area are probably referred from the base. 
We shall reserve the discussion of the abdominal symptoms and the 
“shaking” attacks until we have completed a brief study of the succeeding 
two cases (Cases 17 and 18). 
Case 17.—A. S., aged 26, male, married, says that he knows of no infec- 
tion except measles, although he does recall that ten years ago he had pains 
in the legs lasting two weeks. His work consists in carrying heavy bundles. 
He smokes about ten cigarettes daily. The first cardiac symptoms consisted 
in occasional rapid heart action while at work. For four years he has had fre- 
quent peculiar night attacks. They would start with midsternal pains 
radiating to the back, accompanied by belching and sometimes vomiting. He 
would then have to get up and “stretch,” and the pain would not be relieved 
until it passed “down the chest.” The attacks lasted minutes or hours; 
they were usually followed by tachycardia. Neither diet nor exercise seemed 
to influence the onset nor the severity of the attacks. CARDIO-VASCULAR CLINICS 
533 
Examination.—As in the previous case you note that this patient is tall 
and spare. The physical signs also are quite similar in both: The typical 
Corrigan pulse, the throbbing carotids and aorta, the immense precordial 
heave, the systolic thrill over the right base, aorta and over the carotids, the 
diastolic murmur heard over the right base and along the left sternal margin, 
the thrill-like jerky ventricular impact, the massive ventricular hypertrophy 
and the nocturnal attacks of pain. There is no precordial or epigastric 
tenderness; no edema of the legs. The urine is normal. 
Case 18.—I. L., aged 20, had articular rheumatism, with remissions, from 
his sixth to his eighth year. He has rarely had rheumatic attacks since then. 
He has had “heart trouble” for ten years. Until two years ago the symp- 
toms consisted mainly in rapid heart action without dyspnoea. During the 
last two years, he has had peculiar attacks with increasing frequency. These 
are usually preceded by a day or two of anorexia and lassitude. The attack 
itself is usually nocturnal and is ushered in by a feeling of epigastric pressure 
which then radiates to the back, abdomen and legs. It is frequently accom- 
panied by tachycardia. There is no vomiting. The pressure gives way to 
pain which becomes extremely intense, so much so that he literally writhes 
in agony as he actually did in one attack in which I saw him. Pressure 
over the abdomen seems to bring him some relief; for example, in the attack 
of which I speak, I found the patient’s mother actually lying across his abdo- 
men with her full weight. There is no precordial distress or vomiting during 
the spell. Mild attacks last several hours; severe ones, two to three days. 
It requires about a week for thorough recuperation and return to his old status. 
Examination.—You observe how tall and lanky this boy is. The physical 
signs that you will find upon inspection, palpation, percussion and ausculta- 
tion are quite similar to those of Cases 15 and 16. 
It would be difficult to find a group of three patients with double rheuma- 
tic aortic lesions, in whom the physical findings Were more similar or classical. 
The murmurs, the tremendous ventricular hypertrophy, the youth of the 
patients, the throbbing carotids and aorta, and the Corrigan pulse are the 
outstanding features. 
It has always puzzled me to understand why the aortic valves become the 
site of such severe rheumatic disease in some young individuals. The 
patients we have just examined are of the thin, graceful type, with graceful 
rounded and slender extremities. Such individuals are regarded by some as 
belonging to the “lymphatic” type, with hypoplastic vessels and heart. If 
that be so, one can conceive that such substandard cardio-vascular systems 
may the more readily become the site of rheumatic infection. My own exper- 
ience has been that the majority of severe rheumatic aortic cases in the male 
belong to this lymphatic type. 
What caused the attacks in Cases 16, 17 and 18 with their accompanying 
phenomena? If rheumatic manifestations such as tonsillitis and articular 
pains had directly preceded the attacks, one might assume an added infective 534 
CARDIO-VASCULAR CLINICS 
insult to the heart as the primary agent. But such a history is absent. 
Rheumatic manifestations had not recently been present in any of the 
patients. From the history and course of the attacks, dietary indiscretions, 
excitement, and streptococcemia could also be excluded as etiological factors. 
What appears to me as the fundamental cause and the most likely one, is a 
continued progressive pathological change either in the cardiac muscle or in 
the endocardium. Where the damage is already as wide-spread as in these 
cases, and proper cardiac functioning is, even at its best, tremendously handi- 
capped, increasing destructive changes need not necessarily be severe in order 
to still further compromise the circulatory mechanism. For example, inter- 
ference with the coronary arteries by the hyperacting aorta or even their 
possible partial temporary occlusion by the massive weight of the heart 
might sufficiently alter the intracardiac circulation to evoke painful attacks. 
In addition, patients with marked aortic lesions are extremely susceptible 
to extraneous influences, such as excitement, as well as to pathological insults 
to the endocardium and myocardium. There apparently exists a hyper- 
susceptibility of the nerve mechanism controlling the heart, brought about 
by constant excitation of the rich nerve supply surrounding the root of the 
aorta; this is caused by the tremendous hyperpulsatile activity of that vessel 
with consequent continued mechanical excitation of its surrounding nerves. 
Thus morbid impulses are sent to the corresponding dorsal segment of the 
spinal cord, and a vicious reflex arc is set up between the diseased aorta on 
the one hand, and a hyperexcitable spinal segment on the other. 
It is such reasoning, admittedly theoretical in part, which I believe best 
explains the various phenomena exhibited by Cases 16, 17, and 18 during 
their attacks. For example, in Case 16 the intestinal symptoms were such 
as to sometimes resemble intestinal obstruction. Spastic constipation has 
often been ascribed to changes in the nerve control of the intestines; indeed, 
such patients have occasionally been operated on for intestinal obstruction 
although no mechanical cause has been found at operation. I believe the 
intestinal symptoms in Case 15 which always began with palpitation, con- 
stitute an instance in which the intestinal nerves became reflexly excited. In 
Case 17 the symptoms were those of esophago-spasm—sharp, midsternal pains 
radiating to the back, accompanied by belching—while in Case 18 the pains 
consisted of exceedingly severe intestinal colic. It is interesting to note that 
in all three, the patients attempted various mechanical procedures in order 
to relieve the pain: Shaking the body, the pressure on the abdomen, walking 
up and down. 
CASE 19.—BEGINNING RHEUMATIC DOUBLE AORTIC LESION—CONTINUANCE 
OF THE LESION DESPITE TONSILLECTOMY 
C. W., male, aged 7, has had ‘growing pains’ for the last two years. The 
mother is positive that he has had only one attack of tonsillitis. One year 
ago both tonsils were removed. Soon thereafter he developed measles, CARDIO-VASCULAR CLINICS 
535 
and a few weeks later, frequent attacks of rheumatic pain in the knees and feet. 
These attacks were accompanied by fever lasting several days, and by an 
itching rash somewhat resembling measles. The child has been kept in 
bed for his heart and rheumatism for several weeks at a time. It is important 
to emphasize that the child himself does not complain of a single cardiac 
symptom. 
Examination.—This stocky youngster as you see does not impress one as 
being ill. His teeth are in good condition. Upon examining the pharynx, you 
observe that both tonsils have been radically removed. Upon inspection 
of the neck and chest, you notice the over-active aorta in the jugulum; there 
is also some cardiac hyperactivity noticeable in the apical region. Upon 
auscultation you hear a distinct systolic and diastolic murmur over the base 
of the heart, especially to the left. Both murmurs are transmitted slightly 
downward. At the apex, you hear a slight short presystolic murmur; this is 
probably the so-called Flint murmur. The remainder of the physical exami- 
nation reveals nothing abnormal. The knee reflexes and the urine are nor- 
mal. There is no edema of the legs. You find upon palpating the knees 
that both are somewhat tender, probably from a mild rheumatic process now 
present. 
The orthodiascopic tracing being passed around shows a large and 
abnormally broad aorta. There is also moderate left ventricular hyper- 
trophy. This is evident not only from the enlargement to the left but also 
from the contour of the left ventricle which is almost square in shape. It is 
evident that the boy is suffering from a double rheumatic aortic lesion. My 
main reason for presenting him is to have you observe the effect of the tonsil- 
lectomy. Just how large the tonsils were before operation we of course do 
not know. The history states definitely that the child has had but one attack 
of tonsillitis during his whole life, so that unless some marked, gross change in 
the tonsils had been present, I question the advisability of tonsillectomy after 
one attack of tonsillitis. You also recall from the history that soon after 
the tonsils were removed, the child suffered from rheumatic attacks. We 
know that such rheumatic attacks are apt to be accompanied by exacerba- 
tions of endocarditis. One may therefore speculate as to whether the opera- 
tion did not do real harm instead of good. As I have already pointed out to 
you in discussing other cases, I feel that nowadays tonsillectomies are done 
much too often with the idea of controlling rheumatic infections and endo- 
cardial lesions. In cases which suffer frequently from tonsillitis or in those 
in whom the tonsils are particularly enlarged and look ragged and fleshy, 
tonsillectomy is no doubt indicated. But the time for doing the operation 
must be properly chosen, for if done during the active stages of endocarditis, 
or when rheumatic manifestations are still active, it may be followed by just 
such rheumatic and endocardial recrudences as we see in this boy. The 
operation should be done, if at all, when rheumatic and endocardial manifes- 
tations have ceased for some weeks or even months. The fact that practi- 536 
CARDIO-VASCULAR CLINICS 
cally every tonsil, when removed, shows some disease should cause no surprise, 
for lymphoid tissue situated at the portal of the pharynx must almost of 
necessity show some pathological change. Palpably diseased tonsils or those 
frequently inflamed should of course be removed, but as just pointed out, the 
time chosen for operation should be a properly chosen one, during a quiescent 
period of endocarditis if possible. 
CASE 20.—TYPICAL LUETIC AORTITIS 
A. F., male aged 55, says that ten years ago he had gonorrhoea lasting 
several weeks. Some years ago, he was abed with “rheumatism,” which 
lasted about a month. He had previously smoked as many as fifty cigarettes 
a day; at present, he smokes ten daily. For the last two years, he has had 
gradually increasing attacks of dyspnoea accompanied by precordial pains 
which radiate to the left arm. The attacks occur especially when he is 
aggravated, when walking in the cold air, or after sexual intercourse. He 
sleeps well at night. His appetite is good. He has not lost weight. 
Examination.—You notice the patient is well preserved and is not dysp- 
noeic when at rest. The radial arteries do not feel thickened, the pulsation 
is equal on both sides. Upon raising the arms above the head you note a 
tendency to the water-hammer pulse. The systolic blood pressure is 140; 
the diastolic is 40. Upon inspection you observe some overaction of the 
carotids. The aortic pulsation is not visible or palpable in the jugulum. 
Upon palpation there is no precordial sensitiveness, nor is there any abnormal 
pulsation over the mitral or aortic area. Upon auscultation over the right 
base you hear a typical double aortic murmur, a rough systolic and a loud 
diastolic, both of which are transmitted downward to the cardiac apex. 
Except for this transmitted murmur, the sounds at the apex are normal. 
There is some tenderness to pressure over the epigastrium. The edge of the 
liver is palpable slightly below the free border of the ribs. The pupillary 
light reflexes are sluggish. The knee jerks are normal. There is no edema 
of the legs. The urine is normal. The orthodiascopic tracing, as you readily 
observe, shows marked enlargement and broadening of the first part and 
arch of the aorta. The left ventricle is only slightly enlarged. The Wasser- 
mann blood reaction is 4 plus. 
I have presented this case to you chiefly because the physical signs are 
so typical of aneurismal dilatation of the aorta. A double aortic murmur 
in a middle-aged individual is in itself suggestive of syphilitic aortitis. A 
rheumatic double aortic lesion without marked ventricular hypertrophy is 
rare in the middle-aged. This case illustrates a fact that I have often observed, 
namely, that extensive ventricular hypertrophy is by no means a necessary 
accompaniment of luetic aortitis; it may be present or the ventricles may be of 
normal size. On the other hand, the aorta is involved in almost every case 
of cardiac syphilis. CAKDIO-VASCULAR CLINICS 
537 
The therapy required in this patient is obvious. He should be put upon 
iodides and mercurial injections. He should also be given salvarsan injec- 
tions, at first in small, later, in full doses. If the treatment be continued, 
the prognosis is good; the precordial pains and dyspnoea will probably 
disappear within several weeks. The aortic enlargement is permanent, but 
if further luetic inflammation be controlled and the disease be not far 
advanced, all the symptoms will probably recede. 
CASE 21—SYPHILITIC MYOCARDITIS—CARIES OF TEETH—GINGIVITIS— 
PYORRHCEA—REMARKS UPON THE CONNECTION BETWEEN HEART 
DISEASE AND PYORRHCEA 
Gentlemen.—This man is forty-seven years old. He has been married 
eighteen years, his wife has never been pregnant. He had gonorrhoea many 
years ago; he denies syphilis. He had double pneumonia at one time. Five 
years ago he had “rheumatism” in the muscles of the shoulder and forearm. 
For the last seven years, there has been sugar in his urine in amounts up to 
i per cent.; it is always readily controlled by proper diet. He had trouble with 
his teeth for many years; at various times he has been treated for pyorrhoea. 
All of the teeth of the lower jaw have been extracted; there is considerable 
bridge work in the upper. Despite local treatment by good dentists, pyo- 
rrhoea is still present. Cardiac symptoms began about two years ago. 
These consisted chiefly in a feeling of oppression on the chest, of dyspnoea, 
and of frequent expectoration of blood-stained sputum. He has also had 
several attacks of sudden dyspnoea with expectoration of frothy sputum. 
He has had epigastric pain and tenderness for several months; these symptoms 
were ascribed to indigestion by his family physician. 
Examination.—As the patient removes his set of lower false teeth, you 
note that the gums of the lower and upper jaw are spongy; they bleed readily, 
pus can be squeezed out of the upper tooth sockets. ' The patient is slightly 
dyspnoeic when at rest, the respiration rate is 25 per minute. He looks well 
nourished. Inspection of the precordium reveals nothing abnormal. Upon 
palpation we note there is slight overaction in the apical region, there are no 
abnormal pulsations over the right base or in the jugulum. Superficial or 
deep pressure over the heart elicits no pain or sensitiveness. Auscultation 
reveals a normal first sound over the right base, the second aortic is-somewhat 
metallic in character. At the apex, with the patient sitting up, the first and 
second sounds are distant and indistinct; when the patient lies down, you note 
the increased dyspnoea; the cardiac rate rises to 100 per minute. When the 
patient is in the recumbent position, you hear at the apex, typical “gallop 
rhythm,” a generic, and, I believe, an unscientific name given to any redu- 
plicated sound. In our case I think the gallop rhythm is due to a redu- 
plication of the first sound, a matter of some importance in establishing the 
diagnosis of myocarditis. The cardiac area is somewhat enlarged to per- 
cussion. The systolic blood pressure is 130; the diastolic, 60. The lower 538 
CARDIO-VASCULAR CLINICS 
border of the liver is palpable two inches below the free border of the ribs. 
There is distinct epigastric tenderness to pressure. The knee reflexes are 
normal. There is no edema of the legs. The urine is normal. There are a 
few scattered rales at the bases of both lungs. The radials at the wrist are 
not thickened. 
You observe that in this case there are but few physical signs upon which 
to base even a generic diagnosis of heart disease, let alone of myocarditis. 
We must therefore depend chiefly upon the symptoms and the history. The 
prominent symptom is dyspnoea, especially upon walking. There is nothing 
in the lung examination, urine or blood pressure which sufficiently accounts 
for the dyspnoea. The frequent hemoptyses, and the attacks of extreme 
dyspnoea and frothy expectoration no doubt indicate edema of the lungs of 
varying severity, and point to the heart as their cause. 
What are the physical findings which substantiate myocarditis? As 
already stated, the physical findings are merely suggestive, not definite. 
They consist in slightly rapid heart action, especially with the patient in a 
recumbent position; in distant heart sounds and in the reduplicated first 
sound at the apex (so-called gallop rhythm). These physical signs are in 
themselves not sufficient evidence upon which to base a diagnosis of 
myocarditis, but they must be studied in conjunction with the history and 
symptoms. I consider the so-called “indigestion” and the epigastric sensi- 
tiveness valuable evidence, not of gastric but of heart disease. I have fre- 
quently found such signs in other frank cases of cardio-vascular disease. 
Indeed I am always suspicious of cardiac, not of gastric disease, if, when 
coupled with dyspnoea a patient complains of “indigestion,” or has epi- 
gastric pains when walking as well as on abdominal palpation. Such pains 
are commonly ascribed to pressure of the stomach against the diaphragm and 
the heart. My roentgenographic studies of such cardiac cases with opaque 
barium meals have led me to believe that the pains are not caused by such 
assumed pressure of the diaphragm against the heart, for I have often found 
the stomach small and hypertonic, containing only small, normal amounts 
of air; hence undue pressure against the diaphragm could scarcely be a factor 
in disturbing the circulation. Although I possess no definite proof, my clin- 
ical observations incline me strongly to the belief that most cases of epigastric 
pain with heart disease are instances of referred and reflex phenomena having 
their origin in the heart. 
I am usually loath to call a case myocarditis unless there are other unmis- 
takable evidences of severe cardio-vascular disease: Such as frank decompen- 
sation, hypertension, cardiac hypertrophy, aortitis, etc., but I believe the 
symptoms and history of the present case are sufficient for the diagnosis of 
myocarditis, without other evidence. 
Etiology.—Here again this patient is of great interest, because the only 
apparent cause for the disease lies in the condition of the gums and teeth. I 
belong perhaps to the small minority who feel that the role of the teeth as the CARDIOVASCULAR CLINICS 
539 
cause of heart disease has been tremendously overestimated. I have seen 
heart disease as frequently in those with, as in those without decayed teeth 
and pyorrhoea. It is one thing to find all sorts of pathogenic and pyogenic 
bacteria in the gums and carious teeth, and another, to prove that these have 
entered the blood stream or have produced toxins and thus cardiac damage. 
On the other hand, occasionally one cannot deny the possible etiological con- 
nection between a pus focus in the mouth and heart disease. I believe, how- 
ever, that in every instance, connection between heart disease and carious 
teeth must be definitely proven, before a patient can be said to have heart 
disease from bad teeth. The case before us seems to offer no other cause for 
the myocarditis than the foul condition of his mouth. His “rheumatism” 
several years ago may well have come from the same cause. I shall, however, 
have a routine Wassermann blood test made to exclude syphilis as a possible 
etiological factor. 
Report and Examination Two Months Later.—You recall, gentlemen, this 
case of myocarditis that I demonstrated to you several weeks ago. You 
recall also that I believed this a rare instance in which pyorrhoea was the 
probable etiological factor of heart disease. Two days after you saw this 
man, I had a Wassermann blood test done; the report stated that it was 
4 plus. I immediately put the patient upon vigorous anti-luetic treatment— 
iodide of potash in increasing doses, intra-muscular injections of salicylate of 
mercury and salvarsan intravenously. He has had three doses of the latter, 
the first dose was two decigrams and the others were six decigrams each. 
He no longer has any dyspnoea, he can now walk rapidly, as you see, without 
shortness of breath, the blood-tinged morning expectoration has ceased; even 
his gums and pyorrhoea are much improved in spite of frequent mercurial 
injections. The physical signs of the heart are about the same, except that 
the heart is not as rapid, and you hear the reduplicated first sound only after 
exercise. The case, therefore, gentlemen, is one of syphilitic myocarditis— 
the positive Wassermann and improvement under anti-luetic treatment have 
proven that. Despite the history and the condition of this man’s mouth, our 
protean friend, syphilis, is after all the cause of this patient’s heart disease. 
CASE 22—AORTIC ANEURISM AND AURICULAR FIBRILLATION 
M. F., male, aged 47, a hard-working individual, had never complained 
of his heart until three months ago. He then had “ palpitation.” The 
doctor who saw him at that time says that the patient had an attack of edema 
of the lungs. Since then he has been unable to work because of tachycardia, 
dyspnoea and epigastric distress when walking. He denies any gonorrhoeal, 
luetic, rheumatic or tonsillar infection. The only previous illness he remem- 
bers is a slow healing ulcer of the leg following a trauma some years ago. 
Examination.—You observe that the patient is slightly short of breath 
even when at rest. On looking very carefully with the eye on the level of the 
chest, you note a slight pulsatile rise in the second and third right intercostal 540 
CARDIO-VASCULAR CLINICS 
spaces. There is no pain on precordial pressure. In the apical region you 
feel the irregular ventricular activity—strong and weak, fast and slow beats 
following each other with no regularity. The pulse is also quite irregular. 
This irregular pulse and heart action is typical of auricular fibrillation. Upon 
auscultation you hear a soft systolic murmur over the second, third and fourth 
right interspaces; but I want you especially to hear the resonant, twanglike, 
accentuated second sound over this same area. There is no diastolic murmur 
over the right base. The sounds over the mitral area are normal. The 
systolic blood-pressure of most of the effective beats is around 190; the dias- 
tolic, around 130. The liver is not palpable. There is sensitiveness to 
pressure in the epigastrium. There is no edema of the legs. The urine is 
normal. 
How shall we interpret the physical signs? Let us attempt to do so 
even before we fluoroscope the patient. I believe that the pulsatile rise of the 
tissues in the right intercostal spaces, combined with an accentuated second 
sound over the same area is indicative of aneurismal enlargement of the 
first portion of the aorta; the enlarged aorta acts here somewhat as a resonator 
or sounding board in producing the accentuation. 
Fluoroscopy discloses as you see, much more enlargement than I had 
suspected. There is not alone aneurismal dilatation of the first portion of 
the aorta, but there is a large sacculated aneurism of the first portion, arch 
and descending thoracic aorta. The left ventricle is only moderately 
enlarged. The process is undoubtedly luetic. We shall get a Wassermann 
report of the blood in a day or so. 
How shall we explain the fact that the patient had been able to work for 
years and then was suddenly attacked with pulmonary edema and subsequent 
decompensation? I believe that the actual cardiac complaints date from the 
onset of fibrillation, for to judge from the size of the aneurism, the lesion 
must have been a steadily progressive one. Without a more exact previous 
history than we have been able to obtain, it is impossible to state the cause 
of fibrillation. However one may well imagine the final involvement of some 
vital cardiac structure such as the coronary arteries, as the culminating cardiac 
“insult” which produced the arrhythmia. I do not believe that there is 
sufficient myocarditis present to cause auricular fibrillation. The X-ray does 
not show massive ventricular enlargement; and progressive myocarditis 
would probably have been accompanied by signs or symptoms of decompen- 
sation long ere this. 
Dating probably from the occurrence of fibrillation, we have the sudden 
change of a man with a very large aneurism without cardiac complaints to 
one who is now dangerously ill. It is necessary to emphasize again a proper 
understanding of the importance of slow progression of an organic disease. 
Thus this aneurism was undoubtedly of many years steady growth. But 
it had not caused any undue pressure upon surrounding structures, and, to 
judge from the absence of cardiac symptoms, there has been no inflammatory CARDIOVASCULAR CLINICS 
54i 
exacerbations; the only handicap the heart and circulation had suffered was 
the purely physical one of sacculation of the root and arch of the aorta. 
You recall the fluoroscopic picture of only moderate ventricular enlarge- 
ment. In my experience, I believe that the degree and constancy of ven- 
tricular hypertrophy which accompanies aortic aneurism has been very much 
overestimated. Indeed, I have examined patients with large aneurisms in 
whom there was no appreciable ventricular enlargement. The usual im- 
pression of huge hypertrophy is doubtless gained by the exaggerated ven- 
tricular thrust against the chest wall during systole, and by the low and 
forward position of the ventricles which are commonly crowded downward 
and to the left by large aneurisms. 
Later Report.—The Wassermann report came back 2 plus. The patient 
was placed upon large doses of the tincture of digitalis. Salvarsan injections 
and mixed treatment were to have been instituted by the family physician 
in a few days. Before proper treatment could be carried out the patient had 
a sudden severe attack of epigastric pain, vomited and died within a few 
minutes. Coupled with the previous history, the cause of death seemed due 
to a coronary infarct. 
CASE 23.—LUETIC AORTITIS—CONSTANT PRECORDIAL PAIN 
I present this case in contrast to Case 22 because constant and long 
continued pain is the main symptom. 
H. P., male, aged 44, complains of very severe, almost constant substernal 
pain for two years. When pain is especially severe, it radiates to the left arm 
and back and is accompanied by dyspnoea. The attacks are occasionally 
relieved by nitrite of amyl. In addition the patient often finds it necessary to 
take 24 of a grain of morphine sulphate every night. The last Wassermann 
reaction was 4 plus. He has had six neo-salvarsan injections with no effect 
upon the symptoms or upon the cardiac status. The urine contains a trace 
of albumen but no casts. 
Examination.—You readily see, even from a distance, the throbbing caro- 
tid and brachial arteries. The systolic and diastolic pressures of the right 
and left brachials are respectively, 170-20, and 150-40. The patient is now 
having one of his usual attacks of pain. We shall immediately give him 
five minims of nitrite of amyl contained in a pearl, and study its effect upon 
the blood pressure. The systolic blood pressure in the right arm has fallen 
to 100. This fall is but momentary, lasting as you note, just one minute; 
none the less, the inhalation seems to have afforded the patient some relief, 
for he says that he feels better and that his attack is over. Upon inspection 
of the chest you observe the pulsatile rise of the aorta in the jugulum, and the 
tremendous ventricular hyperactivity. These observations are readily 
confirmed upon palpation. Upon auscultation you hear a rough, rasping first 
sound over the right base and in the jugulum, and a markedly accentuated 
and resonant second sound over the right base. The orthodiascopic tracing 542 
CARDIO-VASCULAR CLINICS 
being passed around shows aneurismal dilatation of the first part and arch of 
the aorta, and extreme left ventricular hypertrophy. The electrocardiogram 
shows normal rhythm with evidence of left ventricular preponderance—a 
negative deviation in the third lead. The liver is palpable but not tender. 
There is no edema of the legs. 
In contrast to the previous case (Case 22) this patient has been suffering 
from almost continuous precordial pain for two years. He uses as many as 
one dozen 5 minim nitrite of amyl pearls daily, and although he fights against 
the use of morphine as much as possible, he finds it necessary to take one dose 
at night time, otherwise the pain becomes unbearable. 
The diagnosis is of course plain: The patient has an aortic aneurism and 
marked left ventricular hypertrophy. The direct source of the pains seems 
to be due to involvement of the coronaries; this etiology appears more prob- 
able by the relief the patient finds in amyl nitrite. 
The outlook for the cure of the precordial pains seems remote. Thorough 
anti-luetic treatment has brought the patient no amelioration. This prob- 
ably means that the cardiac tissue, especially the coronaries, have reached 
such a stage of sclerosis that they can no longer be influenced by anti-luetic 
therapy. However I shall advise proper digitalization of the patient in the 
hope, rather than the expectation of helping the intra-cardiac circulation. 
Mixed bromides in large doses, and tablets containing nitro-glycerin and 
atropine sulphate will also be advised. 
Later Report.—The family physician reported to me that the patient 
was not benefited by the medication and is still clinging to amyl nitrite and 
morphine. 
CASES 24, 25, 26.—SENILE CARDIO-SCLEROSIS—LOUD SYSTOLIC MURMUR 
OVER THE ENTIRE ANTERIOR SURFACE OF THE CHEST-GENERAL COM- 
MENT 
I shall first present to you a brief history of each of the three cases, after 
which we shall discuss in detail the peculiar and interesting physical findings 
of all. 
Case 24.—C. L., male, aged 68, suffered from moderate dyspnoea at the 
time of hospital admission. The systolic blood pressure is 130: The diastolic, 
100. The urine contains a trace of albumen. The cardiac rhythm is normal; 
the rate between 76 and 80 per minute. Over the entire middle anterior 
aspect of the chest, you will hear a loud, rough systolic murmur transmitted 
slightly to the left axilla and along the carotids. The roentgenogram reveals 
an aortic arch almost twice the normal width, and a somewhat enlarged left 
ventricle. 
Case 25.—M. C., female, aged 64, complained of cough and dyspnoea. 
Six months prior to hospital admission she suffered from some precordial 
distress, the exact nature of which could not be determined. The tempera- 
ture was 1020; there was moderate dyspnoea; and there were physical signs CAKDIO-VASCULAR CLINICS 
543 
of general bronchitis. The fever and bronchitis lasted two weeks. Upon 
examination, you wall find that the cardiac area is somewhat enlarged to 
percussion; a loud, rasping, systolic murmur is heard over the entire precor- 
dium; it is especially intense over the right base. The murmur is transmitted 
along the carotids and laterally to the left axilla. It is also heard as a 
muffled systolic bruit posteriorly in the upper interscapular region. The 
systolic blood pressure is 220; the diastolic, 140. The urine contains a moder- 
ate amount of albumin and some hyaline casts. The roentgenogram reveals 
not only slight dilatation of the aortic arch but also aneurismal dilatation 
of the entire descending thoracic aorta. The latter as you see is a prominent 
shadow on the left side of the chest from the second to the fourth left inter- 
space; at that point it is lost behind the shadow of the left ventricle. 
Case 32.—J. M., male, aged 66, complains of epigastric pain, dizziness, 
headache and sdme dyspnoea. There are old scars, possibly syphilitic, on 
the forearm. The lungs appear normal. Over the entire precordium you 
hear a loud, rough systolic murmur. The cardiac area is somewhat enlarged 
to percussion. A roentgenogram reveals moderate enlargement of the aortic 
arch. The cardiac rhythm is normal. The systolic blood pressure is 135; 
the diastolic, 95. The urine contains a slight trace of albumin. 
I am grouping these cases because, as you observe, they present the same 
auscultatory phenomenon, namely, a loud, rough, systolic murmur which is 
heard over the entire anterior surface of the chest. 
Perhaps I had better define the conception—cardio-sclerosis—because it is 
apt to be loosely used. When I use this term I refer to marked pathological 
changes involving the cardiac muscle, the valves, the aorta, and the coronaries 
and their branches. The damage is by no means equally distributed among 
these structures; frequently the aorta and the coronary system are chiefly 
affected. 
To return to our patients. You observe they all possess the usual 
characteristics of generalized arterio-sclerosis; thickened, palpable and 
tortuous arteries. Pulsation of the aortic arch in the jugulum is a prominent 
visible and palpable physical sign in all. 
The systolic murmur—the special reason for presenting these three 
cases—is rough and loud, and is heard over the entire front of the chest. 
Its areas of greatest intensity are over the right base and the lower precordium. 
It is also transmitted along the carotids and the lower left axilla. In Case 25 
it is heard posteriorly as a soft, muffled sound in the upper interscapular 
region. 
After but a casual examination, one may be inclined to ascribe the murmur 
to the presence of a large sacculated aneurism or to aneurismal dilatation of 
various parts of the aorta. Both types of aortic enlargement, however, are 
usually accompanied by diastolic, as well as systolic murmurs, the area of 
greatest intensity being over the right base of the heart. In aneurismal 
dilatation of the descending thoracic aorta—a rare, isolated condition—one 544 
CARDIOVASCULAR CLINICS 
usually finds the double murmur loudest in the third left interspace near the 
sternum; from this location, it tails away toward the apex and base. This 
characteristic is absent in Case 31. In cardio-sclerosis, the loud systolic mur- 
mur is heard with or without aortic enlargement; the diastolic murmur is 
absent. In addition, careful auscultation reveals a marked difference in the 
intensity of the murmur over the precordium. It is very loud over the right 
base, losing in intensity over the midsternum, again becoming louder at the 
cardiac apex and to the left. It thus seems as if the murmur is made of two 
components—an aortic and a mitral. The former is probably caused by 
such arterio-sclerotic changes as deformities and thickening of the wall of the 
aorta. The mitral component of the murmur may be ascribed to the char- 
acteristic degenerative changes affecting the mitral valve and the mural 
endocardium of the mitral ring, with consequent production of a typical 
mitral regurgitant murmur. The aortic and mitral components are both 
systolic in time; hence, when the pathologic changes are of the gross nature 
above outlined, a loud systolic murmur results, which may be of fairly equal 
intensity over the entire front half of the chest, or there may be an area of 
less distinctness and intensity over the midsternum. 
CASES 27, 28—CARDIO-SCLEROSIS IN THE MIDDLE-AGED—LOUD SYSTOLIC 
MURMUR OVER THE ENTIRE SURFACE OF THE CHEST 
Case 27.—C. H., female, aged 50, buxom in appearance, has had three 
children and no miscarriages. For years she suffered from severe rheumatic 
(?) neuralgic headaches. For one year she had precordial oppression and 
attacks of severe precordial pain radiating to the jaw, back and left arm. A 
rest cure lasting several weeks brought no relief. The blood Wassermann is 
negative. 
Examination.—The systolic blood pressure is 170; the diastolic, no. 
The report of the blood chemistry states that the non-protein nitrogen and 
other constituents of the blood are normal in amount. You notice that there 
is no dyspnoea when the patient is at rest. On palpation, slight overaction 
of the carotids and of the aortic arch is evident. Over the right base, you 
hear a loud, rough systolic murmur transmitted along the carotids; it is also 
heard posteriorly in the mid-dorsal region to the right of the spine. Below, 
anteriorly, it becomes less intense and is merged with an extremely loud sys- 
tolic murmur, most prominent and distinct over the mitral area. The ortho- 
diascopic tracing reveals an enlarged aortic arch and a somewhat globular 
and enlarged left ventricle. 
Case 28.—A. B., a physician, aged 54, of vigorous appearance, con- 
tracted nephritis following a grippe infection about twenty years previously. 
Cardiac complaints began about four years ago. They at first consisted of 
occasional hemoptysis and of slight dyspnoea. Of late months the dyspnoea 
has increased and is accompanied by a sense of weight on the chest. The 
Wassermann blood reaction is negative. CARDIO-VASCULAR CLINICS 
545 
Examination.—You observe that the apex beat is diffuse. Over the entire 
anterior aspect of the chest you hear a loud, muscial systolic murmur, most 
intense over the right base and the lower precordium; it is least intense over 
the midsternum. It is transmitted along the carotids, and is also heard pos- 
teriorly at the third dorsal vertebra. The orthodiascopic tracing reveals an 
enlarged aorta as you see, and a hypertrophied left ventricle. 
I am briefly demonstrating these two middle-aged patients in the same 
group with the three patients of the senile cardio-sclerotic group (Cases 24, 
25, 26) for in both the physical signs are the same, except that the thickening 
and tortuosity of the radials and temporals are absent in these middle-aged 
cases. Indeed, to judge merely from the facies, both patients, C. H. and 
A. B., appear in robust health and give no inkling of the profound cardiac 
disease we find upon examination. Their comparative youth speaks for the 
fact that the pathological inroads upon the heart took place at a relatively 
rapid rate, thus apparently causing more serious and progressive loss of the 
normal cardiac functions.1 
CASE 29.—CARDIO-SCLEROSIS—REMARKS ON THE CAUSE OF SYMPTOMS IN 
SENILE CARDIO-SCLEROSIS 
Mrs. E., aged 73, gives the following history. She has had five children, 
no miscarriages. She had pneumonia twelve years ago. She does not recall 
any other acute illness. While a young woman she suffered from attacks of 
diarrhoea for two years. She finally developed gastric symptoms: Belching, 
eructations, and a dry, irritating cough; the latter was often accompanied by 
belching. Since five years, she has what she describes as a cold feeling in the 
left chest anteriorly. This feeling is often relieved by belching. Several 
weeks ago, she had a severe hemorrhage following the extraction of a tooth. 
She has always been active in business, attending to her work as a designer 
for years. Five weeks ago, immediately after moving a heavy piece of furni- 
ture, she experienced a sudden sharp pain in the left breast. Since then she 
has a “faint,” sore feeling in the left chest, is dyspnceic and has occasional 
“palpitation.” The precordial sensations are often relieved by belching. 
Examination.—You observe, gentlemen, that this elderly patient is well 
preserved, with the keen and active intelligence of a much younger person. 
Yet even superficial inspection shows marked evidence of general arterio-scle- 
rosis, as well as of cardio-sclerosis. The temporal and radial arteries are 
j visibly and palpably thickened. Inspection reveals overacting carotids, and 
l| a pulsatile heave of the tissues in the jugulum from the overacting aorta. 
As I raise the left breast, you observe the diffuse precordial heave due to the 
enlarged heart. The apex beat is markedly displaced, being near the axillary 
line in the sixth interspace. Upon palpation the ventricular impulse is felt 
as a diffuse overforceful shock. There is a small area in the left precordium 
1 Both patients died of edema of the lungs within a few months of the time they were 
demonstrated. 546 
CARDIO-VASCULAR CLINICS 
that is sensitive to moderate pressure. Upon auscultation over the right base 
the first sound is rough, the second, bell-like. Over the apex there is a 
systolic murmur accompanying the first sound. There is slight edema of the 
legs. The liver is palpable two inches below the free border of the ribs. The 
blood Wassermann is negative. The urine contains a slight trace of albumin, 
a few granular casts, and no sugar. The systolic blood pressure is 180; the 
diastolic, 70. The orthodiascopic tracing being passed around shows aneu- 
rismal enlargement of the first portion of the aorta and marked left ventricu- 
lar hypertrophy. 
This patient, like several others we have studied, has typical generalized 
arterio-sclerosis and cardio-sclerosis with massive ventricular hypertrophy. 
It must have taken many years for these pathological changes to have 
occurred. Two main questions are of interest to us in this case: (1) Why was 
this patient free from cardiac symptoms for so many years? (2) What 
caused the sudden onset of the symptoms? 
Regarding the first question, it is often puzzling to understand why 
patients with apparently similar lesions suffer from such diverse symptoms. 
I have shown you other patients with extreme cardio-sclerotic changes who 
have suffered from severe cardiac symptoms and decompensation for years. 
What appears to me of prime importance in the production of cardiac 
symptoms in cardio-sclerotics, is the rate of progress of the disease. One can 
readily conceive that rapid destruction will quickly overwhelm the function 
of an organ and will soon cripple it, whether that organ be the heart, liver, 
kidneys, or any other. But when, for any reason the pathological process 
attacking the cardio-vascular system is slow in its progress, and no vital part 
is attacked, the function may be so gradually interfered with, that the 
normal reserve power of the heart—its “factor of safety”—is only very 
gradually weakened. Such a view, of course, considers the heart chiefly from 
the standpoint of function. This is oft-times advisable, for when the mind, 
eye, and ear are too engrossed in minute pathology, we are prone to forget the 
importance of the validity and power of the still remaining healthy portion 
of an organ. For instance, I have little doubt that our patient has 
marked coronary changes. The aortic changes, the physical signs and the 
generalized arterio-sclerosis indicate the likelihood of such coronary damage; 
yet a gradually progressive coronary change may only slowly cut off the 
vascular supply of the cardiac musculature. It may thus give time for the 
beginning of a collateral circulation, for we no longer regard the coronaries as 
end-arteries. Sudden infarction in coronaries not nearly as diseased as we 
assume those of this patient to be, may end in sudden death. We thus see 
how it is possible for some patients with severe cardio-sclerosis to live fairly 
comfortably despite their severely damaged hearts. You also see that 
even minute physical examination does not tell us everything about a 
patient, and that at times broader view-points must be considered in order to 
understand a case from all angles. CARDIOVASCULAR CLINICS 
547 
With reference to the second question, “ What caused the sudden onset of 
the symptoms?” The history clearly states that the pushing of a heavy piece 
of furniture suddenly brought on the cardiac symptoms: Pain, dyspnoea and 
palpitation. It is probable that any great effort in a person with a severely 
damaged heart makes sudden demands upon the circulation by quickly 
raising the blood pressure and by increasing the force and rapidity of ventricu- 
lar action, thus initiating cardiac symptoms. I have observed a similar 
case in a much milder instance of cardio-sclerosis; precordial pain followed 
the lifting of a heavy bundle. Such conditions cannot be better character- 
ized than by calling them by the somewhat unscientific and generic term, 
cardiac strain. The amount of strain required to produce cardiac symptoms 
will naturally vary with the amount of circulatory reserve; this in itself is a 
variable factor, and is rarely determinable in advance of the supreme circu- 
latory effort that finally produces cardiac symptoms from overstrain. 
I believe that for the present this patient should be given as much physical 
rest as possible. This does not necessarily mean in bed, for some old people 
become restive and worried when in bed; they feel that their last days have 
come, and that they will never be about again. Such views may seem old- 
fashioned to you, but they are very real to the patients, so that unless 
definitely indicated, it is unwise to put older patients to bed. They may lie 
upon sofas, or rest in easy reclining chairs. This patient should be given 
intensive digitalis therapy for one week: About a drachm and a half of the 
tincture of digitalis for four days, followed for three days by theobromine 
sodium salicylate and a restricted fluid intake. If dyspnoea, edema and 
precordial pain be benefited, the chances for the re-establishment of excellent 
compensation are good, and it may even be possible for the patient to again 
take up, at least partially, her old employment of designer. 
Later Report.—The patient remained at home several weeks. The dysp- 
noea soon ceased and the edema disappeared after two weeks. The precor- 
dial sensitiveness has almost entirely gone. The patient at first was allowed 
to walk about the room, then upon the street, and finally permitted to go to 
business for a few hours each day. The family physician reports that now, 
several months from the time we first saw her, she is again at business, quite 
as active as formerly and rarely complains of any of her heart symptoms. 
CASE 30.—CARDIO-SCLEROSIS— CHOLECYSTITIS 
M. J., female, aged 64, seven years ago had an attack of right-sided abdo- 
minal pain of three months’ duration. There was no jaundice. Several 
years thereafter, she developed midsternal pains, especially when walking in 
the open against the wind; the pains usually radiated to the right shoulder 
and right breast. Three months ago, she developed gastric symptoms; 
belching after meals, and rather constant epigastric distress aggravated by 
eating. She has lost 25 pounds in weight during the last year. She has 548 
CARDIO-VASCULAR CLINICS 
been sent here to determine whether the epigastric pains are of gastric or 
cardiac origin. 
Examination.—The systolic blood pressure is 160; the diastolic, 80. 
The urine is normal. Inspection of the chest reveals as you notice nothing 
abnormal. Upon palpation, there is a small area in the midsternum sensitive 
to pressure. Over the right base and over the mitral region, you hear a loud, 
rough systolic murmur, most prominent when the patient is lying down. 
The orthodiascopic tracing shows a somewhat enlarged aorta; the other cardiac 
outlines are normal in form and size. There is no edema of the legs. Ab- 
dominal examination reveals tenderness over the gall bladder region, with 
the pain radiating to the right side of the back. 
I do not wish to enter into the details of the abdominal examination, 
except to state that the latter is very suggestive of cholecystitis. The 
loud murmur and the hypertension present definite evidence of cardio- 
sclerosis. And yet, as you see, there is no decompensation: The patient 
is not dyspnoeic and she can walk comfortably about the room. I believe 
that the cardiac nerves of this individual have become hypersensitive because 
of the abdominal condition, whether of cholecystitic or of gastric origin. In 
other words the reflex cardiac arc has become abnormally excited and has 
thus been rendered hyperirritable. That is to say, the midsternal pains 
are not necessarily indicative of severe coronary disease, but are symptomatic 
of a hypersensitive reflex arc, and hence the morbid reaction—pain—even in 
the presence of mild coronary disease. 
The cardiac condition presents no contraindication to operation if such 
be indicated because of the abdominal complaint. There is no decompensa- 
tion, nor are the cardiac symptoms suggestive of any acute inflammatory 
disturbance. 
CASE 31.—ALCOHOLIC CARDIO-SCLEROSIS 
J. K., aged 63, married, has three grown up, healthy children. He 
considered himself well until two years ago. He then had what the doctor 
told him was an attack of edema of the lungs. About that time dyspnoea 
began. At first it was nocturnal in character; later it was also present 
by day. Of late, with exacerbations and slight remissions, dyspnoea has 
been a constant feature. He also has a dry cough. He denies any venereal 
history. Until his fortieth year, he drank an average of three or four glasses 
of red wine daily; he had never been intoxicated. 
I have had this patient under observation for one year. His condition 
when I first examined him was quite different from that at present. There 
was then definite evidence, on palpation and percussion, of considerable 
left ventricular hypertrophy. There was a loud systolic murmur over the 
mitral area and at the second right interspace. The cardiac rate was no 
per minute with occasional extrasystoles. There were signs of fluid at the 
right base posteriorly. The liver was very much enlarged. There was slight CARDIO-VASCULAR CLINICS 
549 
edema of the legs. The urine contained a slight trace of albumin and a few 
casts. The blood pressure was then 140 systolic and 7c, diastolic. A Wasser- 
mann blood test was negative. A nitrogen partition test of blood showed 
that the non-protein nitrogen, creatinin and uric acid were normal in 
amount. The phthalein output for two hours was also normal. 
The patient was put upon intensive digitalis and theobromin sodium 
salicylate therapy. The tincture of digitalis was given in twenty-drop doses, 
three times daily for one week, followed for three days by theobromine 
sodium salicylate in one-half gramme doses four times daily. The fluid 
intake, chiefly water and weak tea, was restricted to about 500 c.c. (one pint) 
in twenty-four hours. At the end of several weeks, there was marked 
improvement in the patient’s condition. The dyspnoea almost entirely 
disappeared; the liver diminished in size; edema of the legs also disappeared 
and the patient was able to walk about comfortably. 
This favorable status continued several months. Gradually, however, 
the condition in which you now find him supervened. You note his apathy, 
his somewhat cyanotic lips and the brief attacks of dyspnoea, during which 
the entire facies becomes more cyanotic. The cardiac examination reveals, 
even upon cursory inspection, the diffuse precordial heave betokening mas- 
sive ventricular hypertrophy. Upon auscultation the murmurs I described 
as being plainly heard a year ago are now scarcely audible; this is probably 
due to weakness of the heart action. The regular rhythm is frequently inter- 
rupted by what appear to be extrasystoles occurring in groups of three or 
four. There is massive edema of the lower extremities. The urine contains 
a slight trace of albumin and some granular casts. 
To sum up—this patient presents a definite clinical picture of cardio-sclero- 
sis. I believe the predominant pathological change is in the heart muscle, 
the patient has marked myocarditis. While the etiological factor is not 
absolutely certain, I think that the habitual drinking of wine in earlier 
manhood is responsible for the present cardiac status. Syphilis can be 
excluded, not only because of the negative Wassermann, but also because he 
has not responded to mixed treatment given him before coming under my 
observation. About a generation ago, alcoholism was held largely responsi- 
ble for many cases of heart disease. According to the modern conception, 
the pendulum has swung very far in the opposite direction, and alcoholism 
is now regarded as a very rare cause of cardiac damage. Both views are 
extreme I believe. Each case must be studied on its merits; the habits of 
the patient must be very carefully investigated, and other factors of course, 
must be carefully excluded. From this patient’s history and by a process of 
exclusion, I believe that he is suffering from alcoholic myocarditis. 
Why is this patient so listless? He is apparently not uremic, but just as 
his legs are edematous, so also is the brain probably water-logged and 
edematous. Such a condition naturally interferes with proper cerebral 
functioning. CARDIOVASCULAR CLINICS 
550 
It is of interest to inquire why medication—digitalis and theobromin—at 
first so successful in relieving the decompensation, is at present of no avail. 
It must be remembered that myocardial degeneration of such marked degree 
can never be entirely restored to its normal state. Drugs can only restore, to 
some extent, the driving force, the pumping power of the heart, and the degree 
to which it attains this success must depend upon the amount of healthy 
muscle susceptible to drug action. This presupposes that no sudden cardiac 
accident, like a coronary infarct, has supervened to alter entirely the patho- 
logical picture. The underlying condition, alcoholic myocarditis, is a slowly 
progressive one, and when degeneration is already extreme, drugs can scarcely 
stay or halt the increasing pathological damage. This patient will grow pro- 
gressively worse, and, unless some other accident such as edema of the lungs 
occurs, he will die with the typical picture of heart failure. 
CASES 32, 33.—MYOCARDITIS WITHOUT HYPERTENSION OR PHYSICAL SIGNS 
Case 32.—M. W., male, aged 64, had always led a quiet and regular life 
and was not given to excesses of any kind. He is married. His only pre- 
vious cardiac complaints were occasional left sided precordial pains and 
dyspnoea when taking long walks. Neither was sufficiently severe to cause 
him to seek medical advice. One week ago, while going to business, he felt 
nauseated and later vomited. He was dazed but managed to arrive home 
alone. At home he complained of left sided pains in the chest radiating into 
the left arm. He had no cough. The pains gradually subsided but he had 
several severe attacks of dyspnoea. There was no fever. Two days after 
the attack he developed edema of both legs. His physician states that the 
urine then contained a trace of albumin but no casts. 
Examination.—You note that the patient’s face is somewhat gray. He 
is not dyspnoeic at this moment although the doctor who attended him states 
that he was suddenly called to see him after midnight yesterday because of 
extreme shortness of breath. The dyspnoea must have been intense, for the 
patient himself states that he spent the preceding night in a rocker because 
he could not get his breath. The systolic blood pressure is now 120; the dia- 
stolic, 85. The urine is normal. Inspection and palpation of the precordium 
reveal nothing abnormal. There is no parasthesia or sensitiveness to super- 
ficial or deep pressure over the heart. Upon percussion the heart seems some- 
what enlarged to the left. The first sound at the apex is faint and distant; 
when the patient lies down this sound is reduplicated (so-called gallop rhy- 
thm). You hear a faint systolic murmur which accompanies the first sound 
at the apex. You will find that the murmur becomes somewhat louder when 
the patient is in a sitting position. At the base of the heart the sounds are 
normal. Abdominal examination reveals nothing abnormal. Upon aus- 
cultation of the lungs you hear some mucous rales at both bases. The radial 
arteries do not feel thickened. You see that there is edema of both lower 
extremities, chiefly of the right leg. CARDIOVASCULAR CLINICS 
551 
Re-examination 24 Hours Later.—You now find that the cardiac status of 
the patient is about the same. Despite vigorous stimulation, edema of the 
legs is still present. The patient was uncomfortable and dyspnoeic during 
the night. The rales in both lungs are more numerous and widespread. 
The patient’s mentality is now somewhat dulled. These signs presage 
an early death from heart failure.1 
In this patient I venture the diagnosis of myocarditis for the following 
reasons: The history points to a coronary infarct on the day the patient first 
became ill: The nausea, vomiting, precordial pains and dyspnoea were doubt- 
less due to this cause. A coronary infarct also satisfactorily accounts for the 
resultant cardiac failure—edema of the legs, and, later, pulmonary edema. 
Assuming the diagnosis of coronary infarct as correct, it seems highly 
improbable from the pathological standpoint that coronary disease can be 
present as an isolated lesion unaccompanied by more or less widespread 
disease of the cardiac musculature. It is upon this assumption that I base 
the diagnosis of myocarditis even in the absence of other criteria of the disease. 
The absence of auscultatory evidence of myocarditis will be discussed in con- 
junction wdth the following case. 
Case 33.—E. S.,aged 53, male, was said to have had “heart trouble” when 
he was a soldier in Switzerland at the age of 20. His family physician who 
has had him under careful observation for 10 years, states that he has had 
slight shortness of breath and occasional moderate tachycardia for a number 
of years. In that interval his systolic blood pressure varied from 100 to 143. 
The urine was always normal. The patient never presented any cardiac 
murmurs. He never had any edema of the legs. The only previous illnesses 
of note are an old gonorrhea in his youth and a severe attack of facial 
erysipelas 20 years ago. 
During the past few months the patient has become increasingly dyspnoeic 
and has developed substernal pains. He has great difficulty in climbing the 
hill leading to his home and must often stop because of shortness of breath 
and pains in the chest. Two days ago his physician states that he had a 
typical attack of pulmonary edema. This was relieved by the hypodermic 
administration of morphine sulphate and of digitalis. 
Examination.—As you look at this patient now, he is the picture of health. 
His complexion is ruddy; he has no discomfort in breathing. There are no 
abnormal jugular or carotid pulsations. You hear at the apex a slightly 
reduplicated first sound, more marked when the patient sits up. Otherwise 
the cardiac examination reveals nothing abnormal. There are no rales to be 
heard in the chest. There is no edema of the legs. The systolic blood pres- 
sure is low, it is 80; the diastolic, 60. 
I present these two patients chiefly to demonstrate that both have severe 
cardiac disease—probably coronary disease and myocarditis; yet the most 
careful physical examination elicits no abnormal signs except the gallop 
1The patient died two days later. 552 
CARDIOVASCULAR CLINICS 
rhythm at the apex. These cases illustrate the importance of a minute study 
of such symptoms as dyspnoea and precordial pain, and of the history of 
attacks of edema of the lungs. These of themselves offer sufficient evidence 
of severe heart disease without the usual physical phenomena to be found 
upon cardiac examination. In the first patient (Case 32), the beginning 
symptoms were gastric, and the pains in the chest and arm might have 
been ascribed at the outset to a stomach derangement. But increasing 
dyspnoea and edema of the legs soon cleared up the clinical picture and made 
it apparent that the heart was the offending organ. 
CASE 34.—PREGNANCY WITH CARDIAC DISEASE AND ENDOCARDITIC 
RECRUDESCENCE 
Mrs. W., is now in the fourth month of her fourth pregnancy. The other 
pregnancies and deliveries were normal. The youngest child is ten years old. 
Although she knew she had “heart disease,” she had no symptoms until 
four years ago. At that time she had slight hemoptysis, probably from a 
pulmonary infarct. Since then she has had difficulty in walking because of 
pains in the epigastrium and under the left breast. These symptoms have 
been aggravated during the last six months; they are accompanied by “palpi- 
tation.” During the last few months, she has had severe palpitation during 
coitus. Since her pregnancy, she has had several attacks of cough, fever, 
dyspnoea and blood-streaked sputum. 
Examination.—You see the patient is somewhat dyspnoeic especially when 
attempting to lie flat. Over the mitral area you hear the classical murmurs of 
a double mitral lesion; these are also heard distinctly posteriorly between 
the vertebral column and the angle of the left scapula. The second pulmonic 
sound is accentuated. The cardiac area is not enlarged to percussion. You 
hear distinct signs of localized dry pericarditis over a small area at the third 
left interspace near the left sternal border. The heart is regular; the rate 
ioo per minute. The temperature is 102° per rectum. Over the lungs 
posteriorly, near the scapular angles, you hear localized sibilant breathing 
and mucus roles; over the right side there is in addition distant broncho-vesicu- 
lar breathing. There is epigastric tenderness to pressure. The liver is 
not enlarged. The blood pressure and urine are normal. There is no edema 
of the legs. 
Since the attack of hemoptysis the patient has not been able to walk with- 
out pains or palpitation. During her pregnancy these have become aggra- 
vated. Lung complications have been added—attacks of bronchgpneumonia 
with fever. Dry pericarditis is now present; whether this is a recent or old 
process it is impossible to state. This case exactly fits in with my experience 
that when pregnancy occurs during the active recrudescent phases of endo- 
carditis, it has the effect of aggravating existent symptoms and of adding 
new complications. There are two factors which must always be considered CARDIOVASCULAR CLINICS 
553 
in conjunction with pregnancy and heart disease: Decompensation and endo- 
carditic recrudescences. I believe the latter is the more dangerous and leads 
to more fatalities than mild decompensation. Gestation in some unknown 
manner seems to light up dormant or only partially active endocarditic 
processes. 
I shall advise this patient to have an abortion done at once. I believe it 
unsafe for her to attempt to carry her pregnancy to term.1 
CASES 35, 36.—PREGNANCY WITH CARDIAC DISEASE AND NEUROTIC 
SYMPTOMS 
Case 35.—Mrs. K., aged 21, married one year, is pregnant three months. 
She has had “heart disease” for years. In the past ten years her only com- 
plaint has been occasional attacks of rapid heart action. Since her pregnancy 
she has had frequent crying spells because obsessed with the idea that she 
would die during childbirth. She complained almost constantly of palpitation. 
Examination.—You see a vigorous woman who is not dyspnceic. Upon 
auscultation you hear the typical signs of a double aortic lesion: A rough 
rasping systolic and a softer diastolic murmur over the right base; the latter 
is transmitted to the left and below. There is moderate ventricular hyper- 
trophy. The cardiac rhythm is regular, the rate being between 100 and no 
per minute. Compensation, you observe, is perfect—there is no dependent 
edema and no dyspnoea, despite the tachycardia. 
I shall comment upon this case after the examination of the next patient. 
Case 36.—Mrs. L. is married two years. She is now pregnant six weeks. 
She has had “heart disease” since childhood but has always been able to play 
and romp with other children. Since her tenth year she has never been in 
bed because of her heart. She is of a neurotic temperament and is readily 
frightened. It is when frightened that she suffers from momentary 
tachycardia. 
Examination.—Upon exposing the chest you note even at a distance the 
exaggerated ventricular action. The cardiac rate is no per minute and is 
regular. Typical signs of a double mitral lesion are present: A rough diastolic 
rumble and a loud systolic murmur over the mitral area. There is no evi- 
dence of decompensation. The patient confesses that for nights she does not 
sleep because she dreads that she will not live through her pregnancy and 
childbirth. Her heart is almost always “jumping.” 
What advice should be given to these young women? Should the preg- 
nancy be continued or interrupted? Both have perfectly compensated 
lesions; Case 35 has a double aortic, Case 36, a double mitral lesion. In 
both the lesion has been quiescent for many years. Because of the knowledge 
1 The next day, the gynecologist gave the patient a small injection of scopolamine, and 
dilated and packed the uterus. After several days, the fetus was expelled. Thereafter, 
all signs of bronchitis and bronchopneumonia disappeared; further convalescence was 
uninterrupted; palpitation and precordial pain entirely disappeared. 554 
CARDIOVASCULAR CLINICS 
of their cardiac disease both have become frightened and obsessed by the fear 
of death from childbirth. The result has been quite similar in both; crying 
spells and tachycardia. It is really the tachycardia per se which requires 
symptomatic relief. Without the latter symptoms, I should have unques- 
tionably advised the continuation of pregnancy, for the two grave dangers in 
pregnant women with cardiac disease—decompensation and rheumatic 
endocarditic exacerbations—are here absent. I should consider even this 
patient with the double mitral lesion (Case 36) a safe case for the continuation 
of the pregnancy if tachycardia were absent. I say this, despite the fact that 
patients with mitral stenosis are not usually considered good risks for preg- 
nancy and childbirth. I believe, however, that by careful study and discrim- 
ination, one may select cases in whom pregnancy and childbirth may be 
advised. For example I have advised the continuation of pregnancy in 
several cases of mitral stenosis with no untoward results: Childbirth and puer- 
perium were normal. Besides, we occasionally observe patients with mitral 
stenotic lesions who have gone through several normal pregnancies and who 
never knew that they had heart disease. 
To return to our patients—they are so extremely nervous and fretful 
that I am confident that neither reassurance, medication, nor rest will allay 
or control, even in part, their basic dread of pregnancy and death. 
Since both are in the very early stages of gestation I would advise imme- 
diate surgical intervention for the termination of pregnancy. In this stage 
and with compensated patients, an abortion, skillfully and aseptically per- 
formed, adds no operative risks to the cardiac lesion. I shall, however, 
explain to both these patients, that it was their nervousness, rather than the 
actual condition of their hearts which called for operative interference, 
and that if at some future time their hearts remained as good, and if they 
were less frightened, they would have no “palpitation,” and pregnancy would 
very probably proceed normally.1 A good general rule is that pregnancy 
should not be allowed to continue in those who have shown evidence of decom- 
pensation or of fresh endocarditic attacks within two years of conception. 
CASE 37.—OVERACTING HEART—ABNORMAL PHYSICAL SIGNS—REMARKS 
UPON A RATIONAL METHOD OF OUTLINING THE HEART 
J. H. B., male, aged 14, has grown very much during the last year or two. 
He joins in all sports. His only complaint is occasional left-sided abdominal 
pain after running. There is no history of rheumatism or tonsillitis. The 
boy is supposed to have “heart disease.” 
Examination.—As you see, this patient is quite tall, fairly muscular and 
of the blond type. The teeth and tonsils are normal. The systolic blood 
pressure is 130; the diastolic, 87. Upon inspection of the chest you see sil- 
1 The family physician recently reported to me that Case 35 had had an abortion 
performed. Within a few months, she again became pregnant, and had a normal delivery 
and puerperium. The patient herself is feeling well. CARDIOVASCULAR CLINICS 
555 
houetted quite plainly through the rather thin chest wall, the overacting 
heart, especially at the apical region. Upon palpation you feel a thrill-like, 
slapping apical impulse especially when the cardiac rate is increased by 
exercise. Upon auscultation you hear a thrill-like, split or broken first sound 
at the apex; it is systolic in time and is not accompanied by any murmur. 
The apical thrill is unchanged when the boy lies upon his back. Over the 
second right interspace there is a soft systolic murmur which diminishes in 
intensity with inspiration. 
I now invite your attention to the percussion findings. Following the 
ordinary method of percussion, you observe that there is increased dullness 
to the left, less to the right. This therefore presupposes cardiac enlargement 
to the left. The orthodiascopic tracing, however, which I am now showing 
you, reveals an organ that is quite normal in contour and size, and cor- 
responds with the size of the heart one would expect to find in a boy of his 
physique. The urine and knee reflexes are normal. There is no edema of 
the legs. 
There are two points of special interest in this case: The abnormal physical 
signs upon auscultation and palpation, and the discrepancy between the 
percussion and orthodiascopic findings. 
A thrill-like first sound heard upon auscultation and felt upon palpation 
is by no means infrequent in overacting normal hearts. Its cause is not 
quite clear to me. In some instances, it may be caused by intraventricular 
eddies and swirls so to speak, resulting from abnormally violent heart action; 
at any rate by itself it has no pathological significance and is not indicative of 
any myocardial or endocardial lesion. 
The soft cardio-respiratory murmur at the second left interspace is 
extremely common, especially in the young. 
With reference to the marked discrepancy between the orthodiascopic 
and percussion outlines this is but another example of what careful compara- 
tive studies have long since proven to me; namely that percussion findings 
are very inexact and often valueless as compared with X-ray examinations. 
Orthodiascopy itself undoubtedly gives exact outlines because it deals with 
parallel rays. I have tried many methods of percussion: Ortho-percussion, 
mediate, immediate, stroke, light and heavy—and I have never been able to 
detect any correlation between the cardiac outlines thus studied and the 
actual size of the heart as found by the X-ray. A moment’s thought on the 
physics and acoustics of cardiac percussion will perhaps explain the reason 
for this discrepancy. The heart is a muscular, more or less soft organ, situated 
at different depths from a chest wall of varying thickness. The great vessels 
•—the aorta and pulmonary arteries—with their contained blood are of softer 
consistency than the muscular mass of the heart. An added complicating 
factor is the amount of lung tissue—an air-containing, light substance—be- 
tween the heart and chest. Because of the difference in densities of the cardiac 
structures themselves, and because of the variations in the thickness of the 556 
CARDIOVASCULAR CLINICS 
wall and the intervening lung pad, it seems d priore highly improbable that 
any percussion method, or any combination of methods can give even approxi- 
mate data of the size of the heart and aorta. I have therefore attempted 
to apply the lessons I have learned from fluoroscopy to percussion. I 
reverse, somewhat, the usual routine employed in physical examination. I 
seek first the most prominent visible and palpable apical impulse by inspec- 
tion and palpation. If this point is not sufficiently visible, I auscultate to 
define it more accurately. From fluoroscopy I have learned that the actual 
apex may be from 2 to 6 c.m. below this point. In thick-set individuals there 
is comparatively slight mobility of the diaphragm, while in those with 
graceful chests, diaphragmatic excursion is marked. Hence in the former, 
the actual apex is near the point of maximum impulse, while in the latter 
it is much lower. I have corroborated these facts by frequent fluoroscopic 
examinations. The upper aortic line is next delimited. The finger is placed 
in the jugulum behind the manubrium. If aortic pulsation can be felt, a 
corresponding line is marked on the manubrium. Auscultation, and the 
diagnosis of the cardiac lesion, if there be any, will determine how far the 
aortic pulsation in the jugulum may be regarded as being pathological. 
If such pathological lesion in the aorta cause an undue, overpulsatile rise, the 
result will be an abnormally high level for the palpated aorta. The approxi- 
mate position of the aortic valves is next determined by auscultation over the 
right base. The area at which the aortic sounds are loudest marks fairly 
accurately the position of these valves; the upper limit of the right aortic 
curve is about 2 c.m. above this point. The usual palpation and auscultation 
is then practiced. These with the history and the remainder of the clinical 
findings determine the absence or presence of cardiac disease. If heart disease 
is absent, the remainder of the cardiac outline (between the aortic curve and 
the apex) can be determined and blocked in by a knowledge of the probable 
shape of the heart in the particular type of chest wall. (See Orthodiascopy, 
Chapter XII.) If a cardiac lesion has been diagnosed, the remainder of the 
cardiac contour can also be fairly accurately foretold with the aid of pal- 
pation and other clinical data; it is then drawn on the chest wall by our 
orthodiascopic knowledge of corresponding types of heart disease, with and 
without decompensation. 
I admit that this method has its drawbacks for it is founded partly on 
inferences. However, I have not made any of the gross errors inherent in 
percussion, and while often wrong I have not found wide or wild discrepancies 
between the cardiac outline as determined by my method, and the actual 
orthodiascopic size of the heart. 
I have made this digression because I wanted to justify the fact that in 
previous clinics, I passed over the subject of percussion very cursorily. Let 
us now return to our patient. 
An important factor is that a rapidly beating or overacting heart always 
gives the impression of being larger than it actually is. Such is the case CARDIOVASCULAR CLINICS 
557 
here. The orthodiascopic outlines are normal, although the result of the 
examination by auscultation and palpation gives the impression of consider- 
able cardiac enlargement. 
The physical signs—the thrill-like apical sound heard and felt with 
cardiac systole—are not the result of any cardiac disease in our patient, but 
simple come from cardiac hyperactivity. Other cases that I shall show you 
will also demonstrate abnormal physical signs without organic cardiac disease. 
CASES 38 43.—IRRITABLE HEART WITHOUT ORGANIC HEART DISEASE- 
REMARKS COMPARING THE IRRITABLE HEART IN CIVIL PRACTICE WITH 
THAT OF SOLDIERS 
Case 38.—J. H., male, aged 27, unmarried, says that in his business as 
a grocer he had occasional slight discomfort in lifting heavy boxes. This 
never interfered with his business until five years ago; he then had an attack 
of severe abdominal cramps. He felt faint and his heart action became very 
rapid. The doctor who saw him then and with whom I have communicated, 
stated that his heart action was regular and the rate 180 per minute. Since 
that attack, nervousness, excitement, attempts at hard work, or full and 
hearty meals are accompanied by rapid heart action and precordial pains. 
His appetite is good; he has not lost weight. He is nervous and worried 
about his heart, more so since he has been drafted and accepted for war 
service. 
Examination.—The patient is quite robust and well nourished. His 
thyroid is not palpable. The systolic blood pressure is no; the diastolic, 90. 
Inspection of the chest reveals slight apical overaction. You note upon pal- 
pation in the apical region, a systolic, almost thrill-like shock. There is no 
pain or sensitiveness to superficial or deep pressure. Upon auscultation you 
hear a systolic broken first sound, giving the impression of a thrill. The 
other heart sounds are normal. The cardiac area is normal to percussion. 
The urine is normal. The abdominal examination reveals nothing abnor- 
mal. There is no edema of the legs. The knee reflexes are somewhat 
exaggerated. When at rest the pulse rate is 100 per minute; the rhythm, 
normal. After moderate exercise as for example, walking a dozen paces 
rapidly, the pulse rate is 150 per minute and the patient complains of dysp- 
noea and some precordial distress; after about three minutes of rest, the pulse 
returns to its previous level. 
This case is typical of irritability and instability of the nerve control of 
the heart. The history definitely indicates that an attack of paroxysmal 
tachycardia from some gastric disturbance five years ago initiated the cardiac 
symptoms. Prior to that, the patient was a hard-working individual, his 
only complaint being the not uncommon one of a sense of precordial oppres- 
sion from heavy lifting. Now, excitement or effort is very apt to bring on 
rapid heart action, not of the paroxysmal variety with extreme acceleration, 
but with rates reaching 150 per minute, and accompanied by dyspnoea and 558 
CARDIO-VASCULAR CLINICS 
precordial pain. This tendency has been exaggerated by his dread of active 
war service. Despite the physical signs on palpation and auscultation, I 
believe organic disease can be excluded. I have found identical signs—a 
thrill-like systolic shock on palpation and a thrill-like first sound on ausculta- 
tion—in a number of recruits of draft age in whom, after exercise, cardiac 
action was unduly accelerated or overforceful. The abnormal signs just 
mentioned are not evidence of organic disease in such individuals, for often 
when the cardiac rate or activity can be controlled (for example, by having 
the patient take and hold a deep breath) these abnormalities disappear. 
There is nothing in the patient’s history—no antecedent rheumatic or other 
infection—which can be correlated with organic cardio-vascular disease. 
That is very important from the etiological standpoint, for it helps us to 
distinguish murmurs and thrills due to accelerated and violent action per se, 
from similar signs due to actual heart disease. In other words, we are dealing 
with a condition of hyperirritability and instability of the neurogenic control 
of the heart, originally induced by an attack of paroxysmal tachycardia. 
We shall discuss the general problems of the therapy and etiology of 
the irritable heart later, in conjunction with remarks upon the soldier’s heart. 
Case 39.—J. T., aged 28, a furnace worker, has been married five months. 
His work is very laborious. He has had slight precordial pains, and pains 
radiating into the left arm for some months. The symptoms were aggravated 
after a dispute with a fellow-laborer some three weeks ago. He has lost 
thirteen pounds in weight during the present illness. He has had occasional 
palpitation and dyspnoea. 
Examination.—You note the strong musculature of the thorax and arms, 
indicative of continued hard labor. The lungs are normal. Inspection 
shows slight carotid overaction. There is no pain on palpation; the apical 
impulse is marked. Upon auscultation there is a slight thrill-like systolic 
first sound at the apex. The other cardiac sounds are normal. Fluoroscopic 
examination shows that the heart is normal in size and shape; overaction of 
the pulmonary artery and aorta is also evident. The thyroid gland is not 
enlarged. The abdominal examination reveals nothing abnormal. The 
systolic blood pressure is 142; the diastolic, 72, The urine is normal. 
The knee reflexes are very lively. The pulse rate varies suddenly from the 
normal to 100 per minute. This acceleration occurs with and without effort. 
The acceleration can be considerably, although temporarily, moderated by 
having the patient take and hold a deep breath. I always regard this 
phenomenon as an evidence of good vagus control. 
This patient presents no evidence of organic disease. A dispute with a 
fellow laborer has apparently aggravated a dormant cardiac neurosis. I 
believe the man should give up his work for a week or two, not because the 
work itself would damage his heart, but because his present state of hyper- 
susceptibility requires a rest. Bromides in moderate doses for a few days 
will help in the same direction. CARDIO-VASCULAR CLINICS 
559 
Case 40.'—H. M., aged 26, single, gives a questionable history of rheuma- 
tism in childhood. He had always been well and athletic until five years 
ago when he witnessed the drowning of his brother. He then became hysteri- 
cal and was confined to bed two weeks with hysterical attacks. For two or 
three years thereafter, he had “nervous indigestion,” the main symptom 
being belching. The gastric condition improved. The patient then 
developed cardiac symptoms—“palpitation” and pains in the left chest, 
particularly after excitement. After walking a mile now, he becomes “ tired 
all over.” He has recently been told that his heart is occasionally irregular. 
He is a very rapid eater. His present business—theatrical manager—keeps 
him so occupied that he has no time for relaxation. 
Examination.—The systolic blood pressure is 120; the diastolic, 60. 
The thyroid is not enlarged. You note upon inspection slight carotid over- 
activity, and upon palpation slight exaggeration of the apical impulse. 
The sounds over the base are normal. At the apex, immediately after a 
normal first sound, you hear a sharp, superficial click, which is transmitted 
to the axilla; it disappears upon deep inspiration. Occasionally, a superficial 
pleuro-pericardial rub is also heard in this region. There is no precordial 
sensitiveness. The pulse rate is normal. Rapid walking around the room, 
as you see, produces no dyspnoea. The orthodiascopic tracing which I took 
of him shows that the cardiac outlines are normal in size and contour; the 
ventricular contractions were particularly powerful. There was no roent- 
genographic evidence of pericordial adhesions. The abdomen is not sensitive 
to pressure. The urine is normal. There is no edema of the legs. 
I believe the adventitious sound at the apex is due to an old pleuro-peri- 
carditis, and has no relation to the cardiac symptoms now present; it is 
simply an accidental finding. There is no other sign of cardio-vascular 
disease. The whole demeanor and action of the patient during the examina- 
tion, as you probably observed, was that of an individual who is hyperactive; 
it cannot be better expressed than by the use of the common, though unscien- 
tific expression, “his nerves are tense; he is always on edge.” Indeed, the 
history elicits the fact that he never acts calmly, that he has no time for 
actual rest, that his mind is always busily looking ahead. Whether his entire 
disposition was changed by having witnessed his brother’s drowning, or whether 
the latter incident only intensified an inherent tendency, we cannot state 
because we possess no details antedating the accident. The history however 
leaves no doubt that the original shock, followed by hysteria, was the imme- 
diate starting point for a train of nervous symptoms, first affecting the stom- 
ach, and later, the heart. I want to emphasize again the fact that, 
although the cardiac rate was normal, and was not unduly accelerated after 
exercise, the “palpitation,” although subjective, was actual to the patient, 
and caused the various cardiac symptoms of which he complained. Another 
point of interest is the question, would this patient make a good soldier? 
Since there is no tachycardia, the fundamental question is his attitude toward 560 
CARDIOVASCULAR CLINICS 
the war. If he is imbued with the proper patriotic spirit to take a manly 
part, I believe that camp routine, with its associations and release from the 
hurried and harried life this man has been leading, will cause a reversion to a 
physiological, normal level, that the cardiac symptoms will disappear, and 
that he will only suffer from the usual fatigues incident to the work of the 
soldier. 
Case 41.—L.R., aged 48, married, salesman, has always led a very active 
business life but states that he has always been of a nervous temperament. 
He had “palpitation” when about 20. He has always been fond of exercise 
and sports. He frequently suffers from cold hands and feet. Since several 
months, he has had disputes with his wife because of business reverses. 
He is afraid to exercise now because he believes he has heart trouble. He 
never has any dyspnoea while at his work. His family physician tells me that 
he has had occasional extrasystoles and that an occasional hyaline cast is 
found in the urine. At present the chief symptoms are “palpitation” 
especially at night, and attacks of perspiration with -clammy hands and 
feet. » 
Examination.—You see that the patient is of athletic build. The systolic 
blood pressure is 118; the diastolic, 95. If you feel his hands and feet now, 
you will find them cold and wet despite the warm temperature of the room. 
The pulse is regular, its rate, normal. All the cardiac sounds are normal. 
Rapid walking does not cause any abnormal increase of the heart rate. The 
orthodiascopic tracing now being passed around shows that the aorta is normal 
in size and shape, and that the remainder of the cardiac outline is somewhat 
broader than normal. The knee reflexes are lively. 
I believe that organic heart disease can be excluded. The patient pre- 
sented no arrhythmia during our examination, but the “palpitation” at 
night, and the family physician’s statement that he had detected extrasys- 
toles, make it probable that the night attacks are due to extrasystoles. 
The vasomotor instability—perspiration and clammy extremities—is the 
chief feature of the case. I do not regard the presence of an occasional cast 
in the urine as indicative of renal disease, for such a finding is common enough 
in perfectly healthy and normal individuals. 
The first therapeutic measure I would suggest is to allow the patient to 
go on with his business, to assure him that his heart is sound, and then 
gradually to let him take up his usual athletics again. Of equal importance 
is the avoidance of bickerings at home; unless that source of irritation be 
eliminated, all other therapy will be of no avail. For a time and to hasten 
improvement, the patient should take 30 grains of mixed bromides at night, 
and occasional doses of the solid extract of the suprarenal gland when the 
vasomotor or cardiac symptoms become especially annoying. 
Later Report.—The patient has told me that the directions given were 
faithfully carried out, and that he felt so well after two or three days that he 
is again not only attending to business but is taking up his usual athletics. CARDIOVASCULAR CLINICS 
S^i 
I feel convinced that assurance of the absence of heart disease was the con- 
trolling factor in this rapid cure. 
Case 42.—Mrs. W., aged 52, has had five children and several mis- 
carriages. The menopause occurred two years ago; at that time she had 
occasional slight flushes for two months. Ten years ago she had gall stone 
attacks for which she was treated in Carlsbad; but she has had no recurrence 
in the last few years. Her husband died suddenly in bed two years ago. She 
was very much upset by his unexpected death. Since then she began to have 
palpitation, especially at night, and dreaded going to bed for fear that she, 
too, might die suddenly. She also had palpitation when excited or when 
walking in the street; this was accompanied by sharp substernal pain which 
occasionally radiated to the left arm. The systolic blood pressure, taken at 
different times, varied between 180 and 200. She was told of this hyperten- 
sion and also told that she had arterio-sclerosis. She has been on a rigorous 
diet, and although often hungry (at which times she would experience faint- 
ness and tachycardia) she was afraid to eat for fear of increasing her blood 
pressure. 
Examination.—The patient you see, is a stout woman, she is not dyspnoeic 
when at rest. The thyroid gland is not enlarged. The systolic blood 
pressure is 150, the diastolic, 100. There is overaction of the carotids and 
aorta. There is no pain on superficial or deep precordial palpation. There 
is a strong systolic impact felt at the apex. Upon auscultation you observe 
that all cardiac sounds are normal; there are no murmurs nor accentuated 
sounds. When the patient is at rest, the cardiac rate is no; it is slightly 
decreased upon deep quiet inspiration. Walking causes a rapidity of 120; 
after a few minutes it drops to no. There is no edema of the legs. The 
urine and knee reflexes are normal. The orthodiascopic tracing which I 
here demonstrate to you shows a heart of normal size and form. 
In spite of the history of hypertension and of precordial attacks, I regard 
the case as one of pure cardiac neurosis due to fright, and reflexly aggravated 
by hunger pangs. The latter were probably caused by a starvation diet 
which kept the stomach empty a good part of the time, and induced gastric 
hypermotility. I shall allow the patient a liberal mixed diet, to be eaten at 
regular intervals. I shall prescribe bromides at night and two grain tablets 
of the extract of suprarenal gland for the attacks of tachycardia. 
Later Report.—Within three weeks her condition improved remarkably. 
The systolic blood pressure was constantly around 130, the precordial pains 
disappeared and the cardiac rate fell to 80 per minute. The patient sleeps 
well at night and can walk regularly in the open without discomfort. Reas- 
surance doubtless was a large factor in her improvement. 
Case 43.—Mrs. G., aged 26, has been married one year. She has a baby 
three months old. Seven years ago she had a love affair; she became disap- 
pointed in her lover and gave him up. She then had many hysterical spells, 
finally culminating in attacks of severe nocturnal dyspnoea. Since then she 562 
CARDIOVASCULAR CLINICS 
has had many such attacks. She finally married another suitor and became 
pregnant. While pregnant the attacks ceased entirely, but they have 
recently recurred. Her home life is now a happy and comfortable one. Dur- 
ing a typical attack her hands and feet become cold and the heart action, 
rapid. She becomes dyspnoeic, there is a feeling of palpitation and also of 
abdominal pressure; accompanying these are intestinal hypermotility and 
rumbling. The patient says she tries to control the attacks, which usually 
come on and are severest at night. She is losing weight and is afraid to go 
out because of the attacks. Her appetite is poor. 
Examination.—The teeth and tonsils are normal; the thyroid not enlarged. 
Now the patient states that she has what she considers a mild attack. Her 
hands, you observe are cold and clammy. Inspection of the cardiac area is 
normal. There is a broken, thrill-like systolic shock palpable, and a thrill- 
like sound heard over the mitral area. The other heart sounds are normal. 
The cardiac rate is no per minute; walking about in this room has increased 
it to 120; it fell to its previous level within five minutes. The abdomen pre- 
sents nothing abnormal. The knee reflexes are very lively. There is no 
edema of the legs. The orthodiascopic tracing shows a heart normal in size 
and shape. 
I consider this case a typical example of an irritable heart made so originally 
from the emotional strain of a love affair years ago. The symptoms sub- 
sided during pregnancy, apparently because the pregnant state caused a pro- 
found change in her mental attitude, a common result of pregnancy. A 
hyperfunction of one or more of the endocrine glands may have been the fun- 
damental cause of such change. After childbirth, there was recurrence of 
the old symptoms, chiefly vasomotor instability and dyspnoea. Although 
originally hysterical, I do not consider the present attacks of that nature; 
rapid heart action alone, as you know, can cause dyspnoea. The presence 
of symptoms due to irritability of the vasomotor center seems to indicate 
in addition, a possibility of hyperexcitability of the respiratory center. 
Studied with a respiratory apparatus, such patients are sometimes found to 
be suffering from tachynpoea (simply rapid breathing) rather than from 
dyspnoea. 
My views of cardiac neuroses with full consideration of the etiological 
factors involved and of the abnormal physical signs and phenomena, as well 
as the therapy are given in detail in Chapter XIV and XVIII; hence they 
require no repetition here. 
CASES 44, 45-—FAINTING ATTACKS FROM SO-CALLED WEAK HEART- 
REMARKS ON “WEAK” HEART 
Case 44.—A. L., married, aged 49, fainted five years ago. He then had no 
gastric symptoms. From that time and until the attack of four days ago, he 
felt well. While sitting at a banquet in a room full of smoke, he felt weak and 
lost consciousness. Both fainting attacks were attributed to a “ weak ” heart. CARDIO-VASCULAR CLINICS 
563 
Examination.—This patient you observe is a vigorous man. The sys- 
tolic blood pressure is 138; the diastolic, 72. The urine is normal. You 
find that all the heart sounds are normal. Now that he has walked rapidly 
around the room you also find that the heart action is not inordinately rapid 
nor violent, nor does the patient become dyspnoeic. The knee reflexes are 
normal. There is no edema of the legs. The orthodiascopic tracing being 
passed around shows a normal-sized aorta; the ventricular area is somewhat 
broader than normal, probably because the ventricles are pushed up by the 
diaphragm, a frequent finding in stout individuals; this therefore gives a false 
impression of ventricular enlargement. 
I find no evidence of cardio-vascular disease or of “weak heart” in this 
individual. The fainting was probably caused by cerebral vaso-motor 
changes from breathing impure air in a warm and stuffy room. The patient 
should be allowed to again follow his usual occupation. He requires no 
treatment. 
Case 45.—-S. K., unmarried, aged 27, states that he has suffered from 
fainting spells for years. The sight of blood causes him to faint. These 
attacks are most apt to occur when he is in a warm room. Sometimes there 
is a sense of light-headedness instead of an actual faint. The attacks have 
no relation to diet or exercise; indeed, he is very athletic; plays tennis and 
rides horseback. He is a very moderate smoker. He has no gastric or 
intestinal disturbance. The family physician states that at times the pulse 
is irregular, and that the heart sounds are faint. 
Examination.—You see this patient is an excellent example of an athlete; 
tall and lithe. The teeth and throat are normal. Upon auscultation you 
find all the heart sounds quite normal, without any evidence of “weakness.” 
When the patient lies down, the heart sounds become somewhat louder. The 
pulse and cardiac rhythm are occasionally disturbed by a premature con- 
traction (an extrasystole), of which the patient himself is not aware. 
Inspection and palpation of the precordium reveal no abnormality. The 
blood pressure and urine are normal. There is no edema of the legs. The 
orthodiascopic tracing being passed around shows a normal sized aorta, and 
a large sized heart, but not exceptionally so for an individual of his physique. 
I shall now have you fluoroscope the patient with me. Watch the ven- 
tricular contractions carefully and you observe, not “weak” ventricular 
systoles, but just the reverse. You note the vigorous ventricular contrac- 
tions, as shown by the decided diminution in the size of the ventricle with 
each systole. 
Cardio-vascular disease can be excluded, I believe, as a cause of fainting 
spells and of the extrasystoles; both are probably due to vaso-motor 
instability. I have found that the extract of suprarenal gland is of value in 
these individuals, if it can be given at the first premonition of faintness or 
light-headedness. This patient may continue his business and follow his 
usual exercises, no matter how vigorous or even violent they may be. 564 
CARDIO-VASCULAR CLINICS 
Both cases typify what is popularly termed “weak heart,” yet neither 
has the slighest evidence of cardiac disease, and in the case we examined 
fluoroscopically, you were actually able to see the strong cardiac contrac- 
tions. The importance of vaso-motor instability from whatever cause 
—impure air, gastric disturbances, fright, etc.— as a cause of fainting is very 
frequently overlooked; the heart is accused as the offending organ, and 
patients are sometimes coddled to almost ridiculous degrees because heart 
disease is mistakenly regarded as the source of the trouble. This is especially 
true when some cardiac irregularity—usually extrasystoles—co-exists. Of 
course, the entire cardio-vascular apparatus must be carefully examined in 
these individuals, so as to positively exclude any organic lesion as the cause 
of fainting attacks. The treatment does not consist in rest and quiet, nor 
in giving digitalis. Treatment must be directed to the cause of the vaso- 
motor instability. As indicated, these are manifold. In every case, there- 
fore, it is necessary to search for the special cause and to treat it appropriately. 
CASE 46.—VASOMOTOR INSTABILITY—REMARKS ON SO-CALLED “WEAK 
HEART” 
Mr. L., aged 60, always worked hard. He has never complained of his 
heart. Ten years ago he had a long-continued attack of diarrhoea which he 
attributed to milk. At that time he complained of occasional “ thumping 
in his chest.” Since that diarrhoeal attack and until a month ago his bowels 
have been regular, but there is usually slight abdominal colic immediately 
preceding every evacuation. A month ago, he had another severe attack of 
diarrhoea from some unknown cause. Since then he has had frequent “ weak 
spells” which consist of sweats, of cold extremities, and of a feeling of faint- 
ness. The spells last about one-half hour. They are occasionally accom- 
panied by coliky pains and are sometimes relieved by the passing of flatus. 
The patient has been in bed for several weeks because he had been told that 
he had a “ weak heart.” 
Examination.—The patient is well nourished; there is no dyspnoea even 
when lying flat. The radial arteries are not thickened. The pulse is regular; 
its rate, 60 per minute. The blood pressure is normal. There is no abnormal 
carotid or aortic pulsation. In fact, you will find that the most careful 
physical examination of the heart fails to reveal anything abnormal except 
a very soft systolic murmur at the apex. There is no abdominal tenderness, 
no edema of the legs. The urine and knee reflexes are normal. The ortho- 
diascopic tracing, a copy of which you see, shows no enlargement of the aorta 
nor of the remainder of the cardiac outline. 
The patient’s symptoms I believe are real, not hysterical; an otherwise 
hard-working man is not apt to want to be bedridden. The diagnosis of 
“weak heart,” made by another physician, has undoubtedly frightened him. 
I find no pathological cardio-vascular basis for the symptoms. The heart 
is normal. Of course such a statement can be made only after a most careful CARDIO-VASCULAR CLINICS 
565 
examination, for you know the frequency of cardio-sclerosis at this patient’s 
age. I do not consider the faint apical systolic murmur of any significance; 
it is such a common occurrence that in itself it is no criterion of cardiac disease. 
This patient is suffering primarily from disturbance and instability of the 
vaso-motor mechanism, a symptom-complex frequently attributed to 
so-called “weak heart.” That term is a palpable misnomer, for the heart is 
really not “weak,” there is never any actual decompensation in these individ- 
uals. The vasomotor mechanism is very susceptible to reflex influences, 
and in this patient it was probably reflexly excited by the diarrhoea which 
began several weeks ago. 
It is of prime importance, therapeutically, to assure the patient that there 
is nothing wrong with his heart. He should be given tablets, each containing 
H50 °f a grain of atropine sulphate, three times daily before meals. After 
meals, one half a teaspoonful of an ant-acid powder containing equal parts of 
magnesia usta, bicarbonate of soda and oleosaccharated peppermint should be 
administered; depending upon its action on the bowels, the dose of the powder 
may be increased or diminished. For the vaso-motor attacks themselves, I 
know of nothing better than the extract of suprarenal gland given in tablets 
of two grains each. The diet must be carefully regulated, for anything which 
produces indigestion is very apt to aggravate the vaso-motor symptoms. It 
is therefore advisable to ask the patient what simple nourishment best agrees 
with him, and to have him follow such dietary; but the meals should be small, 
and taken at frequent intervals. Aggravation and excitement readily upset 
these individuals, especially their vaso-motor system, hence mental quietude 
and relaxation must be insisted upon. I shall keep the patient in bed for a 
few days longer, because if allowed on his feet after his long stay in bed, the 
vaso-motor instability is apt to increase, and the symptoms made worse. 
Although the patient is not ill it requires full and detailed knowledge of the 
cause of the symptoms in order to re-establish normal vaso-motor equilibrium. 
Attention to small and apparently trifling details is the sure road to success 
in these cases. I have known of individuals in whom insignificant domestic 
excitement has caused a relapse for several weeks. 
Later Examination.—You saw this patient a few weeks ago. He remained 
abed for a week after you saw him; he then was allowed to walk around. He 
is now able to walk rapidly, and in a day or so will return to his work. His 
recovery has been complete and uninterrupted. 
Case 47.—A. B., physician, aged 32, has had no scarlet fever, genito- 
urinary or other infection except an attack of rheumatism lasting one week; 
this occurred nine years ago. He states that in former years, he had 
occasional extra systoles the cause of which he did not know. About six 
months ago, after riding horse-back for many hours, he suffered from severe 
precordial pains and extrasystoles. The pains were very acute and severe 
CASES 47, 48.—IRRITABLE HEART FROM PHYSICAL OVERSTRAIN 566 
CARDIOVASCULAR CLINICS 
for several hours. They later subsided although still aggravated by walking. 
They gradually disappeared entirely until about three months ago. The 
patient then took a Turkish bath; shortly thereafter, he suffered a recurrence 
of the precordial pains upon walking fast in the open air and upon climbing 
stairs. Otherwise he feels well in every particular although he still has an 
occasional extrasystole. 
Physical Examination.—As you see, the doctor’s teeth and tonsils are 
normal. You will find by careful inspection, that there is some hyperactivity 
of the aorta in the jugulum, and of the left ventricle against the chest wall. 
You can corroborate this by placing one finger in jugulum, and the palm of the 
other hand over the apical region. The cardiac rate is now normal, there is 
no irregularity of rhythm at present. The heart sounds are normal. Upon 
exercise there is no abnormal increase of the cardiac rate. The abdominal 
examination reveals nothing abnormal. The knee and pupillary reflexes are 
normal. There is no edema of the legs. The urine is normal. The ortho- 
diascopic tracing being passed around shows a somewhat large heart. It is 
interesting to note that the fluoroscopic examination showed particularly 
strong ventricular contractions. The electrocardiogram shows normal 
rhythm; the deviations are practically normal in size and form. The ther- 
apy and symptoms will be discussed in conjunction with the following case. 
Case 48.—S. J., aged 24, says that she had scarlet fever and diphtheria 
as a child and that she has suffered for years from severe hemicrania. She 
does not know the cause of the latter. She has never suffered from gastric 
disturbances. She does her own housework. Her menses are regular. She 
has one child. One year ago, after a heavy day’s work, she dragged her 
child on a sled up and down hill for quite some time. The same evening she 
developed rapid heart action which has since continued. It is aggravated by 
overwork, climbing stairs and by excitement. Her appetite is fair, although 
she has lost ten pounds since her trouble began. Her bowels are regular. 
She has an almost constant feeling of dyspnoea and an uncomfortable 
heaviness in the chest. The latter is often accompanied by such vaso-motor 
symptoms as flushing of the face, cold hands and feet. At times her heart 
beats very fast. 
Examination.—The teeth and tonsils are normal as you see. There is a 
slight soft enlargement of the thyroid gland. The systolic blood pressure is 
140; the diastolic, 60. The cardiac rate is 112 per minute and regular. You 
note that when the patient holds her breath at the end of a deep inspiration, 
there is a decrease in the cardiac rate of from 10 to 20 beats per minute. You 
observe even from a distance, the cardiac hyperactivity in the apical region. 
Upon palpation you feel a thrill with the systolic impact, due to ventricular 
hyperactivity. Corresponding to this, upon auscultation the first heart 
sound seems somewhat thrill-like and split. The knee reflexes are very 
lively; the abdominal examination reveals nothing abnormal. The ortho- 
diascopic tracing being passed around shows a heart of normal size and form. CARDIO-VASCULAR CLINICS 
567 
The fluoroscopic examination showed over-action of the aorta, pulmonary 
artery and left ventricle. 
As in Case 47, I do not believe that this patient is suffering from organic 
cardio-vascular disease, despite the abnormal physical signs upon ausculta- 
tion and palpation. 
In Case 47, the original cardiac insult was overexertion from horseback 
riding. After a quiescent period of several months, extrasystoles and cardiac 
pains reappeared following a Turkish bath. The sweating probably acted by 
exciting the vaso-motor mechanism which in its turn upset the as yet scarcely 
stabilized cardiac mechanism. The extrasystoles and cardiac pains were 
the main symptoms. In Case 48 there is a possibility that the history of 
severe hemicrania has some bearing as showing a general neurotic tendency. 
The history of dragging her child for several hours on a sled leaves no doubt 
that this overexertion was the immediate cause of the cardiac symptoms. 
The cardiac irritability has shown itself by tachycardia, dyspnoea and pre- 
cordial heaviness, symptoms and signs similar to those found in the so-called 
soldier’s heart. 
Although the manifestations in Cases 47 and 48 are quite different, they 
both represent a type in which cardiac hyperirritability originates from cardiac 
overstrain. It is as yet a difficult and problematical matter to determine 
how or in what manner such overstrain produces cardiac neuroses. It is 
usually assumed that the onset of these attacks is marked by cardiac dilata- 
tion. Unless the usual accompanying symptoms of cardiac dilatation: Pul- 
monary edema, dyspnoea and cardiac failure are present, it seems quite 
difficult to support this hypothesis. It appears to me that perhaps physical 
cardiac overstrain may so affect the nerves in and about the heart, especially 
the nerve plexuses surrounding the aorta, that the cardio-inhibitory and the 
vaso-motor mechanism becomes reflexly and morbidly excited, with the 
resultant train of symptoms known as the irritable heart. In other words, 
unless actual cardiac dilatation can be proved, the primary result of cardiac 
overstrain may be a neurological, rather than a myocardial “insult.” What 
influence, if any, slight mechanical stretching of the cardiac musculature 
may have in the production of symptoms such as outlined in these two cases 
is as yet unknown. It seems possible nevertheless, that such overstretching 
of cardiac fibers can take place without the production of the usual symptoms 
of acute cardiac dilatation with its decompensation. 
Prognosis.—Case 47 had improved and was practically well, until the 
symptoms recurred after the Turkish bath. The chances are therefore that 
he will again improve rapidly, especially since the present symptoms are mild. 
Case 48 will probably run a longer and more protracted course because of the 
continuance and violence of her symptoms and because her housework does 
not allow her to take sufficient mental or physical relaxation and rest. The 
bromides are of value in both; and in both the extract of suprarenal gland in 
two grain doses is of benefit for the attacks of tachycardia and for the extra- 568 
CARDIO-VASCULAR CLINICS 
systoles. The drug is to be given at the time the symptoms are most violent. 
Digitalis is of no use in either case. Nor is rest in bed of any value except 
perhaps for a short time when the symptoms are most marked. In similar 
cases graded games in the form of play usually offer a happy combination 
of the proper amount of exercise with mental relaxation. 
CASES 49-54.—CARDIAC NEUROSIS (ESPECIALLY TACHYCARDIA) FOLLOWING 
FEBRILE CRISES—GENERAL COMMENT 
Case 49.-—-Miss M. S., aged 38, had a mild influenzal attack three months 
ago. She had very slight fever but had frequent, long continued sweating 
even after her cold was better. Since that time, as she says, she “ knows she 
has a heart.” When trying to do her work as teacher, her heart “thumps,” 
sometimes fast, sometimes slowly but always “accentuated,” as she describes 
it. She woke up some weeks ago with a “thumping heart.” She has 
recently suffered from slight indigestion with fulness in the stomach and 
eructations. She has never had rheumatism or scarlet fever and only occa- 
sional sore throats. 
Examination.—The systolic blood pressure is no; the diastolic, 80. As 
you see the thyroid is not enlarged. You notice that even now, although the 
heart rate is normal, the patient has slight dyspnoea. She is quite thin but 
she says that she has not lost any weight during the last year. As you listen 
to her heart, you find that the sounds are normal, with the exception of some 
exaggeration of the first sound at the apex. Cardiac inspection and pal- 
pation reveal nothing abnormal. As the patient walks about, there is no 
increase in the cardiac rate, although the patient states that she is now con- 
scious of her heart action. Abdominal examination reveals nothing abnor- 
mal. There is no edema of the legs. The knee reflexes are normal, the urine 
is also normal. The orthodiascopic tracing, which I pass around, shows a 
somewhat narrow heart but not abnormally so for this thin-chested indi- 
vidual. 
The diagnosis is plain. There is no cardio-vascular disease. The patient 
has a cardiac neurosis in which the prominent symptom is the annoying 
consciousness of her heart action. I believe the primary cause of the neu- 
rosis is the critical sweating which followed a mild influenza attack a few 
months ago. I shall discuss that factor in detail after I have shown you 
similar cases. I shall advise the patient to go back to her teaching and not 
be frightened by the peculiar sensations produced by her heart. She will 
be given the mixed bromides and the extract of suprarenal gland. 
Later Examination.—You no doubt recall that I presented this patient 
two weeks ago. She now feels perfectly comfortable and is able to teach 
and walk as well as ever without any abnormal cardiac sensations. Indeed, 
as she puts it, she no longer knows nor feels that she has a heart. The medi- 
cation consisted of 15 grains of the triple bromides given twice daily regularly CARDIOVASCULAR CLINICS 
569 
for one week, and five grain tablets of the extract of suprarenal gland, taken 
only when she felt particularly uncomfortable. 
Case 50.—Miss B. S., aged 24, has always been somewhat nervous and 
irritable. About six months ago, during the summer, she had a severe attack 
of tonsillitis accompanied by high temperature and followed by critical 
sweats. Since then she has suffered from tachycardia; according to her 
doctor her heart rate often reaches 140 per minute. She has also had gastric 
disturbances for weeks, the chief symptoms of which were frequent belching 
and a feeling of epigastric distension. At present she feels very weak. She 
has been kept in bed for four months by her family physician who thinks that 
she has an organic heart lesion. For a short period she improved but now 
she feels as badly as ever. The main cardiac complaint at present is palpi- 
tation due to rapid heart action. She also has headache and shooting pains 
in the limbs. She has lost about 20 pounds since her illness. Her 
highest temperature since she has been in bed has been ioo°. 
Examination.—You note that the patient is thin. There is no exoph- 
thalmos or goitre. The teeth and pharynx are normal. You see even from 
a distance that there is ventricular overaction in the mitral region. The 
cardiac area seems normal to percussion. The cardiac rate is very peculiar; 
at times it is between sixty and seventy per minute accompanied by a thump- 
ing action of the heart; then, suddenly and without extrasystoles, the rate 
reaches no to 120 per minute, especially when the patient sits up. You 
notice that even the rather rapid heart rate is not accompanied by dyspnoea. 
Upon palpation you feel a somewhat thrill-like systolic shock over the apex 
even when the heart beats slowly. Upon auscultation you hear a soft sys- 
tolic murmur over the mitral area. The abdominal examination reveals 
slight epigastric sensitiveness to pressure; the abdomen is otherwise normal. 
There is no edema of the legs. The urine is normal. 
The treatment will consist of the administration of fifteen grains of the 
mixed bromides given at bed-time; of the suprarenal gland extract in five grain 
doses three times daily before meals, and of an ant-acid powder after meals. 
Later Examination.—We examined this patient about six weeks ago. Her 
systolic blood pressure is now 140; the diastolic, 90. You observe that she 
has become stouter; the patient states that she has now regained her old 
weight. She no longer feels nervous, her only complaint being occasional 
belching. Upon examination you find that the cardiac rate is around 100, 
and that upon taking a deep breath and holding it, the rate is reduced to 
70 or 80 per minute. There is no thrill nor cardiac hyperactivity. The 
patient has improved very much and sleeps very much better than she did 
formerly. I shall prescribe of a grain of atropine sulphate, three times 
daily before meals, and magnesium usta powder in half-teaspoonful doses 
three times a day after meals. 
Despite the history of tonsillitis, or even assuming diphtheria which 
nitated the cardiac symptoms, I do not think that the patient has or ever 570 
CARDIOVASCULAR CLINICS 
had myocarditis. Myocarditis associated with diphtheria is a very serious 
disease, gives rise to decompensation in its early stages and is often fatal. In 
this case the cardiac symptoms began with critical drops of temperature and 
accompanying sweats, and continued for several months until rational treat- 
ment was begun. The benign course of the case, especially the absence of 
fever, would almost of itself make the diagnosis of actual cardiac disease 
highly improbable. It is interesting to note that the physician who treated 
the patient was apparently led astray in the diagnosis by the abnormal phys- 
ical signs which were present; the thrill and tachycardia. As I have just 
pointed out to you, these have now disappeared. 
General comment will be reserved until all the patients of this group have 
been examined. 
Case 51.—Mrs. T., aged 34, is married five years. Her husband had lues 
some years ago. His Wassermann blood reaction is now 2 plus. Four months 
ago while in the seventh month of pregnancy, she had a very severe attack of 
influenzal pneumonia. She was very ill for a long time; in fact, her life was 
despaired of. Convalesence was accompanied by severe night sweats. Even 
now, four months after the pneumonia, she still suffers from occasional sweats. 
Before her pneumonia she was always athletic and active. At present, 
attempts at walking or at lifting anything heavy cause severe pains under 
the left breast. 
Examination.—You see that the patient is a very strong and vigorously 
built woman, in fact she looks the picture of health. She does not suffer from 
any dyspnoea while at rest. The thyroid gland is not enlarged. The sys- 
tolic blood pressure is 140; the diastolic, 90. Upon precordial inspection and 
palpation, slight ventricular hyperactivity is demonstrable in the apical 
region. You also note that there is no sensitiveness upon precordial pressure. 
The abdominal examination reveals nothing abnormal. There is no edema of 
the legs; the urine is normal. I want you especially to note the orthodiasco- 
pic tracing which I pass around; it shows that the aorta is normal in size and 
form and that the general configuration of the heart is normal. This is 
important in view of the husband’s history of syphilis and of the moderately 
strong positive Wassermann reaction of his blood. 
Despite the history of syphilis in the husband, and the patient’s cardiac 
complaints, I find no evidence of cardiac disease. Indeed, although her 
blood has not yet been examined for syphilis, even if it should prove mildly 
positive I would search for the cause of such reaction in some other organ. 
The history points definitely to the fact that the cardiac symptoms—pal- 
pitation and pain—came at the time of the critical sweats. I believe 
that this patient is another example of cardiac neurosis without actual 
disease. 
Later Examination.—This robust patient you saw four months ago. She 
was given the extract of suprarenal gland, with bromides at night. Very 
soon after medication was begun the cardiac symptoms disappeared. She CARDIO-VASCULAR CLINICS 
57i 
was in the country, has since been active, and has felt well until about a week 
ago. She then developed very slight coryza with slight rise of temperature. 
Within a week, the old cardiac symptoms began, especially the precordial 
pains. These became so severe that at times she was unable to sleep. The 
cardio-vascular examination, as before, shows no abnormality of any kind. I 
believe that the slight cold acted anaphylactically, so to speak, and caused 
the present precordial attacks. In other words, she had slight sweats follow- 
ing the cold, and these acted as a sensitizer, as it were, in causing a relapse of 
the cardio-neurotic symptoms. I shall prescribe atropine sulphate in small 
doses. . I believe that very soon she will again be quite comfortable. 
Case 52.—Mrs. S., aged 28, had influenza three months ago. This was 
followed by critical sweats for two weeks. She then developed rapid heart 
action and precordial pressure, especially when excited. Her appetite is fair. 
The chief complaints are throbbing temples and palpitation. 
You see that at present the patient is slightly flushed. There is some 
throbbing of the carotids. There is no goiter or exophthalmos. The pulse 
rate varies rather rapidly from 90 to no per minute. There is a slight pre- 
cordial thrill to be felt upon palpation, and a soft systolic murmur to be heard 
at the apex. The blood pressure is normal. There is no edema of the legs. 
When the patient holds her breath at the end of a deep inspiration there is a 
momentary but decided decrease of the cardiac rate. The knee reflexes are 
very lively. The abdominal examination reveals nothing abnormal. The 
urine is normal. 
I do not believe that this patient has any cardiac disease. She represents 
another instance of continued tachycardia following the critical sweats inci- 
dental to most pneumonia attacks. Therapeutically I would suggest trying 
to build this patient up—she looks somewhat thin, you see—by giving her 
carbohydrates and fats. I shall prescribe the mixed bromides three times 
daily after meals, and the extract of suprarenal gland, to be taken when pal- 
pitation is particularly severe. 
Later Report.—Her family physician reported to me that the patient 
became very comfortable after one week and that she has no tachycardia at 
present. She is able to go about, to walk and climb stairs, and is very com- 
fortable in every way. Perhaps the assurance to the patient that she had no 
cardiac disease was a large factor in the rapid cure. 
Case 53.—Mrs. S., aged 28, had influenzal pneumonia three months ago. 
She was in bed for one month. Following the pneumonia, she had severe 
sweats for two weeks. Since then she has suffered from rapid heart action 
and palpitation, especially after exertion. She s&ys that her appetite is 
poor. 
Examination.—You notice that the patient is somewhat thin. She has 
no dyspnoea while at rest. The systolic and diastolic blood pressures are 
normal. Aside from a soft systolic murmur at the apex, the cardiac exam- 
ination reveals nothing of note. When sitting quietly, the pulse rate is about 572 
CARDIO-VASCULAR CLINICS 
90 per minute; when walking about the room, it rises to no. This rapidity 
is temporarily controlled by having the patient take a long breath and hold- 
ing it. You have of course observed that during the entire examination 
the patient is readily perturbed, that she cries readily and is very 
excitable. 
The patient is certainly neurotic in the ordinary acceptation of the word. 
I believe, however, that it was the critical sweating following her influenza 
which probably caused the palpitation and tachycardia. There is no evi- 
dence of any cardio-vascular disease. Assurance of that fact to the patient 
will no doubt play a very large role in alleviating her symptoms and in curing 
her. 
Case 54.—Miss P., aged 20, has suffered for two years from occasional 
right-sided pain and indigestion. She has had no abdominal symptoms dur- 
ing the preceding three months. Five weeks ago she suffered from slight 
epistaxis and influenzal bronchitis. Since then she has complained consider- 
ably of weakness, anorexia, occasional sweating and tachycardia. Her 
family physician states that her temperature has been normal and that at 
present she has no expectoration. 
Examination.—You observe that the teeth and throat are normal. You 
hear a slight cardio-respiratory murmur over the pulmonary artery. The 
cardiac rate is 100 per minute; otherwise the cardiac examination reveals 
nothing abnormal. The lungs are clear. Upon abdominal examination you 
can feel a somewhat loose right kidney. This finding is by no means 
uncommon, especially in thin individuals. Despite the history of right sided 
pain, there is at present no tenderness over the appendix. 
I believe that organic cardio-vascular disease can be excluded. Except 
for slight tachycardia, there are no abnormal cardiac signs or symptoms. 
The family physician has kept this patient in bed. I think she will do very 
much better if she gets up and goes about, resting in bed only for one hour 
after meals. Patients of this kind often feel exhausted and therefore need an 
abnormal amount of physical rest. She should be over-fed. A tonic pill 
containing iron, arsenic and strychnine is indicated. The extract of the 
suprarenal gland in five grain doses three times a day after her meals 
would probably help in controlling the tachycardia. The prognosis is 
excellent. 
General Comment.—I have grouped these post-febrile tachycardia cases 
for you, gentlemen, because they are quite frequent and especially because 
tachycardia following any infection is commonly regarded as the result of 
organic cardio-vascular disease, particularly of the myocardium. One of the 
chief causes for this mistake has been that the etiological factor has not been 
properly traced. The usual teaching is that pneumonia or other febrile 
invasions attack the cardiac musculature and thus bring about actual myo- 
carditis. That such organic changes can follow pneumonia is of course true. 
I believe that they are very rare, however, and that when they do occur the CARDIO-VASCULAR CLINICS 
573 
patients do not exhibit symptoms similar to the cases I have just shown you. 
All of the cases that I have presented I consider functional in nature. By 
functional I mean that there are no organic changes in the cardiac valves, 
endocardium or musculature. Indeed I have dwelt upon the fact that the 
physical signs are often quite similar to, or identical with those found in 
cardiac neurosis from other causes, as for example the so-called soldier’s heart. 
In the latter it is now generally conceded that organic disease is very rarely 
present. 
What is the cause of cardiac irritability following critical defervesence? 
I shall not here speculate upon the mechanism of the crises themselves but I 
wish particularly to emphasize that the salient clinical feature is the sweating. 
As you know, taken by itself, this is an evidence of excitation of the sympa- 
thetic nervous system. If any of you have ever had a severe cold you will 
know that the sweats frequently continue for several days or even weeks after 
the cold has run its course. And just as the sweats are due to hyperexci- 
tation of the sympathetic nervous system, so I conceive the cardiac irritabil- 
ity, especially the tachycardia, to be due to a concomitant hyperexcitation 
of the accelerator mechanism of the heart. I wish also to dwell upon the 
important clinical fact that once the cardiac neurosis has started, it may con- 
tinue a long time after the sweating has ceased. Unless one conceives the 
primary cause in the light of an abnormal excitation of the svmpathetics and 
accelerators, I believe it is exceedingly difficult to understand how tachy- 
cardia of this type can be brought about. 
If one regards these cases as actual myocarditis with tachycardia, then, 
may I ask, how can such myocarditis suddenly cease in those in 
whom tachycardia suddenly stops? According to my assumption, an 
“insult” to the sympathetic nervous system may abnormally excite heart 
action for a longer or shorter time. It is in this manner that I view the etiology 
of the vast majority of post-febrile tachycardias. What there is in the indi- 
vidual that produces tachycardia in some and not in others I find it impossible 
to state, except the generic statement that different types of individuals 
react differently to what are apparently similar causes. We also know that 
the nerve balance of some individuals is very readily upset while others 
apparently show no such reaction. In addition, certain types of individuals 
may be called sympathetic-excitive in that their sympathetic nervous sys- 
tems are especially irritable, while others may be termed vago-excitive 
because in them the vague nerves are hyperirritable. 
I have often speculated upon the cause of the good results following the 
use of the extract of the suprarenal gland in the group of cases presented to 
you to-day. A priori one would expect that this drug, itself an excitant of 
the sympathetic nervous system, would be followed by poor results. • I 
believe its great benefit depends upon the fact that it stabilizes the vaso- 
motor system, thus tending to make it less hvpersusceptible to abnormal 
nerve influences. 574 
CARDIO-VASCULAR CLINICS 
CASE 55.—IRRITABLE HEART IN A PATIENT WITH PREVIOUS PAROXYSMAL 
TACHYCARDIA 
O. K., male, unmarried, aged 57, in previous years had always been active 
and athletic. About twenty years ago he felt something “snap” in his 
heart, as he described it. This “snap” was followed by very rapid heart 
action which as suddenly stopped. It was not accompanied by any gastric 
symptoms. He does not know the cause of the original attack. Following 
the first attack, he had many others lasting from one half hour to one day. 
The attacks occurred at varying intervals of from one month to one year. 
Several months ago, he developed gastric symptoms for the first time; namely, 
poor appetite and distention after meals. He feels very “nervous” and says 
he cannot sleep at night. Recently his heart action began to annoy him; he 
has a feeling of palpitation and sometimes his heart “ stops. ” After stopping 
it occasionally pumps hard. 
Examination.—Let me first give you the result of the gastric analysis: 
There is hypersecretion but no hyperacidity: There is no evidence of gastric 
ulcer. You see that the patient though small, is wiry and is very well pre- 
served for his age. The systolic and diastolic blood pressures are normal. 
Auscultation reveals no abnormal heart sounds. Palpation over the heart is 
also normal. The orthodiascopic tracing which is being passed around 
shows a heart normal in size and form. Of most interest is the cardiac rate. 
At times it is rather rapid, about 100 a minute, then it suddenly changes to a 
normal rate. In addition the rhythm is occasionally disturbed by extrasys- 
toles. The patient’s tongue is somewhat coated. There is no edema of the 
legs. The urine contains a goodly trace of indican, it is otherwise normal. 
It is of interest to speculate upon the influence of the prior paroxysmal 
tachycardia on the origin of the extrasystoles which are now present. A 
gastric neurosis such as this patient has is in itself sufficient to produce reflex 
excitation of the heart nerves, with resultant tachycardia and extrasystoles. 
But in view of the old paroxysmal tachycardia, one may assume that the 
patient or rather his cardiac nerves have become hypersusceptible, so that 
now they are more readily influenced and upset by any abnormal reflex 
excitation from a neighboring organ, in this instance, the stomach. 
What this patient especially requires is mental relaxation. He has been 
worried about his work, he feels that because of his heart he may not be able 
to continue at his business as a boat-builder, and this doubtless has an influ- 
ence in causing the sleeplessness and gastric symptoms. I would advise him 
to seek some relaxation such as fishing, and to give up his work entirely for a 
week or two. He should be given bromides for his sleeplessness and atropine 
sulphate in small doses three times a day in order to try to control the cardiac 
irregularity. 
Later Report.—I have heard from the patient’s physician that he is much 
improved, and that he sleeps better. The extrasystoles are still present, CARDIO-VASCULAR CLINICS 
575 
but they no longer annoy him, and he is again partly able to take up his old 
work as boat-builder. 
CASES 56, 57.—CARDIAC NEUROSIS FOLLOWING GASTRO -INTESTINAL 
DISTURBANCE 
Case 56.—M. W., female, aged 41, had always been in the habit of bolting 
her food: She suffered frequently from belching. The patient states that 
acids and sour things do not agree with her. She has two children, her 
menses are regular. Some weeks ago, after bolting a heavy meal she had 
what she called a “gas attack:” Her abdomen felt tense and she belched con- 
siderably. The attack was accompanied by palpitation. Her family phy- 
sician who saw her at the time stated that he found the heart action very 
irregular. After one wreek he noted that the heart became more regular. 
There is no history of rheumatic or other infection. 
Examination.—Upon examining the mouth of this patient, you find that 
the teeth and throat are normal. The systolic blood pressure is 160; the 
diastolic, 100. There is, as you see, no thyroid enlargement. The heart is 
rapid and regular, its rate is 100 per minute; this rapidity may be due to her 
evident nervousness at present. There is a somewhat thrill-like apical first 
sound to be heard, and a thrill-like systolic shock to be felt at the apex; they 
are probably due to rapid and somewhat over-active heart action, for if the 
cardiac rate be decreased by having the patient take a deep breath and hold- 
ing it, you find that both these cardiac abnormal features disappear. The 
orthodiascopic tracing which I am passing around shows a heart normal in size 
and form. The abdominal examination reveals nothing abnormal. The knee 
reflexes are normal. There is no edema of the legs. The urine is normal. 
I believe we can exclude organic cardiac disease despite the abnormal 
thrills heard and felt over the apex. I have shown you many similar cases to 
prove that these abnormalities are very often of functional origin and due to 
an over-rapid or an over-active heart. Although there is no cardiac irregu- 
larity at present, the family physician’s description of the arrhythmia at the 
time he examined her leaves no doubt in my mind that it was due to extra- 
systoles. These have now apparently entirely disappeared but the patient still 
complains of a subjective feeling of “palpitation.” I believe that both the 
extrasystoles and “palpitation” are caused by reflex disturbance of the cardiac 
mechanism from the attack of indigestion. Such cardiac neuroses are some- 
times regarded as toxic in origin. I assume this implies that a certain amount 
of poisonous material is absorbed into the system and that this deleteriously 
affects the cardiac inhibitory apparatus or the heart muscle itself. In my 
opinion, the vast majority of these disturbances of cardiac rhythm are not 
toxic in nature but are simply due to reflex excitation of the cardiac nerves 
following any stomach disturbance. I have found extrasystoles frequently 
in patients who are subject to belching and gastric distension. They are less 576 
CARDIO-VASCULAR CLINICS 
frequent, I believe in those with actual organic gastro-intestinal disease than 
in those with functional derangements. 
I shall prescribe atropine sulphate three times daily in doses of }{oo 
of a grain, and an ant-acid powder to be taken after meals; she should also 
be given 30 grains of the triple bromides before retiring at night. 
Later Report.—I have since heard from the family physician that the 
patient is feeling very well, and that the subjective feeling of palpitation and 
the arrhythmia have entirely disappeared. 
Case 57.—S. B., female, aged 27, gives the following history. Several 
months ago she was shocked by the unexpected death of a friend. A few 
days thereafter she had nausea and vomiting for which she remained in bed 
two days. She then felt well for six weeks. Her family physician stated 
that she later had a hysterical vomiting spell and that the vomiting lasted 
five days. She remained well until three weeks ago. Then after eating some 
“fried stuff,” as she calls it, she became nauseated, and heard noises in her 
ears for several days. Very soon thereafter she complained of tachycardia, 
of extreme dizziness and of frequent belching. Her bowels are constipated; 
her appetite is fair. At the present time her chief complaints are almost 
constant tachycardia and dizziness. 
Examination.—The patient as you notice, gives the impression of being 
very nervous; she is restive and her face is flushed. There is no enlargement 
of the thyroid gland. The systolic blood pressure is no, the diastolic, 70. 
The cardiac rate is 110 per minute. When she holds her breath at the end of 
a long inspiration, you find that the rate occasionally becomes normal in 
rapidity. Her hands are cold. Except for the abnormal rapidity, the heart 
is normal upon auscultation and palpation. The knee reflexes are very lively. 
There is no edema of the legs. The orthodiascopic outline of the heart, as 
you see from this tracing, shows no abnormality of any kind. Upon neuro- 
logical examination, I find there is no ataxia of the upper extremities, nor any 
differences in cutaneous sensibility to touch, heat or cold. The ophthal- 
mological examination reveals concentric contraction of both visual fields. 
I do not find any evidence of organic cardio-vascular disease. This 
patient is a very high-strung woman, and it appears that her entire nervous 
system became upset from the nervous shock of the death of her friend. 
Thereafter she had several gastric attacks, and it seems as if the last spell of 
indigestion disturbed the nervous control of the heart and produced the 
tachycardia of which she has since complained. It is very important to 
determine the cause of the dizziness, especially in view of the ocular findings, 
for some cerebral growth may possibly cause both the dizziness and the con- 
tracted visual fields. From the cardio-vascular symptoms, however, I am 
much more inclined to the view that vaso-motor changes in the cerebrum are 
responsible for the dizziness, the frequent noises of which she complains, and 
even for the contracted visual fields. At any rate, for the present, I shall 
proceed upon this hypothesis and shall treat her accordingly. I shall pre- CARDIOVASCULAR CLINICS 
577 
scribe atropine sulphate three times a day to be taken before meals, bicar- 
bonate of soda after meals, large doses of the mixed bromides each morning, 
and the extract of suprarenal gland in one grain doses for severe attacks of 
dizziness and tachycardia. 
Later Examination.—You recall we saw this patient about two months 
ago. At first she got along very slowly, dizziness and palpitation still being 
the main symptoms. She gradually regained confidence in herself, and with 
this return of confidence, dizziness and tachycardia gradually diminished. 
She finally went to the seashore, where after a time she took ocean baths. 
You notice the marked difference, both in her appearance and in her general 
nervous condition. She has gained very much in weight. If you examine 
her heart you will find that the rate is almost normal. She no longer com- 
plains of dizziness and not only feels better, but as she puts it, she is perfectly 
well. 
This case may be coupled with the preceding one as another instance of 
cardiac neurosis following gastric disturbance in a particularly neurotic 
individual. Both cases show how readily the normal cardiac mechanism 
may be upset by reflex disturbances from a disordered stomach, particularly 
in hypersusceptible, neurotic patients. 
CASE 58.—CARDIAC NEUROSIS—SUBJECTIVE DYSPNCEA 
M. L., female, aged 39, has had five children and no miscarriages. Her 
menses are regular. She herself states that she is of an “hysterical tem- 
perament.” She says that about twelve years ago she heard of the sudden 
death of a child. Since then, when aggravated by any quarrel, she feels 
“palpitation and tightness in the heart.” About two years ago, after some 
trouble with her grown-up son, she was considerably upset; this was followed 
by pain and abdominal colic. She does her own housework, is very exact 
about it, but feels exhausted after doing it. She weighed 200 pounds some 
years ago, she now weighs 185. Besides the abnormal sensations in the heart, 
she complains of a choking feeling in her throat. 
Examination.—You observe that this patient has no dyspnoea while at 
rest. Her teeth and tonsils are normal. The systolic blood pressure is 130; 
the diastolic, 90. The heart, you find, is normal to auscultation and pal- 
pation. , The cardiac rate is absolutely normal, indeed, there is no increase 
of the cardiac rate even when the patient walks around the room rapidly. 
The orthodiascopic tracing, you observe, shows a rather small but flat-lying 
heart. Its posture on the diaphragm is no doubt due to the fact that the 
diaphragm has pushed up the left ventricle. The abdominal examination 
reveals nothing abnormal. The urine and knee reflexes are normal. 
I demonstrate this case to you, not because the patient has any cardiac 
disease, but because she is one of a large group found frequently in private 
practice, who complain of all sorts of subjective sensations in the chest—feel- 578 
CARDIO-VASCULAR CLINICS 
ings of unrest, palpitation without actual tachycardia, a choking and gripping 
sensation etc.— yet who have no actual cardiac disease. A neurotic insult, 
so to speak, plays a large role in producing an outbreak of such symptoms. 
As you see, some special cause can usually be elicited by a careful history. 
Reassurance and suggestion play a very large role in the therapy of these 
cases. They require mental relaxation rather than physical rest. If treat- 
ment along such lines be carried out, almost miraculous and rapid cures 
can be accomplished. 
CASE 59.—CARDIAC NEUROSIS AND PREGNANCY 
Mrs. M. R., aged 35, tells us that she has been nervous for years. She is 
now in the third month of her fifth pregnancy. In previous years when upset 
from any cause, she suffered from tachycardia. Of late months she has had 
occasional pains in the left chest, anteriorly and posteriorly. There had also 
been a recent recurrence of old gastric symptoms, chiefly belching; these have 
ceased since her pregnancy. She has had “ palpitation ” off and on for several 
weeks; she is very much worried now because she has been told that she has 
“heart disease.” 
Examination.—The teeth, throat and thyroid as you see, are normal. The 
systolic blood pressure is 143; the diastolic, 88. The cardiac rate is 100 per 
minute. You observe that holding the breath at the end of inspiration has a 
marked effect in slowing the heart rate. Upon palpation over the heart you 
feel a slight systolic thrill at the apex; a soft systolic murmur is audible over 
the same area. Abdominal examination reveals nothing abnormal. The 
urine is normal. There is no edema of the legs. The knee reflexes are very 
lively. The orthodiascopic tracing being passed around shows a normal- 
sized heart and aorta. Upon carefully palpating the left chest, you will find 
two small sensitive areas in the fifth intercostal space, one anteriorly, the 
other posteriorly, which make the patient wince as you press upon them: 
These are the usual sensitive spots found in intercostal neuralgia. 
I find no evidence of any cardio-vascular disease. The patient has a mild 
intercostal neuralgia. The localized pains, the moderate tachycardia, and 
probably also the soft apical murmur and thrill have apparently been inter- 
preted by another physician as “heart disease.” The latter diagnosis was 
told the patient. She naturally became frightened, and being of a neurotic 
temperament it intensified her nervousness. There is no indication for the 
interruption of pregnancy. The chief “remedy” is assurance to the patient 
that she has no “heart disease.” There is no reason to fear that the mild 
tachycardia will interfere with the normal course of pregnancy or parturition. 
CASE 60.—RECURRENCE OF SYMPTOMS OF EXOPHTHALMIC GOITER AT THE 
MENOPAUSE 
Mrs. 0., aged 49, has had two children; the younger is 25 years old. 
About 18 years ago she had exophthalmic goiter with typical symptoms: CARDIOVASCULAR CLINICS 
579 
Tremor, nervousness, enlarged thyroid and “skipping of the heart. ” A thy- 
roidectomy was done with excellent results. She felt well for many years. 
About three years ago she complained of belching, intestinal rumbling, pain 
across the chest, faintness and dizziness. These symptoms have usually been 
temporarily relieved by gastric eructations. Until two months ago her 
menses were regular. Latterly, after such slight exertion as walking, she 
has suffered from midsternal pains radiating to both arms; she 
feels weak and has “ skipping ” of the heart. In addition she occasionally has 
a burning sensation in the throat. All these symptoms are usually relieved 
by belching. There is no vomiting or regurgitation of fluid. The bowels 
are regular. She has been eating rather heavily of late. The urine contains 
a trace of sugar; it is otherwise normal. 
Examination.—You note the scar in the neck due to the thyroidectomy. 
There is no exophthalmos. There is some carotid overaction. You feel a 
strong, thrill-like impulse at the apex. Upon auscultation over the mitral 
area, there is a broken, cog-like systolic first sound. The other cardiac 
sounds are normal. The cardiac rate is ioo per minute, and is interrupted 
by occasional extrasystoles. The systolic blood pressure is 160; the diastolic, 
70. The abdomen is not sensitive to pressure. The margin of the liver can- 
not be felt. The orthodiascopic tracing, as you see, shows an enlarged aorta 
as well as enlargement of the left ventricle below and to the left. There is no 
edema of the legs. The knee reflexes are lively. 
I shall first discuss the physical signs at the apex: The palpable thrill and 
the broken, thrill-like first sound. These are by no means indicative of a 
valvular lesion Such abnormal sounds are common in rapidly beating, 
violently acting hearts found in typical exophthalmic goiter. They are also 
common in the irritable heart observed in general and military practice. 
Now, with reference to the orthodiascopic findings. Is the enlarged left 
ventricle the result of dilation or of hypertrophy? The form of the heart in 
the tracing is not characteristic of hypertrophy; it has not the large, obtuse, 
egg-shaped form. When I looked at the heart through the fluoroscope, I 
missed the rocking action like a see-saw with the fulcrum in the region of the 
pulmonary artery. This motion is characteristic of the hypertrophied left 
ventricle. Ventricular enlargement such as you see in this tracing is not 
uncommon in exophthalmic goiter. In the earlier stages of the disease, it can 
be scarcely attributed to hypertrophy, for post-mortem examination has 
shown that hypertrophy of the cardiac musculature is rare. I believe the 
aortic enlargement visible in the tracing is due to dilatation of the artery, 
probably from the violence with which the blood is thrown into the 
circulation. 
How shall we interpret and correlate the midsternal pains, the belching 
and the exhaustion? The “skipping” of the heart complained of by the 
patient is readily explained as due to the extrasystoles which we discovered 
upon examination. I believe the pain and the gastric symptoms, especially 580 
CARDIOVASCULAR CLINICS 
the relief following belching, are due to cardiospasm. The cardiac irregu- 
larity may have its reflex origin from that condition. 
I consider that the cardiac and gastric symptoms are the result of a neuro- 
sis accompanying the beginning menopause. In fact, the present symptom 
complex may be considered, in a sense, a recrudescence of the old goiter symp- 
toms; but this time they are of climacteric origin. The therapy should be 
directed mainly to the gastro-intestinal canal. The patient should be given 
an ant-acid powder. She should take simple food frequently rather than 
regular three large meals, and should be given bromides at night. 
Later Report.—Three weeks later her physician stated that she was much 
improved and that she could walk without pains or discomfort. 
CASE 61.—EXOPHTHALMIC GOITER WITH HYPERTENSION 
P. G., aged 27, has been married one year. The menses had been regular 
until six weeks ago. She says she had a goiter and occasional tachycardia 
for some time before marriage. For the first few months after marriage she 
felt well. Latterly she has been tired and ‘‘nervous” and has lost weight. 
Examination.—I present the patient to you as a typical example of exo- 
phthalmic goiter with a so-called goitrous heart. You observe the moderate 
exophthalmos, the flushed facies, the tremor of the outstretched hands, the 
enlarged thyroid. You can also see the tachycardia by watching the rapidly 
throbbing carotids, as well as the heave of the left breast with each ventricu- 
lar systole. The heart rate is 120 per minute. You feel a decided systolic 
thrill at the apex, and you hear a broken, split, thrill-like first sound over the 
mitral area. These abnormal cardiac signs are not necessarily evidence of 
valvular or myocardial disease; they are probably due to the violence with 
which the blood is thrown into the aorta during systole. 
The orthodiascopic tracing, you observe, shows an enlarged aorta; 
the ventricular outline is normal in size and form. 
I present this case to you chiefly because of the marked hypertension. 
The systolic blood pressure, you observe, is 210; the diastolic, 50. The urine 
is normal in every respect. There is no edema of the legs Moderate hyper- 
tension is part of the clinical complex of exophthalmic goiter. Occasionally, 
however, as in this instance hypertension is extreme. But this is not indica- 
tive of renal involvement in patients with exophthalmic goiter; it is probably 
due to an extremely hypersensitive and labile vaso-motor system which reacts 
in an exaggerated fashion to any abnormal stimulus. 
It is a matter of interest to speculate as to whether marriage had any 
relation to the onset of the goitrous symptoms in our patient. From the 
history it is probable that a mild non-toxic goiter was present before marriage. 
We know that pregnancy does occasionally activate a dormant goiter, appar- 
ently by its as yet somewhat mysterious hormonic endocrine influence upon 
the thyroid. However, since it is only six weeks from the date of her last CARDIOVASCULAR CLINICS 
S8i 
menstruation, and since goitrous symptoms have been present several months, 
pregnancy can be excluded etiologically. Is it possible that marital inter- 
course of itself can so affect ovarian function as to profoundly and deleteri- 
ously influence the entire endocrine system, and with it the thyroid, thus 
causing the complex of exophthalmic goiter? Although we are now delving 
into the unknown, it seems possible that sexual intercourse can effect an 
already pathological thyroid in the manner just suggested. On the other 
hand, it must be remembered that sexual intercourse and excitement as such, 
may also conceivably exert a morbid influence upon patients with goitrous 
tendencies by producing general neurotic hyperexcitability. 
Therapy.—Should the patient be pregnant, I would insist upon immediate 
emptying of the uterus. This can and should be done, I believe, under mor- 
phine and not general narcosis. The remainder of the treatment should 
consist essentially in rest, attempts at overfeeding and in the administration 
of large doses of mixed bromides. Intercourse should be interdicted for 
several months at least. Cases such as these run a very protracted course; 
they are very trying both to physician and patient, for care and supervision 
must be exercised for months before marked or indeed any improvement 
becomes evident. Even when these individuals are apparently cured, they 
are apt to have mild or severe relapses if their lives are not carefully regulated, 
especially in the avoidance of all kinds of excitement. I shall not take up 
the advisability of thyroidectomy in this case because it would lead us too 
far afield. 
CASES 62-64.—TOBACCO HEART—GENERAL COMMENT 
Gentlemen, I have grouped for you three cases of so-called tobacco heart 
whose histories and examinations we shall first complete; we shall then discuss 
the etiological and various other factors. 
Case 62.—E. C., male, aged 59, a baker, has always been a heavy cigar- 
ette smoker, often smoking from forty to fifty cigarettes daily. He says that 
he is of a very excitable temperament and easily aggravated. About a year 
and a half ago, following a dispute, he had his first attack of precordial pain. 
Since then these pains have been very frequent, especially when walking or 
driving in the open air. In his bakery he can walk around very rapidly 
without discomfort of any kind. Occasionaly the precordial pains radiate 
to the left shoulder. He has not lost weight, he has no gastric or other 
symptoms. 
Examination.—You note that when the patient is sitting quietly he is 
not dyspnceic nor does he become dyspnoeic when walking about the room. 
The systolic blood pressure is 120; the diastolic, 80. You observe that neither 
upon palpation, percussion nor auscultation does the cardiac examination 
reveal any abnormality, whether the patient be at rest, walking, sitting quietly 
or lying down. The knee reflexes are very lively. The abdominal examina- 582 
CARDIOVASCULAR CLINICS 
tion reveals nothing abnormal. There is no edema of the legs. The urine is 
normal. Despite the fact that this man is broad-chested, the size of the aorta 
and of the heart as shown by the orthodiascopic tracing being passed around is 
surprisingly small. 
In my opinion the patient presents no evidence of organic cardio-vascular 
disease. I believe that the cardio-vascular symptoms can be explained as the 
result of tabagism in a person of neurotic tendencies. 
Later Examination.—This patient you saw about four weeks ago. I 
presented him as a case of “smoker’s heart.” At this examination you will 
discover that the blood pressure and other cardiac findings are the same 
as at the first examination. The patient feels very much better, is able to 
walk in the open, and says he can walk even in cold weather without precor- 
dial pains. I had given him the mixed bromides in 15 grain doses mornings 
and evenings, and a tablet of nitro-glycerine and atropine sulphate three times 
daily before meals. For attacks of precordial pain he took the extract of 
suprarenal gland. 
Case 63.—A. B., aged 54, a physician, gives the following history. Except 
for articular rheumatism some twenty years ago and for occasional attacks of 
lumbago, he has had no antecedent venereal or other infection. He was a 
light smoker until ten years ago; he then began smoking heavily, consuming 
as much as one half dozen cigars and ten to fifteen cigarettes daily. He has had 
occasional slight gastric hyperacidity and vertigo for eight years; both were 
usually relieved temporarily by belching. About five years ago he had a 
sudden severe attack of nausea and vomiting, followed by severe vertigo 
which lasted four weeks. The attack was regarded as due to over-work and 
nervousness. He stopped eating seasoned food. Since several months he 
has had severe midsternal burning pains radiating to the left forearm and 
fingers. When the pains occur while walking, they are sufficiently intense 
to make him stop. The attacks are occasionally accompanied by nausea. 
They usually last two or three minutes. They are not accompanied by 
dyspnoea or palpitation. The pains are most apt to occur when he starts 
walking after a heavy meal. With the cessation of pain, the patient can 
again walk comfortably and even play golf. He has not lost weight, his 
appetite is good, all other functions seem to be normal. 
Examination.—You note, gentlemen, that this large and robust-looking 
man rests very comfortably, showing no dyspnoea when sitting quietly or 
when walking about the room. The systolic blood-pressure is 140; the dia- 
stolic, 90. You find that a most careful examination of the heart by ausculta- 
tion and palpation in the resting or lying position or after exercise, elicits no 
untoward sign or symptom. The urine is normal. The electrocardiogram 
being passed around shows nothing abnormal. The orthodiascopic tracing 
shows a normal sized aorta, the heart is somewhat broad, but not too much 
so for a man of his physique. The Wasserman blood test is negative. 
There is no edema of the legs. CARDIO-VASCULAR CLINICS 
583 
Despite the presence of the precordial attacks from which this patient 
suffers, I feel quite sure that he has no cardio-vascular disease. I attribute 
even the gastric symptoms to the same cause that produced the precordial 
pains, namely tobacco poisoning. 
Later Examination.—You recall this patient and his history, and that he 
was here one week ago. You will find upon examination that there is no 
change in the cardiac status. The blood pressure is normal and all the other 
physical signs are the same as previously. The patient feels very much 
better; he has cut down the amount of his smoking considerably. He finds that 
he can now walk comfortably, and that the midsternal and other pains 
are very much less. The only medication he is taking is atropine sulphate 
tablets in doses of of a grain three times daily before meals. 
Case 64.—M. K., aged 46, a butcher, was sent to us by a well-known 
gastro-enterologist. According to his report, the gastric findings after the 
extraction of a test meal show typical hyperacidity; there is no hyper- 
secretion, and no blood or mucus in the extracted meal. There is no blood 
in the stools after a meat free diet. 
Regarding the history, the patient states that he has smoked since he was 
nine years old. When still a young man fie consumed from fifteen to twenty 
cigarettes a day. There is no previous history of rheumatism or of any 
infection. He was always a quick and hearty eater, and a hard worker. 
About nine months ago, after pushing a very heavy meat cart, he was 
suddenly attacked with severe precordial pains. Since then any exercise, 
especially walking even slowly in the open air, produces midsternal pains 
which radiate to the back and arms. There is in addition slight midsternal 
sensitiveness during or immediately after an attack. Besides these chest 
symptoms, he suffers frequently from belching and faintness. He had been 
on an “ ulcer diet ” for several weeks. Once he broke his diet by eating cheese- 
cake and some sour food; this immediately produced very severe abdominal 
symptoms—colic, and a tympanitic and somewhat rigid abdomen, especially 
upon the right side. He often has sudden hunger pangs and complains of 
frequent and continued intestinal rumblings, probably due to hyper-peristal- 
sis. The Wassermann blood reaction is negative. 
Examination.—Inspection of the mouth, tonsils and gums reveals nothing 
abnormal. With the exception of a small area of midsternal sensitiveness, 
you will find that the cardiac examination reveals nothing abnormal upon 
the most careful inspection, palpation or auscultation. When the patient 
sits quietly, he complains of no pain, but as I allow him to walk around, even 
slowly, he begins to complain of his midsternal pain which as he says is 
beginning to shoot toward the back and the left arm. The present attack, 
the patient says, is somewhat exceptional in that it occurs indoors instead of 
in the open. When you compare the right and left radials, you find that the 
latter seems somewhat smaller than the right, yet despite this difference, 
the systolic blood-pressure of both brachials is equal; it is 145 in both. The 584 
CARDIOVASCULAR CLINICS 
diastolic blood-pressure of the left arm is 84. The orthodiascopic tracing 
being passed around shows that the aorta is normal in size and form, that the 
left ventricle is small, and that the remainder of the cardiac outline is also 
normal in size and form. There is no edema of the legs. The urine is normal. 
The electrocardiogram, which I show you, is likewise normal. 
Despite severe precordial pains, we find no tangible evidence of organic 
disease. I believe the patient is suffering from a cardiac neurosis due to 
tabagism. I want to emphasize the combination of gastric and cardiac 
symptoms in this case as in the other. 
Later Report.—I received a report of this case from the family physician 
some months after we had examined him. The doctor stated that for some 
weeks, the pains remained very severe, despite the tablets of atropine sul- 
phate and nitroglycerine which he took. Gradually, however, the pains 
became less acute and the patient was able to walk in the street in warm 
weather. Latterly, he still further improved in that he was able to drive his 
own automobile. My impression is that improvement will continue so that 
the patient will eventually be able to get about as comfortably as he did 
prior to his precordial attacks. However, he may never be able to again 
take up his laborious work. 
General Comment.—There are two opposite views regarding the effect of 
tobacco poisoning upon the heart. In the one, the more popular view, nico- 
tine, the main deleterious alkaloid of tobacco, is assumed to directly injure 
the cardiac structure, especially the myocardium, thus producing myocar- 
ditis. The other and less commonly accepted theory, the one to which I 
adhere, is that nicotine is a specific neurotropic poison which is especially 
harmful to the nerves of the heart. This theory is partly based upon the well 
known experimental physiological fact that nicotine injected into animals 
acts upon ganglia and nerve structures. 
I have reviewed the existing experimental procedures that sought to pro- 
duce an actual cardiac lesion in animals either by nicotine injections or by 
having animals inhale tobacco smoke for longer or shorter intervals. To say 
the least, I have found this evidence conflicting and of problematical value. 
The meagre pathological data relating to the human subject states that the 
heart of smokers who have died from other causes showed only slight 
muscle changes and that this was attributed merely to the incidental 
tachyardia. 
A clinical argument against the presence of any severe organic cardio- 
vascular change from nicotine is the fact that after the etiology is recog- 
nized and patients stop smoking, the symptoms usually recede, the 
precordial pains become less and the patients soon become more comfortable. 
It is interesting to note that most of the patients I have seen with so-called 
tobacco angina suffer from their precordial pains and disturbances chiefly 
when walking in the open, and not when walking about in a warm room. It 
seems probable that cold air causes some vaso-motor change which reflexly CARDIO-VASCULAR CLINICS 
585 
excites the cardiac nerve control, produces coronary spasm and conse- 
quent precordial pains. 
You will note in the cases that I have presented to you that there seems 
to be some culminating factor which starts cardiac pains and other symptoms. 
In the one case, it was pushing a heavy meat cart; in another, the doctor, it 
followed a severe nerve strain. In other words, anything which can throw a 
physical or nerve strain upon the circulation is apt to be the final factor which 
elicits cardiac symptoms. I have already stated that when smoking is 
stopped the patients are usually relieved of their cardiac and other symp- 
toms. But this is by no means always the case; for as in other instances of 
a labile and disordered nervous mechanism, an injury or insult, once insti- 
tuted, is sometimes apt to cause long continued symptoms for weeks or even 
months. This is well demonstrated in Case 64. This patient will probably 
go through many trials before his vaso-motor system is so stabilized that he 
can walk comfortably and without pain. Such patients must walk slowly at 
first and exercise only in their rooms; if there be no recurrence of severe pains, 
they may venture out in the open, but at the outset only in warm weather. 
It may take months until they, or rather, until their vaso-motor systems 
are so re-trained, that they can walk at their natural gaits in the open air. 
It takes even longer before they can take up more strenuous physical exertion, 
especially hard work. Here also re-training must proceed very slowly. 
Patients with sedentary occupations and severe tobacco symptoms should at 
first work but a few hours each day. Patients with laborious occupations will 
at the beginning have to seek some work which does not require severe 
physical exertion. 
What is the fundamental cause of the precordial pains, the chief symptoms 
from which patients with “ tobacco hearts” suffer? While my own theory of 
its causation is not susceptible to proof, it appears to me that the pains are 
produced only by marked interference with the coronary flow, similar to the 
mechanism assumed in the severe precordial so-called anginal attacks accom- 
panying coronary embolism and thrombosis. I have emphasized and given 
my reasons for the statement that I do not regard actual cardiac or coronary 
disease present in smoker’s hearts. Hence, according to my assumption, 
interference with the coronary circulation can only come from spasm of these 
vessels, a fact apparently depending upon abnormal excitation of the nerves 
controlling their caliber. Remember that nicotine is a neurotoxic and neuro- 
tropic alkaloid. We do not know the paths of the abnormal excitations which 
influence the intra-cardiac blood supply but for the present I believe that the 
clinical facts can be explained in no other way than by assuming interference 
with the coronary flow. 
Therapeutically I have found doses of atropine sulphate given to the limit 
of tolerance the best single drug. This may be taken regularly for weeks or 
even for months; atropine poisoning can be avoided by searching for its well- 
known symptoms from time to time and then if necessary remitting the drug 586 
CARDIOVASCULAR CLINICS 
for a few days. Different patients tolerate the drug differently, so it is 
always wise to start with small doses and increase it as rapidly as possible to 
its full physiological effect. When, in addition to the precordial pains, the 
patients are restive and irritable, occasional doses of the triple bromides have 
a good effect. For special attacks of pain, I have found the extract of the 
suprarenal gland of great benefit. 
I want to recur for a moment to the gastric and enteric symptoms in two 
of our cases. I believe that in both excessive smoking was their cause. Just 
as nicotine can cause poisoning of the heart nerves, so I believe that it 
can occasionally cause poisoning of the gastric nerve supply, with attendant 
violent gastro-intestinal disturbances. Indeed, in Case 64, at one time the 
abdominal symptoms—very severe gastric and intestinal spasms—pre- 
dominated the clinical picture. It seems probable that tabagism can pro- 
duce hypeperistalsis, hyperacidity, gastrospasm, severe abdominal pains and 
other symptoms resembling gastric ulcer by its neurotropic effect upon the 
gastric and intestinal nerve supply. 
The dizziness that many of the patients with tobacco hearts complain 
of is very probably connected with disturbance of the vaso-motor mechanism, 
thus affecting the blood supply to the cerebral center or centers which control 
equilibrium. 
To sum up, while I cannot deny that tobacco poisoning may possibly, 
or to put it another way, can conceivably produce some organic change in 
the cardiac structures, I think that up to the present time, definite proof 
of such organic change is lacking, despite the many clinical and experimental 
papers published upon the subject. On the other hand, upon physiological 
and clinical grounds, I hold that all the symptoms can be accounted for on 
the assumption that the main tobacco alkaloid, nicotine, can act as an almost 
specific neurotropic poison, can thus affect the controlling nerve mechanism 
of the heart, and can consequently produce not only various types of cardiac 
irregularities but also very severe precordial distress from coronary spasm. 
CASES 65-67.—“IRRITABLE HEARTS” IN PATIENTS WITH ORGANIC VALVULAR 
DISEASE—GENERAL COMMENT 
Case 65.—J. I., male, aged 15, has had frequent attacks of tonsillitis. 
As a young child he was a somnambulist. He has grown considerably during 
the past year. He was fairly athletic and always able to run at least a half 
mile without getting out of breath. Two weeks ago he developed fever 
which lasted one week and was accompanied by rapid heart action. A cardiac 
murmur was then detected for the first time. Since then any excitement or 
exertion, even walking, causes tachycardia. 
Examination.—The boy, you observe, is quite tall for his age. The 
thyroid gland is not palpable. The teeth are in good condition. The tonsils 
are somewhat fleshy. Inspection of the precordium shows well marked CARDIOVASCULAR CLINICS 
587 
hyperactivity. There is no thrill or tenderness on palpation. Upon 
auscultation you hear a very faint systolic murmur when the boy sits up; this 
becomes quite loud when he is lying down. When the boy rests quietly, the 
cardiac rate is 90 per minute; after walking about the room once, the rate 
rises to no per minute, but the patient shows no sign of dyspnoea nor does he 
complain of the rapid heart action. 
Now let us fluoroscope him. You observe first a heart normal in size and 
form; second, the ventricular hyperactivity. I wish you to observe carefully 
the effect of deep breathing upon the ventricular activity. He is now holding 
his breath at the end of a deep inspiration. You see not only a much slower 
cardiac rate, but also the deeper, quieter, less violent ventricular systoles. 
This again literally shows you what you have so often heard me describe as the 
effect of breathing on some rapidly acting hearts, namely that it not only 
slows the heart, but may also produce less violent ventricular contractions. 
The latter can sometimes be ascertained by the usual clinical methods of 
examination, but it is important to have an ocular demonstration by the 
X-ray in order to establish the validity of this phenomenon. 
Diagnosis.—The first question to decide is whether the systolic murmur 
is the result of a mitral lesion or is functional in origin. As you know and as I 
have already demonstrated to you, loud systolic murmurs especially over the 
mitral area, are not infrequent in rapid heart action from any cause. I believe 
that in the present case the only decisive criteria indicating endocarditis are 
the frequent tonsillar attacks and the fact that the cardiac symptoms followed 
immediately after a febrile onset. We do not know the exact nature of the 
fever, it is true, but that it was probably not due to tonsillitis. When 
fever is part of the syndrome of a general bacteremia from any cause, the 
endocardium can become infected, often as a terminal event. There is of 
course no such evidence in our patient. Unless fever be of rheumatic, tonsillar 
or scarlatinal origin, I believe that it only rarely causes endocarditis. Hence, 
as a corollary, the vast majority of so-called febrile murmurs are not due to 
actual heart disease. Rheumatic fever occasionally produces only very 
mild, fleeting rheumatic manifestations, and almost immediately attacks the 
endocardium. I believe this boy represents this exceptional course, because 
the physical signs and manifestations of heart disease followed so directly 
upon the fever. I present him to you as an example of a mild, acute, mitral 
regurgitant lesion in which the main symptom is the tachycardia. 
I believe that the prognosis is good because the boy looks well, has no 
fever now nor any subjective symptoms. I assume therefore that the patho- 
logical process is apt to stop soon, and to gradually retrogress so that in the 
course of years, or perhaps even of months, the physical signs of the lesion 
may entirely disappear. I believe this happens more frequently than is 
usually suspected. For example, I have examined the patients of careful 
dependable physicians who assured me that their patients had had typical 
rheumatic endocardial lesions in previous years, with classical physical signs; 588 
CARDIOVASCULAR CLINICS 
yet upon more recent examination, the latter had entirely disappeared. 
Occasional autopsy examinations showing retrogressive changes in the 
mitral leaflets of those with typical rheumatic histories also support the view 
that prior active processes may ultimately retrogress to such an extent as to 
leave very little permanent evidence of the disease. 
Another reason for presenting this patient is to show you how a heart 
with an organic lesion may become hyperirritable in the same manner as a 
heart with purely functional derangements. 
Later Report.—I have heard from a sister of the boy four weeks after we 
had examined him that he was at. the seashore, feeling well but that his heart 
action was still rapid. As I have stated to you, it may be months before 
the cardiac irritability quiets down and the heart rate again becomes normal. 
I prescribed the salicylate of soda and mixed bromides; these were to be 
taken intermittently for several months. 
Case 66.—L. S., female, aged n. Her physician states that she had a 
typical attack of cardiac decompensation two years ago: Edema of the lungs, 
enlarged liver and dyspnoea. This occurred soon after an attack of rheu- 
matism. When a baby she had been subject to tonsillitis; a tonsillectomy 
had been performed a long time before cardiac symptoms began. Her 
cardiac complaints at present consist in the consciousness of rapid heart 
action, and in shortness of breath when climbing stairs, running or after 
skipping the rope. She is also subject to sudden severe attacks of hemicrania. 
Examination.—The child you see is well developed. She is not dyspnoeic 
when at rest. Inspection of the neck and chest reveal nothing abnormal. 
Upon palpation, you feel a systolic thrill-like precordial shock at the apex. 
Upon auscultation, you hear over the mitral area a loud systolic murmur 
which is transmitted to the left axilla, and posteriorly to the left scapular angle. 
You also hear a loud systolic murmur over the pulmonary artery; this is prob- 
ably transmitted from the mitral region. As you know, mitral murmurs are 
occasionally transmitted over large areas, sometimes indeed over the entire 
front of the chest. There is also a soft systolic murmur over the aorta. 
The cardiac area is not enlarged to percussion. The liver is not palpable. 
There is no edema of the legs. The urine is normal. 
Diagnosis, Therapy and Prognosis.—It is apparent that the child has a 
mitral lesion and that she is at present fully compensated. The history 
leaves no doubt that she had an attack of heart failure two years ago. 
The lesion therefore seems now to have reached a quiescent stage. It is 
possible, however, that the occasional attacks of hemicrania are of rheumatic 
origin; and that they represent rheumatic recrudescences sufficient to keep up 
cardiac irritability. You recall that the child’s chief complaint was rapid 
heart action only after rather violent exercise, such as jumping and running. 
Even normally, of course, there is increased cardiac rapidity after such exer- 
tion. Let us see what effect rapid walking across the room has upon the 
cardiac condition. You observe that there is a rather sudden increase of the CARDIOVASCULAR CLINICS 
5^9 
cardiac rate to no, and that cardiac hyperactivity is now plainly visible, for 
you see the violent cardiac impulse against the chest wall even from a dis- 
tance. The child herself, however, does not complain of or notice this 
hyperactive, increased rapidity. In other words, this girl apparently is 
conscious of rapid heart action only when it is excessive. This fact is impor- 
tant in determining what she, or other patients for that matter, mean by 
rapid heart action, for we cannot always examine patients when symptoms or 
complaints are most obvious or severe. Each patient has his own standard, 
his own pathological threshold, so to speak, from which he measures the 
beginning of his complaints. To return to this patient, you observe that the 
tachycardia is somewhat decreased by deep breathing, a clinical evidence of 
vagus control, and always an encouraging sign, I believe, for it shows a tend- 
ency to normal inhibitory control. Since the hemicrania may be of rheu- 
matic origin, and hence an indication that the rheumatic poison is still active 
occasionally, I believe the child should take the salicylate of soda in 15 grain 
doses every night for about a month, and then in decreased doses at longer 
intervals. While the girl should be allowed to walk about, go up and down 
stairs slowly and to attend school, I do not think it wise for the present to 
allow her to romp, nor to do anything which is going to race her 
heart. 
I believe the ultimate prognosis is good. By “good” I mean that the 
lesion is now quiescent or will become quiescent soon, with no or very little 
loss of cardiac reserve, with no hyperirritability, and no abnormal tachy- 
cardia even upon strenuous exertion. When that stage is reached, the prob- 
ability is that the mitral murmur will become less loud, and in the course 
of years may become almost or entirely inaudible. 
Case 67.—Mrs. R. N., aged 33, married, has two children, gives no pre- 
vious history of rheumatism, tonsillitis or scarlet fever. She at no time had 
cardiac symptoms until the fourth month of her second pregnancy. She then 
had precordial pains which the family physician diagnosed as due to pleurisy. 
There was no further trouble during the pregnancy. After the birth of her 
child, over a year ago, she began to complain of precordial pains which radi- 
ated to the left arm and around the chest, and of occasional dry cough. 
These symptoms were aggravated when climbing stairs and walking fast, or 
when she became excited and irritable. 
Examination.—You see that the patient has the appearance of a healthy 
woman, with good color, well nourished and with no dyspnoea when quiet. 
Inspection of the chest and neck reveals nothing abnormal. Upon palpation 
under the left breast, however, you feel the typical presystolic thrill 
indicative of a mitral stenotic lesion. This diagnosis is readily verified upon 
auscultation, for you hear the classical diastolic rumble of mitral stenosis, as 
well as a reduplicated second sound at the apex. Over the pulmonary artery, 
you hear typical pleuro-pericardial friction sounds especially when the 
patient breathes deeply. The teeth and tonsils are normal. There is no 590 
CARDIOVASCULAR CLINICS 
edema of the legs. The urine, knee reflexes and abdominal examination 
reveal nothing abnormal. The lungs are normal. 
The orthodiascopic tracing being passed around shows that the pulmonary- 
artery is widened, that the left ventricle is enlarged downward, and that the 
right auricular curve is somewhat enlarged. 
To sum up, the patient has an old quiescent mitral stenotic lesion of which 
she was not even cognisant until the middle of her second pregnancy, now 
about one and one-half years ago. She then developed an acute pleuro- 
pericarditis accompanied by precordial pains. The pains again recurred after 
the birth of her child. In addition to the pains, exertion and excitement bring 
on what the patient calls “palpitation.” During our entire examination, how- 
ever, you may have observed that there was no abnormal increase of the 
cardiac rate so that what the patient characterizes as “palpitation” is prob- 
ably cardiac hyperactivity. 
I have shown you other patients in whom pregnancy or parturition had a 
definite effect in lighting up dormant quiescent cardiac lesions. I believe 
that the onset of the acute pleuro-pericarditis was the first tangible evidence 
of an endocarditic recrudescence in this individual, and that it served to 
mark the change from the quiescent to a more active cardiac lesion. 
Examination Two Weeks Later.—You examined this patient two weeks 
ago. She feels much better now. The treatment consisted in rest for an 
hour after each meal, very little stair-climbing and a local application of 
mustard paste over the site of the pain. Internally I prescribed a mixture of 
salicylate of soda, bromide of soda and simple syrup. The patient complains 
of very much less pain and “palpitation.” Objectively the presystolic mur- 
mur and thrill are much less pronounced. This of course does not mean that 
there has been any recession in the pathological process in the mitral valve, 
but that the hyperactivity has diminished, with a corresponding diminution 
in the loudness and harshness of the murmur. In other words, the heart is 
probably acting now similar to the way it did in its previous quiescent state. 
General Comment.—I have grouped Cases 82, 83 and 84 because they are 
examples of irritable hearts in patients with actual cardiac lesions. In two 
of these hyperexcitability showed itself by tachycardia. In the third, (Case 
84), the hyperexcitability was evidenced not by tachycardia, but by over- 
forceful action of the heart which the patient characterized as “palpitation.” 
Case 82, to judge from the history, has apparently been neurotic since child- 
hood; the somnambulism in childhood is evidence of this. Indeed this neu- 
rotic taint may be a reason why a comparatively slight and not very active 
lesion produced such marked tachycardia. Case 83 is an example of hyper- 
excitability following an inflammatory lesion a year or two previously. 
Case 84 typifies the results of a local pleuro-pericarditis upon a heart lesion 
which for years had been inactive. 
It is important to know, to study, and to recognize the various kinds of 
individual reaction when the heart becomes affected. In some, cardiac symp- CARDIO-VASCULAR CLINICS 
S9i 
toms recede within a few weeks, or after the inflammatory condition has run 
its course. Thereafter, except for objective changes, cardiac irritability is 
no longer a symptom, and within certain limitations, the circulation is carried 
on with no systemic or subjective disturbances. This of course refers to mild 
endocarditic infections. On the other hand, in patients who are or who 
become neurotic from any cause, it is the neurotic condition which continues 
for months or even years after the inflammation of the heart valves 
becomes quiescent. Indeed in such individuals, any abnormal excitement, 
let alone any rheumatic or inflammatory recrudescence, can immediately 
cause a lighting up of all the old symptoms such as tachycardia, precordial 
pains and dyspnoea. The student must therefore carefully weigh the influ- 
ence of the neurotic condition itself in such patients, and guide his therapy 
and prognosis accordingly. I do not wish it to be understood that I consider 
these patients hysterical; as a matter of fact I have rarely found them so. 
To state the matter in another fashion, the nervous reflex arcs of these 
individuals are hypersusceptible, and react violently and continuously to 
any abnormal stimulus. 
Although the pathological process recedes at the same rate in neurotic 
as in other people with heart disease, the former are “heart sick,” so to speak, 
for a much longer time, the symptoms continue, and they suffer much more 
than ordinary individuals with similar lesions. Therapy along general 
neurological lines, therefore, plays a large role with them. The bromides 
are of value medicinally. These patients are self-centered; therefore it is of 
great therapeutic importance to divert their minds as much as possible. As 
soon as the state of the circulation and of the endocarditis allows it, they 
should be encouraged to seek mental relaxation as well as physical exercise 
by playing games. Billiards and pool when available, suggest themselves 
as the mildest at the beginning. Light calisthenics is also an excellent method 
for diversion as well as exercise. Pitching and throwing ball represents more 
active exercise. Other amusements and exercises will suggest themselves to 
fit individual cases and requirements. 
CASE 68—CONGENITAL PATENT DUCTUS ARTERIOSUS WITH VERY SLIGHT 
CARDIAC SYMPTOMS 
Miss W., aged 22, is the youngest of ten children. She never had rheuma- 
tism or any cardiac symptoms until three years ago. She then noticed an 
occasional “dragging feeling” in the chest, with momentary sharp precordial 
pains radiating to the back. These pains are not associated with exercise. 
She has no dyspnoea when dancing, skating or running. 
Examination.—You note the normal appearance of this young girl; there 
is no dyspnoea or cyanosis. The pulsations in the neck appear normal. 
Upon palpation you feel the overacting pulmonary artery in the second left 
interspace, as well as a somewhat overacting apical impulse. The sounds 
over the right base and mitral area are normal. Over the pulmonary artery 592 
CARDIOVASCULAR CLINICS 
there is heard a rather rough, loud diastolic murmur transmitted downward 
along the fourth interspace. This murmur is not influenced by respiration 
or exercise. It is heard posteriorly between the angle of the scapula and the 
spinal column; the first and second pulmonic sounds are also heard distinctly 
in the same area. There are no pericardial friction sounds. The orthodia- 
scopic tracing you are now examining shows that the aorta is normal. The 
curve of the pulmonary artery is enlarged, and fluoroscopically the artery 
shows vigorous pulsation. The remainder of the cardiac outline is normal. 
The abdominal examination reveals nothing of note. The urine and reflexes 
are normal. There is no edema of the legs. 
The diastolic murmur at the left base indicates pulmonary insufficiency; 
a functional cardio-respiratory murmur frequently found in the same area is 
but rarely diastolic in time and is not transmitted posteriorly. There are 
only two valvular lesions which can produce a diastolic murmur over the 
pulmonary artery: The Graham-Steele, which occasionally accompanies a 
decompensated mitral regurgitant lesion and is due to relative insufficiency 
of the pulmonary valve; and a congenital patent ductus arterious with pul- 
monary insufficiency. In our patient, a Graham-Steele murmur can be 
excluded because there is no evidence of a mitral lesion. The typical thrill, 
the systolic murmur, and cyanosis, all characteristic of a marked case of 
patent ductus arteriosus, are here absent. It is therefore somewhat hazard- 
ous to make a positive diagnosis of a congenital anomaly even by a process 
of exclusion. But it must be remembered that characteristic symptoms 
and physical signs depend entirely upon the degree of patency of the duct; 
if it be of comparatively large caliber, the physical signs indicating stenosis 
may be slight or absent, and the only auscultatory evidence may be that of 
pulmonary insufficiency from a certain amount of blood regurgitating back- 
ward through the pulmonary valves. 
The onset of symptoms in this patient—the occasional precordial pains— 
is difficult to explain. There had been no prior infection to produce endo- 
carditis; there is no evidence of pericarditis. The main danger in very mild 
and favorable cases such as this lies in the common experience that a patient 
with any congenital lesion is particularly prone to attacks of endocarditis. 
Our main therapeutic problem therefore is the prevention of such infection. 
At present we possess no specific method of guarding against this, except 
the general rules regarding tonsillitis and rheumatism, and a thorough 
search for possible foci of infection. Regarding the latter, I am of the opinion 
that there has been too much interference and that too much radical surgery 
has been done to remove or drain assumed infected foci, in the absence of 
any definite correlation between the infection and the cardiac disease. 
CASES 69, 70.—CONGENITAL CARDIAC LESIONS, PROBABLY PATENT INTER- 
VENTRICULAR SEPTUM 
I am fortunate in being able to present to you two cases with similar 
congenital defects. CARDIOVASCULAR CLINICS 
593 
Case 69.—T. M., female, aged 9, is the youngest of three children. There 
is no history of rheumatism, scarlet fever or tonsillitis. She was born a “ blue 
baby.” As an infant her face would become quite dusky when she cried. 
She goes to school now and ranks fairly well in her class. She can walk and 
even climb stairs slowly without dyspnoea or cardiac discomfort. She has no 
cough and in fact has no complaint of any kind. 
Examination.—The child, you see, is well developed. You observe the 
moderately cyanotic hue of the lips, cheeks and ears. The fingers are moder- 
ately clubbed. I want you to note also the interesting congenital anomaly 
of the right pupil; a triangular sector of it is missing. There is no overaction 
of the veins or arteries at the root of the neck. Inspection of the precordium 
reveals no abnormal pulsation. Upon palpation you feel a rough systolic 
thrill, chiefly over the mitral area. This thrill I want you particularly to 
observe is not transmitted to the carotids. Upon auscultation you hear a 
loud ro gh systob’c murmur especially pronounced over, and slightly to the 
left of, the midsternum; from there it diminishes in intensity, although it 
can be heard over the entire front of the chest. It is also transmitted slightly 
posteriorly. The liver is palpable two inches below the free border of the ribs. 
The lungs are normal. The feet are dusky and the toes are clubbed, as you 
see. There is no edema of the legs. 
I want you carefully to observe with me the heart as I fluoroscope the 
patient. In the first place you see that the aorta is normal in size, and that 
there is no aortic overaction. The area occupied by the pulmonary artery, 
which forms the curve immediately beneath the aorta, is only slightly 
enlarged. The left ventricle is moderately hypertrophied. The electro- 
cardiogram is of some interest since it shows the characteristics of left ven- 
tricular preponderance; namely, a negative ventricular deviation in the third 
lead; this is contrary to the usual findings in congenital heart disease. 
Diagnosis and Differential Diagnosis.—The child doubtless has a con- 
genital lesion. There are two principal congenital lesions that can produce 
marked cyanosis—a patent ductus arteriosus and a patent interventricular 
septum. In the former the abnormal physical signs—the murmurs and 
thrills—are especially prominent in the second left interspace over the site 
of the pulmonary artery and are commonly transmitted to the aorta in 
the jugulum. Fluoroscopically, there is usually enlargement and marked 
hyperactivity of the pulmonary artery. On the other hand in those with 
patent interventricular septa, as exemplified in our present case, the abnor- 
mal physical signs are found chiefly over the mitral area, and fluoroscopically, 
there is commonly no hyperactivity or enlargement of the pulmonary artery 
or aorta. 
Case 70.—A. S., male, aged 14, is the younger of two children. He has 
had mumps and chickenpox, but no scarlet fever or rheumatism. When three 
years old his heart was examined; the mother was then told that the child 
had congenital heart disease. The tonsils were removed several years ago. 594 
CARDIOVASCULAR CLINICS 
The only symptoms he complains of are rapid heart action and slight dysp- 
noea when excited or running. He swims and rows without cardiac 
complaints. 
Examination.—The boy, you see, is tall and well set up for his age. 
The systolic blood pressure is 120; the diastolic, 68. In contrast to the other 
patient, this boy shows no cyanosis of the face or hands. The teeth and 
pharynx are normal. Upon inspection you observe some hyperactivity of the 
left ventricle, and of the aorta in the jugulum. Upon palpation you feel a 
marked thrill over the mitral area. Upon auscultation you hear a loud rough 
systolic murmur over the same area. This murmur is transmitted chiefly 
to the left axilla. It is also heard distinctly posteriorly in the upper left 
interscapular region. It is heard faintly over the aorta in the interclavicular 
notch as a soft, distant systolic murmur. The abdominal examination reveals 
nothing of note. The lungs are normal. There is no edema of the legs. 
The urine is normal. The orthodiascopic tracing, as you observe, shows a 
normal sized aorta, a somewhat enlarged pulmonary artery and a moderately 
hypertrophied left ventricle. The right side of the heart is not enlarged. 
Diagnosis.—As in the previous instance (Case 69) the abnormal physical 
signs are most prominent over the mitral area and less or almost entirely 
absent over the aorta and pulmonary artery. Hence my belief that here 
also we are dealing with a similar lesion—namely, a patent interventricular 
septum. 
Prognosis.—Children with congenital lesions come to the physician not 
because the parents are interested in the type of congenital defect—the parents 
already know that there is some congenital heart trouble—but because they 
are interested in the question of longevity; in other words, in what we 
call prognosis. 
I believe the chances that the boy (Case 70) will live at least until adult 
age, are good for several reasons. (1) His range of activity—his cardiac 
reserve power—is excellent; you recall he takes active exercise which is 
not followed by any deleterious effect. (2) He has no cyanosis. This in 
itself bespeaks a favorable cardiac outlook. (3) He has but one congenital 
defect, as far as we can determine. In those in whom more than one cardiac 
anomaly is present, the chances for a long life are greatly diminished. To 
sum up, we may say that thus far the only visible untoward effect of the con- 
genital lesion has been moderate ventricular hypertrophy. This of course 
is a handicap especially at his age, but it is known that ventricular hypertrophy 
not combined with inflammatory disturbances may reach immense propor- 
tions before the circulation finally becomes severely crippled. And if in this 
boy the hypertrophy be only slowly progressive the circulation within certain 
limitations may be carried on fairly satisfactorily for many years. Indeed, a 
patient soon learns what he can and cannot do with comfort. 
A frequent danger in cases with congenital cardiac defects is the possi- 
bility of inflammatory valvular infections to which they are especially prone. CARDIO-VASCULAR CLINICS 
595 
Practically this means those individuals should be shielded if possible from 
rheumatism, tonsillitis and scarlet fever. The boy’s tonsils have already 
been removed. We possess no specific preventative anti-rheumatic measures 
except the usual ones of care against over-exposure to inclement weather. 
The boy may walk and row, and swim in shallow water. He may golf. 
He should not indulge in the more violent sports as running or tennis playing 
because of the danger of the development of tachycardia; rapid heart action, 
once developed, may then become a very annoying symptom and a difficult 
one to control. 
The girl’s chances for longevity seem less bright. The cyanosis and 
clubbed fingers, and the fact that quick walking and stair climbing cause 
dyspnoea are evidence of a markedly disturbed circulation and of crippled 
cardiac reserve. 
CASE 71.—TACHYCARDIA AND COLLAPSE AT PARTURITION 
Mrs. M., aged 35, is a primipera. The only thing of note in her previous 
history is that she has occasionally complained of slight “palpitation” 
when excited or when her stomach was upset. The labor was perfectly 
normal; there was no inordinate amount of bleeding. The doctor in attend- 
ance then followed the usual procedure for the delivery of the placenta, that 
is, he used the Crede method of expression. Apparently the placenta was 
adherent, for even vigorous attempts at expression failed to dislodge it. 
Within a few minutes after this procedure, the patient became pale and dysp- 
noic, and the pulse rate ran up to 130 per minute. There was no evidence of 
any internal or external bleeding. I saw the patient about one hour later. 
The systolic blood pressure was 60; the diastolic, 45. The cardiac rate was 
130 and regular. There was no evidence of any organic cardiac lesion. The 
facies was pale, the patient was listless although she could be sufficiently 
aroused to answer questions. She presented a typical picture of circulatory 
collapse, yet there was no sign of external or internal bleeding. The uterus 
was well contracted although the placenta was still in situ. The placenta was 
extracted manually one hour later and the uterus packed. Even following 
this manipulation, the loss of blood was not more than two or three ounces. 
I gave the patient % of grain of morphine, 1 c.c. of a 1-1000 solution of 
strophanthin, and 1 c. c. of pituritin soon after I examined her. Hot black coffee 
was given by mouth. These had no effect upon the collapsed condition of 
the circulation, nor upon the patient’s sensorium. Improvement began, but 
very slowly, only after the placenta was removed. You see the patient now 
two days after delivery. The temperature is normal. The uterine packing 
has been removed. The uterus is well contracted. If you listen to the heart, 
you find the rate around 95. Except for this slight increase in rapidity, the 
cardiac examination reveals no abnormality The patient is still somewhat 
pale. 596 
CARDIOVASCULAR CLINICS 
The question of interest is the cause of the circulatory collapse and of the 
tachycardia. I believe that active hemorrhage, internal or external, can be 
etiologically excluded because there was no uterine tear nor any other cause 
for bleeding. It seems to me that the pressure upon the abdomen for the 
removal of the placenta was the immediate cause of the circulatory collapse. 
You recall that the history stated that collapse began very soon after this 
manipulation. Such abdominal pressure can probably produce circulatory 
failure either by its direct effect upon the venous trunks, or by its influence 
upon the intra-abdominal ganglia and nerves which control vaso-motor tone. 
The latter hypothesis seems more probable. For example, you have often 
heard of, and no doubt know the mechanism of the circulatory collapse 
following a hard punch in the abdomen. I believe the etiology in our patient 
was quite similar. The “blow” was the pressure of the hand upon the 
abdomen in order to express the placenta; the effect was vaso-motor paresis. 
With over-distended abdominal veins in the splancinic area, or according to 
some, wdth over-filled capillaries thus produced, the arterial tree becomes 
empty, and the patient bleeds into her own veins, or possibly, into her capil- 
laries. The resulting picture is very severe anemia and collapse, as if the 
patient actually had a severe hemorrhage. Should you ask, why such 
accidents do not occur more frequently, I can only answer that so many 
unknown physical factors are concerned in expressing a placenta, that, 
lacking such data, an answer would be a mere guess; just as we do not under- 
stand, and can only surmise why one man is merely stunned by a blow upon 
the abdomen, and another perhaps killed. 
CASES 72, 73.—TRANSIENT HYPERTENSION WITHOUT ORGANIC CARDIO- 
VASCULAR DISEASE OR CARDIAC SYMPTOMS 
Case 72.—M. S., female, aged 57, had six children. She reached her 
menopause six years ago. She has always considered herself “sickly.” 
For years she suffered from hysterical fainting spells and from gastric dis- 
turbances; the latter consisted mainly of belching and of intestinal hyper- 
motility. An X-ray examination of the stomach, made some time ago, 
showed no abnormality. She recently suffered from left sided hemicrania 
and from blurred vision in the left eye. An oculist’s report at that time 
stated that the patient had glaucoma. The systolic blood pressure then was 
175. She recently had two attacks of precordial pain referred to the left 
axilla. She has always been thin and is a very meager eater. 
Examination.—You note that the patient is somewhat emaciated. Upon 
inspection you observe some hyperaction of the carotids in the neck and of the 
ventricle in the region of the left nipple; this overaction may be only apparent 
because the neck and chest wall are thin. There is no pain on pressure over 
the heart. The ventricular overaction is quite noticeable on palpation, in 
fact, there is a slight thrill-like thrust felt by the examining hand. Upon 
auscultation you hear a somewhat thrill-like first sound at the apex. When CARDIO-VASCULAR CLINICS 
597 
the patient lies down, however, this abnormality disappears. The other 
cardiac sounds are normal. The orthodiascopic tracing that I am now 
passing around shows a somewhat enlarged aortic knob; the remainder of the 
cardiac outline is normal in contour and size. The systolic blood pressure is 
now 152; the diastolic, 100. The urine is normal; there is no edema of the legs. 
The knee reflexes are very lively. 
Because of the distinct neurotic history, because of the old attacks of 
hemicrania, and because there is very little, if any, cardio-vascular disease 
present, the hypertension seems to be of functional origin and transient in 
character. This is my belief despite the diagnosis of glaucoma, which as you 
know is sometimes found in patients with cardio-vascular disease. I do not 
think that the abnormal sound at the apex indicates organic disease, for it is 
common in hyperactive irritable hearts. If the glaucoma yields to treat- 
ment, I shall allow the patient to continue with her housework and shall 
put her upon a liberal, fattening diet, consisting chiefly of sweets, starches 
and fats. We shall have the opportunity of examining her again in a few 
days. 
Examination Two Weeks Later.—The physical examination of the 
heart is the same as we first found it. She has been to another ophthal- 
mologist since we examined her one week ago; he found no evidence of glaucoma 
nor of any visual disturbance. This does not necessarily mean that the 
original diagnosis was wrong; the glaucoma may have yielded readily to local 
treatment or the cure may possibly have been concomitant with the fall of 
blood pressure, for the latter was 115 and 118 systolic, at the last two 
examinations. 
This case is another instance of the extreme importance of not making 
a positive diagnosis of permanent hypertension from one examination alone 
—especially if other factors are present which bespeak a marked lability of the 
vaso-motor mechanism. 
Case 73.—A. D., aged 43, laborer, has been a steady whiskey and beer 
drinker for years. He has been very “nervous” for several weeks; he cannot 
sleep, he is unable to work, his hands tremble and he vomits every morning. 
Examination.—The history, the coated tongue and the trembling fingers 
which you observe when the patient’s hands are outstretched, indicate that 
he is suffering from alcoholism. The cardio-vascular, the X-ray and urine 
examination reveals nothing abnormal except the blood pressure, and it is 
for that reason that I present this patient. The systolic blood pressure is 
165; the diastolic, 105. In view of the fact that alcoholism can produce 
nephritis, the high systolic reading is suspicious. On the other hand, the 
patient is on the verge of an attack of delirium tremens, and this alone, with 
its accompanying abnormal nervous state, may also account for the 
hypertension. 
Examination Two Weeks Later.—The patient states that he has stopped 
drinking whiskey; he feels well and has no gastric disturbances. You observe 59§ 
CARDIOVASCULAR CLINICS 
that his fingers do not now tremble when his hand is outstretched. The sys- 
tolic blood pressure is 130; the diastolic, 80. The urine is normal. It is 
therefore evident that the nervous excitement incidental to the incipient 
delirium tremens was responsible for his temporary hypertension. 
CASE 74.—HYPERTENSION—DIABETES—VASO-MOTOR SYMPTOMS 
Mrs. K., aged 68, has hypertension and has consulted various physicians 
for this symptom for ten years. She says that she has had sugar in her urine, 
at times as much as 7 per cent. Despite the hypertension, the patient has 
always been active. For the past few months she has had faint and weak 
spells at irregular intervals; she has also had occasional “palpitation, ” 
dizziness and flushes. There is now precordial distress. Her physician 
states that while at the seashore, the patient was capable of taking long walks, 
and had no symptoms. In the city she is quite excitable and is particularly 
worried because she cannot take active part in the household management; 
she is always fussing about little household matters. Her physician states 
that her usual systolic pressure is around 170 m.m. 
Examination.—You notice the patient is well preserved for her age. You 
observe also her flushed cheeks. The systolic blood pressure is now 145; the 
diastolic, 80—nearly normal figures for her age. The radial arteries are not 
thickened. There is slight aortic overaction in the jugulum. There is no pre- 
cordial sensitiveness. The cardiac area is normal to percussion. With the 
exception of a slight blurring of the first sound at the apex the heart sounds 
are normal. The liver is not palpable. There is no edema of the legs. The 
urine to-day contains per cent, of sugar, no acetone or diace tic acid, no 
casts or albumen. 
From the cardiac aspect the patient presents only one definite physical 
finding—occasional hypertension. Her blood pressure, to-day almost normal, 
has doubtless been higher at various times. Its variability shows that the 
vasomotor system is unstable and labile, and is apparently easily affected by 
various influences. A little nerve upset may readily increase the blood pres- 
sure of such individuals. Since there is no evidence of cardiac disease or of 
cardiac failure, I attribute the patient’s symptoms—flushes, giddiness and 
faint feelings—to the same cause, namely, vasomotor instability. Without 
a study of the blood sugar, and the effect of diet upon the blood and urinary 
sugar, it is impossible to state whether this case is one of actual diabetes or 
whether it is due to changes of vasomotor tone, for the latter may also cause 
glycosuria. On the other hand, diabetes and arteriosclerosis with hyper- 
tension are often concomitant. In our patient, in the absence of any evidence 
of arteriosclerosis I am not inclined to believe that arteriosclerosis produced 
diabetes despite her age. As already stated the primary cause of the gly- 
cosuria as well as the cause of the hypertension may be instability and 
lability of the vaso-motor system. CARDIO-VASCULAR CLINICS 
599 
The main therapeutic indication is to get the patient out of her present 
environment of petty family worries and excitement, and to let her again go 
to the sea shore, or to any other place away from home. There need be no 
limitation of exercise. Regarding the glycosuria, the diet for the present 
should be only moderately restricted. While an advocate of the Allen treat- 
ment for most cases of diabetes, I fear that harm would be done in this case by 
following that treatment now, because the patient would become worried and 
the symptoms probably intensified. Bromides are indicated: The solid 
extract of the suprarenal gland in two grain doses should be given for special 
attacks of weakness and dizziness. 
Later Report.—The patient’s physician told me that she had been out 
West, where she travelled and walked about without any restriction and 
with no household cares or responsibilities. She felt well and had no com- 
plaints of any sort. 
CASE 75.—HYPERTENSION AT THE MENOPAUSE WITHOUT ORGANIC CARDIO- 
VASCULAR DISEASE 
M. M., aged 53, gives the following history. She has had neither ton- 
sillitis nor rheumatism. She has had six children. Her menopause occurred 
two years ago. Before the menopause was finally established, she suffered 
considerably from flushes and perspiration. About 20 years ago she had 
attacks of severe epigastric pain and vomiting; these attacks often came at 
night. She has had no attacks of this kind for 10 years. For the past two 
years she suffered from nausea and pyrosis. Analysis of the stomach 
test meal shows moderate hyperactivity. She is also enteroptotic, as you will 
later see for yourselves. The patient was sent to us by her doctor because 
she has hypertension and extrasystoles; the latter come chiefly upon exertion. 
The history is sufficiently complete regarding her gastric complaints. I 
wish to add, for it is of extreme importance, that the patient herself does not 
complain of her heart; she has neither dyspnoea, oppression nor any cardiac 
symptoms. 
Examination.—The patient, you observe, is not dyspnoic when at rest 
nor when walking about the room. The systolic blood pressure is 175; 
after the cuff pressure has been allowed to remain on for a few minutes, 
it falls to 160; the diastolic pressure is 108. The thyroid gland is not enlarged. 
The urine is normal. All the heart sounds are normal. There is no pre- 
cordial sensitiveness nor other abnormality on palpating the cardiac area. 
When the patient is at rest you hear an occasional premature contraction; 
their number is somewhat increased by exercise. The electrocardiogram 
being passed around shows that the extrasystoles are ventricular in origin. 
The liver is palpable about one inch below the free border of the ribs. 
There is slight epigastric sensitiveness to pressure. The orthodiascopic 
tracing, you observe, shows slight enlargement of the aorta; it is otherwise 
normal. There is no physical or clinical evidence of cardio-vascular disease 600 
CARDIOVASCULAR CLINICS 
despite the extrasystoles and hypertension. I believe that the gastric 
symptoms are functional in origin, and that the arrhythmia and hypertension 
are also of neurogenic nature, caused by nerve instability incidental to the 
menopause. 
Therapeutically, I would suggest atropine sulphate in small doses. This 
usually has a marked effect upon the gastric symptoms; it may thus help 
to break the morbid reflex arc now existing between the cardiac and gastric 
nerves. Appropriate diet for the hyperacidity is also indicated. The patient 
need not limit her exercise, for the extrasystoles are of functional origin and 
are but another evidence of abnormal nerve excitation. 
Case 76.—H. L., aged 53, has been married many years. The patient 
is very intelligent and is able to give us interesting and important details 
not only of her present, but also of her past history. I want to emphasize 
the following significant data taken from her early history: Since childhood 
she has been subject to hemorrhages in the tongue and skin. For some years 
she has suffered from hemicrania and left-sided chest pains; the latter were 
diagnosed as angina pectoris. Seven years ago a laparotomy was performed 
for a large ovarian cyst; she has not menstruated since. Hypertension has 
been present for some years; according to her story, the systolic blood pressure 
has varied from 225 to 150 m.m. The Wasserman blood reaction is negative. 
There is an occasional trace of albumin in the urine but no casts. She becomes 
fatigued very readily. For the last few weeks she sleeps poorly. She 
knows that her pulse has been irregular for some time; this irregularity is more 
pronounced of late. She also suffers from occasional attacks of rapid heart 
action accompanied by dyspnoea. There are no gastric symptoms. 
Examination.—You observe that the systolic blood pressure is now 210; 
the diastolic, 130. Upon inspection you note moderate hyperactivity of the 
ventricle in the apical region, and of the aorta in the jugulum. Palpation 
over the apex gives a somewhat thrill-like sensation during systole. There is 
slight precordial pain upon pressure. The abdominal examination reveals 
nothing abnormal. At present the pulse is rhythmic and of normal rapidity. 
The urine contains a heavy trace of albumin, and an occasional leucocyte 
and hyaline cast. The phenolsulphonenaphthalein output in two hours is 
60 per cent. There is no edema of the legs. The orthodiascopic tracing as 
you see shows a somewhat enlarged aorta; it is otherwise normal in outline 
and size. 
Diagnosis.—Besides hypertension this patient presents several other 
features of extreme interest. You recall the early history of submucous and 
subcutaneous hemorrhages in the tongue and skin respectively, and of hemi- 
crania with precordial pains. Such symptoms have been grouped by Osier 
under the term “visceral crisis,” that is, these individuals are apt to have 
visceral pains and symptoms especially at the time of the hemorrhages. 
Often they present no evidence of actual organic disease. The visceral 
symptoms are sometimes very alarming and almost fulminating in character. CARDIOVASCULAR CLINICS 
601 
In addition these patients occasionally present marked nervous instability 
and are especially susceptible to what may be styled “nerve insults.” To 
apply these considerations to our patient, the hemorrhages, hemicrania and 
precordial pains mark her as particularly prone to react .unfavorably to any 
type of nerve excitation. Hence with the establishment of artificial meno- 
pause following the laparotomy, she became a receptive subject, so to speak, 
for hypertension, tachycardia and extrasystoles—all functional symptoms 
and signs which one may group as a vaso-motor neurosis. 
How shall we evaluate the heavy trace of albumin without casts in the 
clinical picture? The one phthalein test which was done was normal: 
The normal excretion for two hours is, as you know, between 40 and 60 per 
cent. I do not believe we can ascribe the hypertension to nephritic origin, 
in spite of the albumen. The previous neurotic history and symptoms just 
alluded to; the absence of dyspnoea and of edema; the absence of gastric and 
of uremic symptoms all speak against this supposition. On the other hand, I 
believe it possible that hypertension of the type exhibited by this patient may 
in the course of time finally eventuate into an actual nephritis. Recurring 
to the albuminuria, it may possibly be of the so-called orthostatic type, 
which has recently been shown to be of vasomotor origin in almost every 
instance. Only more frequent urinary examinations can clear up this point. 
Another rather common symptom exhibited by our patient is fatigue: 
She is “readily exhausted.” There are days when such individuals are “all 
in” and can scarcely walk or get about without feeling unnaturally tired and 
exhausted. At these times they find it necessary to lounge about and 
rest mentally as well as physically. Even too much talking then annoys 
them. They do not care to read or sew. This condition is sometimes 
precipitated by some untoward, though slight overexertion or excitement. 
Often, however, it cannot be correlated with such factors. These symptoms 
are frequently regarded as hysterical, but neither they nor the patients show 
any of the usual stigmata of hysteria. 
Case 77.—S. A., female, 55 years old, had had “bladder trouble” for 
years until finally relieved by an operation, the nature of which she does not 
know. She has four children. A hysterectomy was performed upon her 
seven years ago. Soon thereafter she developed climacteric symptoms— 
chiefly flushes, and hot and dry feelings over the body. About three years 
ago her present symptoms began: Dyspnoea of varying severity, pain and 
pressure over the precordium, and pain along the left arm. Her blood 
pressure has been high for some time. Occasionally she is awakened by spells 
of tachycardia which may last an hour or two. She counts her pulse very 
often. She says it varies from 70 to 100 per minute. She perspires very 
readily and profusely. She often suffers from attacks of unaccountable 
fatigue. She has many social activities and does not want to “give in.” 
She says that at times sudden painful swellings of the forearm and wrists 
appear. Her appetite is good, she has no gastric symptoms. 602 
CARDIO-VASCULAR CLINICS 
Examination.—The patient who is very intelligent had given me an exhaus- 
tive account of her symptoms which I have condensed for you. She is as you 
see, quite stout. Even now, while she is sitting quietly, you observe that her 
face is flushed and that she perspires freely. The systolic blood pressure is 
210, the diastolic no. The heart action is regular, the rate, iio per minute. 
Upon palpation you will find that there are areas in the third left interspace 
as well as over the cardiac apex which are extremely sensitive to pressure; 
otherwise inspection and palpation of the chest disclose nothing abnormal. 
All the heart sounds are normal, there are no murmurs or accentuations. 
The lungs appear normal. The abdomen shows the scars of previous opera- 
tions, otherwise the abdominal examination reveals nothing of note. There is 
no edema of the legs. The urine and the knee reflexes are normal. The thy- 
roid gland is not enlarged. 
The orthodiascopic tracing being passed around shows a normal sized 
aorta, and a heart which is normal in size and form. The Wasserman blood 
reaction is negative. The urine and knee reflexes are normal. There is no 
edema of the legs. 
In the absence of physical evidence of cardio-vascular disease, I believe 
that all the signs and symptoms—hypertension, precordial pains, occasional 
tachycardia, exhaustion, etc.—are primarily due to the establishment of 
artificial menopause following pan-hysterectomy. I shall prescribe liberal 
doses of the mixed bromides, and shall try various extracts of the endocrine 
glands, chiefly the ovarian and suprarenal, the object being to find a substi- 
tute for the lost ovarian secretion. 
Later Reports.—I saw the patient two weeks later. The systolic blood 
pressure then was 185, the diastolic, 95. The patient seemed less fatigued 
but the pains and symptoms were about the same. I made another examina- 
tion after two weeks. The symptoms were the same; in addition, she had 
typical gouty arthritis involving a big toe. At my last examination, eight 
or nine months later, the systolic blood pressure was 175, the diastolic, no. 
There was marked skin hyperesthesia over the precordium and epigastrum. 
The cardiac and other physical signs were the same. A phenolsulphone- 
phthalein test showed an output of 45 per cent, in two hours. 
I have as yet found no reason to change my opinion as to the fundamental 
nature of the case. I believe that both the hypertension and symptoms are 
of functional origin, and are chiefly if not entirely caused by vaso-motor 
neurosis following artificial menopause. 
Case 78.—N. L., female, aged 49, unmarried, says that she has always 
been of a nervous and “highly fidgety” temperament. Her menses have been 
irregular for the past eight years. Two years ago she ceased menstruating. 
For the last three years she has been suffering from headaches and dyspnoea. 
She says that her blood pressure has been high for several years. A laboratory 
report which she has brought with her shows that the urine contains a slight 
trace of albumen, but no casts, leucocytes or sugar. CARDIO-VASCULAR CLINICS 
603 
Examination.—You notice that the eyes of the patient bulge slightly. 
When the patient extends her hands you observe the coarse tremor which she 
says she has had for many years. The teeth are in excellent condition; 
the throat is normal. The thyroid is not palpable. The systolic blood 
pressure is 200; the diastolic, 135. You observe that there is some hyper- 
activity of the carotids. Upon palpation you feel a thrill-like systolic shock 
at the apex. Upon auscultation you hear a somewhat booming first sound at 
the apex; the second aortic sound is hyperresonant, almost bell-like in quality; 
the other sounds are normal. The liver is not enlarged. There is a large, 
readily moveable non-sensitive tumor in the left hypochondrium; it is prob- 
ably a floating left kidney for it has the general shape of that organ. An 
enlarged or floating spleen would show the characteristic splenic hilus. The 
knee reflexes are exaggerated; other reflexes are normal. The phthalein out- 
put for two hours is 35 per cent. 
The orthodiascopic tracing as you see, shows a slightly enlarged aorta; 
the remainder of the tracing is normal in size and form. 
Diagnosis.—I do not think that the abdominal tumor—probably a 
floating kidney—has any relation to the symptom complex. Again as in the 
other cases of this group, despite the hypertension, there is very little evidence 
of any organic cardio-vascular disease. I believe the onset of the menopause 
is responsible for the hypertension. The somewhat prominent eyes and the 
coarse tremor are suggestive of hyperthyroidism. Prominent eyes, however, 
are natural with some individuals, and the patient insists that the tremor 
is an old one and antedates her present symptoms many years. 
I shall allow the patient to do light housework such as cooking, dusting, 
and light sewing, and advise her for the present to walk slowly. I shall also 
put her upon a liberal lacto-vegetable diet, and limit her protein intake some- 
what. Therapeutically, I shall advise corpus luteum and large doses of the 
mixed bromides. 
Later Report*—I have examined this patient several times since I pre- 
sented her to you. The systolic pressures have varied from 190 to 168, the 
diastolic from 130 to 120. Once she had slight edema of both legs, but the 
urine then showed neither albumen nor casts. I prescribed theobromine 
sodium salicylate in gm. doses four times daily for a few days for the 
edema, the latter disappeared and has not since returned. Despite the hyper- 
tension, the patient is symptomatically improved; she is able to walk better 
and to do light housework—she complains much less of dyspnoea. 
Unless a patient belonging to a group such as we have just examined 
should die of some accident or of an intercurrent disease, and a careful gross 
and microscopic examination of the cardio-vascular organs be made, there 
will always be a lurking suspicion, I presume, that the hypertension may not 
be entirely functional, and that our present methods of examination are not 
GENERAL REMARKS UPON HYPERTENSION AND THE MENOPAUSE 604 
CARDIOVASCULAR CLINICS 
sufficiently refined or thorough enough to disclose the actual underlying 
diseased process. I admit the validity of this viewpoint. But unless 
patients present some of the other common earmarks of actual cardio-vascular 
disease, I believe that for the present at least, the majority of the hyperten- 
sive menopause group must be classed as of functional origin and intimately 
correlated with the cessation of menstruation. 
It must be emphasized that these patients often suffer symptomatically as 
severely and as continuously, as those with hypertension from actual cardio- 
renal disease. Thus Case 77 suffers from exquisite precordial pains and 
hyperalgesia. Dyspnoea is also a common symptom but it is not apt to be as 
continuous as in hypertension with organic disease. Although the patients 
complain of shortness of breath, careful examination will sometimes disclose 
not actual dyspnoea, but rapid respiration, that is, tachypnoea. The latter 
may possibly be due to hyperirritability of the respiratory center resulting 
from vaso-motor changes. 
Intermittent sweating, sometimes severe enough to be called a sweating 
attack, is another fairly frequent and annoying symptom of these hyperten- 
sive patients. The sweating is sometimes combined with flushes and a feel- 
ing of heat in various parts of the body. 
The extreme fatigue and nerve exhaustion have already been discussed in 
conjunction with the presentation of one or two of the cases. I have attemp- 
ted to discover whether there exists any correlation between the type of onset 
of the menopause and the onset of hypertension. As you know, with some 
the cessation of menstruation is slow and gradual; with others, sudden. 
Some of the climacteric hypertensive cases have suffered from the usual 
flushes accompanying the menopause, while others have not; so that as far as 
my observations up to the present have gone, it seems that any patient at the 
menopause may be a potential subject for hypertension. 
The cessation of menstruation undoubtedly causes a profound disturbance 
of the entire nervous system, and in addition, probably affects some link or 
links in the endocrine chain. That there exists a more or less intimate cor- 
relation between the ductless glands is a fairly established clinical fact, but it 
is by no means always easy to determine where the chain has been broken, 
that is, what abnormally functioning gland or glands are responsible for the 
symptoms. For example, in the hypertensive climacteric group under dis- 
cussion, it seems probable that the endocrine glands especially affected are 
the adrenals and the thyroids, as indicated by the hypertension, sweating, 
tachycardia and the labile vaso-motor mechanism. But it must be remem- 
bered that for the present this is only an assumption and not an incontro- 
vertible fact. 
The treatment has already been touched upon in presenting the individual 
cases. Speaking of the entire group, I wish to add that these individuals 
react only indifferently well to medication. I do not refer to the effect of 
therapy on the hypertension itself, for I have not found that medication or CARDIO-VASCULAR CLINICS 
605 
diet has any permanent influence on the degree of hypertension. 
I also made the interesting observation that the patients often feel 
as well when the blood pressure is excessive as when it is only 
moderate. I am referring now especially to medication directed to pre- 
cordial discomfort, dyspnoea and nerve exhaustion. I have found that the 
extract of suprarenal gland in doses of one to five grains, administered only 
when such symptoms become most annoying, is followed by excellent results. 
A priori, suprarenal extract seems contraindicated in hypertension but it often 
acts beneficially nevertheless. The reason for this may be its power to stabil- 
ize the vasomotors, thus rendering them less susceptible to extraneous influ- 
ences. I have only rarely succeeded in giving relief by the administration of 
other organic extracts such as the ovarian, pituitrin and the thyroid extract. 
In addition to the suprarenal gland, I frequently prescribe tablets containing 
atropine sulphate, gr. }^00 to Kso, and nitroglycerine, gr. }{00 to gr. }is, 
three times daily before meals. This often controls the flushes and sweats. 
As for the longevity of the hypertensive climacteric patients, my observa- 
tion has been that their lives do not seem to be seriously jeopardized, appar- 
ently they rarely develop the serious or fatal complications found in the 
hypertension which accompanies actual cardio-vascular disease, such as 
coronary infarcts, uremia, pulmonary edema, cerebral hemorrhage, etc. 
CASE 79, 80.—HYPERTENSION AND VASOMOTOR INSTABILITY WITHOUT 
CARDIO-VASCULAR DISEASE 
Case 79.—This case is quite similar to case 74. C. G., female, aged 69, 
says that she has had high blood pressure, at times as high as 200, for at least 
eleven years. She also has had sugar in her urine at various times, even as 
much as six per cent. During the past few months, she has had “faint-like 
weak spells” which come at irregular intervals; when they occur she is inca- 
pable of doing anything and feels “all in.” She also suffers from occasional 
“palpitation” and dizziness, and from flushes. She has no precordial dis- 
tress or gastric complaints. While living with her daughter she is always 
busy with household duties, continually worrying over very trivial matters. 
When away from the city on a vacation, she is able to take very long walks 
with no distress, discomfort or attacks of any kind. 
Examination.—Despite the history of hypertension which her family 
physician corroborated, the systolic blood pressure is now only 140, the dias- 
tolic, 82. The radial arteries do not feel thickened. You note slight aortic 
overaction in the jugulum. There is no pain or other abnormal sensation 
upon precordial palpation. There is a slight impurity of the first sound at 
the apex; all the other sounds are normal. The cardiac area is not enlarged 
to percussion. The abdominal examination reveals nothing of moment. 
The urine contains no albumen or casts; it contains one per cent, 
of sugar, but no acetone or diacetic acid. There is no edema of the legs. 606 
CARDIO-VASCULAR CLINICS 
You observe that the patient is not dyspnceic when walking around the room 
but she does complain of faintness and giddiness. I want you also to remark 
her extremely flushed face at this moment. 
Diagnosis.—It is perhaps hazardous to state that this woman nearing 
her seventieth year, has no arteriosclerosis; yet from the history and from 
our negative cardio-vascular findings I believe that the hypertension is prob- 
ably of functional origin. You recall the patient’s statement that when 
away from home and not worried and annoyed with petty household matters, 
she walks well, has no giddiness and feels quite comfortable. I have no doubt 
that, as both her physician and she have stated, she has marked hypertension 
at various times. Indeed the fact that the blood pressure is normal to-day 
demonstrates the variability and lability of her vaso-motor mechanism. It is 
perhaps this same instability which causes the glycosuria; for glycosuria, 
as you know, can be produced by various abnormal nerve influences such as 
fright, excitement, etc. It will of course require such further examinations 
as a blood sugar determination and the carbo-hydrate tolerance to test this 
point. 
Therapy.—The patient has followed only a moderately rigorous anti- 
diabetic diet. For the present I shall let her follow her usual dietetic regime. 
I shall give her the mixed bromides and suprarenal extract, the latter to be 
taken only when she feels the “ weak spells ” coming on. I shall advise her to 
go away from home for several weeks, so as to rid her of the irritation of 
petty worries. Then she may walk and exercise as much as she chooses. 
Examination and Report Eight Months Later.—Some of you may recall 
this patient. She left the city upon my advice and lived with her sister out 
west for several months. While there, she felt perfectly well, even though 
she drove and walked around until she was physically tired. The reason she 
returns to us is that a few days ago, she felt a recurrence of the old symptoms, 
giddiness, weakness and “palpitation.” In addition, she complains of sudden 
hunger pangs upon arising, and feels as if her stomach were distended with 
gas. She has pain in the left shoulder and numbness in the left hand. All 
these symptoms began soon after a sudden attack of diarrhoea which was 
produced by some indiscretion of diet. 
We now find a systolic blood pressure of 160; the diastolic, 78. The 
cardio-vascular examination is the same as before; there are no murmurs; 
the urine is normal; the pulse is rhythmical; there is no edema of the legs. 
The orthodiascopic tracing being passed around corroborates our former 
finding based upon percussion, namely, a heart normal in size and 
form. 
Why has this patient a recurrence of her old symptoms, in an even more 
aggravated form? I believe that the patient is now suffering from a gastric 
neurosis caused by the diarrhoea, and that the former has reflexly excited 
the vaso-motor mechanism. It demonstrates how hypersusceptible the 
nervous system of this individual is, that so small a cause can result in such CARDIOVASCULAR CLINICS 
607 
severe discomfort. I shall attempt to attack the symptoms by treating the 
gastric neurosis. I shall prescribe atropine sulphate, of a grain, and 
nitroglycerine 3dso of a grain in tablet form to be taken three times daily before 
meals, I shall also prescribe an antacid powder containing magnesium usta, 
saccherated peppermint powder and bicarbonate of soda in equal parts, to be 
taken in teaspoonful doses after meals. Simple semi-solid food should be 
taken in small quantities about every two or three hours. She is not to wait 
until her stomach is empty; she will thus avoid the hunger pangs of which she 
complains. 
I have since received several reports from her family physician. She soon 
began to improve and is at present feeling well, with no discomfort of any 
kind. 
Case 8o.—M. H., female, aged 49, presents a symptom complex similar 
to the previous case, although the history and the course of the disease 
in the two patients are entirely different. 
This patient has had three children. During the last few months her 
menses have been irregular. For over 1 o years she has complained of heaviness 
in the left arm and of a peculiar “hollow feeling” in the left chest. She is 
readily fatigued. She had a fainting spell four years ago, the cause of which 
is not known. Since then she has felt much worse; she has had more pre- 
cordial pains and can scarcely move without discomfort. Her physican states 
that the heart action is occasionally irregular and that the pulse rate is usually 
around 90 per minute. She has never had rheumatism, tonsillar or other 
infections. At the present time even talking brings on precordial pains and 
heaviness in the left arm. She has no gastric symptoms. She has com- 
plained of insomnia recently. Following the advice of her doctor the 
patient has remained in bed for several weeks. 
Examination.—You see that the patient is very well preserved; she 
scarcely looks her age. Although lying flat in bed you observe that there is 
no dyspnoea. The systolic blood pressure is 170, the diastolic, 80. The 
heart rate is 90 per minute and regular. There is a slight systolic thrill on 
palpation, and a somewhat broken, split first sound on auscultation. As 
already pointed out such abnormalities are not uncommon in irritable hearts. 
Otherwise, percussion, inspection, palpation and auscultation reveal nothing 
abnormal. The lungs, urine, abdominal and neurological examination reveal 
nothing of note. There is no edema of the legs. 
Diagnosis.—There is no evidence in this patient of organic cardio-vas- 
cular disease; indeed, there is no history of any antecedent infection that 
might have caused heart disease. Another point against heart disease is the 
fact that patients with symptoms of actual cardiac disease show almost 
invariably in the course of a year or two one or more of the usual accompani- 
ments of a cardiac lesion, namely, murmurs, dyspnoea, edema of the legs, 
etc. From the history, it seems that the symptoms were aggravated by a 
fainting spell a few years ago. To put the diagnosis briefly, I believe that 608 
CARDIO-VASCULAR CLINICS 
she has no organic cardio-vascular disease, but is suffering from an old cardiac 
neurosis with referred precordial and vaso-motor symptoms. 
In this case we base our diagnosis of cardiac neurosis and vaso-motor 
instability upon the patient’s statements and subjective sensations, and upon 
our negative findings. You may ask, how can we believe in the reality of such 
symptoms as a “hollow feeling” in the heart? Isn’t she hysterical? In 
answer to that, I wish to state that I have examined many other cases, both 
functional and organic, who describe their cardiac symptoms in language 
expressive to them, but which we may not be able to fully comprehend or 
follow. I may mention for example such descriptions as “ empty, tight, gone, 
fading,” “far away” feeling in and about the heart as examples of what 
patients attempt to convey to the examining physician. 
You may also question the patient’s statement that talking, or even being 
talked to, causes precordial symptoms. I have observed just such complaints 
in other individuals. It is the mental rather than the physical effort involved 
which seems to irritate these patients and their morbid, hypersusceptible 
vaso-motor mechanisms. 
This patient does not impress me as being hysterical. She is quite calm 
and is not even worried, although she had been previously told by her doctor 
that she has “heart disease.” On the contrary, she seems very anxious to get 
better and wants to know what can be done for her. 
Therapy.—First, medicinally, I shall prescribe some hypnotic to give the 
patient better nights. Moderate doses of veronal combined with a very 
large dose of mixed bromides, given every evening, or luminal in one and one 
half grain doses will best accomplish this purpose. This should be taken for a 
few nights only. I shall prescribe tablets of the extract of suprarenal gland in 
three grain doses regularly three times a day, and large doses of nitroglycerine 
up to 14 5 of a grain as temporary relief for the precordial symptoms. 
Second, the patient will have to be actually retrained in learning first, 
to sit up in and out of bed, and later to walk about. At the beginning she 
should err on the side of doing too little; if too much is attempted at the outset, 
the patient is apt to suffer a relapse, and that is not only discouraging in 
itself, but it usually requires several days for recuperation. Sitting up in bed, 
raising the arms and legs slowly herself-—in other words, active motion—should 
be the type of exercise at the beginning. Sitting out of bed, standing, and 
finally walking about the room are the next steps. Thus, by gradations, the 
patient regains her vaso-motor equilibrium and relearns to walk. All this 
of course, requires patience and a full understanding of the case on the part 
of the physician. 
Third, Reassurance and encouragement are of vital importance. With- 
out these, other means are of no avail. Such patients are exceedingly apt to 
have recurrences of symptoms of longer or shorter duration; hence, they must 
be encouraged over the periods of depression, for they are often depressed 
when they do not progress steadily. The prognosis regarding longevity is C ARDIO-VASCULAR CLINICS 
609 
excellent, that regarding activity is also good, but progress is slow, tedious and 
usually interrupted by periods of remissions. 
Later Report.—The family physician reported to me two weeks later that 
the patient now walks fairly well and has had practically no precordial 
discomfort. 
CASES 81, 82.—EXTRASYSTOLES WITHOUT ORGANIC HEART DISEASE- 
COMMENT 
Case 8i.—Gentlemen: This woman is 42 years old. She says that the 
marked kyphosis which you see was due to a fall in infancy. She considered 
herself well until seven years ago. At that time her child died quite unex- 
pectedly. The shock made her “nervous” and resulted in occasional 
attacks of “palpitation.” On closer questioning I believe we can interpret 
the ‘‘palpitation” as meaning tachycardia. Before her illness the patient 
weighed 115 pounds; she has since lost about 20 pounds. After two years, 
the nervous symptoms disappeared and she felt comparatively well until a 
few months ago. She then developed “ stomach trouble,” the chief symptoms 
being anorexia, heart-burn immediately after eating, epigastric distress and 
sour eructations. There was then neither dyspnoea, palpitation nor pre- 
cordial distress. 
The patient was brought to this Clinic with the diagnosis of heart block. 
Let us now examine her. We hear no murmurs or other abnormal sounds. 
Upon percussion the heart seems normal in size. On auscultation we find 
the following arrhythmia which doubtless was mistaken for heart block: At 
irregular intervals, either after a few beats or occasionally only after several 
minutes, a premature beat is heard at the apex, but not felt at the wrist. This 
type of arrhythmia is frequently termed “missed beat;” when the heart is 
not auscultated at the same time that the radial is felt, the impression is given 
that the heart has likewise ceased its activity during this interval. As a 
matter of fact, what occurs is that the ventricles anticipate their time for 
rhythmical contraction, and contract prematurely, as evidenced by the pre- 
mature sound heard at the apex; this sound is fainter than the rhythmic 
contraction but is still quite distinct. This is another instance of the impor- 
tance of simultaneous cardiac auscultation and radial palpation. The reason 
that the premature contraction was not felt as a pulse beat was the purely 
physical fact that it was not strong enough to open the aortic valves sufficiently 
to cause a systemic pulse wave and consequent pulse beat. The “missed” 
or “dropped” beat was missed or dropped as a pulse beat, while at the heart, 
a premature contraction or extrasystole had occurred. I do not care what 
term you use, so long as you fully comprehend the pathological physiology 
involved. It is interesting to observe the venous pulsation in this patient’s 
neck, because it is so plainly visible. As you feel the pulse, you observe the 
normal regular jugular pulsations. With each pulse intermission you note 
two premature smaller jugular waves which quickly succeed each other; 610 
CARDIO-VASCULAR CLINICS 
these represent the waves corresponding to the extrasystole or premature 
contraction. If a polygraphic tracing were taken, we should find that these 
smaller premature jugular waves represent a premature auricular, as well as 
a premature ventricular contraction (the a'-c' wave), and constitute evidence 
of an auricular extrasystole. I wish to add that the patient herself is at no 
time cognizant of her cardiac irregularity. 
Let us now summarize our findings. A frail patient has indigestion for 
some months. We find she has auricular extrasystoles which vary con- 
siderably in the frequency of their occurrence. There is no evidence, physical 
or otherwise, of organic cardio-vascular disease. How then, shall we explain 
the arrhythmia? I believe the old history of shock and tachycardia offers us 
the clue. I have found it to be a clinical fact that once the function of the 
cardiac nerves is disturbed, the nerves become extremely susceptible to extra- 
neous influence for years, long after the original attack has passed or has been 
forgotten. I believe the new neurogenic insult, so to speak, is caused by the 
patient’s indigestion, which has again reflexly aroused the old cardiac nerve 
hypersusceptibility and instability, with consequent production of extra- 
systoles. You recall that these are auricular extrasystoles, another probable 
evidence of their functional origin, for it has been found that these are much 
more frequently of functional than of organic origin. 
The therapy should be directed to the stomach, not to the heart. An ant- 
acid powder after meals will probably relieve her indigestion. For the extra- 
systoles, atropine sulphate in doses of to °f a grain three times a 
day before meals may be of value because of its effect in paralyzing the peri- 
pheral ends of the vagus. Digitalis is contraindicated because there are no 
cardiac symptoms nor is there any cardio-vascular disease. 
CASE 82.—VENTRICULAR EXTRASYSTOLES 
In conjunction with the previous case (Case 81), I wish to present briefly 
the following patient. He is 32 years old, has been and is a heavy smoker of 
cigars and cigarettes. He awoke some weeks ago with a feeling of “palpita- 
tion.” The next day and often since he has felt as if his heart were “going to 
stop beating.” This feeling, when pronounced, frightens him. Despite 
these sensations he is able to continue his work, that of chauffeur. He is 
active and has no dyspnoea upon exertion. 
Upon examination we find that there are no cardiac murmurs. There is 
no decompensation. The heart rhythm is occasionally interrupted by pre- 
mature contractions which, in contrast to Case 81, cause small, corre- 
spondingly premature, radial beats. The jugular veins are not prominent in 
this individual, hence the study of the jugular pulsations does not help us as 
before in the differentiation between auricular and ventricular extrasystoles. 
As you are aware, ventricular extrasystoles can'be diagnosed by the presence 
of prominent jugular waves, caused by the coincidence of the auricular and CARDIOVASCULAR CLINICS 
611 
premature ventricular contraction (a'-c' wave). I took an electrocardiogram 
of this patient; it showed that the extrasystoles were ventricular in type. 
To what are the extrasystoles here due? In the absence of cardiac dis- 
ease and in view of the history of tabagism, I believe that smoking is the cause 
of the cardiac irregularity. 
Student: Is that what we understand by a tobacco heart? 
Dr. N.: The term-tobacco heart opens up a very large question. Almost 
all textbooks state that the poison, from tobacco produces very serious patho- 
logical lesions in the heart. I have made a special clinical study of a good 
many cases of so-called “tobacco heart,” and I have never been able to find 
evidence of organic heart disease, in a single instance. I have found arrhyth- 
mias of all kinds: Tachycardias, extrasystoles, and in two individuals, sino- 
auricular block—but no actual heart disease. As a matter of fact, careful 
experimental investigations have shown that animals that have been allowed 
to inhale smoke in an enclosed chamber showed no postmortem evidence of 
any change in the valves, endocardium or myocardium. This is a contra- 
diction to earlier experimental work done to prove that strong and continued 
nicotine injections could produce aortitis^in rabbits. In my opinion, cardiac 
irregularities following tabagism in man result almost entirely from the 
effect of the main tobacco alkaloid, nicotine, upon the heart nerves. It is 
known experimentally that nicotine has a neurotropic effect upon the sym- 
pathetic ganglia, and I believe that in the human being, tobacco arrhythmias 
are caused solely by the toxic effect of nicotine upon the neurogenic control 
of the heart, and not upon the valvular or other structures. The cause of 
precordial pain in tabagism I shall not now discuss. 
The special reason for showing Cases 81 and 82 was to demonstrate the 
important fact that the presence of extrasystoles does not necessarily mean 
heart disease. In one case, tobacco, and in the other,indigestion caused the 
arrhythmia. Heart disease may of course be accompanied by arrhythmias of 
various types; but I want you always to remember that arrhythmias in them- 
selves are not evidence of heart disease, and that other symptoms and signs 
of cardiac disease must be found before you condemn a patient with an 
arrhythmia as having “heart disease.” 
CASE 83.—FUNCTIONAL EXTRASYSTOLES 
Mrs. L., aged 49, had always been active and well until the onset of her 
menopause five months ago. This was at the outbreak of the war when one 
of her sons entered military service. She identified herself with war activi- 
ties and worked incessantly from morning until night. Five years ago, the 
patient had had a mild cholecystitis following gall stone attacks. A few 
months ago she felt her heart “ skipping.” She awoke several times during 
the-night with a feeling of “fluttering in the chest.” The family physician 6l2 
CARDIOVASCULAR CLINICS 
states that after a short rest cure the cardiac irregularity became less 
pronounced. 
Examination.—You note that the patient is quite robust. She has no 
dyspnoea. The systolic blood pressure is 118; the diastolic, 70. Inspection 
of the chest and neck reveals nothing abnormal. There is slight sensitiveness 
to pressure under the left breast. All the cardiac sounds are normal. The 
cardiac rhythm is disturbed by occasional extrasystoles. Some of these the 
patient is aware of and she says that they produce a “ weak sensation in 
the chest.” There is at present no sensitiveness in the gall bladder region upon 
palpation. There is no edema of the legs. The urine is normal. The ortho- 
dia'scopic tracing shows you that the heart is normal in size and form. Walk- 
ing, as you observe, does not affect the frequency of the extrasystoles. 
I believe that organic cardio-vascular disease can be excluded as a cause 
for the premature contractions. In a long conversation which I had with the 
patient before presenting her to you it was made evident that the war and her 
son’s share in it are continually on her mind; these thoughts are further inten- 
sified by her own war activities. I believe that it is this nerve strain, occur- 
ring at her climacteric which is responsible for the cardiac neurosis and the 
consequent extrasystoles. 
Therapeutically, I shall suggest to the patient that she give up her work 
for a short while, and then gradually and less ardently resume her activities. 
To stop her work indefinitely would probably make her very fretful, would 
result in much more anxiety about her condition, and would give her more 
opportunity for introspection and worry. When she resumes her activities, 
she should work in a calm and less hurried way; even in eating, the patient 
should take her time; for bolting food also has a certain effect in keeping up 
cardiac irregularities. The mixed bromides should be given every morning. 
Aromatic spirits of ammonia in teaspoonful doses may be given when she 
finds the “fluttering in the chest” too annoying. The prognosis depends 
entirely upon some rearrangement and curtailment of her work, so that her 
mind and nervous system are not affected by hurry or strain. Indeed the 
therapeutic problem is a neurological rather than a cardiac one. 
CASE 84.—AORTITIS WITH HYPERTENSION—DECOMPENSATION—EXTRA- 
SYSTOLES—NEUROSIS 
Mrs. K., aged 66, had always considered herself well physically, although 
she has been “nervous” of late years. Her nervousness took the form of 
introspective worry about the possibility of sudden death. Several years 
ago she was treated for hypertension. She has had two attacks of “grippe.” 
Since the last one she has complained of palpitation and shortness of breath. 
Her son died about one year ago; this depressed her greatly. She com- 
plains frequently of a feeling of “tightness” in her forehead. CARDIOVASCULAR CLINICS 
613 
Examination.—You note that the patient, although of small stature looks 
well nourished. She is somewhat anemic, yet as she talks her face becomes 
slightly flushed. The systolic blood pressure to-day is 160; the diastolic, 
60. I have taken the blood pressure at various times: The lowest sys- 
tolic has been 145; the highest, 210. Inspection of the neck reveals moderate 
overaction of the carotids. Precordial pressure produces no pain. Aortic 
and ventricular pulsation are normal. Over the right base you hear a loud, 
rough systolic murmur with a somewhat accentuated second sound. The 
other cardiac sounds are normal. The cardiac rhythm is interrupted by 
occasional extrasystoles. These the patient herself recognizes and they no 
doubt constitute the “palpitation” of which she complains, for the cardiac 
rate is normal in rapidity. These extrasystoles, taken electrocardiographic- 
ally, were found to be of ventricular type. The lower border of the liver is 
one and one half inches below the costal margin. There is slight edema of 
the legs. The orthodiascopic tracing shows that the aorta is not dilated, and 
that there is moderate left ventricular enlargement. The urine contains no 
albumen or casts. The Wassermann blood reaction is negative. The 
patient’s scalp, which she says feels so tight, is smooth, not swollen, and is not 
sensitive to pressure. 
There is no doubt that the patient is suffering from actual cardiac disease: 
The edema of the legs and the physical signs over the right base are sufficient 
evidence of that. In addition a marked neurotic element is present. This is 
evident from the history, as well as from the almost constant complaint of 
tightness of the scalp. There is considerable lability of the vaso-motor 
mechanism, as shown by the marked variation in the systolic blood pressure 
from 145 to 210. Of course, you must remember that a neurotic element can 
accompany actual disease; indeed, the latter may be the cause of the former. 
This is especially true of the neuroses which so frequently accompany nephri- 
tis with hypertension. I believe, however, that in this patient, the neurosis 
is simply an added symptom, for with reassurance and local treatment (violet 
ray was given to the scalp), the tight feeling has entirely disappeared. As I 
have pointed out in other cases, extrasystoles can accompany and be an evi- 
dence of decompensation. And indeed the present examination gives one 
that impression. But I have examined the patient at other times when 
there was more tibial edema and hypertension, yet the pulse remained regular 
and extrasystoles were absent. I believe, therefore, despite the cardio-sclero- 
sis that the extrasystoles are mainly of functional origin. The patient has 
done well on digitalis and theobromine. Local treatment for the scalp, 
repeated reassurance—for she frequently harps upon and reiterates her 
symptoms—have had an important share in aiding this patient. This is 
another example of the importance of psychology, especially in neurotic 
individuals. It is always wise to extend hope and sunshine to every patient, 
and to try to judge of the patient’s feelings by the way you might feel under 
similar circumstances. 614 
CARDIO-VASCULAR CLINICS 
CASES 85-87.—PAROXYSMAL TACHYCARDIA WITHOUT ORGANIC DISEASE- 
REPORT AND REMARKS UPON TWO OTHER FATAL CASES 
Case 85.—P. S., physician, unmarried, aged 34, says that for several 
years he has been occasionally awakened from sound sleep by a peculiar 
feeling in his heart. Upon taking his pulse, he always found it regular. 
He has been a heavy drinker and drinks six to ten glasses of beer daily. 
During the last few months he has had five attacks of pulse acceleration, the 
rate at times being 240 per minute. The attacks cease as suddenly as they 
begin. He has not noted any cardiac irregularity which precedes or ends 
them. Between paroxysms he has no cardiac symptoms; during them, 
there is simply an uncomfortable feeling of fluttering in the chest. Three 
attacks came after heavy meals; belching was then a prominent symptom. 
After an attack he usually has a slight drawing sensation in the lowermost 
part of the sternum. During the last few months he has complained of some 
heaviness in the epigastrium, especially after starchy food. The bowels are 
regular. 
Examination.—You note that the patient is rather stout. The systolic 
blood pressure is 148; the diastolic, go. The heart action is regular, the rate 
100 per minute. The thyroid is not enlarged. Upon inspection you observe 
that the cardiac impulse is somewhat exaggerated. There is slight accentua- 
tion of the first sound at the apex and over the right base; otherwise the heart 
sounds are normal. There is no abdominal tenderness, no edema of the legs. 
The urine and reflexes are normal. 
The history and the careful observation of the patient himself make the 
diagnosis of paroxysmal tachycardia unmistakable. I am able to clinch 
that by the fact that once I observed the patient when his pulse rate was 180 
per minute but before I had time to take an electrocardiogram the heart 
action suddenly became normal. 
The question arises, what is the cause of the attacks? Is it to be found in 
the heart itself or in some other organ? The physical examination of the 
heart reveals no evidence of disease. The sounds are normal. There 
is no dyspnoea or other evidence of decompensation. The urine is normal. 
There is no history of any recent infectious disease. The patient has dyspep- 
tic symptoms which require very careful study because the stomach is often 
the organ which, when diseased, can excite heart action and bring on tachv- 
cardial attacks. I have therefore had a gastric analysis of a test meal and an 
X-ray examination made. The former shows slight hyperacidity. The only 
positive finding of the roentgenological examination which included the entire 
gastro-intestinal canal is slight cardiospasm. This very probably causes the 
epigastric discomfort, and especially the substernal pain which accompanied 
the paroxysmal tachycardia. In fact it is probably the cardiospasm which 
initiates the attack. We know that cardiospasms not due to neoplasms are 
brought about by abnormal excitation of the sphincteric control of the lower CARDIO-VASCULAR CLINICS 
615 
esophagus and cardia, and that there exists an intimate correlation between 
the nerves of the stomach and heart. Excitation of one can readily affect 
the other, although with our present knowledge it is impossible to state why 
in some individuals, we find reflex excitation of the accelerators and not of the 
inhibitors. In fact in most instances of gastric disease that I have observed 
in which the cardiac mechanism was reflexly excited, the heart action has 
been slowed as the result of vagus excitation, and not accelerated. 
Our patient, then, requires treatment for his stomach and not for his 
heart. He should be advised to refrain from drinking large quantities of 
fluid of any kind. He should eat moderately and chew his food carefully. 
He should take an alkaline powder after his meals, and atropine or belladonna 
before meals. The cardio-spasm and dyspepsia will thus be cured and the 
tachycardia will probably not recur. 
Case 86.—I. D., female, aged 50, has two children. During the last four 
months the menses have been irregular. Twenty-two years ago, when her 
first baby was born, she had an attack of very rapid heart action similar to 
the present. Since then she has had repetitions about twice yearly*- She had 
a mild attack of typhoid fever seven years ago. There have been no other 
infections. Three weeks ago, after a heavy meal, she awoke at midnight 
feeling nauseated. Later she vomited and fainted. When she recovered 
she complained of rapid heart action which lasted several hours. The family 
physician found the pulse regular; its rate was 180 per minute. 
Examination.—The systolic blood pressure is now 150; the diastolic, 
90. Upon inspection you note a slightly exaggerated ventricular impulse 
and slight overaction of the aorta in the jugulum. There is slight pressure 
sensitiveness over the left breast. The second aortic sound is accentuated, 
the other sounds are normal. There is slight edema of the legs. The urine 
report states that there is no albumen or casts and that the specific gravity is 
1020. 
This patient presents similarities and differences from the previous 
one (Case 85). Both have had attacks of paroxysmal tachycardia. In 
both the attacks followed digestive disturbances. In this patient the attack 
also occurred as the result of acute indigestion. The chief difference is that 
in contrast to the other, this patient shows some changes suggestive of chronic 
nephritis: the systolic blood pressure of 150, slight edema of the legs, and 
the accentuated second sound over the right base. It is now three weeks 
since the tachycardial attack, hence the rapid heart action in itself could 
scarcely account for the edema. Upon the probability of presence of a 
nephritis/even without the urinary changes, I have suggested that the patient 
be placed upon a salt-free, non-protein diet, that she be given theobromine 
sodium salicylate in half gramme doses several times daily for a few days, and 
mixed bromides in 30 grain doses nightly for two or three weeks. The 
bromides are prescribed to diminish, if possible, the sensitiveness of the 
nervous system to any abnormal excitation. 6i6 
CARDIO-VASCULAR CLINICS 
Case 87.—L. D., aged 21, as an infant had sudden sharp attacks of 
vomiting without apparent cause. When six years old she had indefinite 
attacks of “palpitation.” Six years ago she had a mild attack of infantile 
paralysis. She has had no other infections. During the last two years she 
has had several attacks of paroxysmal tachycardia; each began and ended 
with an extrasystole. Such extrasystoles are sometimes called the onset and 
offset of an attack. In addition to the paroxysms she gets milder spells of 
rapid heart action; these are usually controlled by taking a drink of water or 
by resting for a few hours. They often occur after overexercise or when 
frightened. In the last attack acetone was found in the urine. She has long 
been on a diet excluding milk, cream, and to lesser extent, sugars. Menses 
began at 13; they are regular and painless. She has had sudden fainting 
spells of unknown origin. Her hands are usually cold and moist. 
Examination.—I had an opportunity to examine the patient during a 
typical attack of paroxysmal tachycardia which I shall now describe to you. 
The thyroid was not enlarged. The carotids pulsated regularly and rapidly. 
On palpation a thrill-like systolic impulse was felt at the apex. Percussion 
showed that the heart was not enlarged. Upon auscultation a thrill-like, 
rough, systolic first sound was heard at the apex; there was a reduplicated 
second sound at the right base and at the apex. The systolic blood pressure 
was 85; the diastolic, 60. The cardiac rate was 200 per minute and except 
for occasional extrasystoles it was regular. Pressure upon the right vagus, 
or holding the breath at the end of a deep inspiration produced a normal 
pulse rate for a few seconds. 
Upon examining the patient now, you note that the cardiac status is 
normal: The heart sounds are normal, the murmurs that were present during 
the tachycardial seizures have disappeared. The urine is normal. There 
is no dyspnoea or edema of the legs. In other words there is no evidence 
of organic cardio-vascular disease. 
I do not believe that acidosis as shown by acetonuria was an etiological 
factor, because the special diet meant to control it had no effect in decreasing 
the number of attacks. The cardiac nerve control in this case may be likened 
to loosely held reins over a skittish, high-strung horse. Any nervous excite- 
ment such as hilarity, being startled or even dancing, brings on rapid heart 
action. When the tachycardia is mild, rest for a short time sometimes 
stops it; otherwise a severe paroxysm of tachycardia results. The only 
fundamental cause for the attacks seems to lie in the history of nervous 
instability of the vasomotor and vomiting centers since childhood. 
Therapeutically, I would suggest the extract of suprarenal gland in doses 
of five grains three times daily for about a month. Although its use is 
empirical to a great extent, it may act beneficially by stabilizing the vaso- 
motor center. I have found it of value in similar cases. I see no reason for 
the continuance of the dietary restriction, except of course the avoidance of 
heavy foods and of over-feeding. The patient also ought avoid those exer- CARDIO-VASCULAR CLINICS 
617 
tions which in her experience have brought on the milder attacks of cardiac 
rapidity. 
Paroxysmal attacks occurring in patients with normal hearts are rarely 
dangerous to life. The seizure may last several hours, or even several days. 
In the latter, the tachycardia defies all drug and other therapeutic measures. 
The seizure may suddenly cease when life is almost despaired of. For the 
control of the tachycardia, sudden, sharp pressure over the right or left vagus 
may be tried, by pressing the fingers for a few seconds over the carotids in 
the middle of the neck. Pressure upon the eyeballs in order to evoke the 
oculo-cardiac reflex is another procedure which may be of value. Among 
drugs strophanthin intravenously is occasionally of aid because of its effect 
upon the vagus. Another procedure is having the patient take a deep breath 
and holding it as long as possible—this may cause sufficient vagal inhibition 
to stop the attack (q.v. Chapter XI). 
Fatal cases of tachycardia without organic cardiac disease are so rare that 
they deserve detailed study. I shall therefore offer the following. 
REPORTS AND REMARKS UPON TWO FATAL CASES OF PAROXYSMAL 
TACHY C ARDIA 
I recently observed two fatal cases of such sudden arrhythmia—perhaps 
it would not be correct to term them paroxysmal—which occurred in women 
after laparotomies. 
Mrs. P., 30 years old, said that for some years she had had occasional 
spells of “weak heart,” especially when her stomach was upset. Careful 
questioning elicited the important fact that by “weak heart” she meant 
that her heart would suddenly beat very fast, and then would as suddenly 
resume its normal rate. For several weeks she was in bed, suffering from a 
right-sided pyosalpinx with irregular fever. A laparotomy was advised. 
Examination of the heart shortly before operation revealed no murmurs or 
arrhythmia. During narcosis there was no vomiting but the cardiac rate 
reached 120 per minute. Narcosis was stopped before the operation—sal- 
pingectomy—was completed, because of the rapid heart action. After the 
operation, the heart remained regular, the rate 160 per minute, the pulse 
scarcely palpable. When I saw the patient 48 hours afterwards, she was 
lying flat in bed without any dyspnoea. The cardiac area was not enlarged to 
percussion, there were no murmurs. The thyroid was not enlarged. The 
heart rate was 180 per minute; the action, regular. The lips were somewhat 
cyanotic. The lungs were normal. The hands were cold, the pulse scarcely 
perceptible. The patient regurgitated fluid frequently, although there were no 
signs of peritonitis. The rectal temperature was ioo°. The mentality was 
clouded although repeated questioning elicited an intelligent response. The 
diagnosis of paroxysmal tachycardia without organic cardio-vascular disease 
was made. First right and than left vagus pressure in the neck was tried, 618 
CARDIOVASCULAR CLINICS 
but the procedure had no effect upon the cardiac rate. One cubic centimeter 
of /fooo solution of strophanthin and of a grain of morphine sul- 
phate were injected subcutaneously; they also had no effect on the tachycar- 
dia. The patient died one hour later. The cause of the tachycardia will be 
discussed in conjunction with the following similar case. 
Mrs. M., aged 35, gave a definite history of hysteria. She frequently 
complained of her heart during some of these hysterical attacks. She suffered 
from diseased adnexa which required operation. Examination of the heart 
at the surgeon’s office several days before operation revealed a cardiac rate of 
120 per minute; there were no other abnormal findings. The patient was 
very much frightened at the thought of a laparotomy. The heart was rapid 
as she got on the operating table. During the narcosis, the patient became 
somewhat cyanotic. Suddenly, about twenty minutes before the completion 
of the operation the patient had a convulsive seizure lasting about five 
minutes. Immediately thereafter the heart rate was 180 per minute, the 
pulse scarcely palpable. The rate remained the same until I saw the patient 
two days later. The temperature was 103°; she passed 1900 c.c. of urine 
the first day after operation. The patient was talkative and answered ques- 
tions incoherently. The abdomen was ballooned and slightly tense, but not 
sensitive to pressure. The tongue was coated and dry. There was no 
vomiting. The leucocytes were 10,000 per cubic centimeter, the differential 
count was normal. The cardiac rate was 160 per minute, the action regular. 
There was a systolic murmur at the apex, common to patients with rapid 
heart action. The systolic blood pressure was 75; the diastolic, 65. Despite 
warm rectal Murphy drips of glucose solutions, vagus pressure, digitalis 
in large doses, and adrenalin chloride subcutaneously, the patient died 
within 24 hours after my examination. 
My first impression was that the patient was suffering from sepsis; but the 
onset of the violent tachycardia during narcosis, ushered in as it was by a 
convulsive seizure, apparently indicates that in some manner the tachycardia 
was the fundamental cause of the other symptoms. 
Regarded mechanically, sudden overloading of the large deep abdominal 
veins with blood causes lack of blood to the systemic arteries, and hence to the 
heart. The heart is therefore never sufficiently filled with blood, and even 
when beating rapidly, as in tachycardia, there is insufficient arterial blood 
pumped through the systemic circulation. In itself, this may conceivably 
account for various abdominal symptoms and for improper functioning of the 
viscera because of lack of arterial blood. Indeed both fatal cases may be 
compared with some phases of shock as seen on the battlefield: The low systolic 
blood pressure, the rapid heart action, the assumed overfilling of the venous 
trunks and the ineffective ventricular systoles resemble those shock cases in 
which there is an abnormal distribution of the blood volume, the preponder- 
ant amount being found in the veins of the splanchnic area or possibly in 
the capillary bed. CARDIO-VASCULAR CLINICS 
619 
It would be of great importance to know the exact cause of the inception 
of rapid heart action in these fatal cases. With our present incomplete 
knowledge the discussion must be perforce hypothetical. Both cases gave 
histories of attacks of tachycardia prior to operation. It is of course not 
unusual to find patients, especially nervous women, with tachycardia induced 
by the fright of operation. In the great majority of these the narcosis, by 
dulling sensibilities and (speaking physiologically) by diminishing the thresh- 
old of the higher cerebral centers to reflexes, tends to make the cardiac rate 
resume its usual pre-operative level. In both of these fatal cases, nothing in 
the operations themselves could have affected the heart rate; both operations 
were skilfully performed, there was no undue loss of blood nor any especially 
forceful intra-peritoneal manipulations. In fact in both tachycardia 
occurred before the operations were completed. Narcosis itself often pro- 
duces cyanosis, but unless extreme, it rarely causes tachycardia. However 
it is impossible to state the effect of even slight cyanosis upon sensitive cardio- 
inhibitory centers already functioning improperly. 
Although the question of shock in its many manifestations is still 
unsettled, its frequent and most damaging effect is sudden overdistension of the 
abdominal reservoirs; a bleeding into a patient’s own veins, with all the seri- 
ous consequences of an actual external hemorrhage. Another view is that 
the blood stagnates in the capillaries. It is in some such aspect, I believe 
that these fatal cases must be conceived. The laparotomy may have been 
the culminating factor by producing changes in the venous circulation of the 
abdominal viscera. That tachycardia, once established, can become per- 
sistent even after the original cause has ceased, is evident from Cases 85 and 
86. In one of these as you recall, tachycardia continued for hours after the 
original gastric attack had ceased. 
CASE 88. PAROXYSMAL TACHYCARDIA DUE TO GASTRIC NEUROSIS AT THE 
MENOPAUSE 
Mrs. S., aged 52, passed her menopause three years ago. Since then she 
has had attacks of severe left-sided hemicrania and rapid heart action. From 
the patient’s description the latter seems to have been typical paroxysmal 
tachycardia. These seizures usually occurred when she was hungry, several 
hours after an early breakfast. There are no gastric symptoms. The 
patient is constipated, sleeps very poorly, and feels so fatigued that she must 
go to bed early. She usually awakes at about one o’clock with a start, and 
then is awake the remainder of the night. She is out of bed at six. She has 
not lost in weight. 
Examination.—You note that the patient is well nourished. There is 
no dyspnoea. The systolic blood pressure is no; the diastolic, 70. Cardiac 
examination reveals nothing abnormal. The reflexes and urine are normal; 
there is no edema of the legs. The orthodiascopic tracing, as you see, shows 620 
CARDIO-VASCULAR CLINICS 
that the aorta is normal and that the ventricle lies somewhat flat on 
the diaphragm. 
There is evidently no actual cardio-vascular disease to account for the 
attacks of paroxysmal tachycardia. I believe that the cause of the latter is 
to be found in the sharp hunger attacks from which the patient suffers 
every morning. Although I shall not enter at any length into the subject 
of the sensations of hunger, you know they are the result of nerve influence, 
probably from the vagus upon gastric secretion and motility. In this simple 
phenomenon lies the etiology of this patient’s tachycardia, the cardiac accel- 
erators become reflexly excited with consequent production of tachycardia. 
The fundamental cause of the nerve instability is probably the climacteric, 
which may also be the cause of this patient’s insomnia, exhaustion and 
hemicrania. 
The patient must take more rest and sleep. The stomach should not 
be allowed to become empty. Abnormally hungry feelings should be guarded 
against by frequent small feedings; milk answers this purpose very well. 
The patient may continue with her housework. She should lie down for 
one hour after lunch. Such simple measures will probably cure the patient 
of her paroxysms of rapid heart action. 
CASE 89—DISCUSSION OF AURICULAR FIBRILLATION WITH AN ILLUSTRATIVE 
CASE 
This man is 45 years of age. The previous history states that at the age 
of three, he had some bone infection in his left knee which resulted in an 
operation and subsequent fistula. There is no history of any other infection 
—no growing pains, no scarlet fever, no rheumatism, no sore throats except 
one very mild one which lasted a day or so. He gives a moderate alcoholic 
history. There is nothing otherwise in the history which has any relation 
to his present trouble. The Wassermann blood reaction is negative. 
The complaint which brings him to the hospital began rather acutely 
about five months ago. He then became short of breath; he could not walk; 
his abdomen began to swell. 
Let us first study the heart action. Please listen to the heart, not for 
murmurs at present, but with the primary idea of telling me what you think 
of his arrhythmia. 
Student: There is very rapid, irregular heart action; the first sound seems 
to me to be very strong. 
Dr. N.: For the present I am interested in the rhythm alone. 
1 st Student: The rhythm is irregular, rapid, and at times seems to be 
skipping. 
2nd Student: His heart is very irregular; first it is slow, then rapid, then 
it skips. 
3rd Student: It seems paroxysmal. CARDIO-VASCULAR CLINICS 
621 
Dr. N.: I notice, in the first place, that none of you gentlemen felt the 
patient’s pulse; that in itself is a very grave error. Every time you examine 
a heart, particularly when studying and looking for arrhythmias, always feel 
the pulse at the same time. If you do that in this case, you will notice not 
only that the heart action is irregular but that the pulse is also irregular; 
furthermore with every heart beat there is a pulse beat; that is, the pulse is 
just as irregular as the ventricular action. You will further note that not 
only is there an irregularity in time but also in the strength of the ventricular 
beats. There are scarcely two successive beats of equal force or rhythm. 
The type of arrhythmia which produces such gross irregularity of force 
and rhythm of the heart and a corresponding irregularity of the pulse is 
called auricular fibrillation. 
There are various experimental methods by which auricular fibrillation 
can be produced. A common method is to faradize the auricles directly. 
As a result, instead of having the physiological orderly rhythmical auricular 
contractions followed by regular systolic contractions of the ventricles, there 
results irregular discordant auricular activity. Different parts of the auricle 
contract at different times and with varying intensity; indeed, as the technical 
term denotes, the auricles actually fibrillate. At the same time the auricles 
are in a state of dilatation. What is the result upon the ventricular activity? 
In the normal rhythmical heart as you know the impulse starts at the sino- 
auricular node, the so-called pacemaker, and spreads thence through theauricles 
to the auriculo-ventricular conduction system consisting of the auriculo- 
ventricular node, and of the bundle of His with its branches. The ventricles 
are thus incited to rhythmic orderly contraction. In auricular fibrilla- 
tion, there is as it were a bombardment of the auriculo-ventricular conduction 
system by a great number of discordant auricular impulses. As many as goo 
of these per minute have been counted in the electrocardiograms of patients 
with auricular fibrillation. Comparatively few of these impulses can pass 
through the conduction system. Those which do pass incite the ventricle 
to irregular, tumultuous activity. That is true in the case we are studying. 
Indeed because of this man’s thin chest wall and enlarged ventricles, you may 
actually see that the ventricular contractions are irregular in strength and 
rhythm. One may even venture a diagnosis of auricular fibrillation by mere 
careful inspection of the cardiac area. Please remember that you never see 
or hear the auricles fibrillate but that you make the diagnosis of auricular 
fibrillation by the characteristic effect of the latter upon ventricular activity. 
What is the result of this irregular ventricular activity upon the systemic 
circulation? Some of the ventricular contractions are so weak that they 
cannot open the aortic valves and therefore cannot produce corresponding 
pulse waves in the radials. Another reason for the non-opening of the aortic 
valves may be that the ventricular systoles, otherwise sufficiently strong, 
do not properly direct the blood toward the aortic valves. In either case, it is 
apparent that there will be more heart than pulse beats. The consequent 622 
CARDIOVASCULAR CLINICS 
lack of correspondence between the number of ventricular systoles and the 
pulse rate is sometimes called pulse deficit. I prefer the more descriptive 
name of abortive beats. The stronger ventricular systoles open the aortic 
valves in the usual fashion and produce correspondingly strong pulse beats. 
But since even these effective ventricular systoles vary in force and rhythm 
there is a corresponding variation in the propagated arterial waves as shown 
by a pulse which is also irregular in force and rhythm. 
Let us now verify all these observations by again examining the patient. 
You will note that some ventricular systoles are followed by pulse beats, 
while others are not. I wish to impress upon you again that this simply 
results mechanically from the fact that some of the ventricular systoles do 
not open the aortic valves. 
Why do patients with auricular fibrillation so frequently decompensate? 
It has been shown experimentally that the reason depends primarily upon the 
resultant irregular ventricular activity. When the latter is present the blood 
cannot be thrown into the systemic circulation in an orderly fashion, and 
it is this which finally produces what we call heart failure or decompensation 
in patients with this arrhythmia. 
Clinically, the incidence of auricular fibrillation may be roughly grouped 
as occurring, first, in rheumatic endocarditis; second, in cardiosclerosis; and 
third, in patients without cardiac disease—the extracardiac group. All these 
groups will be discussed in detail in succeeding Clinics. Here I wish to state 
briefly that the rheumatic valvular lesion most apt to produce auricular fibril- 
lation is mitral stenosis. Further, that by cardio-sclerosis I mean a generic 
term which includes gross pathological changes in all the cardiac structures— 
valves, endocardium, muscle, aorta and coronaries. It occurs chiefly in 
older individuals with general arteriosclerosis, with or without hypertension. 
The third group—those without actual disease—is the smallest in number. 
Auricular fibrillation comprise approximately 70 per cent, of all arrhyth- 
mias, hence the importance of understanding and diagnosing it. It will also 
be much easier for you to grasp and comprehend the others if you thoroughly 
recognize this irregularity. Another practical reason why it is so important 
to grasp the fundamentals of auricular fibrillation is that it is the one which 
may most often be benefitted therapeutically. We know that digitalis has 
the power of blocking many of the auricular discordant impulses which bom- 
bard the auriculo-ventricular conduction system in auricular fibrillation. 
These impulses are thus to a great extent cut off, so that the ventricles are 
restored to some condition of orderliness in rhythm and force. In addition 
digitalis also helps by increasing the 'contractile power of the heart. The 
great advantage of digitalis, however, in fibrillation arises from the aforesaid 
power to block the manifold auricular impulses, thereby producing more 
regular heart action. Quinidine has the remarkable power of occasionally 
restoring the normal rhythm in some cases of auricular fibrillation. I shall 
later present some cases to demonstrate its action to you. CARDIOVASCULAR CLINICS 
623 
Thus far we have concerned ourselves only with the general diagnosis of 
and the problems arising from the arrhythmia itself. I should now like to 
have you listen to the heart with a view to distinguishing the abnormal 
sounds you hear. 
ist Student: The sounds are accentuated; there is a murmur. 
2nd Student: The first sound is replaced by a loud murmur; a systolic 
one. I do not think the second sound is accentuated. 
3rd Student: There is a murmur which seems presystolic, and at the 
same time one hears a sharp first sound. The second sound is accentuated. 
Dr. N.: Upon auscultation, I find as follows: In an area surrounding 
the left nipple I hear a rather loud systolic murmur. A little lower and near 
the cardiac apex I hear a somewhat distant diastolic murmur which occupies 
the latter half of the diastolic period. Will you please listen now in order to 
corroborate these auscultatory findings? 
The patient’s heart action was so rapid when first admitted to the hospital 
and before putting him on digitalis, that no murmur could be distinguished. 
But as I have just pointed out we now hear in the left nipple region a rather 
loud systolic murmur, and in the apical region, a relatively distant diastolic 
murmur of a somewhat rumbling character. In the presence of auricular 
fibrillation they are typical of a double mitral lesion: The systolic, of mitral 
regurgitation; the diastolic, of mitral stenosis. 
And now as to the size of the heart. Even without percussion you note 
the size of the organ as it is silhouetted against the chest wall. The apex is 
in the fifth interspace in the axillary line. 
The liver is enlarged; its lower border can be felt at the umbilicus. There 
is very slight edema at the ankles. 
Let us now search the history for the cause of the valvular disease in this 
patient. The great majority of cases of mitral disease is caused by rheuma- 
tism, tonsillitis or scarlet fever. The patient says he had a slight attack of 
sore throat some months ago shortly before his cardiac symptoms began. 
Such widespread cardiac mischief, however, could not possibly have been 
produced by so recent and mild an attack. It is possible that this patient 
represents one of those in whose childhood there had been so-called “growing 
pains”—in other words, rheumatism— and that the patient does not recall 
them. Or the old bone infection in childhood may be the cause of this mitral 
lesion. Under such circumstances however, patients are not apt to have such 
exceedingly long quiescent periods for, as you remember from the history, 
this man until recently never had any cardiac symptoms. Indeed, he had 
never consulted a doctor about his heart until a few months ago, a very 
unusual story of an endocarditis resulting from a septic bone infection. With 
reference to the alcoholic history in this case, he has been only a moderate 
drinker. The role of alcoholism as a cause of endocarditis has been, as we 
now know, overemphasized; and, even conceding alcoholism as an etiological 
factor, it is difficult to conceive it as producing such a typical mitral valvulitis. 624 
CARDIOVASCULAR CLINICS 
Weighing all probabilities it seems most likely that the cause of the lesion is 
rheumatism, the details of which the patient has forgotten. 
This patient has received altogether a little over two drachms of the tinc- 
ture of digitalis. This has already produced a very marked change in his 
condition. The heart beats less frequently and there is a greater tendency 
to regularity. The edema of the ankles is less; the liver is smaller. The 
man can breathe more comfortably, and as he says he “ feels fine.” He would 
scarcely have to tell us that because a cardiac patient who breathes as com- 
fortably as he does always “feels fine.” I am now going to put him upon 
rather large doses of digitalis, a half teaspoonful three times a day for about 
three days, and then for the following two days, upon theobromin sodium 
salicylate with a limited fluid intake. 
Regarding further care of this and similar cases, I should advise that 
after compensation has been restored, the patient consult a physician about 
every two or three weeks. We know that, given properly, digitalis may be 
taken for a number of years. This patient may be made so comfortable that 
he may even be able to follow some light pursuit. Some become so accus- 
tomed to taking digitalis that they themselves are able to approximate the 
proper amount of the drug needed. The average amount of the tincture of 
digitalis required to restore compensation is one ounce. I am in the habit of 
giving one drachm a day in the usual mild case of decompensation with auricu- 
lar fibrillation. In more urgent cases I prescribe much larger doses. 
Student: Does the pulse rate influence you in the amount of digitalis to 
be given? 
Dr. N.: If I do not get the proper effect, that is, the restoration of com- 
pensation, I would continue digitalis up to the one ounce amount, even 
though the ventricular rate were to fall as low as 45 per minute. As a matter 
of fact in order to investigate that point for myself, I had under observation 
some three or four years ago, a series of cases of fibrillation in whom I con- 
tinued digitalis despite the fact that the ventricular rate was between 40 
and 50 per minute. One patient told me he had never felt better in his life: 
He left the hospital with a heart rate of 35 per minute. 
Student: How often would a case of this sort have to be seen in private 
practice? 
Dr. N.: Ordinarily once daily while in the acute stage. As the patient’s 
condition improves, say at the end of four or five days, he may be visited less 
frequently. 
Student: Do you give tincture alone? 
Dr. N.: I always give the tincture alone and undiluted. You can keep 
a good tincture several months without deterioration. 
Student: How long do you keep such a patient in bed? 
Dr. N.: That depends on the severity of the case. This particular patient 
will probably improve sufficiently in about ten days so that he will then be 
able to sit out of bed, and in a few days thereafter, walk around. CARDIOVASCULAR CLINICS 
625 
Student: Does he feel very weak? 
Dr. N.: The usual complaint is shortness of breath. The weakness is 
not more marked than that of other bed ridden patients. If I allow this 
patient to get up and walk around without continuing digitalis in smaller 
doses, he will again decompensate in a comparatively short time, probably 
in several weeks. Incidentally, what I have just said proves to you that the 
old theory of the danger of continuing digitalis when a patient is walking 
about is an erroneous and exploded one. 
GASES 90-92.—DISCUSSION, DESCRIPTION, AND TABULATION OF VARIOUS 
TYPES OF AURICULAR FIBRILLATION WITH ILLUSTRATIVE CASES 
To-day I shall continue the subject of auricular fibrillation and shall 
illustrate it with several additional cases. 
Case 90.—This patient has already been examined by some of you. 
M. H. is a typical example of a decompensated double mitral lesion with 
auricular fibrillation. You will recall that I advised the continuation of 
medication even after compensation was restored. He has not taken any 
digitalis since he left here three weeks ago; he re-entered the hospital several 
days ago, decompensated and dyspnoeic. Two or three days after the second 
admission he developed a left-sided hemiplegia; you see he cannot raise his 
left arm or his left leg. Upon listening to his heart you hear, just beneath 
the left nipple, a loud systolic and a distinct, though somewhat distant dias- 
tolic rumble followed by a reduplicated second sound. The pulse and heart 
action are grossly irregular in force and rhythm. The liver is enlarged; there 
is no edema of the legs. This case, therefore, represents auricular fibrillation 
with a double mitral lesion probably due to an old rheumatic infection. 
The prognosis is now complicated by the hemiplegia, which no doubt 
is due to an embolic infarct from one of the mitral vegetations. The point I 
wish to emphasize at this juncture is that the patient did not follow my direc- 
tions regarding digitalis. I had stated that despite the fact that he was thor- 
oughly compensated when he left the hospital, he would have to continue 
medication. This the patient did not do, and I am therefore not surprised 
to find that he returned very much decompensated. It is indeed probable 
that the irregular violent ventricular action such as is even now present was 
the controlling mechanical factor which loosened one of the mitral vegeta- 
tions. If the heart had been beating more quietly and less irregularly under 
the influence of digitalis, an embolic infarct would have been less likely to 
occur. 
Case 91.—A. B., male, 76 years old, came to the hospital for a skin disease 
which has no connection with his cardiac status. I wish to demonstrate 
him as illustrating a cardiac type very frequently found among the old and 
senile. He has emphysema and he also has a very irregular pulse. I want you 
to feel his pulse and to listen to the heart at the same time, a procedure always 
to be followed when studying arrhythmias. You will find that unless the 626 
CARDIO-VASCULAR CLINICS 
patient sits up, you can scarcely feel the heart beat. The sounds are very 
faint, probably because the organ is covered by emphasematous lung. The 
radial and temporal arteries are thickened. You note that the pulse is irregu- 
lar both in rhythm and force, an almost infallible sign of auricular fibrillation. 
The underlying pathological lesion is cardio-sclerosis, a very frequent finding 
in elderly individuals. Very often such patients have no cardiac symptoms. 
In this case, for example, despite the fact that the pulse is grossly irregular, 
there are absolutely no cardio-vascular symptoms—no dyspnoea, no edema, 
no decompensation. 
Case 92.—This man, 53 years old, a tailor, tells us that except for very 
slight, temporary ailments, he had never been ill until about five years ago. 
At that time he sought admission to another hospital and stayed there for 
two weeks. The symptoms then were shortness of breath and cough. He left 
the hospital and soon thereafter noticed that his eyes began to bulge, although 
he felt absolutely well and was able to continue at work for several years. 
Heathen sought re-admission to the same hospital because of the recurrence 
of the original symptoms. After several weeks he left and was again well 
until about six weeks ago. At that time he developed diarrhoea and short- 
ness of breath. The latter has continued up to admission to this hospital 
five days ago. 
Let us now examine the patient. First, by inspection you note that the 
patient is very dyspnoeic and that he has very marked exophthalmos. You 
further note very prominent and irregular pulsations in the neck; the larger 
and more vigorous are due to the carotids. The jugular pulsations are 
irregular but less prominent. You likewise observe that there is a fullness 
of the neck in the region of the thyroid; both lobes of this gland are consider- 
ably enlarged. In the chest you observe that the apical impulse is diffuse 
and is very rapid and irregular in the time and force of its systoles. 
Second, Palpation: By placing the palm of the hand over the precordium 
you are able to feel and corroborate what you have just observed by inspec- 
tion; namely, the diffuse irregular impulse produced by ventricular systoles 
which are irregular in rhythm and force. In other words the ventricular 
action is grossly arrhythmic. No thrill is felt over the precordium. 
Third, Auscultation: We hear no cardiac murmurs but we do hear some 
moist, crepitant rales probably due to congestion and edema of the left lung. 
You also note that some of the ventricular beats do not reach the wrists. 
That is due to the fact, already pointed out in a previous Clinic, that some of 
the systoles are not strong enough to open the aortic valves or that they do not 
throw the blood in a proper direction towards the aortic valves. Either 
reason is sufficient to prevent opening of the latter and hence prevents a 
corresponding pulse wave. 
Finally, The size of the heart: The apical impulse is most prominent in 
the sixth interspace, twelve centimeters from the midsternal line, a point 
near the anterior axillary line; this is evidence of enlagement. CARDIO-VASCULAR CLINICS 
627 
The liver is considerably enlarged; its lower border is two inches below 
the umbilicus. There is marked edema of the legs. The urine shows hyaline 
and granular casts. The Wassermann blood test is negative. Regarding 
therapeusis, I wish to mention that, despite digitalis, morphine and bromides, 
all given in large doses, there has been no improvement in the patient’s 
condition. 
This case is one of auricular fibrillation as shown by the absolutely 
irregular ventricular action. Because of the exophthalmos, the enlargement 
of the thyroid, the absence of any rheumatic or infectious history, the sharp 
attack of diarrhoea antedating the present illness, and because the patient 
had several attacks of decompensation, I believe that the auricular fibrillation 
and consequent heart failure are due to exophthalmic goiter (“Basedow’s 
disease”). I shall shortly explain my reasons for this view. 
I ask you now to study this tabulation with me, in which I divide the 
subject of auricular fibrillation as follows: 
Table i 
A. Experimental causes of auricular fibrillation. 
1. Stimulation of the vagus. 
2. Stimulation of the sympathetic. 
3. Direct faradization of the auricles. 
4. Injection of thyroid extract intravenously (1 experiment). 
Table II 
B. Some abnormal factors found, in or productive of auricular fibrillation in the human being. 
1. Enlarged and dilated auricles. 
2. Pathological changes in the pacemaker (sino-auricular node). 
3. Changes in nerve tone in the pacemaker. 
(a) From destruction of nerve fibrils and ganglia. 
(b) From abnormal impulses reaching the pacemaker. 
Table III 
C. A uricular fibrillation is found clinically in: 
1. Cardio-vascular disease. 
(a) Valvular disease—chiefly mitral stenosis. 
(b) Cardio-vascular—chiefly senile (in both, auricular fibrillation is usually per- 
manent). 
2. Extra-cardiac causes in patients with normal and abnormal hearts. 
(a) Toxins. 
Biological—chiefly in pneumonia (auricular fibrillation usually temporary). 
Chemical—tobacco, sulphuretted hydrogen (isolated observations). 
(b) Reflex—chiefly, from gastro-intestinal disease (auricular fibrillation usually 
temporary). 
(c) Exophthalmic goiter (A. F.1 usually in attacks or permanent). 
(d) Drugs—chiefly digitalis (A. F.1 usually temporary). 
(e) Emotions—fright, fear, excitement (A. F.1 in attacks). 
(/) As part of, or during attacks of paroxysmal auricular tachycardia. 
1 A. F. = auricular fibrillation. 628 
CARDIOVASCULAR CLINICS 
I assume that you know what I mean by the pacemaker, the normal 
rhythm center or the sino-auricular node—all interchangeable terms. You 
know that its arterial supply is a rich one, the node being supplied by its 
own special artery. It is also rich in nerve ganglia and fibrils. 
I want to stress the importance of the knowledge we now possess, that 
fibrillation may be temporary or may appear in attacks. The older writers 
regarded auricular fibrillation as a perpetual arrhythmia. 
You of course observe that Cases 90, 91, and 92, all fibrillators, belong in 
different etiological categories. I shall briefly discuss some of the clinical 
conditions in which auricular fibrillation is found. 
Mitral stenosis is one type of valvular disease in which fibrillation is quite 
common. Usually in decompensated mitral stenosis, where fibrillation has 
appeared for the first time, the ventricular action is quite irregular, and the 
rate, 100 per minute or more. Decompensation, as I have already empha- 
sized in a previous Clinic is brought about by the irregular ventricular action 
which results from fibrillation, and it is the irregular ventricular action 
which is of such extreme practical importance. That is to say, the thing 
which disturbs the patient clinically, which causes the dyspnoea, the anasarca, 
the bronchitis, etc., is the irregular ventricular activity which prevents the 
blood from being thrown into the general systemic circulation with any 
degree of regularity. 
Although I use the term senile cardio-sclerosis, it must be under- 
stood that this pathological type is by no means infrequent in the earlier 
decades of life. Senile cardio-sclerosis is also frequently accompanied by 
auricular fibrillation. It is uncommon to have, as in Case 91, rather 
irregular heart action with rates which do not exceed the normal ventricular 
rate. The pulse and cardiac irregularity, if you will recall the examination 
of Case 91, is not nearly as marked in rhythm or force as, for example, in 
Case 92, the patient with the exophthalmic goiter. That probably accounts 
for the fact that patients such as the former do not often suffer from much 
disturbance in the systemic circulation despite fibrillation. Case 91, 
indeed, came to the hospital for an entirely different disease; the irregular 
pulse was only an incidental finding. There are, however, senile cardio-scler- 
otic cases which do have very irregular heart action with fibrillation, and 
those are the patients who suffer most from dyspnoea and other signs of 
decompensatory disturbances. 
We shall now discuss, in conjunction with Case 92, the question of exoph- 
thalmic goiter with auricular fibrillation. By correlating the tabulated 
experimental (Table I), with the probable fundamental causes of fibrillation 
(Table II), we may be able to find the cause of the fibrillation in Case 92. 
I want to preface, however, that what I am going to tell you about fibrilla- 
tion in exophthalmic goiter is to some extent hypothetical, because, though we 
have some experimental data, the facts are not sufficiently known to enable 
us to draw exact clinical conclusions. CARDIOVASCULAR CLINICS 
629 
You note from the Table that, experimentally, stimulation of the sympa- 
thetics has produced auricular fibrillation, and clinically, that changes in 
the rhythm center from abnormal impulses reaching it may also produce 
fibrillation. We know that exophthalmic goiter is sometimes accompanied 
by mild pathological changes in the myocardium; in rare and exceptional 
instances these may amount to extreme cardiac hypertrophy without involve- 
ment of valvular or arterial structures. Furthermore exophthalmic goiter is 
almost invariably accompanied by evidence of hyperexcitation of the 
sympathetic system. Observe, for example, the usual tachycardia and 
sweating in exophthalmic goiter. We know, also, that there are undoubted 
instances in which sudden emotions such as fright or excitement, form the 
starting points of exophthalmic goiter. Case 92 states that preceding his 
last attack of cardiac failure, he had severe diarrhoea uncontrolled by medica- 
tion and having no relation to diet. I believe that this symptom, intestinal 
hypermotility, was another evidence of hyperexcitation of his sympathetic 
nerves. 
To summarize: The goiter, the exophthalmos, the fibrillation with conse- 
quent decompensation, and the diarrhoea are the results of disturbances of 
the sympathetic system. I profess, however, no knowledge as to the funda- 
mental cause of the sympathetic disturbance in this case. Regarding ther- 
apy, I am not surprised that digitalis has not had the slightest effect upon 
the irregular and rapid ventricular activity nor upon the heart failure. We 
have.no specific, nor anything like a specific at present, which can influence 
continued fibrillation in patients with goiter.1 The primary therapeutic 
effort must be directed toward some drug which can control the hyperexcit- 
able sympathetics. I have tried digitalis in several other cases of goiter with 
fibrillation and heart failure without benefit. 
The discussion of Case 92 shows the importance and need of correlating 
all factors and data in the study of the individual cases of auricular fibrilla- 
tion which you may be called upon to diagnose and treat. If a case of decom- 
pensation is due to auricular fibrillation with mitral stenosis you will find, 
with few exceptions, that digitalis acts almost as a specific. I prefer to give 
the tincture as already outlined in a previous Clinic. I want to emphasize 
again the importance of keeping such cases for an indefinite period of time 
under the influence of this drug, otherwise they will again decompensate. 
Case 91 is an excellent example of that fact. 
Let us now take an instance of auricular fibrillation in senile cardio-sclerosis 
with fairly marked irregular and rapid ventricular activity and with signs 
of decompensation There again digitalis will probably have a beneficial 
effect. I say “probably” because one must understand that in senile cases 
there are usually advanced pathological changes in the myocardium, endo- 
cardium and the coronaries, thus there is often not enough healthy heart left 
1 The specific action of quinidine was not known at the time this and other cases of 
fibrillation were presented. 630 
CARDIO-VASCULAR CLINICS 
upon which the digitalis can act. Such changes constitute, I believe, the 
most potent reason for disappointment in the action of digitalis in these 
individuals. Digitalis may indeed block the discordant impulses coming 
from auricle to ventricle in fibrillation, and hence help steady the ventricular 
action; but it cannot well increase the contractile power of a considerably 
damaged heart. 
I shall now briefly discuss some of the salient extra-cardiac causes of fibril- 
lation in patients with otherwise normal hearts. Some years ago I observed 
a case of fibrillation without dyspnoea in a tobacco smoker with an organically 
sound heart. A similar case has been reported in the literature. An instance 
of transient auricular fibrillation has been reported in a laborer who while 
working in a vat was overcome by hydrogen sulphide gas; his heart was organ- 
ically normal. We also occasionally observe patients with absolutely normal 
heart, blood vessels and kidneys, who apparently set up fibrillation as the 
result of reflex causes arising from stomach or intestinal disturbances. An 
illustrative case is the following: About two years ago, I was consulted by a 
lady fifty-nine years of age. She had suffered from belching and regurgitation 
of food for many years. About ten years ago she had colitis and abdominal 
cramps. Five years thereafter she had pains over the sigmoid. She was 
operated upon for appendicitis. Adhesions were found; the pains over the 
sigmoid persisted. During the past summer she was considerably oppressed 
by the heat. She went to Atlantic City, and while resting in a rolling chair, 
she had a fainting spell lasting about five minutes. Her family physician, 
an excellent and careful practitioner, assured me that the summer before, 
her pulse had been perfectly regular. I saw her some weeks after the fainting 
attack; the pulse and heart action were grossly irregular; sometimes slow, 
sometimes fast. She had attacks of tachycardia during which the heart 
rate was over 160 per minute; the rhythm was irregular. Only at such times 
was there slight dyspnoea. At other times the patient complained of a sub- 
jective feeling of “palpitation.” The gastro-intestinal symptoms consisted 
of belching, colicky pains and intestinal rumbling. A polygraphic tracing which 
I took revealed auricular fibrillation. In the absence of any evidence of 
organic cardiac disease—no decompensation, no edema, no bronchitis, no 
cyanosis, no hypertension, no abnormal constituents in the urine, no cardiac 
enlargement, no murmurs, and because of the old though still present gastro- 
intestinal symptoms, I made the diagnosis of auricular fibrillation arising 
reflexly from the gastro-intestinal canal. Therapy was directed chiefly to the 
latter. Bromides were prescribed. A good prognosis was given, although 
no time limit was set as to the duration of the fibrillation. The patient was 
allowed to sit out of bed, then to walk and gradually to resume her old activi- 
ties, even including golfing. The arrhythmia lasted several months. The 
pulse and heart action finally became regular and remained so. This case is 
given in detail, partly because of its interest, partly to impress upon you the 
great importance of obtaining a good, careful previous history, and finally, the CARDIOVASCULAR CLINICS 
631 
importance of studying, correlating and weighing all data before arriving at a 
diagnosis. 
Returning to Table III, you note that auricular fibrillation may occur as 
part of or during an attack of paroxysmal auricular tachycardia. The latter 
means that the auricles are beating regularly at a rate between 180 and 250 
per minute. The ventricles may beat at the same speed or not, depending 
upon whether the ventricle responds to every auricular impulse. When the 
ventricle does not regularly respond it denotes that heart block is present. 
It is not unusual to have paroxysmal auricular tachycardia as the result of 
minor gastric complaints in patients with perfectly normal hearts. Diges- 
tive disturbances, in some as yet unknown manner cause abnormal impulses 
in the rhythm center in the auricle with the resultant production of paroxysmal 
auricular tachycardia. The occurrence of auricular fibrillation found momen- 
tarily in such occasional cases denotes, I believe, that the abnormal impulses 
have tended to race the auricles at a speed beyond that of auricular tachy- 
cardia, so that the auricles can no longer beat rhythmically, and in its place 
the disorderly activity implied by auricular fibrillation occurs. 
Regarding fibrillation from fright and other emotional causes (Table III), 
I myself have never observed such cases, but they have been reported, and I 
have no doubt that they occur because the more one deals with graphic 
methods, the more one encounters irregularities of almost all types. These 
irregularities in previous years were simply diagnosed as arrhythmias but are 
now more exactly classified. 
Digitalis (Table III) may produce auricular fibrillation. I had one such 
case under observation several years ago. A boy with a decompensated 
mitral regurgitant lesion and an otherwise rhythmic heart showed fibrilla- 
tion every time he was under the maximum effects of the tincture of digitalis. 
Polygraphic tracings left no doubt as to the type of the arrythmia. I tried 
the digitalis experiment several times; when the drug was discontinued, 
fibrillation stopped and the pulse became regular at the end of a day or so; 
when it was again administered the auricles again fibrillated. It is interest- 
ing to note that, though the auricles were fibrillating, the patient felt perfectly 
well and compensation was completely restored. In this case the toxic action 
of digitalis upon the vagus was probably responsible for the arrhythmia; at 
the same time the contractile power of the heart, that is its pumping power— 
was considerably improved by the drug. It has been shown experimentally 
that if the entire gastro-intestinal tract of a cat be removed from esophagus 
to anus, and digitalis be injected intravenously, the cat will go through the 
action of emesis. In other words, the drug apparently possesses some 
action upon the cerebral center. Thus, the vomiting caused by digitalis may 
be similarly explained in patients to whom we have given too much digitalis, 
or who are particularly susceptible to the drug. It offers a more plausible 
explanation than the usual one that digitalis causes vomiting by irritating 
the gastric mucosa. 632 
CARDIO-VASCULAR CLINICS 
Referring again to Table III, I now wish to discuss the relation between 
toxins and fibrillation. Fibrillation occasionally occurs in pneumonia in 
adult and older individuals, in those with normal hearts, as well as in those 
with valvular and other cardiac disease. I presume the usual impression of 
pneumonia toxins is that they possess a destructive influence upon the cardiac 
muscle, valves and coronaries. In almost every postmortem in pneumonia, 
there is some cloudy swelling of the cardiac muscle, but it does not differ in 
degree or kind from that found in other infectious fevers. In my opinion 
auricular fibrillation occurring during pneumonia is not due to such 
pathological change, but is caused by some damage to the nervous mechanism 
—i.e., to the neurogenic control of the heart. In what way toxins may thus 
act, I cannot tell you. Though we use the term frequently, we possess so 
little knowledge about toxins and their effects on nerve structures that 
further discussion along these lines would be purely hypothetical. But it has 
been my clinical experience (and clinical experience after all is important) 
that fibrillation occurring in pneumonia in patients with previously 
normal hearts do not, even in after-years show any damage to the heeart as 
the result of the arrhythmia. I do not wish to leave you with the impression 
that pneumonia may not produce wide-spread damage to the myocardium 
and other cardiac structures. As a matter of fact I believe that this disease is 
often the insidious and first cause of a good deal of cardio-vascular damage 
which shows itself only in later life. This statement is scarcely susceptible 
to proof because the process is so insidious and slow. For example in a patient 
whom I saw some years ago, there was no doubt as to the correlation between 
a severe pneumonia contracted some years previously and the very gradual 
onset of cardio-sclerosis. In pneumonia with fibrillation, it seems difficult 
to conceive of severe cardiac damage which would not show itself immediately 
after the pneumonia had run its course; in the cases I have observed I could 
discover no sign of cardiac disease either during fibrillation or immediately 
thereafter. 
In concluding the remarks on fibrillation, I wish again to emphasize the 
importance of bearing in mind some such scheme as the Tables which give 
the physiological, clinical and experimental causes. Always try to correlate 
etiology with the case in hand. In that manner you can attack the thera- 
peutic and prognostic problems more readily and rationally. Such study 
will also help eliminate mistakes in the application of drugs. 
Student: What preparations of digitalis do you prefer and why? 
Dr. N.: The action of all the digitalis bodies is alike. I prefer the tincture 
because it can be given in smaller doses, because of its uniform strength, and 
because it is fairly stable by reason of its alcohol content. Next I prefer; 
digipuratum or digitan tablets because they are standardized preparations. 
In an emergency, I prefer strophanthin for its quick effect; one ampule con- 
taining one cubic centimeter is injected intravenously or intramuscularly; 
it should be injected slowly. It is particularly indicated at the onset of severe CARDIO-VASCULAR. CLINICS 
633 
decompensation or when auricular fibrillation comes suddenly with signs of 
circulatory failure, but it should never be administered in cases to whom fairly 
large amounts of digitalis had already been given. Digalin is variable in 
strength and hence is not as good as the other preparations just mentioned. 
Student: Does the effect of strophanthin last as long as digitalis? 
Dr. N.: No, it does not. Its effect lasts 12 to 24 hours; therefore it is 
necessary to follow it with digitalis. Sometimes it has a most remarkable 
and beneficial action within an hour or two. 
CASE 93.—AORTITIS WITH ATTACKS OF AURICULAR FIBRILLATION 
M. G., male aged 52, is married and has two grown children. He gives 
the following history: He has never had rheumatism. Twenty-five years 
ago he had a severe attack of jaundice. Thereafter he suffered from pyrosis 
and abdominal pain. About five years ago he suddenly was awakened at 
night by his first “heart attack;” this consisted of a feeling of “thumping in 
the chest” lasting several minutes. Some years later he was operated upon 
for appendicitis and purulent cholecystitis. Since these operations he has had 
no gastric symptoms except when eating fatty food; he then has some belching 
and pyrosis. Seven years ago he had typhoid fever, and four years thereafter, 
pneumonia. During the last two years the “heart attacks” are more fre- 
quent, occurring even daily. They last much longer than formerly, sometimes 
for hours. He has been a smoker in moderate amounts but he does not smoke 
at all now. He is a very poor sleeper; his sleep is often disturbed by erections, 
by thoughts of business or by introspection regarding his heart. Digitalis 
in small doses has improved his cardiac condition somewhat. The bromides 
produce restful nights. He wakes up hungry and feels worse before breakfast 
when washing and dressing. When not annoyed by “heart attacks,” he feels 
well and is able to attend to business. 
Examination.—The patient has given us a very intelligent and continuous 
story of his abdominal and cardiac complaints. The first point to determine 
is the nature of these “ heart attacks.” I was fortunate enough to examine the 
patient during one of the paroxysms. The heart at first beat rhythmically; 
then, while the patient was sitting quietly, he said, “I am having an attack.” 
The pulse and heart action suddenly became grossly irregular and rapid, with 
all the clinical characteristics of auricular fibrillation. An electrocardiogram 
which I immediately took confirmed the type of the arrhythmia. There was 
no dyspnoea, the patient simply complained of an uncomfortable feeling 
of “palpitation.” The attack lasted several minutes. I was able to decrease 
the cardiac rate slightly by sudden sharp momentary pressure upon the left 
and right vagus but the irregularity continued unchecked. 
At present the patient, as you see, is perfectly comfortable. He is a very 
well preserved man for his years. The blood pressure, urine and lungs are 
normal. The heart and pulse are now regular. Inspection and palpation 
of the cardiac area reveal nothing abnormal. Upon auscultation, the first 634 
CARDIOVASCULAR CLINICS 
sound over the right base is rough; all the other cardiac sounds are normal. 
Except for the scars of previous operations, the abdomen presents nothing 
abnormal. There is slight edema of the legs, as you note by the pitting upon 
pressure. The orthodiascopic tracing which I here show you presents definite 
evidence of enlargement of the first portion of the aorta; the remainder of the 
cardiac outline is normal in size and contour. 
To Summarize.—The patient, many years ago, suffered from painful 
digestive symptoms and from “heart attacks.” The former were cured by 
operation. The latter were at first infrequent but during the last two 
years, they have increased in frequency and duration. Insomnia has been 
an added symptom, probably because the patient is worried about his attacks. 
We have no means of deciding whether the “ heart attacks ” years ago were 
of the same nature as the recent ones. From the patient’s description of both, 
the probability is that they are identical. The original paroxysms of auricular 
fibrillation—for such is the type of the present arrhythmia—may have been the 
result of reflex excitation of the cardiac nerves from the old dyspepsia. 
The dyspepsia itself was due to appendicitis and cholecystitis. You gather 
from the history that even now the patient is sometimes awakened by abnor- 
mal hunger sensations. 
Why are the paroxysms more frequent of late? The cardiac examination 
may offer the correct explanation. The rough first aortic sound, the dilated 
aorta, and the edema of the legs are probably due to aortitis with cardiac 
insufficiency. The irregular heart action per se may also have caused the 
edema, but the latter seems more likely a part of the composite picture of mild 
cardiac decompensation. The changes in the aorta are probably compara- 
tively recent, otherwise there would not have been this long remission of 
cardiac symptoms. The aortitis may have had its origin in the attack of 
pneumonia three years ago. Such gradual progressive changes following 
pneumonic infections are, I believe, by no means infrequent. They rarely 
appear immediately after or during the pneumonia, but are one of the late 
sequelse. The pathological changes in the aorta—possibly also involving 
the coronaries—can account for a recrudescence of the old attacks in more 
severe form. The fact that the patient feels worse upon arising and before 
breakfast is also of interest. I have observed similar instances in other 
types of heart disease. It seems due to the fact that it requires an added 
effort, and is a tax on the weakened cardiac reserve to carry on the circulation 
properly when the patient first moves about mornings. The hunger experi- 
enced in the morning may also cause reflex vasomotor disturbances which 
deleteriously affect circulatory stability. 
Therapeutically I would first reassure the patient. There is no harm 
in giving him bromides at night for the insomnia. I should also advise him to 
take a glass of warm milk before retiring so that the stomach be not too empty 
mornings. He should have a glass of warm milk given to him every morning 
while still in bed. I should treat him intensively with digitalis for one week, CARDIOVASCULAR CLINICS 
635 
instead of the irregular dosage he has been taking. For this purpose, he 
should have two digipuratum or digitan tablets daily for one week. This 
would have the effect not only of helping the circulation but also of increasing 
the tone of the vagus. The latter is one of the effects of digitalis. You remem- 
ber in this connection that I had stated that pressure on the vagus decreased 
the cardiac rate during a fibrillation attack; the mechanical pressure prob- 
ably also acted as a stimulus to the vagus. 
Later Report.—The family physician reported to me that the patient 
followed the treatment outlined, and that the “heart attacks” have thus far 
been very infrequent and of short duration. 
CASE 94.—MYOCARDITIS—AURICULAR FIBRILLATION—DECOMPENSATION- 
THERAPEUTIC RESULTS 
M. K., male, aged 45, gives the following history: He considered himself 
well until two years ago. He is a moderate smoker. There is no history of 
scarlet fever, rheumatism or of venereal infection. Two years ago he began 
to cough and to have shortness of breath; later he developed epigastric pains 
and “palpitation” upon walking. His legs are often considerably swollen. 
Examination.—You note at once the patient’s orthopncea. Upon inspec- 
tion of the chest, you observe the diffuse irregular ventricular activity; 
corresponding to it the pulse is also completely irregular in force and rhythm; 
in other words the patient has auricular fibrillation. The radial arteries are 
not thickened. Corresponding to the irregularity in force of the ventricular 
systoles, the blood pressure of the various beats fluctuates considerably. The 
majority of the beats registers a systolic blood pressure of less than 150 m.m. 
There is no pain on precordial palpation. Upon auscultation you hear a soft 
systolic murmur at the apex; there are no thrills or other abnormal sounds 
to be heard during systole or in the occasional long diastolic pauses. The 
liver is moderately enlarged. There is tenderness upon pressure in the 
epigastrium. There are bubbling mucous rales and sibilant breathing over 
the chest. At present there is no edema of the legs. The urine contains some 
albumen with granular and hyaline casts. The orthodiascopic tracing reveals 
no enlargement of the aorta, but as you see, the left ventricular and right 
auricular curves are considerably enlarged, giving the cardiac contour a some- 
what rounded appearance. 
It is evident that the patient is suffering from severe decompensation as 
shown by the dyspnoea, the auricular fibrillation, and the signs of bronchial, 
pulmonary and hepatic congestion. The anatomical cardiac lesion is less 
easy to diagnose. The only abnormal sound is the soft systolic apical mur- 
mur. Perhaps, if the heart action can be made more regular and slower by 
drugs, especially digitalis, we may hear other abnormal sounds not audible now. 
The renal condition may be the primary disease, although it is more probably 
the result of circulatory congestion. For the present I believe we must 
regard the cardiac condition as due to myocarditis, for the following reasons: 636 
CARDIOVASCULAR CLINICS 
The absence of physical signs of an endocardial lesion, the orthodiascopic 
evidence of ventricular enlargement, the absence of aortic enlargement, and 
the absence of any rheumatic or other history which would be likely to cause 
an endocardial lesion. 
The results of therapy in this case will practically depend upon what we 
can accomplish by intensive digitalis and theobromine medication during the 
next week or two. The patient tells us he has received digitalis, but from his 
account I believe in insufficient quantity. I shall prescribe the tincture of 
digitalis in teaspoonful doses three times daily for three days; then he will be 
placed for two days upon a strict Karrel diet, and take theobromin sodium 
salicylate in seven grain doses, four times daily. If this intensive medication 
is followed by good results, the digitalis will be continued in smaller doses, 
and the theobromin and Karrel days will be prescribed at more frequent 
intervals. 
Later Examination.—This patient you saw four weeks ago, markedly 
decompensated and dyspnoic. The therapy I then suggested had been 
carried out. As you can see even without a detailed examination there has 
been marked improvement in the patient’s condition. He tells us he feels 
quite well and comfortable. He is able to walk without dyspnoea or palpita- 
tion. The rales in the chest have almost entirely disappeared. The liver is 
much smaller; there is no epigastric sensitiveness. The ventricular rate is 
now 60 per minute; it is fairly regular in force and rhythm. Upon ausculta- 
tion no murmurs are heard. The urine contains no albumen. The average 
systolic blood pressure is now 160 m.m. 
This patient shows the brilliant result of digitalis therapy. He is now in 
excellent condition and may even do some physical work. He will have to 
continue taking digitalis, and occasionally theobromin and a Karrel day for 
an indefinite time, in order to prevent a recurrence of decompensation and 
dyspnoea. Digitalis in his present condition may be given in ten minim doses, 
once daily; the theobromin and Karrel diet for two days every month. In 
the absence of any cardiac murmurs even now with the slow heart action, I 
believe our original diagnosis of myocarditis is correct. 
CASES 95-97.- TRANSIENT AURICULAR FIBRILLATION 
In a previous clinic I demonstrated to you several cases of transient auricu- 
lar fibrillation. I now have the opportunity of showing you three others. 
Case 95. Transient Auricular Fibrillation Due to Cofee.—S. K., aged 35, 
physician, was a heavy smoker in former years but stopped because smoking 
produced precordial pains. He had influenzal pneumonia some months ago; 
this was not accompanied by any arrhythmia. The night before I saw the 
patient, he said that he drank two cups of very strong, almost black coffee, a 
very rare thing for him. He recalled that the coffee was very strong because 
it required an exceptional amount of sugar in order to sweeten it. One hour 
after drinking the coffee, he felt a “fluttering around his heart;” he took his 637 
CARDIO-VASCULAR CLINICS 
pulse and found it irregular. He had no dyspnoea and slept well the entire 
night. He had no subjective symptoms the following day. He kept to his 
bed for precautionary reasons, simply because his pulse was still irregular. 
Examination.—You observe that the patient is quite comfortable now, 
being neither dyspnoic nor suffering from any distress. In fact, to judge from 
his laughing countenance, he considers the whole matter a joke. The highest' 
systolic blood pressure registered by the strongest beats is 120. This excludes 
hypertension. I am not going to attempt to find the average blood pressure, 
a process which requires some calculation because I consider it unnecessary 
in this case. You note that both pulse and heart action are completely irregu- 
lar in time and rhythm, the characteristics of auricular fibrillation that I 
have so frequently pointed out to you. Aside from the arrhythmia, there is 
not the slightest evidence of cardio-vascular disease; there is no dyspnoea, there 
are no murmurs, there is no precordial or epigastric sensitiveness, the fiver is 
not enlarged, there is no edema of the legs, the lungs are normal, the urine is 
normal and there is no history of rheumatic infection. 
I believe that the auricular fibrillation is due solely to an overdose of coffee, 
and not to any organic heart disease. I have never seen or heard of a similar 
case due to coffee poisoning, but the history is so clear and unmistakable that 
I think this diagnosis is justifiable. The further progress of this case will 
probably substantiate or upset the diagnosis. If the arrhythmia be of func- 
tional origin and due to an overdose of coffee, the auricular fibrillation should 
disappear within a day or so, that is, after the coffee has been eliminated 
from the system. I do not believe any medication is necessary at present. 
Examination Next Day.—You observe, gentlemen, that the patient’s 
pulse and heart action are regular now and that all the heart sounds are normal. 
He feels perfectly well. The disappearance of the arrhythmia justifies our 
original diagnosis, I believe, namely that it was caused by an overdose 
of coffee. 
Coffee is known to cause extrasystoles occasionally , probably by increasing 
excitability of the cardiac nerves. Although the mechanism of their action 
may be entirely different, caffein seems also to have an effect upou the heart 
somewhat similar to that of digitalis, in that both can produce extrasystoles 
and auricular fibrillation in susceptible individuals. 
CASE 96.—AURICULAR FIBRILLATION FROM FRIGHT 
Mrs. D., aged 70, had an attack of influenza some months ago; otherwise 
she does not recall any recent illness. Yesterday she suddenly became dizzy 
and fell. This frightened her very much. Soon thereafter her heart began 
to “palpitate” and there has been “palpitation” ever since. I can get no 
further details from her. 
Examination.—You observe, gentlemen, that although the patient looks 
her years, she has not the thickened radial and temporal arteries common in 
the old. Nor is she very dyspnoeic. Her heart and pulse action are typical 638 
CARDIOVASCULAR CLINICS 
of auricular fibrillation: Both are completely irregular in force and rhythm. 
The heart sounds, the urine and the lungs are normal. There is no edema of 
the legs, there is no precordial or epigastric sensitiveness. The heart is 
apparently not enlarged to percussion. 
The question now arises, what is the cause of the sudden onset of auricular 
fibrillation? Two main probabilities suggest themselves; either this patient 
may have had a coronary infarct, an accident not so very infrequent in older 
people and not uncommonly associated with auricular fibrillation; or sudden 
fright following the dizzy spell and fall may have caused the arrhythmia by 
some acute circulatory disturbance in the brain, in the neighborhood of the 
cardio-inhibitory center. I am inclined to the latter hypothesis despite 
the greater chances of coronary disease in a person of advanced age; indeed, 
the original attack of giddiness may even have been of cardiac origin. In 
favor of a functional cause—fright—is the absence of dyspnoea and of gastric 
disturbances, and the fact that the arrhythmia immediately followed the fall. 
I shall prescribe digipuratum tablets, one three times daily. We shall 
re-examine the patient in a day or two; perhaps the further course of the 
case will indicate the correct diagnosis. 
Examination Two Days Later.—This patient, you recall, I presented as a 
case of transient auricular fibrillation. You notice now that the pulse and 
heart action are normal. There are no murmurs. The patient is quite 
comfortable. I shall discharge her and let her follow her usual occupation. 
I believe that the cause of the auricular fibrillation was fright, for I do not 
think that digitalis would so quickly have cleared up the arrhythmia, had it 
been due to a coronary infarct. When the latter interferes sufficiently with 
the intra-cardiac circulation to produce auricular fibrillation it would almost 
of necessity cause other cardiac symptoms such as pulmonary edema and 
precordial pains. 
Assuming that the arrhythmia is of functional and not of organic cardio- 
vascular origin, let us theorize for a moment regarding the possible mechanism 
which induced the auricular fibrillation. One may, for example, hypotheti- 
cate that the fall itself, by causing a sudden change of blood pressure, pro- 
duced sufficient disturbance in the vasomotor tone and in the cardio-inhibitory 
center to have induced the arrhythmia. Or, subsequent to the fall, there 
was vasomotor instability, thus upsetting the usual control of this center. 
Even giddiness per se may conceivably reflexly alter the vasomotor tone and 
thus produce an arrhythmia. I realize of course that we are heaping up theoret- 
ical assumptions with a meager substratum of facts. But it is a rather 
common clinical experience that sudden fright, for example, produces severe 
tachycardia and extrasystoles, and I see no reason why it may not also cause 
auricular fibrillation in exceptional instances. The more I observe and study 
arrhythmias, the more lam impressed by the fact that the most bizarre as well 
as the most common types can follow functional derangements. I have 
even observed a case of heart block of functional origin. I was able to follow CARDIO-VASCULAR CLINICS 
639 
that patient to autopsy, for he was killed in an elevator accident. Careful 
macroscopic examination of the heart showed no lesion in the auriculo- 
ventcicular conduction system nor in any other part of the heart. 
CASE 97.—TRANSIENT AURICULAR FIBRILLATION—PERMANENT HYPER- 
TENSION 
A. K., married, aged 58, had been a moderate smoker. He had gonorrhoea 
many years ago. He has not had any recent acute diseases. He had always 
been athletic. Except for cardiac “ attacks,” of which this is the fourth, 
he had never had any cardiac symptoms. The first attack occurred four years 
ago. The patient believes it was the result of too much swimming. The 
second he believed followed too much smoking. 
For several weeks past he has been worrying over financial matters. 
One night he suddenly noticed that his heart beat very irregularly, at which 
time he also became dyspnoic. Prior to this, even though working hard, he 
never was short of breath. 
Examination.—This is the fourth day, the patient tells us, that his pulse 
and heart action have been irregular. You observe that he is not dyspnoeic 
now, although he is lying rather flat. Both heart and pulse are irregular in 
time and rhythm, typical of auricular fibrillation. When you listen to the 
heart, you will find that the second sound over the right base is somewhat 
accentuated; the other cardiac sounds are normal. There is no pain on pre- 
cordial pressure nor does the patient suffer from any subjective precordial 
discomfort. The systolic blood pressure of most of the effective beats ranges 
between 160 and 170. The liver is not palpable. The urine is normal. The 
Wassermann examination of the blood is negative. There is no edema of the 
legs. The eye grounds, as reported by the ophthalmologist, show no evidence 
of arterio-sclerosis. The orthodiascopic tracing being passed around shows 
moderate enlargement of the first portion and arch of the aorta. The 
remainder of the cardiac outline is normal in size and form; in other words, 
there is no evidence of ventricular hypertrophy. 
To summarize: This patient has auricular fibrillation now; the other 
past “attacks” may also have been examples of the same arrhythmia. The 
definite cardio-vascular abnormalities that the patient presents are an accen- 
tuated second aortic sound, an enlarged aorta as demonstrated by the X-ray, 
and moderate hypertension. I believe that the aortitis is of the slowly 
progressive type, for there would otherwise not be such long remissions of 
cardiac symptoms. You see the patient looks very robust for a man of his 
years and even now, despite fibrillation, he does not feel ill. You may recall 
that I have already shown you one or two examples of aged individuals with 
very much enlarged aortas who were suffering from very few cardiac symp- 
toms. Our patient seems to belong to that group. I believe that financial 640 
CARDIOVASCULAR CLINICS 
worry has much to do with the onset of this last pulse irregularity. As I 
picture the case it seems to me that the neurotic element may have been a 
factor in causing arrhythmia, and even the hypertension. I shall place the 
patient upon digipuratum or digitan for several days; for three days, I shall 
give him two tablets daily, and then for six days, one daily. He is also to 
receive fifteen grains of the triple bromides every night. I believe the arrhy- 
thmia will disappear soon and that the blood pressure will become normal. 
I shall report to you the further progress of the case at some future time. 
Report Four Months Later.—The patient took the medication I had 
authorized. I then sent him to the sea-shore for several weeks. I have seen 
him often during the intervening four months. One week after the examina- 
tion, the pulse rhythm became normal and has remained so. The blood 
pressure varies between 190 and 200 systolic, and from 130 to 100, diastolic. 
Our examination of the phenolsulphonephthalein output for two hours was 
40 per cent. This is the lower normal limit. The patient is again active, but 
is not rushing about quite as much as formerly. His only complaint is slight 
dyspnoea upon walking stairs, and slight palpitation. These symptoms 
seem to have no correlation with the height of the systolic or diastolic pres- 
sures. From all present indications the hypertension seems to be permanent. 
Whether it antedated the time we first saw him, we have no means of ascertain- 
ing, because the patient had not had his blood pressure taken for many years. 
I scarcely believe that a latent interstitial nephritis plays an important 
role in the hypertension of this patient because none of the usual earmarks 
of nephritis are present. Neither the dyspnoea, pallor, 'anemia, gastric nor 
precordial symptoms, eye-ground changes, norlowphthalein output is present. 
On the other hand I do not wish to diagnose the case as one of so-called func- 
tional hyperpiesis, for the enlarged aorta is distinct evidence of some organic 
arterial change. 
Later Note.—Some months later, I saw the patient in an attack of moder- 
ate dyspnoea with severe precordial pain radiating to the left arm. The 
temperature was normal. Heart action was rhythmical. The only physical 
sign in addition to the old murmurs was a localized area of dry pericarditis 
in the fourth left interspace. This was undoubtedly due to an inflamed 
pericardium covering an infarcted myocardial area from occlusion of a small 
coronary. In view of this definite evidence of coronary disease, I believe 
that the previous attacks of temporary auricular fibrillation may also have 
been results of coronary stoppage from embolism or infarct. The precordial 
attacks also clear up, I believe, the cause of the hypertension, for the latter 
is by no means an infrequent accompaniment of aortitis without clinical evi- 
dence of nephritis. Indeed, cases of aortitis with cardio-sclerosis have been 
described in which postmortem examination of the kidneys both macro- and 
microscopically did not show sufficient changes to warrant the assumption 
that the slight nephritis was the cause of the hypertension. CARDIO-VASCULAR CLINICS 
641 
CASES 98-104.—THE USE AND ADMINISTRATION OF QUINIDINE SULPHATE IN 
AURICULAR FIBRILLATION 
Gentlemen: I have waited several weeks until I was able finally to 
gather together several cases of auricular fibrillation so that we could 
observe together the effect of quinidine on the rhythm. Where it was found 
necessary, the cases have first been properly digitalized, for it is very impor- 
tant to put the patients in as good a state of compensation as possible before 
quinidine is given. Hence, digitalis is first administered to those who present 
evidence of heart failure. It will perhaps simplify our problem if I take up 
briefly our present knowledge of quinidine—its action, dangers, disadvan- 
tages, etc. 
Since quinidine first came into fairly general use in 1921 because of its 
extraordinary power to restore the normal rhythm in a certain proportion of 
cases of auricular fibrillation, there have been case and experimental reports 
dealing with the fundamental method of action of quinidine. In an excellent 
paper dealing with the experimental phase, Lewis and his co-workers draw the 
following conclusions regarding the effects of quinidine sulphate in auricular 
fibrillation as found in man. They state that the drug has two actions: 
(1) Direct action upon the auricular musculature by which it lowers the sino- 
auricular rate; depresses and prolongs conduction time from auricle to ventri- 
cle; and lengthens the refractory period of the auricular musculature. The 
last is of most importance. (2) It causes partial paralysis or release of the 
vagus. In this it is opposite in effect to digitalis which increases vagal control 
and inhibition. 
I call your attention now to the new fact that auricular fibrillation is 
regarded as basically due to irregular blocking of a continuous “circus’’ 
wave of excitation, the normal method of spread of impulse through the auri- 
cles. Although the circus wave still continues, blocking of it depends upon 
differences and defects in conductivity and irritibility of various portions of 
the auricular musculature. The consequence is what we clinically know as 
auricular fibrillation. Before normal rhythm is restored by quinidine, there 
is usually a significant decrease in the number and irregularity of the fibrilla- 
tory waves as determined by electrocardiograms taken by direct chest leads; 
there is also preliminary stage of increased ventricular rate, whether the normal 
rhythm be restored or not. This action seems due to release of vagus control, 
a factor just mentioned. Occasionally the ventricular action becomes very 
rapid, irregular and violent, in consequence of which there may be marked 
dyspnoea. This, and the fact that quinidine can cause gastro-intestinal 
disturbances, such as nausea, vomiting and diarrhoea, and that it has occa- 
sionally produced cerebral embolism from sudden slowing of the blood 
current in the auricles coincident with the restoration of normal rhythm, 
are possible dangers following the employment of the drug. As an instance 
of tachycardia, there is a recent report of a case of auricular fibrillation in a 642 
CARDIO-VASCULAR CLINICS 
patient with mitral regurgitation who was given quinidine sulphate, 8 grains 
daily for three successive days. In all 24 grains were given. On the second 
and especially on the third day, there was evidence of severe decompensation 
with auricular fibrillation still present. It took thorough digitalization to 
slowly restore compensation. I wish again to emphasize that it shows that 
there probably exists a drug idiosyncracy to quinidine in some individuals, 
as indeed is true of all powerful drugs. Quinidine undoubtedly increases the 
tendency to decompensation or actually causes heart failure by its occasional 
action in causing marked increased rapidity of the heart action. 
I have had occasion to use quinidine sulphate in hospital practice in 
patients with auricular fibrillation in all types of cardio-vascular disease. 
Many were old individuals with marked cardio-vascular and cardio-renal 
changes, some with, others without hypertension. Many were decom- 
pensated. The net result of quinidine administration was temporary restora- 
tion of normal rhythm in a few of these cases. A few complained of nausea. 
One or two vomited. Some exhibited an increase of tachycardia, but none 
to any alarming extent. Some of the patients had two or three courses of 
quinidine—but the results were the same. All of the patients were properly 
digitalized before the quinidine was given. I had not expected permanent 
restoration of the rhythm in these advanced cases of cardio-sclerotic disease, 
for it was my clinical impression that quinidine was of value chiefly in younger 
individuals without far advanced degeneration of the heart muscle, in other 
words, mainly those with valvular disease. My routine administration 
consisted in giving the quinidine sulphate in 5 grain doses every hour for 
three doses. I examine the patient after the first dose to see whether there is 
any hypersensibility. I again observe the patient after the third dose. If 
then there are no untoward symptoms—no vomiting, diarrhoea or undue 
tachycardia—5 grain doses at hourly intervals are repeated for three more 
doses. Thus altogether 30 grains are given in one day. 
I have found this method and dosage satisfactory and have up to the 
present not noticed any ill effects from this method, although I have often 
observed some alarming symptoms from the quinidine as such. Two cases 
I shall later report to you. The method itself seems safe because any 
important drug idiocyncracy will probably show itself after the first five or 
after the 15 grains, a dose which seems well within safe limits. 
Case 98.—Mrs. F., a widow 46 years old, has to support herself and 
does much laborious work carrying bundles and climbing stairs. She has 
complained of frequent attacks of bronchitis and dyspnoea for several years. 
She reached her climacteric two years ago; it was accompanied by sweats, 
flushes, menorrhagia and rapid heart action. Of late months, dyspnoea has 
become more marked. She has had “bluish” hands for years. She sought 
hospital admission chiefly because of her dyspnoea and fainting spells. 
Examination.—You note that when at rest in bed there is only slight 
dyspnoea. Her hands and lips are moderately cyanotic. There is no evi- CARDIOVASCULAR CLINICS 
643 
dence of bronchitis or of pulmonary congestion. She had already received one 
and one half ounces of the tincture of digitalis. Despite that, you notice 
that the heart action is still quite irregular both in force and rhythm, the 
usual clinical evidence of auricular fibrillation. The urine is normal. Most 
of the beats register a blood pressure around 180, therefore I believe we are 
safe in saying that hypertension is present. In the fluoroscope I found that 
the heart was practically normal in size for one of her physique. You hear 
no heart murmurs on auscultation. There is no edema of the legs. My 
impression is that the laborious work and nerve disturbances incidental to the 
menopause are more responsible for her cardie condition than advanced cardio- 
vascular disease. This is based upon the absence of such physical evidence 
as is usually found in cardio-sclerosis. The heart is not enlarged; there are no 
murmurs; there are no precordial tenderness and pains, so significant of serious 
coronary disease; there is no pulmonary edema or edema of the legs. I have 
already pointed out to you in other Clinics that women at the menopause are 
particularily susceptible to arrhythmias and hypertension, especially if there be 
some pathological changes in the cardio-renal vascular system. These 
changes, however, need not necessarily be marked or advanced. It is only 
the correlation and careful observation of all the data—the history, the 
duration of symptoms, the physical examination—which helps in the deter- 
mination of how much the symptoms are due to organic changes, and how 
much to superimposed functional changes. In our present case the fainting 
attacks may have been due to severe paroxysms of tachycardia from her 
hard work. 
Quinidine Administration.—A five grain quinidine capsule had been 
given about one half hour ago. The patient does not complain about nausea. 
The cardiac condition is the same as when we saw her before the drug was 
given. We shall therefore give her two more 5 grain doses one hour apart. 
. . . Examination after 15 grains of quinidine sulphate. The patient, as 
you observe, has a heart rate slightly more rapid than previously. I believe 
it is perfectly safe to go ahead with the other 15 grains this afternoon, to be 
given in the usual 5 grain doses at hourly intervals. We shall see her 
again tomorrow. 
Examination Next Day.—The house physician reports that the patient 
complained of a little “ throbbing” in the head, that she felt nauseated yester- 
day afternoon and that she vomited during the night. He found the rhythm 
normal this morning. Let us examine the patient. She says that she now 
feels quite well. The heart and pulse are perfectly regular, the rate is 75 per 
minute. The blood pressure is quite different from the previous readings, 
for the systolic is 100 and the diastolic 80. In other words, at present, she has 
hypotension, not hypertension. Although the reason for this change is not 
quite clear to me, it serves to emphasize what I said about the influence of 
purely functional derangements: Perhaps the hypertension as well as the 
fibrillation were chiefly functional in origin, hence the drop in systolic blood 644 
CARDIOVASCULAR CLINICS 
pressure when fibrillation ceased and normal rhythm was restored by quinidine. 
That the low systolic blood pressure is not due to myocardial failure is shown by 
the fact that the patient is comfortable and has no dyspnoea. 
Later Report.—-The next day the rhythm was still normal, there were 
however, occasional extrasystoles. I have no opportunity here to take 
electrocardiograms. It is known, however, that extrasystoles are not uncom- 
mon after the normal rhythm has been restored by quinidine. By graphic 
tracings these have been found to be usually auricular premature contrac- 
tions. This is another clinical evidence of the after-effect of quinidine on the 
auricular, rather than on the ventricular musculature. I saw the patient 
again after two days. She was again fibrillating, the ventricular rhythm 
resembled what we found at our first examination. This then is an 
instance in which the drug had but temporary effect. Perhaps patients 
of this kind should be kept under the effect of quinidine by continuing the 
drug in smaller doses.1 
Case 99.—Mr. B., aged 54, came under my observation for the first 
time about one year ago. He was then extremely decompensated and had 
been so for several months. He presented the usual evidences of advanced 
heart failure: Cyanosis, pulmonary and leg edema, congested liver, dyspnoea. 
He had auricular fibrillation. The cardiac lesion was an old mitral regur- 
gitation. He improved remarkably under rest and digitalis, so much so 
that he was finally able to resume his work as tailor. I had written him to 
return to the hospital to study with you the effect of quinidine in his case. 
Examination.—You observe that the patient is not dyspnoeic. The 
cardiac action is irregular, the rate 80 per minute. Most of the systoles 
come through at the wrist as pulse beats, that is, there is very little pulse 
deficit. The liver is scarcely palpable; there is no pulmonary edema or 
edema of the legs. There is a loud systolic murmur over the mitral area. 
The patient is still taking his digitalis. 
Quinidine Administration.—We shall now proceed with quinidine sulphate 
as in the previous case. He had his first 5 grain capsule one half hour ago. 
His condition is the same as when I examined him early this afternoon. We 
can safely give him his other two doses. . . . Now after 15 grains there 
is as yet no change in the condition: No undue tachycardia, no dyspnoea, 
no nausea. He may therefore receive the other 15 grains in 5 grain doses at 
hourly intervals. We shall examine again tomorrow. . . . The house 
physician reported no untoward symptoms except slight nausea. He said 
that he found the rhythm normal on his morning rounds. You observe that 
the heart action is rapid although regular. The rate is 110 per minute. The 
patient is also conscious of his rapid heart action, and says that he does 
1 After the patient left the hospital, her family physician gave quinidine under my 
direction. Quinidine was administered in daily 5 grain, and later in 5 grain weekly doses 
after the primary 30 grain dose. In this manner the rhythm has remained normal and the 
patient is very comfortable. CARDIOVASCULAR CLINICS 
645 
not feel better or even as well as before the quinidine. This is probably due 
to the fact that his ventricular rate is more rapid now than when under 
digitalis alone, for as you know dyspnoea and other symptoms occurring 
with auricular fibrillation depend upon the resultant rapidity and irregularity 
of ventricular action and not on the auricular fibrillation as such. 
Later Report.—The regular rhythm lasted two days, after that interval, 
auricular fibrillation again set in as before the quinidine. 
Case ioo.—I got the following previous history of this patient, Mrs. J., 
aged 34, the mother of two children, from her family physician. She has 
had a mitral stenotic lesion for years. The lesion has always been com- 
pensated; the rhythm normal. She is of a high strung temperament. 
During the last week she has been very busy and active, taking a prominent 
part at a charity bazaar. She ate very irregularly and was on her feet a good 
part of the day. The work and responsibility exhausted her very much. 
Two days ago while at the bazaar in the evening she noticed that her heart 
became irregular. The physician says it has been irregular since. 
Examination.—You observe that the patient is somewhat dyspnoic. On 
examination you will find the typical physical signs of mitral stenosis with 
auricular fibrillation—heart action irregular in force and rhythm. There is 
a distinct rough diastolic murmur. The heart does not appear enlarged. 
There is no edema. Since the patient is not decompensated, I believe we can 
safely dispense with digitalis and start at once with quinidine. 
Quinidine Administration.—The patient has been given a 5 grain capsule 
one half hour ago. You observe that there is no change in the cardiac con- 
dition, the irregularity is the same as before. She shall get two other 5 grain 
quinidine sulphate capsules one hour apart, making in all 15 grains. We 
shall again examine her then. . . . The rhythm you now observe is 
perfectly regular, the rate is 70 per minute. The patient has herself 
remarked the absence of the annoying feeling of “palpitation.” Since the 
normal rhythm has been restored, it will not be necessary to continue the 
quinidine in this case. 
Later Report.—I have seen this patient at intervals for two weeks since 
our last examination. The rhythm has remained regular except for occa- 
sional extrasystoles. The patient is otherwise perfectly comfortable. The 
extrasystoles are regarded as clinical evidence of a tendency for quinidine 
to lose its effect with a possible return to auricular fibrillation. It may 
therefore be expedient to attempt to continue the quinidine effect by giving 
the drug, say 5 grains every second day. If then the extrasystoles disappear, 
it may be safe to discontinue the drug entirely. 
Case 101.—Mr. B., aged 29, a shoe clerk, had articular rheumatism 
seven years ago, since which time he dates his “heart” trouble. He had 
always been able to follow his occupation without cardiac symptoms till sev- 
eral months ago. At that time he took another position which required 
some stair climbing. He soon noticed that he suffered from “palpitation” 646 
CARDIO-VASCULAR CLINICS 
and shortness of breath. These complaints brought him to the hospital. 
Examination.—Here again we have a typical mitral stenotic lesion with 
auricular fibrillation. The sounds over the aorta are normal. The liver is 
moderately enlarged. There is moderate dyspnoea. He has already been 
digitalized. 
Quinidine Administration.—He got his first 5 grain capsule one hour ago. 
It apparently has not altered the cardiac condition, nor has the patient shown 
any especial drug hypersusceptibility. . . . Now 15 grains have been 
given altogether. There is no significant increase in the tachycardia, no 
nausea or other unusual symptom, hence we shall continue with the other 15 
grains at hourly intervals. . . . The rhythm is still irregular. We shall 
examine him again tomorrow. . . . The house physician reports that the 
pulse and heart were regular on his morning rounds, and that the patient felt 
slightly nauseated. You observe that the heart action is now rhythmical, 
the rate is normal. You also hear the typical mitral stenotic murmur. In 
addition, it now becomes evident for the first time that there is another 
valvular lesion—aortic regurgitation—for you can hear the typical diastolic 
murmur of that lesion not only at the right base but also at the second and 
third left interspaces. It is therefore evident that the previous irregular 
ventricular action either masked other murmurs; or what seems more prob- 
able that the irregular ventricular action did not allow sufficiently long 
diastolic intervals for the regurgitant back flow from the aorta to be heard 
as a murmur. What influence the aortic lesion will have with the now 
rhythmical heart is problematical. Probably not much, however, for the 
diastolic pressure is not very low, there is no water hammer pulse, and all 
the clinical signs point to mitral stenosis as the clinically predominant 
lesion. 
Later Report.—The patient has been walking around the ward for two 
weeks and feels quite comfortable. He says that he occasionally feels his heart 
“skip.” I have been able to corroborate that the “skipping” was due to an 
occasional extrasystole. This probably means that the quinidine is beginning 
to lose its effect. I therefore advised one 5 grain quinidine capsule every morn- 
ing for three days and then a capsule twice weekly. These doses are purely 
arbitrary, for enough experience has not been accumulated to be able to 
predict the proper dosage in such individuals. We do know however, that 
quinidine passes out of the system at the end of two or three days. Hence the 
occasional necessity for frequent repitition of the drug in order to keep up its 
effect. I again examined the patient at the end of another week. The 
heart rate was normal and rhythmical, there were no extrasystoles. He was 
then discharged from the hospital. 
Case 102.—Mr. G., aged 41, a painter, was admitted to the hospital 
several months ago with the same complaint that he has nowr; dyspnoea, 
cough, slight edema of the legs. Compensation was restored with digitalis. 
He has again been digitalized now. CARDIOVASCULAR CLINICS 
647 
Examination.—You note the typical irregularity of auricular fibrillation 
as well as the typical mitral stenotic lesion. The cardiac rate is 70 per minute, 
the beats are fairly regular in force. There is no edema of the legs. There 
are no rales or pulmonary congestion. In other words, digitalis had again 
restored compensation. 
Quinidine Administration.—One hour ago he got his first 5 grain dose of 
quinidine. Since his condition is unchanged we shall proceed with the other 
10 grains. . . . The patient complains of some dyspnoea; you will 
observe that the heart rate is somewhat more rapid and irregular, this 
probably causes the dyspnoea. I believe that after several hours we may 
give the other 15 grains. . . . The house physician reported that the 
patient vomited during the night. The patient complains that he still feels 
somewhat nauseated. You observe on examination that fibrillation is still 
present and that the cardiac rate is what it was at our first examination, 
about 70 per minute. I shall again try quinidine in a few days. 
Later Report.—A week after our last quinidine attempt, I again tried the 
drug in our usual method of administration, 30 grains in divided doses of 5 
grains each. The effect was the same, at first, increase of tachycardia with 
some dyspnoea; later, vomiting. The rhythm was not restored to normal. 
It is safe to again try quinidine in such cases after a week or two because it 
has been shown that the drug passes out of the system within three days. 
In some cases I have made repeated attempts, but in a general way it may 
be stated that if normal rhythm is not restored at the first trial, it will prob- 
ably not succeed in the other trials. 
Case 103.—This patient, Mr. F., aged 64, scarcely looks like a promising 
case for beneficial results from quinidine. His present cardiac condition 
is very much better than when he entered the hospital, several weeks 
ago. From his old cardiac history, we learn that for several years he has 
suffered from recurring attacks of articular rheumatism, for which he was 
admitted several times to another hospital. Despite these frequent rheu- 
matic attacks he never had any cardiac symptoms until three years ago when 
his son was drafted for war service. This upset him very much. Imme- 
diately thereafter his cardiac complaints began; palpitation and shortness of 
breath. These finally eventuated into severe and continued heart failure; 
cough, edema of the legs, constant dyspnoea, palpitation. On hospital 
admission, the patient was extremely cyanotic and orthopnoic. There were 
moist crackling rales and sibilant breathing over the entire chest. There 
was a soft systolic murmur at the right base followed by a diastolic 
murmur; the latter was not transmitted. Over the mitral area there was 
a blowing systolic murmur. The blood Wassermann reaction was negative. 
Auricular fibrillation was present. It took several weeks of digitalization, 
theobromine sodium salicylate with restricted fluid intake, and various 
expectorant mixtures to bring about what might be called a fair state of 
compensation. 648 
CARDIO-VASCULAR CLINICS 
Examination.—You observe that the patient is still cyanotic and moder- 
ately dyspnoic. You hear the aortic and systolic murmur. The liver is 
still considerably enlarged as the result of venous stasis. There are soft 
mucous rales to be heard over the lungs at various areas. X-ray examination 
of the chest shows that the aorta and left ventricle are considerably enlarged. 
Theie is no edema of the legs at present. The rhythm is characteristic of 
auricular fibrillation. The entire cardiac condition may be summed up as 
rheumatic mitral and aortic regurgitation, myocarditis, emphysema, con- 
gested liver and chronic decompensation. Shock and anxiety over his son 
seemed to be the factors which initiated the cardiac symptoms. 
Quinidine Administration.—Five grains had been given one hour 
previously. There are no untoward results, the patient is still fibrillating. We 
shall give him io more grains in two doses and then examine him. . . . 
Now, 24 hours after the first dose you observe that the heart is perfectly 
regular and that the patient feels comfortable. The murmurs are the same 
as before, rales are still present but the patient feels less palpitation. This 
was a rather unexpectedly favorable result in a patient with such advanced 
disease. 
Later Report.—The rhythm remained normal for four days and then 
fibrillation again began. Perhaps at some future time, I shall again 
administer quinidine for a longer period in order to try to get a lasting effect. 
Case 104.—Miss E., aged 59, states that she had “kidney trouble” 
one year ago. She has been complaining of gastric derangements, 
chiefly belching, distension after meals and pyrosis for a number of years. 
The cardiac symptoms began a few weeks ago. These were a sense of 
oppression in the chest and dyspnoea. Dyspnoea, however, is correlated not 
with exercise but with ingestion of meals, it is more marked after eating and 
even directly after swallowing fluids. The house physician states that on 
admission a few days ago, the heart was very irregular and rapid, the rate 
was around no. She was immediately digitalized. The ventricular rate 
fell to 80 and later to 40; it has been between 40 and 50 since then. 
Examination.—You observe that the patient is not dyspnoeic. The lungs 
are normal. There are no murmurs over the mitral area. The second 
aortic sound is accentuated. The urine contains a heavy trace of albumin 
and a few hyaline and granular casts. The systolic blood pressure is 150, the 
diastolic, 80. The Wassermann blood reaction is negative. There is no 
edema of the legs. The orthodiascopic examination shows a prominent aortic 
arch, no aneurism, and a heart moderately enlarged to the left. Having 
given you these data, let us pay particular attention to the arrhythmia. It 
is not as easy to diagnose as in our other cases because the heart action is slow 
(the rate just now is 50 per minute) and because the heart beats fairly regu- 
larly. On listening for a while, however, you will hear some beats that are 
weaker, as well as occasional definite but irregularly spaced breaks in the 
rhythm. On carefully examining the jugular in the neck you wall find that CARDIO-VASCULAR CLINICS 
649 
there are no jugular pulsations that correspond to the normal auricular pulsa- 
tions, in other words, the a wave is absent; instead of the normal a-c- 
fl-waves found in rhythmic heart action there are but two: The c and v. 
These characteristics serve to characterize the rhythm here present as auricu- 
lar fibrillation with slow and fairly regular ventricular action. Perhaps 
the latter was due to the digitalis. 
Quinidine Administration.—One 5 grain dose has already been given. 
. . . Now 15 grains have been given. The cardiac condition is the same. 
The other 15 grains will be given later. We shall see the patient to- 
morrow. . . . The house physician reported that the rhythm was regular 
this morning. It is regular now, for you will find on auscultation that the 
action is perfectly rhythmical and that the rate is 65 per minute. 
Later Report.—The pulse remained regular one day. Fibrillation then 
recurred, but the ventricular rate was then 70, not around 50. Quinidine 
in the usual manner was again administered and the next day the rhythm 
was again normal, the rate between 55 and 70. Quinidine in 5 grain daily 
heart doses was then advised, to see whether recurrences of fibrillation 
could be avoided. 
It is interesting to inquire into the possible correlation between the gastric 
symptoms and the cardio-vascular condition. The patient apparently 
has nephritis, aortitis and moderate hypertension. The symptoms are 
recent and always showed definite correlation between food ingestion and 
dyspnoea. I have already pointed out to you the intimate nerve relationship 
between the vagus supply to the stomach and heart. It is well exemplified 
in our case. It is evident in the marked effect that digitalis had in depressing 
the ventricular rate. It also accounts for the increased dyspnoea, the feeling 
of substernal oppression after meals and after cold drinks. The latter pre- 
sumably cause esophagospasm and cardiospasm, which again reflexly excite 
the cardio-inhibitory center and cause the referred symptom-complex. 
Comment and Summary.—Let us now summarize the effects of the quini- 
dine on the seven cases we have studied together. Three had mitral stenosis. 
Using the word “permanent” in the limited sense of several weeks, normal 
rhythm was permanently restored in two, it had no effect on the third. There 
were two cases of mitral regurgitation, one of whom was severely decompen- 
sated. There was temporary restoration of the normal rhythm in both. 
There were two cases of cardio-sclerosis, with temporary restoration of the 
normal rhythm in both. 
With more extended experience, it may be possible later to attain a perma- 
nent result in some of these temporarily restored cases. In some forty 
cardiac cases of all kinds with auricular fibrillation that I have, up to the 
present, quinidinized, I have only exceptionally seen harmful effects of the 
drug if the patient is first digitalized and if one has the opportunities to 
observe the case after the first and after the third dose, in order to avoid 
unpleasant or possibly dangerous results. Indeed I feel so secure in this 650 
CARDIO-VASCULAR CLINICS 
method of administration that I have advised it under the supervision of the 
attendant physician in those cases of auricular fibrillation that I saw either in 
office or outside consultation. If the doctor is made aware of the possible 
dangers and he is told how to recognize them clinically, the drug will gradually 
assume its proper place not only in hospital practice where it is now almost 
exclusively used, but also in private practice in the hands of the general 
practitioner. 
There is a possible danger to which I have not as yet alluded. I myself 
have not had any personal experience with it. An occasional case may be 
found in which administration of quinidine is followed by a shower of ven- 
tricular extrasystoles—ventricular tachycardia. The arrhythmia may not 
show itself at once; it apparently may come at any time during treatment. 
Its danger lies in the fact that it may possibly portend and be a forerunner of a 
fatal arrhythmia—ventricular fibrillation. We have as yet no clinical guide 
in differentiating in advance those patients who may react in this danger- 
ous and possibly fatal manner. 
It may be asked of what advantage is it to the patient with auricular 
fibrillation who often feels comfortable to have the normal rhythm 
restored. As a matter of clinical observation most of those with restored 
rhythm lose the feeling of palpitation due to irregular beating of the heart 
and are able to do much more work and be more active than when fibrillation 
is present. 
Keeping in mind the exceptional case, and the various dangers and 
contraindications to quinidine, I believe that quinidine, like digitalis has a 
large sphere of usefulness in every case of auricular fibrillation. (Contra- 
indications are given in Chapter XX.) 
Having summed up the advantages and indicated to you some of the 
disadvantages of quinidine, it remains to give you the details of the two 
cases in which quinidine was followed by untoward results. 
Mrs. W. age 32, patient of Dr. N. gave a history of frequent tonsillitis. 
Her tonsils were removed one year ago. Total hysterectomy was performed 
two years ago since which time she gained 20 pounds in weight. No reason 
for the operation could be obtained. She had rheumatism one year ago. 
She had complained of frequent attacks of dyspnoea and tachycardia for some 
time; they were not always the result of overexertion. The attacks have 
been worse of late months. On examination the blood pressure was normal. 
There was a typical mitral stenotic lesion present; the rhythm was disturbed 
by occasional extrasystoles; electrocardiograms showed them to be auricular in 
origin. The orthodiascopic tracing revealed moderate enlargement of the pul- 
monary artery, right auricle and left ventricle. There was no decompensation. 
Under luminal and extract of suprarenal gland, there was gradual improve- 
ment in the dyspnoea and tachycardia so that the patient was capable of 
doing a moderate amount of walking. The patient was then laid up in a 
hospital for two weeks with an attack of pneumonia. I saw her again shortly CARDIOVASCULAR CLINICS 
651 
after she left the hospital. Electrocardiograms then taken showed auricular 
fibrillation with moderate tachycardia. Twelve digitan tablets were prescribed 
to be taken once four times daily. These had no decided effect in decreas- 
ing the cardiac irregularity. A luminal tablet was then given at night, and 
for the next day, 8-5 grain quinidine sulphate capsules in two hour intervals 
was prescribed. Her family physician reported that there was some increase 
of the tachycardia and dyspnoea. The fibrillation remained uninfluenced. 
The increased tachycardia disappeared in a day or two. Two days after 
quinidine was stopped, the patient complained of sudden pain in the right 
arm and of a cold feeling in the right hand. The radial pulse could not be 
felt. The blood pressure in the right brachial could not be obtained. It was 
apparent that she had an embolus in the right brachial artery. The 
patient passed out of observation. 
It is a well known clinical observation that embolism as the mechanical 
result of breaking off of vegetations of an infected valve, especially in mitral 
stenosis, is by no means infrequent. It can occur with or without auricular 
fibrillation. It is not always the result of tachycardia. Some years ago for 
example I saw a case of embolism of the popliteal artery from mitral steno- 
sis in a patient with no arrhythmia and no rheumatic exacerbation. In 
our patient, however, since the accident occurred two days after the 
increased tachycardia from quinidine, it is only fair to assume that the more 
rapid and perhaps more violent heart action had a marked influence in causing 
the embolism. 
Mrs. K., 74 years old, had been an occasional sufferer from phlebitis for 
years. Her heart has been irregular for some time; the type of the irregularity 
as determined by the electrocardiogram was auricular fibrillation. She also 
suffered from occasional tachycardial attacks at night; these were usually 
accompanied by gastric distention. There was slight edema of the legs, and 
mucous rales at both bases. She had been digitalized at various times 
during the preceding months; this generally controlled the tachycardia and 
to some extent lessened the edema and pulmonary signs. The orthodiascopic 
tracing showed an enlarged aorta and moderate left ventricular hypertrophy. 
The auscultatory signs were those of aortitis, the clinical diagnosis was aortitis 
and cardio-sclerosis. After she had been thoroughly digitalized for the last 
time, she was given quinidine sulphate in 5 grain doses according to the 
method I have already outlined. There were no specially alarming symptoms 
on the quinidine day. The blood pressure was normal. The next morning 
the fibrillation had ceased entirely, the pulse and heart action were regular 
with the exception of occasional extrasystoles. The systolic blood pressure 
was 130, the diastolic 180. The patient felt perfectly comfortable in every 
way. Early in the evening the patient vomited and soon thereafter fainted. 
There were many single as well as grouped extrasystoles; for several minutes 
at a time there was typical coupled rhythm. After the first fainting attack 
the patient was taken with generalized convulsive seizures. She became 652 
CARDIO-VASCULAR CLINICS 
markedly cyanotic. She was unconscious with widely dilated pupils. There 
were comparatively long periods of apnoea. The urine contained a rather 
large quantity of albumin for the first time. There was no special change 
in the superficial or deep reflexes. The convulsive seizures though less violent 
than the initial attack, continued at irregular intervals during the night. 
During the whole of this time the patient was in coma. When I saw her the 
next morning her mentality was again perfectly normal. There was no 
dyspnoea. The urine contained albumin and casts. Coupled rhythm was 
present. My impression was that she had entirely gotton over the serious 
phenomena of the night before, and that she would probably slowly recuper- 
ate. She simply complained of her tongue which she had bitten during her 
convulsive seizures. The patient died suddenly late in the evening. An 
autopsy could not be obtained. The cause of the convulsions and circulatory 
collapse may be attributable to two possible causes: First, the toxic quinidine 
effect on the cerebrum somewhat similar to what occasionally happens when 
overdoses of quinine are given. Second, the toxic effect of quinidine upon the 
heart muscle. In my opinion the latter was the cause of circulatory collapse, 
as well as of death. It seems to me that the convulsive seizures were prob- 
ably caused by some secondary cerebro-circulatory disturbance, possibly a 
temporary thrombosis in the larger cerebral veins. The consequent distur- 
bance of the cerebral blood current may be a conceivable cause of the convul- 
sive seizures, general cyanosis and circulatory collapse. The sudden clearing 
of the cerebral blood stream may also have accounted for the temporary 
remission of all the serious symptoms as well as for the normal mentality 
of the patient on the day following the convulsions. I can scarcely conceive 
of quinidine acting as a cerebral poison and producing circulatory symptoms, 
and then suddenly, with the remission of all symptoms for several hours, 
produce sudden death. The urinary changes (albumin and casts) were 
probably congestive changes secondary to the acute circulatory collapse. 
This case should act as a warning, for, as has been pointed out in a previous 
chapter (Chapter XX), patients who have venous thromboses of the legs are 
bad subjects for quinidine and are apt to have disagreeable or alarming 
symptoms during the administration of the drug; in such patients quinidine 
should not be given unless there is some very strong and very definite 
indication such as in our case where digitalis was losing its usual effect in 
restoring compensation. 
CASE 105.—HEART BLOCK 
Gentlemen, this young woman gives the following history. She is thirty- 
two years old and has had “heart trouble” since her fifteenth year. She 
has had typical attacks of inflammatory rheumatism and a “weak heart” 
for many years. She has had three children. Her first two pregnancies 
proceeded normally. During her third pregnancy, she suffered from rheu- CARDIOVASCULAR CLINICS 
653 
matism and fever for about two months. She has again had articular 
rheumatism since the birth of the last child. During the past year her heart 
feels “weaker” and annoys her more than formerly. She now has “spells” 
in which she can feel her heart beat very fast and then she becomes dizzy 
and feels faint. The Wassermann blood test is negative. 
Inspection.—We see a small, frail-looking woman who is not dyspnoic 
while resting quietly in bed. Upon inspecting her chest we see quite plainly 
a very marked, diffuse systolic precordial heave, the lowest and most promi- 
nent point of which is actually in the axillary line over the seventh rib. We 
note further that the ventricular impact occupies about three-quarters of the 
left chest. We observe in the neck marked vigorous pulsations, some of 
which are due to the carotids and others to the jugulars. 
Palpation.—Over the right base there is a very marked rough, readily 
palpable systolic thrill particularly prominent in the third right interspace 
about two inches to the right of the mid-sternal line. This systolic thrill is 
also palpable, but fainter, to the left of the sternum for a similar distance and 
over a similar area. In the apical region we find a strong diffuse impact 
with a suggestion of a systolic thrill. 
Auscultation.—Corresponding to the area where the thrill is most marked 
there is a loud rasping, rough systolic, and also a fainter diastolic murmur. 
The former is transmitted to the carotids, and to the aorta in the interclavicu- 
lar notch. Over the mitral area, besides hearing the boom of the strong 
apical thrust, there is a thrill-like systolic murmur and a fainter diastolic one. 
In addition there is occasionally heard in the apical region a short faint sound 
quite distinct from the other two aforementioned mitral murmurs. These 
faint sounds come approximately in mid-diastole. The physical signs at the 
base are characteristic of a double aortic lesion. The murmurs at the mitral 
area are probably transmitted from the aortic region, athough it is possible 
that an actual mitral regurgitant lesion is also present. But the prominent 
physical signs over the aorta together with the tremendously hypertrophied 
heart indicate unmistakably that the main valvular lesion affects the aortic 
valves, and that a mitral lesion, if present at all, is of secondary importance. 
This patient entered the hospital with a rhythmical pulse rate of 35 to 40 
per minute, a rate she has since maintained. You have heard from the 
patient herself about the “spells” she has had. I want you now to notice 
that the pulse at the wrist is regular, and that you do not feel any extrasystolic 
beats at the wrist nor at the apex, as in some cases of abortive extrasystoles 
which are heard over the heart but missed at the wrist. I also want you to 
observe that there are two jugular pulsations to every heart beat. You can 
verify this by placing your finger m the suprasternal notch where you can 
distinctly feel an aortic thrill. Every time you feel the thrill, you see two 
jugular pulsations—one comes at about the same time as the aortic pulsa- 
tions, the other about equidistant between it and a succeeding one. In other 
words there are two venous pulsations to every arterial one. Since the 654 
CARDIOVASCULAR CLINICS 
jugular pulsations are of course produced by the auricle, and the aortic pulsa- 
tions by the ventricle, it denotes that there are two auricular to every ventric- 
ular contraction. Such an arrhythmia is called heart block with a two-to-one 
ratio. One can make a diagnosis of heart block readily in this case without 
graphic methods because the carotid and jugular pulsations are so pro- 
nounced and obvious. Probably the above mentioned faint murmur or sound 
heard in mid-diastole is caused by the auricular pulsation falling between 
the two ventricular contractions, an auscultatory phenomenon fairly often 
present in heart block. 
And now you observe that the patient’s history and symptoms are readily 
correlated with the physical findings. There is a history of rheumatism, 
“weak heart,” and latterly of “spells.” These “spells” are doubtless 
examples of Stokes-Adams syndrome, common in heart block, and due to 
cerebral anemia. Probably the attacks of dizziness occurring without abso- 
lute loss of consciousness represent mild Stokes-Adams complexes. The 
patient has not had attacks of any kind while in the Hospital. 
Let us now try to discover why this patient developed heart block. The 
rheumatism unquestionably produced the valvular lesions. Her cardiac 
condition antedates the last pregnancy by many years. This is evident 
not only from the history but also from the tremendous cardiac damage. 
As a result of the last attack of rheumatism, the added pathological “insult” 
presumably consisted of myocardial inflammation and infiltration (so-called 
submiliary myocardial nodules or “Aschoff bodies”), in or near one of the 
component parts of the auriculo-ventricular conduction system. Heart block 
can come from other causes, for example, from infarcts, gummata, tumors 
and calcareous infiltration which destroy the junctional tissues, but in this 
case rheumatic myocardial changes seem the most probable. 
The liver of the patient is enlarged; there is no edema of the legs. 
To Summarize.—This patient has an old double aortic lesion, an old 
hypertrophied heart, recurring rheumatic attacks, and a two-to-one heart 
block, the latter probably recent. Incidentally you will have observed that 
by eliciting a good history, by careful inspection of the chest and neck, and 
by palpation over the right base and in the jugulum, we have obtained almost 
complete information of the cardiac status. Auscultation added, so to speak, 
corroborative and confirmatory testimony. 
Therapy.—If the cardiac lesion were syphilitic in origin, the heart block 
might be improved by anti-luetic treatment. In the case before us, however, 
the old rheumatic history, the very advanced valvular changes and ventricu- 
lar hypertrophy, and the advent of heart block usually denote the begin- 
ning of permanent decompensation. This patient may continue for some 
time in fair comfort, but she will probably never be able to resume her usual 
duties and occupation. 
With reference to the use of digitalis, if she were dyspnoic or edematous, 
or if signs of decompensation were now present, I would use the drug and CARDIOVASCULAR CLINICS 
655 
expect some benefit from it. But actual heart failure is not now present, 
hence digitalis would probably be of no value. One may try to overcome the 
heart block by administering large doses of atropine, thus perhaps influencing 
any functional disturbances arising from the vagus. I observe from the 
history chart that atropine was used without any effect upon the heart block. 
I think it advisable to use large doses of salycilate of soda because of the 
rheumatic history. I would push it to its full physiological limit. 
It is still a moot question whether digitalis should be used in incomplete 
heart block because it is said that the use of digitalis may change an incom- 
plete into the complete form. To obviate this possibility, I give atropine 
with digitalis; if digitalis is given after meals, give the atropine before meals. 
My opinion is that digitalis is indicated in all types of heart block when cir- 
culatory failure is present. 
Student: If heart block is due to infiltration of the bundle of His, how may 
atropine help? 
Dr. N.: Atropine will not help if the only cause of the block is the 
assumed infiltration of the bundle of His, but some cases of heart block are 
partly functional and partly organic. Even in heart block of purely func- 
tional origin, atropine may have no effect upon the arrhythmia. I had one 
such case under observation some years ago. Autopsy showed that the 
heart and the conduction system were normal, yet atropine given frequently 
in large doses during life had no effect upon the block. 
Student: How did you recognize that the auricular was twice the ventricu- 
lar rate? 
Dr. N.: I recognized that from the pulsations in the neck. In the notch 
you may feel the aortic pulse; at the same time you can plainly see two jugular 
pulsations to the one carotid. In other words, there are two auricular con- 
tractions to one ventricular. 
Student: How do you explain the pulsation of the veins in the neck? 
Dr. N.: The auricle is in a sense continuous with the jugulars through 
the intervention of the superior vena cava; when the auricle contracts, there 
is a reflux flow in the jugulars which becomes visible as a pulsation. Very 
often in less obvious cases, it is necessary to resort to graphic methods—the 
polygraph or the electrocardiograph—in order to study and decipher the 
jugular or auricular pulsations. 
Student: In a case of heart block, can you expect the greater enlargement 
to the right or to the left? 
Dr. N.: That depends entirely upon the underlying cardiac disease and 
not upon the heart block as such. Here the heart block is an added insult 
to an already tremendously hypertrophied heart, but you need not neces- 
sarily get marked hypertrophy in heart block. 
Student: What is the mechanism of Ducroziez’s sign ? 
Dr. N.: That depends upon the amount of aortic regurgitation. If 
with the quick systolic ventricular contractions, there be a marked back- 656 
CARDIO-VASCULAR CLINICS 
flow into the ventricle because of aortic leakage (that is, because of aortic 
regurgitation), the arterial pulse wave is but a momentary one and the arterial 
walls quickly collapse, a fact clinically recognized as the pistol shot pulse. 
When heard and felt at the femoral artery, it has received the name of Ducro- 
ziez’s sign. One may also occasionally feel the hyperpulsation and collapse 
in the digital arteries. This sign can be best elicited by gently clasping the 
patient’s fingers between your thumb and other fingers. 
Student: Is the capillary pulsation due to hypertrophy of the heart? 
Dr. N.: No. It is due to the quick filling and collapse of the entire arte- 
rial system, even including the capillaries. 
In complete heart block the ventricular rate is usually between 25 and 30 
per minute, and the auricular rate is between 60 and 80. There are, however, 
cases of complete and incomplete heart-block in whom the ventricular rate 
is between 15 and 20, and the auricular rate between 80 and 90. 
Student: What would you consider, in a general way, the contraindica- 
tions to the use of digitalis? 
Dr. N.: I do not know of any. If there is circulatory failure which comes 
from cardio-vascular disease the drug should be used. I am not afraid of 
hypertension, or of slow pulse rates, or of digitalis poisoning as possible con- 
tra-indications. Indeed in hypertension digitalis often reduces the blood 
pressure, especially when cyanosis is present. Of course, I do not mean that 
digitalis is always followed by beneficial results. 
As another instance of aortic disease, I may mention the case of a man 
of thirty-eight who consulted me recently. He was in the habit of taking 
vigorous exercise. He was refused life insurance. He thought he had a slight 
valvular lesion. As a matter of fact he had a typical Flint murmur, that is, 
a short pre-systolic thrill at the apex with marked ventricular hypertrophy, 
yet he had no cardiac symptoms. In that case the etiological factor could not 
be determined. It is rare to have a patient at that age feel so well with an 
aortic regurgitant lesion and advanced hypertrophy. I may add that it is 
in just such quiescent cases that a streptococcus viridans infection is apt to 
develop in later years. 
CASE 106.—COMPLETE HEART BLOCK 
This man, M. H., is 69 years old. He says that until three years ago he 
was always able to work very hard. He had never previously complained 
of dyspnoea or of other cardiac symptoms. Then, quite suddenly, he had a 
“weak spell” and lost consciousness. Since that time he has had such spells 
very often, occasionally falling down during them. From the inception of 
these attacks he has been unable to work because of dyspnoea on exertion, 
dizziness, and a tendency to fall when he walks up stairs. The patient is too 
ignorant to give us further details. Let us examine him in the routine 
manner. CARDIOVASCULAR CLINICS 
657 
Inspection.—You note that the patient when at rest is not very dyspnceic. 
Upon scrutinizing the neck you distinctly observe two types of pulsations. 
The venous is exemplified in the pulsations of the enlarged inferior thyroid 
veins as well as in the dilated jugulars which you see plainly bulge in the 
supraclavicular hollow to the right. The carotid pulsations are slow; their 
rhythm is occasionally disturbed, as you observe, by premature contractions. 
Auscultation.—Let us now auscultate the heart. I wish again to impress 
upon you the necessity of always keeping your fingers on the pulse during the 
entire time that you listen to the heart. If you make that a part of your 
routine, you will more readily diagnose the presence of arrhythmias and. 
recognize their type as well. 
The ventricular pulse rate is 45 per minute. Some of the extrasystoles 
(more properly called premature contractions) which you hear at the apex 
are felt as definite pulse beats at the wrist, while others are not felt at all. 
This simply means that the weaker extrasystoles do not open the aortic 
valves sufficiently to propagate a systemic pulse wave. There are occa- 
sionally two premature beats to be heard at the apex. Let us again carefully 
study the neck pulsations and find out whether we can now properly interpret 
the arrhythmia. When you gently press the thumb and index finger of one 
hand over the corresponding carotids, you feel a slight thrill with every 
ventricular systole. Corresponding to the premature beats that are heard 
at the apex, you feel the extra carotid pulsation synchronous with them. It 
is of special interest to watch the dilated inferior thyroid veins in this individ- 
ual. Take notice that they pulsate oftener than the carotids; as you know, 
these venous pulsations are synchronous with and are caused by auricu- 
lar systoles. In other words, the pulsations of the neck, which are so promi- 
nent, tell us that the auricles are beating much faster than the ventricles. 
Occasionally you observe that the carotid and auricular components of the 
venous wave fall simultaneously, producing a summation wave. Expressed 
polygraphically, the c and a wave fall at the same instant to make one large 
wave. 
The electrocardiographic and polygraphic tracings show that there is 
no ratio between the auricular and ventricular contractions, an evidence of 
complete heart-block 
Having studied the arrhythmia, let us examine and auscultate carefully 
for the presence of abnormal sounds and murmurs. Over the lower precor- 
dium and towards the left axilla there is a systolic murmur. There is also 
a rough systolic murmur over the right base in the second and third inter- 
spaces; it is this which is transmitted to the carotids and which we felt as a 
thrill in these arteries. The apical murmurs and those at the base are heard 
better when the patient is sitting down. Auricular beats falling between the 
ventricular systoles are not heard. Such sounds are heard as faint taps in a 
fair proportion of cases of heart block. When the patient is in the recumbent 
position, aside from the arrhythmia, there are no visible abnormalities. Upon 658 
CARDIOVASCULAR CLINICS 
having the patient sit up, one sees a poorly defined, diffuse impulse below 
and to the left of the nipple. Upon precordial palpation, there are no abnor- 
mal thrills. The aortic pulsation in the jugulum is not palpable. 
The right border of the heart is about an inch and a quarter to the right 
of the midsternal line; the apex beat is heard most plainly in the 6th inter- 
space about an inch below and one-half inch to the left of the left nipple. 
The blood pressure which had been previously taken was 200 systolic and 
160 diastolic. The liver is enlarged and reaches about halfway between the 
lower border of the ribs and the umbilicus. There is marked edema of the 
legs. 
How shall we interpret the auscultatory phenomena—the rough aortic 
and the mitral murmurs—in terms of the cardiac pathology in this case? 
What lesion or lesions are present? In view of the hypertension, the decom- 
pensation (as shown by the enlarged liver and edema), the presence of heart 
block, the absence of a rheumatic history, the fact that the cardiac symptoms 
started late in life, and the age of the patient, we may be sure that he has 
cardio-sclerosis, a composite of myocarditis, and of sclerosis which affects 
the endocardium, the aorta and the coronaries. The mitral systolic murmur 
is the result of sclerotic changes. Because of the abnormally slow heart 
action, there is insufficient blood supply to the brain, therefore cerebral ane- 
mia results, and in its. train follows the Adams-Stokes syndrome. The 
latter may vary from attacks of momentary semi-consciousness to rather 
long-continued absolute unconsciousness, coma and convulsive seizures. 
The patients rarely die during a paroxysm. 
It is interesting to speculate upon the lack of cardiac symptoms for so 
many years in this individual, and upon the final pathological “insult” 
which caused heart block. We must of course assume that the cardio- 
sclerosis had been present for many years prior to the inception of the cardiac 
symptoms three years ago; for, unless the pathological process can be attri- 
buted and traced back to some definite, severe, and comparatively recent 
infection, wide-spread changes as are here present take many years to evolve. 
Such data of recent infection are absent. The man was steadily at work 
until his “spells” began. I believe that the secret of the absence of symp- 
toms in this and similar cases lies in the fact that the pathological process is 
often a very slow and insidious one; thus cardio-vascular functions are only 
very slowly and gradually damaged; thus also the cardiac reserve force, the 
socalled factor of safety, is sufficiently large to accommodate itself to the dam- 
age, until the disease becomes very wide-spread, or until some vital area is 
involved. 
What special damage caused the heart block? The “insult” was appar- 
ently a sudden one, for until the “weak spells” began, the patient felt well, 
despite a considerably damaged heart. My assumption is that there was 
infarction of the small special branch of the coronary which supplies the 
atrio-ventricular conduction system, thus suddenly interfering with the CARDIO-VASCULAR CLINICS 
659 
latter’s nutrition. Such an accident would at once nullify the specific power 
of the bundle to carry impulses from auricle to ventricle; in other words, heart 
block results, and the ventricle follows its own slow,idio-ventricular rhythm. 
x\nother possible cause of the block would be advanced interstitial myocarditis 
in the immediate neighborhood of the bundle; this, by pressure, might also 
prevent proper functioning of the latter. But it seems unlikely here be- 
cause such patients usually show the classic signs of severe heart failure long 
before the onset of complete heart block. 
How should this patient be treated? The blood Wassermann was nega- 
tive. This does not absolutely preclude the presence of syphilis unless sev- 
eral examinations should be negative, and an examination of the spinal fluid 
should also be negative for syphilis. I did not have the opportunity to make 
such examinations in this individual. I therefore tried the actual “thera- 
peutic test” of giving the patient the iodides and bichloride of mercury; 
these had no effect upon the symptoms. The importance of making the diag- 
nosis of syphilis naturally lies in the fact that there is much better chance 
for improvement, possibly a cure. Nevertheless our therapeutic efforts 
may be balked because the luetic sclerosis and endocarditis may be so far 
advanced, and scar-tissue be so prevalent, that even vigorous mixed treat- 
ment and salvarsan injections have no effect upon the process. 
In every case of heart block, atropine injections in large physiological 
doses should be tried for its effect upon the block. In purely functional cases, 
or in those without far-advanced disease it occasionally releases the block and 
produces normal rhythm. I have tried atropine in this patient with no 
effect. 
For decompensation, patients with complete heart block should be 
treated similarly to those with cardio-sclerosis and normal rhythm— 
i.e., they should be given digitalis in proper doses. When edema is marked, 
administration of theobromin sodium salicylate in one half gramme doses, 
four times daily and restricted fluid intake for several days are also of value. 
Atropine should also be used in the attempt to prevent the Stokes-Adams 
attacks. Once these attacks appear, we possess no drug to cut them short, 
especially when digitalis has already been given. 
The prognosis here is very poor. The great chances are that the patient 
will die within a year or so. Digitalis can help the circulation for a time, but 
it cannot replace damaged tissue, nor can it have much action on a heart so 
diseased that there is no healthy tissue left to act upon. 
CASE 107.—COMPLETE HEART BLOCK 
A. G., male, is now 69 years old. I saw him for the first time in 1913, 
with the following history: He had small-pox when a child and gonorrhea 
35 years ago. In 1903, following an injury, he had a slow-healing ulcer of the 
leg. When a young man, he had “indigestion” lasting some years. He had 660 
CARDIO-VASCULAR CLINICS 
always been able to work until 1913; he then complained of feeling tired. 
Actual symptoms first occurred in September, 1912, when he began to have 
“flashes in the head” while walking, and also complained of general “weak- 
ness.” In May, 1913, while walking, he suddenly fell unconscious in the street 
and had to be taken home. He noticed no weakness of the limbs after recovery 
from this attack. During the same month he had two other weak and dizzy 
spells, but no unconsciousness. At the time of the first spell his doctor told 
him that his pulse was very slow; the patient himself had no knowledge that 
the pulse had ever been slow before this. He has never had any convulsions 
or twitchings. Abdominal complaints began after his attack in May, 1913. 
These consisted at first of pains over the gall bladder region and in the epi- 
gastrium. He was constipated, never vomited, but was occasionally nau- 
seated. Gastralgia began within one half hour after meals and lasted about 
two hours; “flashes in the head” usually accompanied these pains. His 
tongue was frequently coated. After rest in bed for two weeks the gastric 
symptoms and constipation disappeared, the tongue became less coated and 
the appetite improved. Dyspnoea was slight and an almost negligible 
symptom. 
My notes of the examination in 1913 are as follows: A well-nourished 
man, pupillary and other reflexes normal; no dyspnoea, no dependent edema. 
There were at times vigorous carotid pulsations; jugular pulsations were not 
prominent. Palpation, inspection and percussion of the cardiac area revealed 
nothing abnormal. Upon auscultation, there was a loud rough systolic 
murmur over the mitral area. Over the right base, there was also a rough 
systolic murmur which was transmitted to the carotids. The aortic pulsa- 
tion in the jugulum was not abnormally prominent. The ventricular action 
was slow, regular and usually about 40 per minute; faint, distant sounds were 
occasionally heard at the apex in the inter-systolic periods. The lungs 
were normal. The systolic blood pressure taken at different times varied 
from 180 to 130 m.m., the diastolic from 90 to 50. The urine occasionally 
contained a trace of sugar; otherwise it was normal. The stools were normal. 
The Wassermann blood test taken several times was negative and the Wasser- 
mann reaction of the spinal fluid was also negative, but showed distinct increase 
of mononuclear cells. The eyegrounds showed retinitis. 
I did not see this patient again for five years. The intervening history 
showed that except for occasional attacks of indigestion he had felt quite well. 
There had been no cardiac symptoms or flushes for some years. About a 
week before I last saw him, he said that after drinking two glasses of cold 
water there were epigastric pains with almost constant hiccough; since then 
he has had abdominal discomfort and cough. 
To summarize: There had been sudden onset of a slow pulse accom- 
panying an attack of unconsciousness; there were rather frequent vasomotor 
symptoms (flushes); otherwise there were no circulatory complaints, no dysp- 
noea, no edema. There was auscultatory evidence of changes in the aortic CARDIOVASCULAR CLINICS 
661 
and mitral valves. There were painful gastric symptoms which have since 
disappeared. 
Let us proceed with the present examination. This man, now 69 years 
old, is, as you see, well nourished and able to lie quite flat without dyspnoea. 
The jugular pulsations on the right side of the neck are somewhat more prom- 
inent than on the left, but on neither side are they sufficiently distinct 
to be accurately counted. You see along the inner border of the right sterno- 
mastoid the pulsatile rise of the tissues synchronous with the carotid pulsa- 
tions. Now, as I press upon the root of the jugulars on the right side, the 
pulsations become more prominent, so that one can count their number 
fairly accurately. You observe that while the excursion of most of the 
jugular pulsations is small, there are occasional ones which are more marked. 
Upon inspection of the chest, the cardiac apex is seen to beat an inch below 
and slightly to the left of the left nipple, the heart is beating regularly, slowly, 
and by actual count, at a rate of 56 per minute. There is no pain upon 
precordial pressure. Upon auscultation a rough systolic murmur is heard 
over the mitral area, occasionally followed after a slight interval by a scarcely 
audible sound. Over the right base, a rough loud systolic murmur is heard; 
this is transmitted chiefly to the right infra-clavicular region. In other words 
the physical signs are about the same as at my first examination five years 
ago. 
It is very important in the auscultation of a patient with arrhythmia, to 
disregard the latter for the time being, and to concentrate one’s attention on 
the heart sounds only, for the purpose of establishing the presence or absence 
of abnormal sounds. 
Before we go into the interpretation of the faint sound following the 
ventricular systole, let us discuss the significance of the loud systolic murmur 
heard practically over the entire anterior surface of the chest. It is loudest 
over the upper sternum and tails away toward the mid-sternum; the mitral 
murmur also diminishes toward the mid-sternum, so that at the latter area 
there is a small space in which no murmur is heard. I believe this patient 
belongs to the group of cardio-sclerotics in whom the murmur is due to degen- 
erative and sclerotic changes in the mitral valves, and in the aortic valves 
and walls. The former causes a regurgitant systolic murmur with the area 
of transmission just described; the latter, a loud rough and sometimes rasping 
systolic murmur diminishing toward mid-sternum. I may have an oppor- 
tunity to show you such cases at a later clinic. 
Let us now interpret the little extra sound occasionally heard in the 
inter-systolic intervals at the apex. It sounds almost like the faint tap of 
a fetal heart. It is due to the auricular systoles which occur in these per- 
iods. In other cases of heart block that I have examined, the auricular 
sounds were more distinct and audible than in this individual. 
The margin of the liver is palpable about two inches above the umbilicus 
in the median line. 662 
CARDIOVASCULAR CLINICS 
The slow and regular pulse and heart action, the frequent jugular pulsa- 
tions, the auricular sounds occasionally heard at the apex—all these indicate 
heart block. The Wassermann reaction of the blood and spinal fluid are 
negative. There is no reason to suspect a neoplasm pressing on or invading 
the bundle of His. Besides, the existence of heart block for five years, as 
in this patient, precludes such a diagnosis. How, then, shall we interpret 
the etiology of this heart block? With cardio-sclerosis, as instanced in the 
previous case there is always co-existent myocarditis and often marked 
changes in the main coronaries or their subsidiaries. We know that the 
bundle of His has its own separate arterial supply. The question to decide 
is, has the block been brought on by some sudden change in this arterial 
supply, or has it been the result of myocardial changes affecting the inter- 
ventricular septum, along which course the main branches of the bundle of 
His? Although a positive answer is impossible, I am inclined to the former 
view because of the sudden onset of the block without any prior history 
of decompensation. 
The orthodiascopic tracing of this patient shows some enlargement of 
the first part and arch of the aorta, and moderate left ventricular hyper- 
trophy. The electrocardiogram shows complete heart block with a ventricu- 
lar rate of 45 and an auricular rate of 80 per minute. The patient recently 
had [some evidence of decompensation—mucous rales at both bases and 
edema of the legs. Both have disappeared under the use of digitalis and 
theobromin sodium salicylate. You see that despite the long continued heart 
block and his age, the patient looks exceptionally well preserved, and is 
certainly no worse off than a good many other patients with similar cardio- 
sclerosis and rhythmic heart action. 
Student: What is the etiological factor of the entire condition? Is it 
specific? 
Dr. N.: I do not believe it is specific, because several Wassermann tests, 
carefully done, were found to be negative. We know, as a result of post- 
mortem examinations, that there are other changes, mostly of an arterio- 
sclerotic, non-luetic nature, in or near the auriculo-ventricular conduction 
system, which may also cause heart block. Besides, the patient had been 
placed upon vigorous antiluetic treatment, with no effect upon his condition. 
Atropine sulphate in large doses likewise had no effect upon the arrhythmia. 
Student: What has been the primary agent in this case of cardio-sclerosis? 
Dr. N.: I do not know. Such changes are so slow and insidious that it is 
often impossible to ferret out the primary factor. Infections are frequently 
the starting-point of cardio-scleroses. This individual had small-pox when 
a child; the pit-marks are still evident. In the absence of other infections 
and factors, even such an old infection cannot be positively excluded in the 
etiology. Aside from the arrhythmia, his cardio-sclerosis is no different from 
that found in a great majority of individuals with this lesion. We are at 
present very much in the dark as to the cause of the so-called senile changes CARDIO-VASCULAR CLINICS 
663 
in the arteries. We do know that certain conditions are especially prone 
to produce change in the coronaries and in the cardiac musculature—syphilis, 
alcoholism, nephritis, are the chief of these; articular rheumatism in the 
aged is another. Abnormal metabolism with abnormal amounts of non- 
protein nitrogen in the blood is another possible cause. Infections can bring 
on changes slowly, which may not be noticeable for years after the original 
attack has run its course. That is true, for example, of pneumonia. If 
examined soon after the pneumonia, there are no evidences of any cardio- 
vascular changes, yet within two or three years there may be recognizable 
signs of this disease. I have seen several characteristic instances in which 
I was positive that an old pneumonia was the etiological factor of a marked 
cardio-sclerosis. 
CASE 108.—HEART BLOCK AND AURICULAR FIBRILLATION, WITH POST- 
MORTEM SPECIMEN. COMMENT ON THE ETIOLOGY OF AURICULAR 
FIBRILLATION 
Gentlemen: This woman, aged 80, was admitted to the ward Aug. 7, 
1920. Except that she entered the hospital acutely ill and that she had been 
in normal health prior to admission, no history was obtainable which threw 
any light upon the present illness. 
The house physician made the following notes: “ Shortly after admission, 
the pulse rate was around 150 and very irregular. The patient was 
cyanotic. She was given 1 drachm of the tincture of digitalis and 
gr. nitroglycerine every five minutes for one hour. The total amount of 
the tincture thus administered was 1% ounces. After a short time, 
the cardiac rate dropped to 40 per minute and gradually became 
slower until the rate was 28 per minute. It remained at that rate for a few 
days, to again gradually increase to 40 per minute. Upon admission, she 
had an attack lasting two or three minutes during which breathing almost 
entirely ceased, and pulse and heart action were scarcely perceptible. These 
spells were rather frequent during the first two days; they became less 
frequent, and disappeared entirely on the fourth day.” The patient died 
Nov. 15, 1920 of a terminal pneumonia. 
I examined the patient for the first time about one week after admission. 
The heart action then was slightly irregular, the rate, 45 per minute. On 
succeeding days and until the time of death, the ventricular rate remained 
between 40 and 50 per minute. As a terminal illness the patient developed 
lobar pneumonia, with fever ranging to io4°F; during this period, the pulse 
varied from 40 to 65 per minute. 
Examination: At my first examination a few days ago, the patient was in 
the same condition as you see her now. You note that there are no cardiac 
murmurs. There is no edema of the legs. There are a few mucous rales at 
both bases. The ventricular rate is 45 per minute and fairly regular. The 
patient is fairly comfortable and not very dyspnoeic. I took the first electro- 664 
CARDIOVASCULAR CLINICS 
cardiogram two weeks after admission (Aug. 21), and then another on Nov. 10, 
one week before death. Both were alike and showed auricular fibrillation 
and heart block (Fig. 300). 
Because the patient, a city ward, died without leaving relatives or friends, 
the heart could not be obtained for several weeks after her death. A bit of 
ventricular musculature was then excised, hardened and sectioned to discover 
Fig. 300.—Typical section of a long electrocardiogram showing auricular fibrillation 
and heart block. The ventricular action is slightly arrhythmic, the predominating rate 
is 46 per minute. 
whether the heart could still be used for microscopic study; it was found that 
the musculature was in too poor a state of preservation for such purpose. 
You see the heart here. The gross pathology is quite apparent (see Frontis- 
piece) and it is questionable whether microscopic examination would have 
added anything of importance. The heart is slightly enlarged. The wall 
of the left ventricle is slightly thicker than normal: The right ventricle is 
abnormally thin only toward the apex. The right ventricular cavity is 
somewhat dilated. There are small areas of thickening in the mitral cusps. 
You note especially that there is surprisingly little interstitial fibrotic change 
throughout the entire musculature. The auricles are not enlarged or thick- 
ened. The region of the sino-auricular node—the pacemaking area at the 
junction of the superior vena-cava and right auricle—shows no macroscopic 
change: The artery of that node is not visible or palpable. CARDIOVASCULAR CLINICS 
665 
The chief pathological changes (see Frontispiece), undoubtedly the ones 
that finally caused the cardiac disturbances, you observe are found in the coro- 
naries, in the artery of the auriculo-ventricular node (the node ofTawara) 
and in the musculature surrounding the node. The coronary is thickened 
and sclerosed, although slightly patulous. The most important pathology 
lies in the artery supplying the auriculo-ventricular node, the beginning of 
the auriculo-ventricular conduction system, the normal conveyer of impulses 
from auricle to ventricle. That artery you note is completely calcified. The 
artery is seen occupying a position somewhat lower than the normal site of the 
node, but surrounding the artery (and probably as the result of its calcifica- 
tion) may be seen a distinct zone of degenerated musculature which undoubt- 
edly includes the node, either in whole or in part. 
Comment.—It is of great pathological and clinical importance, especially 
in those suffering from what I may term impending “ coronary failure,” to note 
how long the final pathological “insult” can hold off before complete occlu- 
sion of the coronaries or their subsidiaries occurs. Undoubtedly the calcify- 
ing process in the coronary and particularly in the artery of the node has been 
going on for many years, yet the patient at the time of her death was 80 years 
old and had lived in cardiac comfort until sudden heart failure supervened; 
in all probability the latter resulted from final complete closure of the calcified 
artery supplying that node. This patient is but another illustration of the 
fact that the slow process of intracardiac arterial disease had never at any 
time sharply interfered with the factor of safety of the heart, and that 
ample time had probably been given for establishment of coronary anasto- 
mosis; for, contrary to older teachings, it is now known that the coronaries 
are not end arteries and that many deeply seated anastomoses exist. 
Before proceeding to the clinical aspect of the case, it may perhaps be well 
to recall certain pertinent physiological attributes of cardiac musculature. 
One of these is cardiac irritability. This does not depend upon the strength 
of the stimulus. It is however considerably influenced by other factors, 
especially by the state of nutrition of the cardiac musculature at the time of 
stimulation. Cardiac tissue is refractory to all stimulation during its period 
of contraction, hence the heart is irritable in the physiological sense during 
its diastolic or resting period alone. Conduction, another important attri- 
bute, varies considerably in different parts of the heart; it is best in the spe- 
cialized tissues, the sino-auricular node (the rhythm center) and the 
junctional tissue (the auriculo-ventricular conduction system). 
The chief clinical interest in our case centers in the occurrence of heart 
block and auricular fibrillation, but especially in the etiology of the latter. 
The heart block was the cause of the slow ventricular activity. This is 
readily explicable from the gross pathological changes: The calcified nodal 
artery and the myocardial changes in and near the atrio-ventricular node. 
These focal changes undoubtedly destroyed the conducting function of the 
atrio-ventricular node. The massive digitalis therapy— the tincture 666 
CARDIOVASCULAR CLINICS 
within one hour—may have been a factor in continuing the slow ventricular 
activity, although there is a definite note of the house physician stating that 
there were attacks of apncea with scarcely perceptible heart action (Stokes- 
Adams syndrome) upon admission. Nor does it seem probable that digitalis, 
even in such massive doses, could have continued a depressant action upon the 
ventricles during the remainder of the patient’s life, approximately three 
months. 
Regarding the auricular fibrillation in our case, we have no exact data 
as to its onset, except that the rapid and irregular pulse at the time of admis- 
sion was probably indicative of this type of arrhythmia. Whether it had been 
present before hospital admission, we do not know; from the obtainable his- 
tory, however, there is no evidence of any prior attack of dyspnoea or heart 
failure. Toxic causes (such as are encountered, for example, in exophthalmic 
goitre), reflex disturbances, etc.—need no consideration here as possible 
etiological factors of the auricular fibrillation. 
The possible causes of auricular fibrillation with heart block in this case 
may perhaps best be discussed under the following headings: 
1. Structural changes in the pacemaker. 
2. Primary nutritional disturbances in the pacemaker. 
3. Interference with and blocking of the normal spread of auricular 
impulses from a normally functionating pacemaker. 
1. Structural changes in the pacemaker—Several observers (Cohn and 
Lewis, Falconer and Dean, Draper, H. Freund and others) had previously 
made careful serial microscopic examinations of the pacemaker and of the 
pacemaking area in cases of auricular fibrillation with and without heart 
block, and had ascribed decided etiological significance to more or less 
extensive pathological changes in the sino-auricular node. Such changes— 
usually degenerative and sclerotic in nature—where marked, undoubtedly 
may be predisposing causes of auricular fibrillation. In some cases of auric- 
ular fibrillation however, the sino-auricular nodal region was found normal 
or almost so. Hence where marked sclerotic changes are absent, other causes 
for this arrhythmia must be sought. You recall that in our specimen a 
macroscopical examination showed no evidence of any gross or extensive 
change in the pacemaker. 
2. Primary Nutritional Disturbances in the pacemaker—This would here 
refer practically to calcification and consequent occlusion of the artery of the 
pacemaker, or to occlusion of one of the coronaries which occasionally gives 
off a branch to this node. The former change was absent in our case. 
Regarding the latter, while the coronaries were thickened and sclerosed, they 
were still patulous, and hence would scarcely have interfered sufficiently with 
the arterial supply to the pacemaker, even assuming that a branch of the 
latter was given off by one of the coronaries. 
3. Interference with and the blocking of the normal spread of auricular 
impulses from a normally functionating pacemaker. Garrey quotes Porter 667 
CARDIOVASCULAR CLINICS 
as stating that “fibrillary contractions may be due to interruption of the 
contraction waves.” Working independently, Garrey and Mines have shown 
experimentally that if the auricles be thrown into a state of fibrillation by 
direct faradization (the usual method), and if then a portion of auricular 
tissue (e.g., the auricular appendix) be temporarily clamped off, fibrillation 
will continue in the remainder of the auricular tissue. When the clamp is 
removed, the entire auricle again fibrillates. Garrey and Mines have also 
found that if the auricle be incised trouser-fashion so that sufficiently broad 
auricular bridges remain, and then the auricle be faradized anywhere, contrac- 
tion of the various auricular strips will continue long after faradization has 
ceased. Garrey calls such contractions “ circus contractions,” for he assumes 
that such an excitation wave travels in a continuous circuit, and that the 
impulse spreads from fiber to fiber. In the experimentally slit auricle, these 
circus excitation waves are irregularly and sinuously blocked because of the 
difference in refractory periods of the incised fiber groups and because impulse 
conduction is interfered with. Thus while the circus excitation as an excita- 
tion impulse continues, the auricular strips are actually contracting at vary- 
ing times and with varying energies. The result is incoordinate contraction, 
the irregular auricular tremor characteristic of fibrillation. Lewis and his 
co-workers have recently corroborated Garrey’s observations in a series of 
experimental and clinical papers. 
The theory of Garrey and Mines seems to explain some entities in which 
auricular fibrillation occurs frequently and in which auricular mass as such 
may act as a factor. Thus, in rheumatic mitral stenosis in which auricular 
hypertrophy and distension is common, and in cardio-sclerosis in which 
accompanying sclerotic changes in the auricular musculature are not infre- 
quent, simple mechanical interference with the propagation of a “circus 
wave” may finally throw the auricle into fibrillation. My tentative inter- 
pretation in such instances is that there occurs mechanical hindrance to the 
spread of the excitation wave similar to what happens in the experimentally 
slit auricle: The excitation wave cannot spread evenly and ripple-like 
because auricular conductivity and irritability are interfered with by the 
diseased or distended auricular strips, hence the excitation wave is irregularly 
and sinuously blocked and fibrillation results. 
In addition to pathological or mechanical changes in the auricular mus- 
culature, and excluding all toxic causes, it seems of clinical importance to 
attempt a correlation of the theory of “circus waves” to disease primarily 
found not in the auricles but in the ventricles. It is for example no uncom- 
mon experience to find auricular fibrillation as a temporary or terminal arrhy- 
thmia with or without slow ventricular action in cases of coronary disease 
during an attack of occlusion (coronary failure) with or without pulmonary 
edema. Such sudden disturbance in intracardiac circulation with resultant 
impaired nutrition in the auricular musculature would seem sufficient to 
interfere with and impair the normal physiological rhythmic excitation wave 668 
CARDIOVASCULAR CLINICS 
in the latter by producing local differences in the refractory periods and con- 
duction time of the auricular excitation wave: Thus a patho-physiological 
basis for auricular fibrillation would be laid. In our case there was coronary 
disease with occlusion, the ventricles were beating automatically (heart 
block) and the auricles were fibrillating. The possible influence of digitalis 
has already been discussed. Ordinarily in heart block with coronary disease, 
the auricles beat regularly and approximately at a normal rate. My 
assumption in such cases is that auricular nutrition is not sufficiently damaged 
to prevent the normal spread of impulses and excitation waves. Where 
auricular fibrillation occurs with heart block, the assumption seems fair that 
auricular disease or at least poor coronary circulation (coronary failure) so 
damages the entire intracardiac nutrition—auricles as well as ventricles— 
that auricular excitation waves are irregularly blocked similar to the blocking 
of the experimental circus waves. As a result the auricles are thrown into 
that state of fibrillary contraction we designate clinically as auricular 
fibrillation. INDEX 
a wave, 84 
normal, cause of, 84, 85 
variations in, 86 
a-c-v waves, 80, 83, 84 
Abdomen, paracentesis of, 381 
Abnormalities, cardiac, in life insurance 
examination, 476 
Acardia, 31 
Accelerator nerve, anatomy of, 19 
physiological influence and action of, 40 
Acidosis, auriculo-ventricular heart block 
due to, 199 
in heart failure, 272 
surgical wound shock and, 430 
Aconite, 379 
Adrenalin, cardiac hypertrophy and, 59 
in extrasystoles, 196 
in heart disease, 379 
Alcohol, effect of, on arterial blood pressure, 
432 
on circulation, 379 
heart disease due to, 64 
in cardio-sclerosis, 389 
Alcoholic cardio-sclerosis, case, 548 
Alcoholism cause of heart disease, 396 
Amino-acids, in blood, heart disease due to, 
66 
Ammonia, aromatic spirits of, 379 
Amyl nitrate, 378 
Anacrotic pulse, 92 
Anacrotic radial pulse in auricular fibrilla- 
tion, tracing, 146 
Anaphylaxis, heart block produced by, 199 
Anatomy of heart, 1. See under Heart, 
anatomy of. 
Anemia, secondary, following sharp hemor- 
rhage, sinus arrhythmia due to, 193 
Aneurism, aortic, of rheumatic origin, 322 
true, 58 
arteriosclerotic, 323 
atheromatous, 323 
of ductus arteriosus, 30 
of undefended space, 27 
sacculated, precordial pain in, 418 
Aneurismal dilatation, atheromatous, 323 
of aorta, 58 
Aneurismal dilatation, of aorta, left ven- 
tricular hypertrophy, electro-cardio- 
gram, iis 
of descending thoracic aorta, 313. 
See also under Aortic dilatation, 
of first part and arch of aorta, 312. 
See also under Aortic dilatation, 
syphilis and, 58 
•prognosis of, 322 
Angina pectoris. See Precordial pain of 
cardio-vascular origin, 
types of, 407 
Aniline dyes poisoning, heart disease due 
to, 64 
Annulus ovalis, embryonic, 3 
Anoci-association, surgical wound shock 
due to, 450 
Anomalies affecting entire heart, 31 
Aorta, aneurism of, true, 58 
aneurismal dilatations of, 58 
left ventricular hypertrophy, electro- 
cardiogram, 115 
of arch of and descending thoracic 
aorta, orthodiascopic tracing, 237 
syphilis and, 58 
ascending, atresia of, 29 
ascending thoracic, diffuse aneurismal 
dilatation of, orthodiascopic tracing, 
234 
x-ray of, 235 
co-arction of, 31 
descending thoracic, aneurismal dilatation 
of, 313. See under Aortic dilata- 
tion. 
with left ventricular hypertrophy, 
236 
enlargement and low implantation of 
first portion of, with moderate enlarge- 
ment of left ventricle, orthodiascopic 
tracing, 233 
fetal beginnings of, 3, 4 
first part and arch of, aneurismal dilata- 
tion of, 312. See under Aortic dilata- 
tion. 
malposition of, 30 
pressure within, 74 
669 670 
INDEX 
Aorta, rheumatic lesions of, orthodiascopy 
of, 227 
tracings, 228 
septum of, defects of, 29 
Aortic and mitral disease, combined, ortho- 
diascopy of, 229 
tracings, 230 
Aortic aneurism, case, 496 
due to rheumatism, 322 
case, 322-323 
sacculated, 3x8 
concomitant signs of, 320 
pathological process of, 318 
physical characteristics of, 318 
physical signs of, 319 
prognosis of, 322 
as to cure, 322 
as to operative procedure, 322 
site of aorta affected, 319 
symptomatology of, 320 
x-ray examination in, 320 
with auricular fibrillation, case, 539 
Aortic arch, anomalies of, 31 
dilatation of, and left ventricular hyper- 
trophy, orthodiascopic tracings, 231, 
232 
Aortic bulb, embryonic, 2 
Aortic dilatation, aneurismal, of descending 
thoracic aorta, 313 
cases, 313 
diagnosis of, 313 
differential criteria of, 315 
symptomatology of, 313 
of first part and arch of aorta, 312 
causes of, 312 
symptoms of, 312 
prognosis of, 322 
symptomatology of, 315 
bronchial asthmatic attacks in, 317 
cases, 317-318 
due to cardiac decompensation, 318 
dyspnoea in, 316 
gnawing pains in, 316 
treatment of, 321 
Aortic hypoplasia, 31 
Aortic incompetence, murmurs of, 260 
Aortic lesions, in pregnancy, 465 
orthodiascopic tracings of, 230-234 
rheumatic double, beginning, case, 534 
Aortic pulsation, inspection of, in physical 
examination of heart, 245 
palpation of, 248 
over left base of heart, 248 
Aortic pulsation, palpatation, of, over right 
base of heart, 248 
Aortic regurgitation, case, 528 
decompensated, 299 
clinical syndromes of, 299 
dynamic considerations of, 299 
in case of left ventricular hypertrophy, 
electrocardiogram, 116 
mitral regurgitation, acute pericarditis, 
case, 529 
murmurs of, 260 
reduplicated apical impulses in, 268 
Aortic septum, embryonic, 3 
bulbar swellings, proximal and distal, 
in, 3, 4 
septum aorta-pulmonale in, 3, 4 
truncus arteriosus in, 3, 4 
maldevelopment of, 30 
Aortic stenosis, 299 
cardiac hypertrophy in, 61 
clinical syndrome of heart failure in, 299 
congenital 358 
dynamic considerations of, 299 
left ventricular hypertrophy and, electro- 
cardiogram, 116 
murmurs of, 260 
with regurgitation, rheumatic, cases, 531 
Aortitis, hypertension and, case, 612 
of first portion and arch of aorta, and 
extreme left ventricular hypertrophy, 
orthodiascopic tracing, 232 
orthodiascopy of, 229 
rheumatic, cases, 495 
syphilitic. 311 
affecting aortic arch, with left ventric- 
ular hypertrophy, orthodiascopic 
tracings, 233, 234 
and myocarditis, case, 494 
aneurismal dilatation of aorta. See 
Aortic dilatation, aneurismal. 
of ascending thoracic aorta, 313 - 
of first part and arch of aorta, 312 
diagnosis of, 311 
Wassermann reaction in, 311 
sacculated aneurisms of aorta, 318 
treatment of, 321 
of decompensation, 321 
digitalis in, 321 
of the pains, 321 
of underlying infection, 31 x 
mercury in, 321 
potassium iodide in, 321 
salvarsan in, 321 INDEX 
671 
Arrhythmias produced by abnormal 
sequence of contraction of auricles 
and ventricles, heart block, incom- 
plete, 178 
prolonged conduction time, 177 
shortened conduction time, 178 
sino-auricular block, 175 
sinus arrhythmia, 172 
pulsus alternans, 188 
pulsus paradoxus, 190 
surgery and, 452 
true bradycardia, 170 
types of, 130 
ventricular, 160 
automatic ventricular activity, 163 
interpolated ventricular extrasystoles, 
161 
paroxyzmal tachycardia of ventricular 
origin, 167 
ventricular extrasystoles, 160 
ventricular incoordination, 168 
bundle-branch lesions, 169 
ventricular fibrillation, 168 
Arrhythmic heart, surgery and, 452 
electrocardiogram in, 453 
in cardio-vascular disease, 452 
in decompensation, 452 
in hypertensive cardio-renal disease, 
453 
in functional arrhythmias, 452 
in hypertensive cases, 452 
Arsenic poisoning, heart disease due to, 64 
Arterial blood pressure, 426 
abnormal, in organic cardio-vascular dis- 
ease, 433 
classification of, 433 
hypertension with myocarditis, 433 
with labile vasomotor mechanism, 
433 
hypertension with uremia, 433 
myocardial disease without hyperten- 
sion, 434 
premature arteriosclerosis, 435 
senile arteriosclerosis, 435 
valvular disease and myocardial insuffi- 
ciency with and without hyperten- 
sion, 434 
abnormal, of extra-cardiac origin, 435 
cyanosis, 435 
exophthalmic goiter, 435 
functional hypertension, 435 
case, 436 
functional hypotension, 436 
Aortitis, syphilitic, with precordial pain, 
case, 541 
treatment of, 321 
typical, case, 536 
with auricular fibrillation, case, 633 
with enlargement of first portion and 
arch of aorta, and left ventricular 
dilatation, 231 
Apical impulse, reduplicated, 267 
Apical region, inspection of, in physical 
examination of heart, 243 
Apoplexy in heart failure, 279 
Appendicitis, bradycardia in, 197 
followed by peritonitis, extrasystoles in 
195 
Arborization block, 121 
electrocardiogram, 121 
QRS complex prolonged in, 121 
R wrave in, broadening of, 122 
cause of, 124 
electrocardiograms, 123 
Aromatic spirits of ammonia, 378 
Arrhythmias, 130. See also under specific 
names. 
arterial blood pressure in, 436. See also 
under Arterial blood pressure, 
auricular, 131 
auricular extrasystoles, 131 
auricular incoordination, 142 
auricular fibrillation, 142 
auricular flutter, 153 
incoordination, intermediate, be- 
tween flutter and fibrillation, 157 
paroxyzmal tachycardia of auricular 
origin, 139 
causes of, 130 
classification of, 130 
clinical etiology of, 193 et seq. See under 
separate names, 
functional, surgery and, 452 
hemisystole, 190 
in cardio-sclerosis, 331 
in coronary disease, 410 
in pneumonia, 458 
in tobacco smokers, 420 
nodal extrasystoles, 159 
produced by abnormal sequence of con- 
traction of auricles and ventricles, 
172 
backward conduction from ventricle 
to auricle, 178 
blocked auricular beat, 176 
heart block, complete, 178 672 
INDEX 
Arterial blood pressure, abnormal, of extra- 
cardiac origin, hypertension at men- 
opause, 436 
intracranial tension, increased, 435 
lead poisoning, 435 
basic cause of, 432 
clinical estimation of, 428 
of brachial artery, 430 
auscultatory method, 431 
five phases in, 431 
graphic method, 430 
palpatory method, 430 
visual method, 430 
sphygmomanometers in, 428 
Baumanometer, 428 
Oliver mercurial compressed air 
manometer, 429 
Tycos aneroid, 429 
factors concerned in estimation of, 426 
cardiac energy, 426 
elasticity of arterial wall, 426 
lymphatic system, 427 
peripheral resistance, 427 
venous system, 427 
viscosity of blood, 428 
volume of circulating blood, 427 
factors influencing, 432 
alcohol, 432 
cyanosis, 432 
excitement, 432 
exercise, 432 
hypertonus, 432 
smoking, 432 
hypertension in, treatment of, 438 
absence from business in, 440 
at spas, 440 
diathermy in, 440 
drugs in, 439 
erythrol tetranitrate, 439 
iodide of potash, 439 
nitroglycerin, 439 
sodium nitrate, 439 
electric light baths in, 440 
exercise in, 440 
general considerations of, 438 
hydrotherapy in, 439 
percussion over seventh cervical 
vertebra, 440 
hypotension in, treatment of, 440 
venesection in, 439 
in cardiac arrhythmias, 436 
coupled rhythm, 437 
in auricular fibrillation, 437 
Arterial blood-pressure, in cardiac arrhyth- 
mias, coupled rhythm, in extrasys- 
toles, 437 
sinus arrhythmia and heart block, 437 
in life insurance examinations, 480 
maximal normal, 431 
physiological variations in, 432 
Arterial tonus a cause of hypertension, 472 
Arterial trunks, deviations and transposi- 
tions of, 30, 31 
Arteriosclerosis, cardiac hypertrophy and, 
60 
diabetes and, 65, 66 
myocarditis and, case, 496 
premature, 417 
causes of, 418 
high blood pressure in, 435 
symptoms of, 417 
senile, high blood pressure in, 435 
precordial pain in, 418 
tobacco and, 389 
Arteriosclerotic aneurism, 322 
Aschoff’s bodies, 67 
in rheumatic infections, 207 
Ascites, paracentesis for, 381 
Asphyxia, auriculo-ventricular heart block 
due to, 199 
Asthma, cardiac, 275 
Atheromatous aneurism, 323 
Atresias, 29 
Atrio-ventricular conduction system, 8. 
See Conduction system, 
and cardiac nerve supply, 22 
Atropin in digitalis administration, 364 
cases, 364, 365 
in extra-systoles, 196 
in heart block, 186, 201 
in paroxysmal tachycardia, 205 
in sino-auricular block, 194 
in treatment of bradycardia, 197 
Auricles, pressure within, 74 
Auricular arrhythmias, classification of, 130 
extrasystoles, 131 
Auricular complex in electrocardiogram, 101 
Auricular enlargement, right-sided mur- 
murs of, 262 
cases, 262-263 
Auricular extrasystoles, clinical recognition 
of, 138 
coupled thythm in, 139 
from auricular fibrillation, 139 
from normal beats, 133 
from ventricular extrasystoles, 138 INDEX 
673 
Auricular extrasystoles, clinical recognition 
of, isolated extrasystoles, 139 
frustrane or abortive, 134 
general nature of, 131 
normal site of, 137 
reasons for, 136 
tracing and electrocardiograms, 134, 135, 
137, 138 
Auricular fibrillation, 142 
absence of P waves in, 149 
cause of, 158 
clinical etiology of, 201 
clinical recognition of, 151 
from auricular extrasystoles, 139 
from auricular flutter, 157 
from extrasystolic arrhythmia, 153 
from sinus arrhythmia of non-respira- 
tory type, 172 
diagnosis of, in older prople with cardio- 
sclerosis, 150 
discussion, with illustrative cases, 620, 
625 
due to digitalis, coupled rhythm in, 139 
due to fright, case, 637 
ectopic beats in, 151, 153 
electrocardiograms, 148, 149, 150 
fibrillatory waves in, 149 
heart block with, tracings, 182 
in aortic aneurism, case, 539 
in aortitis, case, 633 
in coronary disease, 410 
in heart block, 663 
in myocarditis, case, 635 
in normal hearts, 202 
in pneumonia, 458 
in pregnancy, 465 
incoordination between auricular flutter 
and,157 
irregularity of pulse in, 142 
murmurs of mitral stenosis in, 259 
permanency of, 202 
polygrams, 143, 144, 145, 146, 147 
quinidine in, cases, 641 
regularity of pulse in, following digitalis 
medication, 149 
transient, 151 
due to coffee, case, 636 ■ 
with permanent hypertension, case, 
639 
treatment of, 203 
digitalis in, 362 
Auricular flutter, 153 
auricular fibrillation in, 151 
Auricular flutter, clinical etiology of, 206 
clinical recognition of, 156 
from auricular fibrillation, 157 
heart block in, 153, 155 
electrocardiogram with both complete 
and incomplete block, 155, 156 
incoordination between auricular fibrilla- 
tion and,157 
polygram, 153 
tracings, 154, 155, 156 
treatment of, 206 
digitalis in, 362 
Auricular incoordination, 142. See also 
under specific names, 
auricular fibrillation, 142 
auricular flutter, 153 
intermediate between flutter and fibrilla- 
tion, 157 
Auricular systoles, ectopic, 136 
ventricular response in, 136 
Auricular tachysystole, 153. See Auricular 
flutter. 
Auricular wave, 84 
Auriculo-ventricular conduction system, 
8, 36. See Conduction System. 
Auriculo-ventricular conduction time. See 
Conduction time. 
Auriculo-ventricular heart block, clinical 
and experimental causes of, 197 
clinical etiology of, 197 
cardiac causes, 198 
destruction of main branch of con- 
duction system, 198 
severe myocardial degeneration, 198 
treatment of, 198 . 
extra-cardiac causes, 198 
abnormal pressure on the cardio- 
inhibitory center, 200 
abnormal pressure on the vagus, 
200 
asphyxia, 199 
chemical poisons, 199 
drugs, 198 
endocrine disturbances, 200 
interference with cerebral circulation, 
199 
vagal inhibition, increased, 200 
by digital pressure, 200 
by reflex peripheral excitation, 200 
treatment of, 201 
Auriculo-ventricular valves, anomalies of, 
29 
atresia and stenosis of, 29 674 
INDEX 
Aviator’s heart, 445 
reduction of oxygen in, 447 
conclusions on, 448 
physiological circulatory reaction in, 
447 
pulmonary reaction in, 447 
size of heart in, 447 
systolic blood pressure in, 447 
reduction of oxygen tests for, 447 
with Henderson re-breathing appara- 
tus, 447 
with steel chamber apparatus, 447 
Bacterial agents and conditions, cardio- 
vascular diseases due to, 66 
diphtheria toxins, 66 
focal infections, 69 
mouth injections, 68, 69 
pneumococci, 66 
pyrogenic abscesses, 70 
pyorrhoea alveolaris, 68 
rheumatism, 67 
tonsillitis, 68 
typhoid fever in, 67 
Bacterial endocarditis, acute, 70, 303 
as a secondary process, 303 
duration of, 305 
etiology of, 303 
organisms, 70 
extent and frequency of, 309 
symptoms of, 304 
blood cultures in, 308 
cardiac, 308 
clinical course of cases in which the 
coccus has not been recovered during 
life, 308 
clinical features of Streptococcus viri- 
dans infection in, 305 
hematological finding, 307 
mucous membrane petechiae, 306 
onset in, 306 
painful erythematous nodules, 306 
pyogenic emboli, 306 
skin petechiae, 306 
general clinical picture in, 304 
fever, 304 
left heart affected, 304 
sepsis, 304 
septic infarcts, 304 
nervous manifestations in, 307 
pathological features of Streptococcus 
viridans infection in, 305 
cerebral lesions, 305 
Bacterial endocarditis, symptoms of, path- 
ological features of Streptococcus 
viridans infection in, in heart, 305 
renal infarcts, 305 
pneumonic complications in, 308 
splenic enlargement in, 307 
urine changes in, 307 
treatment of, prophylactic, vaccination 
in, 309 
symptomatic, 304 
vaccine therapy in, 309 
Barbitol, 380 
Baths, 384 
carbon dioxide, 385 
hot, 385 
Nauheim, 386 
home preparation of, 386 
oxygen, 386 
tepid, 384 
Benzl benzoate, 379 
Biot type of respiration, resemblance to 
Cheyne-Stokes respiration, 273 
Blocked auricular beat, 176 
causes of, 176 
electrocardiogram, 177 
extrasystoles differentiated from, 176 
sino-auricular block differentiated from, 
176 
Blood, chemical examination of, in cardio- 
renal disease, 393 
viscosity of, and surgical wound shock 
450 
factor in estimation of arterial blood 
pressure, 428 
volume of, factor in estimation of arterial 
blood pressure, 428 
Blood pressure, 426. See Arterial blood 
pressure. 
tests for cardiac efficiency, 287 
Blood transfusion in heart disease, 382 
“Blue babies,” 353 
Bradycardia, true, 170 
causes of, 170 
clinical etiology of, 196 
clinical recognition of, 171 
definition of, 170 
differentiated from slow heart action in 
heart block, 171 
electrocardiagrams, 170, 171 
tracings, 171 
treatment of, 197 
Breathing, phasic variations with, in elec- 
trocardiogram, 113, 114 INDEX 
675 
Broad heart. See Heart, broad. 
Bromids for extrasystoles, 196 
in heart disease, 380 
in tachycardia, 203 
Bronchitis, in heart disease, 277 
influenzal precordial pain in crises of, 
424 
Brown, N. W., method of estimation of 
venous blood pressure, 441 
Bulbar swellings, distal and proximal, 
embryonic, 3 
Bundle branch lesions, description of, 169 
differentiation of electrocadiogram of, 
from cardiac hypertrophy, 170 
electrocardiograms, 169, 170 
c wave, normal, cause of, 85 
variations in, 87 
Calisthenics, 383 
Camphor, 379 
Cannon theory of capillary stasis as cause 
of surgical wound shock, 450 
Capillary circulation, 441 
Capillary electrometer, 94 
Capillary sphygmograph, 81 
Capillary stasis, 442 
as cause of surgical wound shock, 450 
Carbon dioxide baths, 385 
for reduction of hypertension, 439 
Carbonated brine baths, 386 
home preparation of, 386 
Cardiac asthma, 275 
Cardiac clinics, 402 
care of school children in, 403 
classification of cardiac disease by, 403 
convalescent country home an adjunct to, 
404 
cooperation in, 402 
exercise among children in, 404 
physical examinations in, 402 
scheme for case reports in, 404-405 
social service department in, 402 
Cardiac cough, 274 
Cardiac cycle, 91 
Cardiac displacements, effect of, on electro- 
cardiogram, hi 
Cardiac efficiency tests. See Functional 
efficiency tests of heart. 
Cardiac energy in estimation of arterial 
blood pressure, 426 
Cardiac hypertrophy, 59. See Hyper- 
trophy, cardiac. 
Cardiac neuroses, 338. See also Heart 
failure, neurotic element in, 338 
factors in, 338 
following febrile crises, cases, 568 
following gastro-intestinal disturbance, 
cases, S7S 
goitrous heart, 349 
in labor in pregnancy, 468 
irritable heart, 341. See Irritable heart, 
subjective dyspnoea, case, 577 
vasomotor neurosis, or “weak” heart, 
338. See Vasomotor neurosis. 
Cardiac overstrain in heart failure, 284 
in normal hearts, 285 
symptoms of, 285 
Cardiac pain, 278 
Cardiac reserve, 75, 76 
Cardiac reserve power, dilatation of heart 
and, 76 
Cardiac strain and labor in pregnancy, 
466 
Cardiac syphilis, 57, 3x1, 417 
aneurismal dilatation of aorta. See 
Aortic dilatation, aneurismal. 
of descending thoracic aorta, 313 
of first part and arch of aorta, 312 
aortitis in, 311 
presence of, characteristic, 311 
causes of precordial pain in, 417 
diagnosis of, 311 
Wassermann reaction in, 311 
parts attacked by, pathology of, 311 
sacculated aneurisms of aorta, 318. See 
Aortic aneurism, 
treatment of, 321, 417 
Cardiac tonus, influence of, on volumetric 
ventricular curves, 75 
Cardio-inhibitory center, heart block due 
to abnormal pressure on, 200 
Cardio-nephritis, case, 495, 496 
Cardio-renal disease, 56 
chemical examination of blood in, for 
non-protein nitrogen, creatinin and 
uric acid, 394 
examination of urine in, 391 
elimination of lactose injected intraven- 
ously in, 391 
iodide of potash excretion test in, 391 
nephritic test diet in, 392 
phenolsulphonephthalein test in, 391 
quantitative, for urea, salt and water 
output, 392 
hypertensive, surgery and, 453 676 
INDEX 
Cardio-sclerosis, 56 
alcoholic, case, 548 
auricular fibrillation in, 202 
cases, 495, 496, 497 
coffee, tea and alcohol in, 389 
digitalis in, 368 
due to mouth infections, 69 
in pneumonia, a late sequel, 461 
case, 462 
in the middle-aged, cases, 544 
murmurs of, 261 
“acute accidents” in, 333 
amount of pathological damage and 
amount of healthy tissue in, 332 
arrhythmias in, 334 
general, 331 
in coronary disease, 334 
cardiac hypertrophy, 336 
embolism, 334 
extent of concomitant cardiac dam- 
age, 335 
hypertension, 336 
precordial distress, 335 
uremia, 335 
ventricular fibrillation, 336 
of complications, 331 
progress of pathological damage in, 333 
physical signs of, 327 
auscultatory sounds, 327 
apical, 327 
normal, 328 
characteristic, 327 
diagnostic loud rough systolic mur- 
mur, 328 
of pericardial adhesions, 329 
inspection, 327 
palpation, 327, 328 
pneumonia and, 195 
prognosis of, 331 
senile, 418 
cases, 542 
cause of symptoms in, case, 545 
percordial pain in, 418 
true bradycardia in, 196 
symptomatology of, 326, 329 
arrhythmias, 330 
dyspnoea, 329 
endema of legs, 330 
enlarged congested liver, 330 
epigastric sensitiveness, 330 
precordial pains, 329 
pulmonary edema, 330 
pulmonary examination, 330 
Cardio-sclercsis, tobacco and, 389 
with cholecystitis, case, 547 
with hypertension, auricular fibrillation 
in, 151 
with left ventricular hypertrophy, case, 
284 
Cardiospasm with temporary hypertension, 
421 
cases, 422 
evidence for exclusion of organic disease 
in, 422 
mild, 421 
painful deglutition in, 421 
symptoms of, 421 
Cardio-vascular clinics, cases, 505 et seq. 
Cardio-vascular disease, 56 
due to alcoholism, 64 
due to bacterial agents, 66. See Bac- 
terial agents, 
due to diabetes, 65 
due to gout, 66 
due to metabolism, 66 
due to thyroid gland, 71 
senility and, 71 
surgery and, 452 
Carotid pulse, inspection of, in physical- 
examination of heart, 244 
Carotid wave, 85 
Catarrhal febrile affections, acute, extra- 
systoles in, 195 
Catarrhal jaundice, true bradycardia in, 196 
Cathartics, saline, 381 
Cerebral circulation, auriculo-ventricular 
heart block due to interference with, 199 
Cerebral hemorrhage in heart failure, 279 
Cerebral thrombosis in heart failure, 279 
Cerebral tumor, extrasystoles in, 194 
Chauveau, early studies of, in measurement 
of pulsations, 78 
Chemical agents as causes of heart disease, 
63 
alcohol, 64 
diabetes, products of, 65 
gout, products of, 66 
industrial poisons, 64 
metabolism, products of, 66 
metallic poisons, 63 
tobacco poisoning, 65 
Chest, right lower, inspection of, in physical 
examination of heart, 246 
Cheyne-Stokes respiration, 273 
definition of, 273 
Chloral hydrate, 380 INDEX 
677 
Circulation, fetal, 25 
in surgical wound shock, 448. See Shock, 
surgical wound. 
Circulatory defects or abnormalities in life 
insurance examinations, 477 
Circus contractions, 158, 159 
Clubbing of fingers and toes in congenital 
heart disease, 354 
Codein in tachycardia, 203 
Coffee drinking, auricular fibrillation due to, 
case, 636 
in cardio-sclerosis, 389 
Cohn, A. E., on classification of arrhyth- 
mias, 130 
Cohnheim’s classification of cardiac hyper- 
trophy due to disease, 61 
Colds, endocarditis and, 68 
Collapsing pulse, 92 
Colloidal silver preparations, 382 
Coma in heart failure, 279 
Conduction, backward, from ventricle to 
auricle, 178 
electrocardiogram, 179 
Conduction system in cardiac musculature, 
anatomy of, 7 
blood supply in, 12 
dissection and demonstration of, n 
main branches in, 8-11 
main stem in, 8 
nerve supply in, 12 
node of Tawara in, 8 
Conduction time, prolonged, 177 
causes of, 177 
clinical etiology of, 201 
electrocardiograms, 177 
shortened, 178 
clinical etiology of, 201 
Conductivity of heart musculature, 35 
Congenital dextrocardia, effect of, on elec- 
trocardiogram, 112 
Congenital heart disease, 353 
congenital aortic stenosis, 358 
general characteristics of, 353 
clubbing of fingers and toes, 354 
cyanosis, 353 
dyspnoea, 354 
hemoptysis, 354 
patent ductus arteriosus, 354 
cases, 355, 356, 591 
symptoms of, 354 
cyanosis, 355 
“machinery murmur,” 355 
Congenital heart disease, patent inter- 
ventricular septum, 356 
cases, 356, 357, 592 
symptoms of, 356 
physical signs of, general, 354 
in congenital pulmonary stenosis, 354 
in patent interventricular septum, 354 
Congenital malformations, defects and 
anomalies of the heart, 25 
developmental defects, varieties of, 25 
septal defects, 26 
aneurism of undefended space, 27 
anomalies affecting the entire heart, 31 
anomalies of the aortic arch, 31 
aortic hypoplasia, 31 
co-arction of the aorta, 31 
congenital dextro-cardia, 32 
defects and anomalies of the ductus 
arteriosus, 30 
defects of interauricular septum (pat- 
ent foramen ovale), 26 
defects of interventricular septum 26 
defects of septum of the aorta, 29 
deviations and transpositions of arterial 
trunks, 30 
entire absence of aortic septum (trun- 
cus arteriosus), 29 
entire absence of interauricular and 
interventricular septa, 28 
septal and valvular anomalies, 29 
valvular stenosis and atresia, 29 
Contractility of heart musculature, 37 
Copper poisoning, heart disease due to, 
64 
Cor biventriculare triloculare, 28, 29 
Coronary arteries, large, occlusion of, and 
pericarditis, 408 
smaller, complete obliteration of, 53 
Coronary arteritis, 53 
Coronary circulation, anatomy of, 15 
Coronary disease, a cause of precordial pain, 
407 
arrhythmias accompanying, 410 
coronary spasm in, 409 
diagnosis of, 407 
digitalis in, 368 
gastric symptoms in, 410 
dyspnoea, 410 
epigastric pains, 410 
vomiting, 410 
gastro-intestinal paresis in, 411 
general considerations of, 408 
in myocarditis, case, 494 678 
INDEX 
Coronary disease, mottling of extremities 
or venous thrombosis in, 41 r 
nephritis, transient, and dependent 
edema in, 411 
occlusion of smaller coronary branches in, 
408 
pains in, referred, 409 
to epigastrium, 409, 410 
to left shoulder, 409 
to precordium, 409 
precordial pain dominant feature in, 
407 
pulmonary edema, acute, in, 411 
Coronary embolism, 53 
Coronary endarteritis, 53 
Coronary lesions, 53 
in etiology of myocarditis, 53 
in infectious diseases, 53 
Coronary occlusion, 53 
Coronary plexus, anterior, 19 
posterior, 19 
Coronary sclerosis, 53 
Coronary spasm, 409 
Coronary thrombosis, 53 
Corrigan pulse, 92 
Cough in heart failure, 274 
Coupled rhythm, 139 
digitalis in, 363 
high blood pressure in, 437 
Creatinin, blood, test for, 394 
Crehore, micrograph of, 483, 484 
Crile’s theory of anoci-association as cause 
of surgical wound shock, 450 
Crista terminalis, 4 
Cyanosis, causes of, 276 
dyspnoea with, 276 
high blood pressure in, 435 
in congenital heart disease, 353 
cause of, 353 
occurrence of, 353 
in heart failure, 276 
influence of, on arterial blood pressure, 
432 
Decompensation, cardiac, tachycardia in, 
203 
definition of, 271 
symptoms of, 271. See Heart failure, 
symptoms of. 
Deep cardiac plexus, 19 
“Delayed rise” test of cardiac efficiency, 
286 
Delirium cordis, 151 
Depressor nerve, anatomy and functions 
of, 19 
Derivations, electrocardiographic. See 
Leads. • 
Dextrocardia, acquired, electrocardiogram 
of, 113 
congenital, 32 
effect of, on electrocardiogram, 112 
Diabetes, heart disease due to, 65 
Diastole, volumetric changes during, 74 
Diathermy in hypertension, 440 
Dicrotic notch, 89 
height of, 90 
Dicrotic pulse, 92 
Dicrotic wave, 89 
cause of, 89 
reflect, 90 
Diet in heart disease, 360, 389 
Karrel diet, 377 
in myocardial insufficiency, and dyspnoea 
without edema, 390 
in obesity, in cardio-vascular disease, 390 
Digitalis, administration of, 360 
action in, 360 
effect upon atrio-ventricular conduc- 
tion system, 361 
effect upon cardiac contractile power, 
360 
inhibitory effect on nervous mechan- 
ism of heart by vagal action, 361 
as a diuretic, 365 
atropin in, 364 
cases, 364, 365 
cumulative effect in, 367 
dangers in, 367 
hunger pangs in, 361 
in aortic lesions with extreme ventricular 
hypertrophy, 369 
slight or moderate ventricular hyper- 
trophy, 369 
in auricular fibrillation, 362 
with completely irregular and rapid 
pulse, 366 
in auricular flutter, 362 
in cardio-sclerosis with decompensation, 
370 
in cardio-sclerosis with hypertension, 368 
in coronary disease, 368 
in coupled rhythm, 363 
in endocarditis, 369 
in extrasystoles, 363 
in heart block, 362 INDEX 
679 
Digitalis, administration of, in mitral lesions 
with auricular fibrillation, 369 
with rhythmic hearts, 369 
in older patients with cardio-sclerosis and 
decompensation, 367 
in pericarditis, 369 
in pulsus alternans, 363 
in rhythmical pulse action with decom- 
pensation, 366 
with decompensation and moderate 
tachycardia, 366 
in unnecessarily large doses over long 
periods, 367 
in valvular lesions, 368 
general classification, 369 
persistence of action in, 367 
regulation of, 365-366 
summary of, 370 
vomiting in, 361, 364 
atropin in, 364 
cases, 364, 365 
Digitalis, auricular fibrillation due to, 139 
auriculo-ventricular heart block due to, 
198 
blocked auricular beat due to, 176 
bradycardia due to, 197 
cardiac hypertrophy and, 59 
effect of, on T wave, 125 
extrasystoles following use of, 196 
in auricular fibrillation, 149, 203 
in case of heart block, effect of, 184 
in extrasystoles, 196 
in sino-auricular block, 176 
in tachycardia, 203 
prolonged conduction time due to, 177, 
201 
pulse alteration due to, 190 
sino-auricular block due to, 193 
ventricular escape and, 164, 167 
Digitalis preparations, 365 
chloroform-soluble fraction, 365 
digitan tablets, 365 
infusion, 365 
non-chloroform-soluble fraction, 365 
powdered leaf, 365 
tincture, 365 
Digitan tablets, 365 
Dilatations, acute cardiac, effect of cardiac 
rate on, 76 
effect of exercise on, 75 
effect of venous pressure on, 76 
factors affecting diagnosis of, 76 
cardiac reserve power, 76 
Dilatations, acute cardiac, factors affecting 
diagnosis of, cardiac strain, 76 
cardiac tonus, 76 
mechanism of, 75 
surgical wound shock and, 451 
ventricular, effect of, on electrocardio- 
gram, 117 
Diphtheria, heart in, 444 
destruction of myocardium in, 444 
marked, 444 
mild, 444 
sudden death in, 445 
treatment of, 445 
Diphtheria toxins, cardio-vascular disease 
due to, 66 
Displacements, cardiac, effect of, on elec- 
trocardiogram, hi 
Diuretin, 376. See Theobromine sodium 
salicylate. 
Drop hearts, 218 
effect of, on electrocardiogram, 107 
electrocardiogram of, no 
orthodiascopic tracings of, 219 
Dropped beats, 131, 134 
Drugs in cardio-vascular disease, 360. See 
also drugs under separate names, 
aconite, 379 
adrenalin, 379 
alcohol, 379 
amyl nitrate, 378 
aromatic spirits of ammonia, 379 
benzl benzoate, 379 
bromides, 380 
caffein and derivatives, 375 
camphor, 379 
digitalis, 360-370 
erythrol tetranitrate, 378 
for treatment of hypertension, 440 
Hoffman’s anodyne, 379 
luminal, 380 
mannitol hexanitrate, 378 
morphine, 380 
nitroglycerine, 378 
potassium acetate, 380 
quinidine, 371 
saline cathartics, 381 
sedatives, 380 
sodium acetate, 380 
sparteine, 379 
squills, tincture of, 371 
strophanthus, crystalline, 370 
tincture of, 370 
strychnine, 378 680 
INDEX 
Drugs in cardio-vascular disease, suprarenal 
extract, 379 
theobromine sodium salicylate, 376 
vasodilators, 378 
Ductless glands, cardiovascular disease due 
to, 71 
Ductus arteriosus, aneurism of, 30 
patent, 354 
case, 355, 356, 591 
electrocardiogram, 116 
symptoms of, 354 
cyanosis, 355 
“machinery murmur,” 355 
persistant patency of, 30 
Ductus Botalli, 30 
Dyspnoea, clinical study of, 273 
cyanosis with, 276 
factors composing, 273 
in cardio-vascular examination of war 
recruits, 475 
in congenital heart disease, 354 
in heart failure, 271 
causes of, mechanism, 272 
clinical etiology of, 271 
in life insurance examination, 477 
paroxysmal, in heart failure, 274 
Edema in heart failure, 277 
causes of, mechanical, 277 
character of, 277 
diagnosis of, 278 
Edema, pulmonary, acute, in coronary 
disease, 411 
in heart failure, 275 
Einthoven, differentiation of, between ac- 
tual and manifest size of deviations, 498 
on pulsus alternans, 190 
work of, on electrocardiograph, 96 
Electric light baths in hypertension, 440 
Electrocardiogram, 101 
auricular complex in, 101 
clinical, method of taking, 103-105 
description of, 101 
effect of variations in cardiac muscula- 
ture on, 106 
cardiac displacements, rn 
congenital dextrocardia, 112 
deviation of R wave, due to changes of 
position, 106 
drop hearts, 109 
horizontally disposed hearts, 107 
phasic variations with breathing, 113 
squatty hearts, 107 
Electrocardiogram, effect of variations in, 
cardiac musculature on, summary, 
127 
ventricular dilatation, 117 
ventricular hypertrophy, 114 
ventricular mobility, abnormal, 118. 
See also Ventrical mobility, 
vertically disposed hearts, 109 
leads or derivations of, 98 
mathematical considerations underlying, 
498 
manifest size of deviations, 498 
measurements of angles made by leads 
and electrical axis, 499 
method of taking, 98 
normal, 101 
interpretation of, 103 
normal variations from standard, 102 
P wave in, 101 
QRST deviations in, 101, 102 
U wave in, 102 
ventricular complex in, 101 
Electrocardiograph, 95 
description of, 96 
principles of, 95 
Electrometer, 94 
capillary, 94 
Embryology of heart, 1. See under Heart. 
Emphysema, chronic, heart in, 337 
symptoms of, 337 
treatment of, 337 
Endocardial lesions, decompensated, in 
pregnancy, 465 
Endocarditis, 46 
colds and, 68 
digitalis in, 368 
due to pyogenic abscesses, 70 
due to pyorrhoea alveolaris, 68 
etiology of, rheumatism, 397 
tonsillitis, 397 
tooth infection, 398 
infectious. See Endocarditis, acute bac- 
terial. 
malignant. See Endocarditis, acute bac- 
terial. 
aneurism of undefended space and, 27 
septic. See Endocarditis, acute bac- 
terial. 
tachycardia, persistent, in, 203 
tonsillectomy in, indications for, 397 
routine and radical practice inadvisable 
in, 398, 508 
time for, 398 INDEX 
68i 
Endocarditis, tonsillectomy in, value of, 
398 
tonsillitis a cause of, 68 
tonsils portals of entry of infection in, 397 
tooth extraction in, routine and radical, 
uncalled for, 399, 508 
ulcerative. See Endocarditis, bacterial 
acute. 
valvular, in children, diseased teeth and, 
69 
Endocarditis, acute mycotic or malignant, 
49) 50 
bacterial origin of, 50 
pathological changes in, 50 
Endocarditis, acute simple (rheumatic) 
46-50, 290 
bacterial origin of, 46 
clinical phenomena in, 290 
arrhythmias, 291 
endocarditic, 291 
myocardial, 291 
rheumatic, 290 
exacerbations and recurrences of, 293 
extrasystoles in, 194 
pathological changes in, 46 
prolonged conduction time due to, 177 
symptoms of, 291 
anemia, 291 
fever, 291 
onset, 293 
physical signs, 292 
prodromal, 292 
pulse, 292 
subjective, 292 
ulcerative, 48, 49 
verrucous, 48 
Endocarditis, bacterial, acute, 70, 303 
as a secondary process, 303 
duration of, 305 
etiology of, 70, 303 
extent and frequency of, 309 
symptoms of, 304 
blood cultures in, 308 
cardiac, 308 
clinical course of cases in which the 
coccus had not been recovered 
during life, 308 
clinical features of Streptococcus 
viridans infection, 305 
hematological finding, 307 
mucous membrane petechiae, 306 
onset in, 306 
painful erythematous nodules, 306 
Endocarditis, symptoms of, clinical features 
of Streptococcus viridans infec- 
tion, pyogenic emboli, 306 
skin petechias, 306 
general clinical picture in, 304 
fever, 304 
left heart affected, 304 
sepsis, 304 
septic infarcts, 304 
nervous manifestations in, 307 
pathological features of Strepto- 
coccus viridans infection in, 305 
cerebral lesions, 305 
in heart, 305 
renal infarcts, 305 
pneumonic complications in, 308 
splenic enlargement in, 307 
urine changes in, 307 
treatment of prophylactic vaccination 
in, 309 
symptomatic, 304 
vaccine therapy in, 309 
Endocarditis, bacterial subacute, 50 
Endocarditis, chronic, 50 
pathological changes in, 50, 51 
valvular disease and, 51 
Endocarditis, rheumatic, 67, 68 
acute, 4x5-417 
cases, 415, 513, 521 
causes of, 415 
symptoms of, 415 
. treatment of, 415 
without decompensation, therapy of, 
3 00 
chronic, aortic regurgitation in, decom- 
pensated, 299 
clinical syndromes of, 299 
dynamic considerations of, 299 
aortic stenosis in, 299 
clinical syndrome of heart failure in, 
299 
dynamic considerations of, 299 
decompensated mitral regurgitation in, 
293 
clinical syndrome of, 294 
dynamic considerations of, 293 
decompensated mitral stenosis in, 297 
clinical syndrome of, 295 
auricular fibrillation in, 298 
embolism in, 298 
paralysis of vocal cord in, due to 
paralysis of left recurrent 
laryngeal nerve, 295 682 
INDEX 
Endocarditis, rheumatic, chronic, decom- 
pensated mitral stenosis in, clinical 
syndrome of, paralysis of vocal 
cord in, cases of, 296 
theories of, 295-296 
paroxysmal tachycardia in, 298 
dynamic considerations of, 295 
symptoms of, 293 
without decompensation, therapy of, 
301 
prognosis of, 302 
in acute stage, 302 
in chronic stage, 303 
in quiescent stage, 302 
in subacute stage, 302 
prolonged conduction time in, 201 
valvular murmurs in, 257 
Endocardium, degenerative changes in, 45 
amyloid degeneration, 45 
atheromatous degeneration, 46, 47 
fatty degeneration, 45 
sclerosis, 45 
histology of, 44 
inflammation of, 46. See also Endo- 
carditis. 
acute mycotic or malignant, 50 
acute simple endocarditis, 46-50 
bacterial, acute, 70, 303 
subacute, 50 
chronic, 50 
rheumatic, 67, 68 
acute, 415-417 
chromic, 293, 295, 297, 299, 303 
subacute endocarditis, 50 
Endocrine disturbances, cardio-vascular dis- 
ease due to, 71 
Engelmann, experimentation in heart phy- 
siology by, 35 
Enlargement of the heart, 59. See Hyper- 
trophy. 
Epicardium, histology of, 44 
Epigastric pulsation, inspection of, in 
physical examination of heart, 246 
Epilepsy, true bradycardia in, 197 
Epileptic seizures, extrasystoles in, 196 
Erythrol tetranitrate, 378 
Esophageal disease and spasms, precordial 
pain from, 423 
case, 423-424 
Etiology of heart disease, 63 
bacterial agents in, 66 
bacterial endocarditis, 70 
Etiology of heart disease, chemical agents 
in, 63. See also Chemical agents, 
classification of causes in, 63 
endocrine disturbances in, 71 
senility in, 71 
spirochetal infection in, 71 
Examination, cardio-vascular, of war 
recruits, 471. See War recruits, 
life insurance, 476. See Life insurance 
examinations. 
of aviation recruits. See under Aviator’s 
heart. 
Examination, physical, of heart, 244 
auscultation in, 257 
murmurs in, extra-cardiac, of non- 
organic origin, 265 
intra-cardiac, of non-organic origin, 
263 
differentiated from mitral organic 
regurgitant murmurs, 264 
of cardio-sclerosis, 261 
reduplicated apical impulse, 267 
reduplicated heart sounds, 266 
right-sided, from auricular enlarge- 
ment, 262 
cases, 262-263 
valvular, of aortic regurgitation, 260 
of aortic stenosis, 260 
of mitral regurgitation, 257 
of mitral stenosis, 258 
of pulmonary insufficiency, 261 
of pulmonary stenosis, 261 
of rheumatic endocarditis, 257 
of tricuspid lesions, 260 
inspection in, 244 
of aortic pulsation, 245 
of apical and precordial region, 245 
of carotid pulse, 244 
of jugular pulsation, 244 
of right lower interspaces, 246 
epigastric pulsation, 246 
liver pulsation, 247 
right lower chest, 246 
mapping out on chest of cardiac outline, 
a rational method, 252 
normal heat sounds in, 242 
first sound, cause of, 242 
significance of, 243 
second sound, cause of, 243 
significance, of 243 
third sound, 243 
of patient lying down, 242 
of patient sitting, 241 INDEX 
683 
Examination, physical, of heart, palpation 
in, 247 
of aortic pulsations, 248 
of mitral lesions, 248 
over left base of heart, 248 
over right base of heart, 248 
past history record in, 240 
percussion in, 249 
inaccuracy of, 250, 251, 252 
physical signs of ventricular hypertrophy 
in, 268 
left, 269 
right, 269 
Exercise, effect of, on acute cardiac dilata- 
tion, 75 
for the cardiac, 399 
fundamental considerations in, 399 
in hypertension, 440 
Exophthalmic goiter, and goitrous heart, 
349, 35° 
and irritable heart, 346 
auricular fibrillation in, transient, 151 
high blood pressure in, 435 
recurrence of, at menopause, case, 578 
tachycardia in, 203 
tracings, 140, 141 
with hypertension, case, 580 
Extrasystoles, auricular, 131. See Auricu- 
lar extrasystoles. 
blocked auricular beat distinguished 
from, 176 
clinical etiology of, 194 
clinical recognition of, 138 
coupled rhythm in, 139 
differentiation between auricular and 
ventricular extrasystoles, 138 
from normal beats, 133 
of isolated extrasystoles, 139 
digitalis in, 363 
frustrane or abortive, 134 
functional, of extra-cardiac origin, etiol- 
ogy of, 194 
general nature of, 131 
in acute endocarditis, 194 
in acute myocarditis, 194 
in life insurance examinations, 477 
nodal, 159 
reasons for, 136 
tracings, 160, 161 
treatment of, 194, 196 
ventricular, 160. See Ventricular extra- 
systoles. 
Extrasystoles, without organic heart 
disease, cases, 609, 611 
Eyeballs, pressure over, to control paroxys- 
mal tachycardia, 205 
Fat embolism, surgical wound shock due to, 
449 
Fatty degeneration of heart due to phos- 
phorus poisoning, 64 
Fatty heart, 53, 336 
causes of, 336 
symptoms of, 337 
Fetal circulation, 25 
Fibrillation, auricular, 142. See Auricular 
fibrillation. 
ventricular, 168. See Ventricular fibril- 
lation, 168 
Fibroid heart, 453 
fibroid uterus and, 453 
Fluoroscopy. See Orthodiascopy. 
Flutter, auricular, 153. See Auricular 
flutter. 
Focal infections, cause of heart disease, 68, 
399 
removal of foci of infection unneces- 
sary in, 399 
Food, improper, cause of heart disease, 
396 
Foramen ovale, 4 
patent, 26 
Frank mirror capsule in sphygmograph, 
79, 80 
Frank segment capsule, 484-485 
Fright, extrasystoles in, 196 
Functional efficiency tests of heart, 285 
delayed rise test, 286 
Graupner method, 287 
Herz muscle-contracting test, 287 
Katzenstein test, 286 
Mendelsohn-Graupner test, 286 
objections to, 278 
Plesch’s method, 287 
pulmonary reserve test, 286 
stair-climbing test, 286 
systolic blood pressure test, 285 
Gaertner method of estimation of venous 
blood pressure, 441 
Gall-bladder and bile ducts, acute inflam- 
mation of, extrasystoles in, 195 
Galvanometer, string, 95 
Ganglia, intracardiac, 19 
stellate, physiological action of, 40 684 
INDEX 
Garrey, experimentation of, on auricular 
fibrillation, 158 
Gaskell, experimentation of, on heart 
physiology, 35 
Gastric diseases, acute, extrasystoles in, 194 
precordial pain in, 420 
clinical picture of, 420 
treatment of, 421 
Gastro-intestinal disturbances, paroxysmal 
tachycardia in, 203 
tachycardia in, 203 
true bradycardia in, 197 
Gastro-intestinal paresis in coronary dis- 
ease, 411 
Gerhartz’s sound registration apparatus, 
482, 483 
Globular heart. See Heart, globular. 
Goiter, exophthalmic, auricular fibrillation 
in, 151 
high blood pressure in, 435 
Goitrous heart, 349 
etiology of, 349, 350 
symptoms of, 350 
dyspnoea in, 351 
exophthalmic goiter and, 350 
extrasystoles in, 351 
hypertension in, 351 
overforceful and rapid heart action in, 
350 
pulse in, 350 
treatment of, 351 
Goldscheider, orthopercussion method of, 
249 
Gout, heart disease due to, 66 
Graupner functional test, 287 
Grippe, extrasystoles in, 195 
Gross, investigation of, on coronary circula- 
tion, 15 
“Growing pains,” 397 
Gymnastics, medical, 383 
h wave, 87 
Hatcher, chloroform-soluble and non- 
chloroform-soluble fraction of digitalis of, 
365 
Heart, anatomy of, of coronary circulation, 
IS 
of lymphatics, 15 
of musculature, 5 
conduction system in, 7 
blood supply of, 12 
dissection and demonstration of, ix 
main branches in, 8-11 
Heart, anatomy of musculature, conduction 
system in, main stem in, 8 
nerve supply of, 12 
node of Tawara in, 8 
deeper layers in, 6 
superficial fibers in, 5-6 
of nerve supply, 19 
accelerator nerve, 19 
coronary plexus, anterior, 19 
posterior, 19 
deep cardiac plexus, 19 
depressor nerve, 19 
extrinsic, 19, 20 
and atrio-ventricular conduction sys- 
tem, 22 
and sino-auricular node, 22 
intracardiac ganglia, 19 
superficial plexus, 19 
sympathetic nervous system and, 19, 
21 
vagus nerve and, 19, 21 
of rhythm center or pacemaker, 12 
of sino-auricular node, 12 
of veins, 15 
portal system and, 17, 18 
pulmonary system and, 17, 18 
systemic circulation and, 16, 17, 18 
valves in, position of, 23 
Heart, anomalies affecting entire, 31 
broad, 218 
orthodiascopic tracing of, 217 
Heart, embryological considerations of, 1 
aorta, 3, 4 
aortic bulb, 2 
aortic septum, 3 
bulbar swellings, proximal and distal, 
in, 3, 4 
septum aorta-pulmonale in, 3, 4 
truncus arteriosus in, 3, 4 
cardiac tube, 1 
fetal septa, 2 
interauricular, 2 
interventricular, 3 
musculature, 4, 5 
development of, 3. See also Heart, 
anatomy of, of musculature, 
musculi pectinati, 4 
myocardium, 4 
pars membranacia, 3 
pulmonary artery, 3, 4 
valves, 4 
Heart, energy of, in estimation of arterial 
blood pressure, 426 INDEX 
685 
Heart, functional efficiency tests of. See 
under Heart failure, symptoms of. 
Heart, globular, 223 
disproportionate right- and left-sided 
enlargement, 223, 225, 226 
extreme, 223 
orthodiascopic tracings, in decompen- 
sated mitral lesions, with auricular 
fibrillation, 221, 222 
moderate, in double mitral lesions with 
auricular fibrillation, 223 
orthodiascopic tracings, 224 
moderately enlarged, 223 
orthodiascopic tracings, 224 
Heart, in diphtheria, 444. See Diphtheria, 
in pneumonia, 455. See under Pneu- 
monia. 
Heart, long and narrow, 218 
orthodiascopic tracing of, 217, 2x9 
Heart, normal, orthodiascopic tracing of, 
2x3, 214 
normal in size and contour, with compen- 
sated mitral lesions, 223 
orthodiascopic tracings, 220 
Heart, orthodiascopic standard of, 216, 218 
outline of, rational method for deter- 
mination of, by mapping out on chest, 
252 
Heart, physical examination of, 244 
auscultation in, 257 
murmurs in, extra-cardiac, of non- 
organic origin, 263 
intra-cardiac, of non-organic origin, 
263 
differentiated from mitral organic 
regurgitant murmurs, 264 
of cardio-sclerosis, 261 
right-sided, from auricular enlarge- 
ment, 262 
cases, 262-263 
reduplicated apical impulse, 267 
reduplicated heart sounds, 266 
valvular, of aortic regurgitation, 260 
of aortic stenosis, 260 
of mitral regurgitation, 257 
of mitral stenosis, 258 
of pulmonary insufficiency, 261 
of pulmonary stenosis, 261 
of rheumatic endocarditis, 257 
of tricuspid lesions, 260 
inspection in, 244 
of aortic pulsation, 245 
of apical and precordial region, 245 
Heart, physical examination of, inspection 
in, of carotid pulse, 244 
of jugular pulsation, 244 
of right lower interspaces, 246 
epigastric pulsation, 246 
liver pulsation, 247 
right lower chest, 246 
mapping out on chest of cardiac outline, 
a rational method, 252 
palpation in, 247 
in mitral lesions, 248 
of aortic pulsations, 248 
over left base of heart, 248 
over right base of heart, 248 
percussion in, 249 
inaccuracy of, 250, 25r, 252 
physical signs of ventricular hypertrophy 
in, 268 
left, 269 
right, 269 
Heart, physiological experimentation, 34 
size and weight of, 22 
in cardio-vascular examination of war 
recruits, 473 
spirochetal injection of, 57 
tables of average measurements of, 238, 
239 
Heart, physiology of, 84 
accelerator center in, 40 
action and influences of cardiac nerves, 39 
accelerator, 40 
ganglia, 40 
vagus, 39 
cardio-inhibitory center in, 40, 41 
myogenic or neurogenic impulse in, 41 
of musculature, 35 
conductivity in, 35 
contractility in, 37 
irritability in, 38 
rhythmicity in, 35 
tonicity in, 38 
reflex excitation in, 40, 4T 
Heart block, auriculo-ventricular, clinical 
etiology of, 197 
cardiac causes, 198 
extra-cardiac factors, 198 
experimental, causes of, 197. See 
Auriculo-ventricular heart block, 
case, 652 
clinical recognition of, 188 
complete, 178 
cases, 656, 659 
description of, 178, 184 686 
INDEX 
Heart block, complete, tracings, 180, 181, 
182, 184, 185, 187 
with slow ventricular rhythm, in pneu- 
monia, 458 
digitalis in, 362 
effect of, case, 186 
in case of peritoneal tuberculosis, 188 
incomplete, 178 
clinical recognition of, 178 
description of, 178 
differentiated from sino-auricular block, 
188 
tracings, 179 
slow heart action in, differentiated from 
true bradycardia, 171 
ventricular rates in, 186 
with auricular fibrillation, case, 663 
tracings, 182 
Heart disease, cardiac clinics for, 402. See 
Cardiac clinics, 
causes of, 396 
alcoholism, 396 
focal infections, 399 
improper food; 396 
infectious diseases, 396 
rheumatism, 397 
scarlet fever, 396 
syphilis, 396 
tonsillectomy, 397 
tonsillitis, 397 
tooth infection, 398 
chronic, dietetic regime in, 389 
prevalence of, 289 
classification of, by cardiac clinics, 403 
congenital, 353. See Congenital heart 
disease, 
diet in, 360 
drugs in, 360. See also under separate 
names. 
exercise in, 399 
fundamental considerations in, 399 
marriage problem in, 463. See Marriage, 
occupation in, 400 
handicaps in, 400 
importance of, 401 
list of suitable occupations, 401 
occurrence of, 396 
tobacco in, 389. See also Tobacco, and 
Smoking. 
Heart failure, acidosis in, 272 
acute, extrasystoles in, 194 
definition of, 271 
diet in, 360 
Heart failure, glucose injections in, 
intravenous, 360 
in life insurance examination, 477 
symptoms of, 271 
cardiac overstrain, 284 
cerebral manifestations, 279 
Cheyne-Stokes respiration, 273 
cough, 274 
bronchial, 275 
cardiac, 274 
cardiac asthma, 275 
cyanosis, 276 
dyspnoea, 27r 
causes of, mechanical, 271 
clinical etiology of, 271, 274 
clinical study of, 273 
factors composing, 273 
edema, 277 
functional efficiency tests in, 285 
delayed rise test, 286 
Graupner method, 287 
Herz muscle-contracting test, 287 
Katzenstein test, 286 
Mendelsohn-Graupner test, 286 
objections to, 278 
Plesch’s method, 287 
pulmonary reserve test, 286 
stair-climbing test, 286 
systolic blood pressure test, 285 
neurotic element in, 279 
direction of action of, 284 
general considerations of, 279 
in case of cardio-sclerosis with left 
ventricular hypertrophy, 284 
in case of rheumatic aortic regurgita- 
tion, 282, 283 
psychic disturbance in, 281 
in cases of mitral stenosis, 281, 282 
orthopnoea, 274 
paroxysmal dyspnoea, 274 
precordial pain, 278 
pulmonary edema, sudden, 275 
renal involvement, 278 
visceral congestion, 277 
Heart sounds, normal, in physical examina- 
tion, 242 
first sound, cause of, 242 
significance of, 243 
second sound, cause of, 243 
significance of, 243 
third sound, cause of, 243 
reduplicated, 266 
Hemicardia, 31 INDEX 
687 
Hemisystole, 190 
Hemoptysis in congenital heart disease, 354 
in mitral stenosis, 277 
Henderson re-breather apparatus, 446, 447 
Henderson’s theory of acidosis as cause of 
shock, 450 
Hepatic congestion in valvular lesions, 277 
Herz muscle-contracting test, 287 
Histology of heart, 44 
of endocardium, 44 
of epicardium, 44 
of myocardium, 44 
History record, 240 
Hoffman’s anodyne, 379 
Holowinski, application by, of principle of 
Newton’s interference rings to sound 
registration, 483 
Howell, experimentation on heart physiol- 
ogy by, 34 
Hunger pangs in digitalis administration, 
362 
Hydrotherapy, 384. See Baths. 
in hypertension, 439 
Hydro thorax, paracentesis for, 381 
Hyperdicrotic pulse, 92 
Hypertension, and aortitis, case, 612 
and vasomotor inability without cardio- 
vascular disease, cases, 605 
at menopause, cases, 599 
high blood pressure in, 436 
diabetes and, vasomotor symptoms, case, 
598 
differentiation between cardiac and cere- 
bral types, 434 
extrasystoles in, 196 
in examination of war recruits, 472 
in high arterial blood pressure, 433 
with myocarditis, 433 
and vasomotor mechanism, 433 
with uremia, 433 
permanent, with transient auricular 
fibrillation, case, 639 
surgery and, 452 
transient, without organic cardio-vascu- 
lar disease or cardiac symptoms, cases, 
596 
treatment of, 438 
absence from business in, 440 
at spas, 440 
diathermy in, 440 
drugs in, 439 
erythrol tetranitrate, 439 
iodide of potash, 439 
Hypertension, treatment of, drugs in, 
nitroglycerin, 439 
sodium nitrate, 439 
electric light baths in, 440 
exercise in, 440 
general considerations of, 438 
general remarks on, 438 
hydrotherapy in, 439 
percussion over seventh cervical verte- 
bra in, 440 
venesection in, 439 
with myocardial insufficiency, precordial 
pain in, 412 
case, 413 
cause of, 412 
symptoms of, 412 
treatment of, 412 
in uremic group, 414 
with labile vasomotor mechanism, 
4i3 
Hyperthyroidism, cardio-vascular disease 
due to, 71 
Hypertonus, influence of, on arterial blood 
pressure, 432 
Hypertrophy, cardiac, 59 
clinical interpretation of, from electro- 
cardiogram showing normal rhythm, 
127 
differentiation of electrocardiogram, from 
bundle branch lesions, 170 
of adolescent growth, 60 
pathological, 61 
classification of types of, 61 
following chronic renal lesions, 62 
in valvular lesions, 61, 62 
physiological, 59 
diagnosis of, caution in, 61 
etiology of, 59 
alcoholic myocarditis, 64, 65 
arteriosclerosis in, 60 
drugs in, 59 
nervous system in, 59 
physical exertion in, 59 
Hypertrophy, ventricular. See Ventricular 
hypertrophy. 
effect of, on electrocardiogram, 114 
physical signs of, 268 
left, 269 
right, 269 
Hypotension, functional, arterial blood 
pressure in, 436 
treatment of, 440 688 
INDEX 
“Ideal” heart in life insurance examina- 
tions, 476 
Incompetency, definition of, 271 
Indigestion, acute, paroxysmal tachycardia 
in, 203 
Industrial poisons, heart disease due to, 64 
Inefficiency, definition of, 271 
Infectious diseases, cause of heart disease, 
396 
coronary lesions in, 53 
crises of, transient auricular fibrillation 
in, 151 
Influenzal bronchitis, precordial pain in 
crisis of, 424 
Insufficiency, definition of, 271 
Interauricular septum, absence of, 28 
defects of, 26 
fetal, 2 
Intercostal neuralgia, precordial pain in, 425 
Interference rings of Sir Isaac Newton, 483 
Interventricular septum, absence of, 28 
defects of, 26 
fetal, 3 
maldevelopment of, 30 
patent, 356 
cases, 356, 357, 592 
physical signs of, 354 
symptoms of, 356 
Intracranial pressure, increased, high blood 
pressure in, 435 
Intraventricular block, due to abnormal 
ventricular mobility, 121 
electrocardiogram, 121 
QRS complex, prolonged, in, 121 
R wave in, broadening of, 122 
causes of, 124 
electrocardiogram, 123 
Iodide of potash excretion test of urine, 391 
Irregularities, cardiac, in life insurance 
examination, 476 
Irritable heart, 341. See also Heart failure, 
neurotic element in. 
causes of, mechanical, 346 
endocrine changes in, 347 
exophthalmic goiter in, 347 
hyperexcitation of sympathetic sys- 
tem in, 346, 347 
discussion of term, 342 
etiology of, 342, 345, 346 
in civil life, 343, 345 
’in military life, 342 
muscular exertion in, 342 
nerve fag in, 343 
Irritable heart, following paroxysmal 
tachycardia, case, 574 
from physical overstrain, cases, 565 
in organic valvular disease, cases, 586 
physical findings in, 345 
symptoms of, 343, 345 
instability of vasomotor and acceler- 
ator mechanism in, 343 
pulse in, 344 
treatment of, 345, 348 
without organic disease, cases, 557 
Irritability of heart musculature, 38 
Jaundice in valvular lesions, 277 
Jugular pulsation, inspection of, in physical 
examination of heart, 244 
Jugular pulse, normal, waves of, 83 
a wave, 84, 85 
cause of, 85 
c wave, 85 
cause of, 85 
h wave, 87 
v wave, 86 
cause of, 86 
variations in, 85 
Junctional tissues, 8. See Conduction 
system. 
Karrell diet, 377 
modification of, 377-378 
use of, in myocardial insufficiency with 
edema, 390 
Katzenstein test, 286 
Keith on transpositions of arterial trunks, 
3i 
Keith-Flack, node of, center of rhythmicity, 
35 
Kidneys, action of digitalis on, 365 
in Streptococcus viridans infection, 58 
involvement of, in heart failure, 278 
lesions of, chronic, cardiac hypertrophy 
following, 62 
Koenig, manometric flames of, 482 
Korotkow, estimation of arterial blood pres- 
sure by auscultatory method, 431 
Kraus’s theory of paralysis of vocal cord 
in mitral stenosis, 295 
Labor, in pregnancy, heart in. See Preg- 
nancy. 
Lactose elimination test of urine, 391 
Laryngeal nerve, left, paralysis of, paralysis 
of vocal cord due to, 295 689 
INDEX 
Lead poisoning, heart disease due to, 63 
high blood pressure in, 435 
true bradycardia in, 196 
Leads, electrocardiographic, definition of, 
98, 100 
description of, 100 
Life insurance examinations, 476 
blood pressure in, 480 
cardiac abnormalities in, 476 
cardiac irregularities in, 476 
circulatory defect or abnormality in, 477 
constant rapid heart action in, 478 
definite organic lesions in, 481 
extrasystoles in, 477 
heart failure in, 477 
ideal heart in, 476 
murmurs and thrills in, 478 
murmurs at apex, 478 
over left base, 479 
over right base, 479 
thrills over base, 479 
split, thrill-like sounds, 479 
shortness of breath in, 477 
size of heart in, 480 
standard heart in, 476 
Liver complications in valvular lesions, 277 
Liver pulsation, inspection of, in physical 
examination of heart, 246 
Locke’s solution for heart experimentation, 
34 
Luetic valvulitis, 57 
Luminal, 380 
in extrasystoles, 196 
Lymphatic system, in estimation of arterial 
blood pressure, 427 
Lymphatic system of heart, 15 
M complex in abnormal ventricular mobil- 
ity, 119 
interpretation of, 127 
“Machinery” murmur, 355 
Mackenzie ink polygraph, 81 
description of, 81 
method of using, 82 
Magnesia, sulphate of, 381 
Mall, on malposition of the inferior septum 
and endocarditis, 27 
Mannitol hexanitrate, 378 
Manometric flames of Koenig, 482 
Mapping out of cardiac outline on chest in 
physical examination, 252 
Marey, early studies of, in measurement of 
pulsations, 78 
Marey, sphygmograph of, 79 
Marriage, heart disease and, 463. See 
Pregnancy. 
in decompensation, 463 
in quiescence of lesion, 464 
Massage in heart disease, 383 
Mechanism of the heart, 73 
in acute cardiac dilatation, 75 
summary of, 77 
valve closure, 73 
volumetric ventricular curves, 74 
Mediastinal tumors, precordial pain in, 425 
Mendelsohn-Graupner test, 286 
Menopause, exophthalmic goiter at, recur- 
rence of, 578 
hypertension at, cases, 599 
high blood pressure in, 436 
paroxysmal tachycardia due to neurosis 
at, case, 619 
precordial pain accompanying vasomotor 
disturbances at, 424 
Mercury poisoning, heart disease due to, 64 
Metabolism, heart disease due to, 66 
Metallic poisons, heart disease due to, 63 
Micrograph of Crehore, 483-484 
Mines, experimentation of, on auricular 
fibrillation, 158 
Mirror transposition of heart, 33 
Missed or dropped beats, 134 
Mitral incompetency, 293. See Mitral 
regurgitation, decompensated. 
Mitral lesions, compensated, 223 
orthodiascopic tracings of, showing 
heart of normal size and contour, 220 
decompensated, with auricular fibrilla- 
tion, 223 
orthodiascopic tracings of, showing 
extreme globular hearts, 221, 222 
double, acute pericarditis, case, 523 
double, decompensation, streptococcemia, 
case, 524 
double, orthodiascopy of, 227 
tracings, 224, 225 
double, with auricular fibrillation, 223 
orthodiascopic tracings, 224 
orthodiascopy of, 223 
palpation of, in physical examination of 
heart, 248 
with aortic disease, orthodiascopy of, 229 
tracings, 230 
Mitral regurgitation, cardiac hypertrophy 
in, 61, 62 
with decompensation, murmurs of, 257 690 
INDEX 
Mitral regurgitation, with decompensation, 
orthodiascopy of, 227 
tracings, 226 
compensated, with variable auscultatory 
signs, 511 
coronary involvement of undetermined 
origin, 525 
decompensated, in chronic rheumatic 
endocarditis, 293 
clinical syndrome of, 294 
dynamic considerations of, 293 
murmurs of, 257 
differentiated from non-organic mur- 
murs, 264 
simple, in pregnancy, 465 
with pericarditis, cases, 507, 508 
Mitral stenosis, atypical history and 
symptoms, case, 518 
auricular fibrillation in, 151, 202 
cardiac hypertrophy in, 61 
decompensated, 297 
clinical syndrome of, 295 
auricular fibrillation in, 298 
embolism in, 298 
paralysis of vocal cord in, due to 
paralysis of left laryngeal nerve, 
295 
case of, 296 
theories of 295-296 
paroxysmal tachycardia in, 298 
dynamic considerations of, 295 
hypertension, neurasthenia, case, 520 
murmurs of, 258 
notched P wave in, 121 
psychic element in, cases, 281, 282 
pulmonary infarct, gastric and vasomotor 
symptoms, case, 516 
rheumatic, auricular fibrillation accom- 
panying decompensation in, 201 
in pregnancy, 464 
sudden onset of vasomotor symptoms, 
case, 515 
with auricular fibrillation in pregnancy, 
465 
with rheumatic recrudescence, case, 512 
Morphine, auriculo-ventricular heart block 
due to, 199 
in heart disease, 380 
Mosenthal’s nephritic test diet, 392 
Mouth infections, cardio-vascular disease 
due to, 68, 69 
Miinchener Bierherz, 64 
Murmurs, extra-cardiac, of non-organic 
origin, 265 
in cardio-vascular examination of war 
recruits, 474 
in life insurance examinations, 478 
intra-cardiac, of non-organic origin, 263 
differentiated from mitral organic 
regurgitant murmurs, 264 
due to aberrant fibers in ventricle, 264 
occurrence of, 264 
soft, blowing systolic murmurs, 265 
of cardio-sclerosis, 261 
right-sided, from auricular enlargement, 
262 
cases, 262-263 
systolic, loud rough, diagnostic of cardio- 
sclerosis, 328 
valvular, of aortic regurgitation, 260 
of aortic stenosis, 260 
of mitral regurgitation, 257 
of mitral stenosis, 258 
of pulmonary insufficiency, 261 
of pulmonary stenosis, 261 
of rheumatic endocarditis, 257 
of tricuspid lesions, 260 
Musculature of heart, development of, nor- 
mal, 4, 5 
conduction system in, 7 
of the adult, 5 
deeper layers in, 6 
superficial fibers in, 5-6 
physiology of, 35 
conductivity in, 35 
contractility in, 37 
irritability in, 38 
rhythmicity in, 35 
tonicity in, 38 
variations in, as affecting electrocardio- 
gram, 106 
cardiac displacements, in 
congenital dextrocardia, 112 
deviation of R wave, due to changes of 
position, 106 
drop hearts, 109 
horizontally disposed hearts, 107 
phasic variations with breathing, 113 
squatty hearts, 107 
summary, 127 
ventricular dilatation, 117 
ventricular hypertrophy, 114 
ventricular mobility, abnormal, 118. 
See also Ventricular mobility, abnormal, 
vertically disposed hearts, 109 691 
INDEX 
Musculi pectinati, fetal, 4 
Myalgia, intercostal, precordial pain in, 425 
Myocardial degeneration, in pneumonia, 460 
prolonged conduction time due to, 201 
Myocardial fibrosis, 54 
Myocardial incompetency, definition of, 271 
Myocardial insufficiency, auricular fibrilla- 
tion in, 202 
definition of, 271 
due to alcoholism, 64 
dyspnoea and, without edema, diet in, 390 
pulsus paradoxus in, 190 
with edema, Karrell diet in, 390 
without hypertension, precordial pain in, 
4i3 
case, 415 
symptoms of, 414 
treatment of, 414 
Myocarditis, 54 
acute, extrasystoles in, 194 
symptoms of, 323 
acute interstitial suppurative, 54 
chronic, diagnosis of, 326 
symptoms of, 323 
chronic fibrous interstitial, 54 
clinical interpretations of, from electro- 
cardiogram showing normal rhythm, 
127 
coronary lesions in, etiology of, 53 
due to alcoholism, 64 
due to pyorrhoea alveolaris, 68 
high blood pressure in, without hyper- 
tension, 434 
occlusion of main coronaries and, 408 
prolonged conduction time and, 177 
Myocarditis, rheumatic, 55, 67 
syphilis and, 57 
syphilitic, with tooth infections, case, 537 
toxic, extrasystoles in, 195 
sinus arrhythmia due to, 193 
with arteriosclerosis, case, 496 
with auricular fibrillation and decompen- 
sation, case, 635 
with coronary disease, case, 494 
with syphilitis aortitis, case, 494 
without hypertension or physical signs, 
cases, 550 
Myocardium, degenerative changes of, 52 
brown atrophy, 52 
fatty degeneration, 52 
fatty infiltration, 53 
parenchymatous or albuminous degen- 
eration, 52 
Myocardium, degenerative changes of, 
simple atrophy, 52 
fetal, 4 
histology of, 44 
inflammation of, 54. See Myocarditis, 
coronary lesions in. 
Myogenic vs. neurogenic theory of impulse, 
4i 
Narrow heart. See Heart, long and 
narrow. 
Nauheim baths, 386 
for reduction of hypertension, 439 
home preparation of, 386 
Nephritic test diet, 392 
Nephritis, in coronary disease, transient, 
411 
with excessive amounts of non-protein 
nitrogen in blood, treatment of, 394- 
395 
Nerve shock, heart failure due to, 281 
Nerve supply of heart, anatomy of, 19. 
See also under Heart, anatomy of. 
Nervous seizures, extrasystoles in, 196 
Neuralgia, intercostal, precordial pain in, 
425 
precordial, of unknown origin, 425 
Neurogenic vs. myogenic theory of impulse, 
4i 
Neurotic element in heart failure, 279 
cases of, 281-284 
direction of action in, 284 
general consideration of, 279 
psychic disturbance in, 281 
Newton, Sir Isaac, interference rings of, 483 
Nicotine. See Smoking. 
selective action of, on nerve mechan- 
ism of heart, 445 
Nitroglycerine, for heart failure, 378 
Nodal extrasystoles, electrocardiogram, 159 
tracings, 160 
Nodal rhythm, 142 
Node of Tawara, 8 
Non-protein nitrogen in blood, test for, 394 
Obesity, cardio-vascular disease in, diet in, 
390 
reduction of weight, 390 
restrictions in diet, 390 
Occupation for cardiacs, 400 
handicaps in, 400 
importance of, 401 
list of suitable occupations, 401 
Oertel treatment, 384 692 
INDEX 
Ohm’s gelatine membrane apparatus for 
sound registration, 482 
Onychograph, 81 
Orthodiascope, 211, 212 
Orthodiascopic standards, 216 
size of heart in, 216, 218 
Orthodiascopic tracing of normal heart, 
advantages over teleroentgenographic 
plates, 213 
Orthodiascopy, 210 
of aortitis, 229 
of broad heart, 218, 221-223 
of combined aortic and mitral disease, 229 
of heart in mitral lesions, 220-227 
of narrow heart, 218, 2x9 
of normal heart, 213, 214 
of rheumatic aortic disease, 227-229 
procedure in, 210, 213 
Orthopercussion of Goldscheider, 249 
Orthopnoea, 274 
Ortner’s theory of paralysis of the vocal 
cord in mitral stenosis, 295 
Ostium primum, embryonic, 2 
Ostium secundum, embryonic, 2, 3 
Overacting heart, case, 554 
Oxygen baths, 385 
for reduction of hypertension, 439 
P wave, 101 
absence of, in auricular fibrillation, 149 
notching of, due to asynchronous auricu- 
lar activity, 120 
splitting of, due to asynchronous auricu- 
lar activity, 120 
Pacemaker, anatomy of, 12 
center of rhythmicity, 35 
Paracentecis of abdomen, 381 
of thorax, 381 
Paralysis of vocal cord in mitral stenosis, 
296 
case of, 296 
theories of, 293-296 
Paroxysmal tachycardia, case, 204 
clinical etiology of, 203 
control of, by pressure over vagus, 40 
due to gastric neurosis at menopause, 
case, 619 
of auricular origin, 139 
clinical recognition of, 141 
definition of, 139 
description of, 140 
differentiated from ventricular tachy- 
cardia, 168 
Paroxysmal tachycardia, of auricular origin, 
electrocardiogram, 157 
origin of paroxysms in, 140 
of ventricular origin, description of, 167 
electrocardiogram, 166 
polygram, 140 
treatment of, 204 
without organic disease, cases, 614 
Pars membranacia, embryonic, 3 
Passive motion in heart disease, 383 
Patent ductus arteriosus, congenital, case, 
59i 
Patent foramen ovale, 26 
Patent interventricular septum, cases, 592 
Percussion wave of radial pulse, 89 
Pericardial adhesions in cardio-sclerosis, 
auscultatory signs of, 329 
Pericarditis, digitalis in, 369 
occlusion of main coronaries and, 408 
precordial pain in, 425 
with effusion, pulsus paradoxus in, 190 
Periodic respiration, 273 
Peritonitis, extrasystoles in, 195 
Phenolsulphonephthalein test, 391 
Phonocardiogram, 485 
description of, 485 
normal, 486 
time relationship of murmurs tran- 
scribed by, 489 
value of, 488, 489 
with simultaneous electrocardiogram, 
488 
Phosphorus poisoning, heart disease due to, 
• 64 
Physical examination. See Examination, 
physical. 
Physiology of heart, 34. See under Heart. 
Plesch functional efficiency test, 287 
Pleurisy, precordial pain in, 425 
Plumbism, heart disease due to, 63 
Pneumonia, auricular fibrillation in, transi- 
ent, 151 
cardio-vascular disease due to, 66, 194 
crisis of, precordial pain in, 424 
extrasystoles in, 195 
heart in, 455 
cardio-sclerosis a late sequel in, 461 
case, 462 
circulatory irregularities in, 458 
arrhythmias, 458 
auricular fibrillation, 458 
complete heart block with slow 
ventricular rhythm, 458 INDEX 
693 
Pneumonia, heart in, extent of area of 
pneumonic involvement in, 456 
functional power of, 460 
case, 461 
general considerations of, 455 
in crisis, 457 
in digitalis medication, 458 
in lytic resolution, 457 
in toxic cases, 456 
myocardial degeneration in, 460 
treatment of, 455, 459 
cardiac stimulation in, 455, 459 
of arrhythmias, 459 
results of, 460 
in pandemic, 460 
hypostatic, in valvular lesions, 277 
Poisons, industrial, heart disease due to, 
64 
metallic, heart disease due to, 63 
Polygraphs, 81 
Mackenzie ink polygraph, 81 
Portal system, anatomy of, 17, 18 
Potassium acetate, 380 
Potassium iodide excretion test of urine, 391 
Pott’s disease, precordial pain in, 425 
Precordial pain, of cardio-vascular origin, 
407 
causes of, 407 
basic, 407 
factors in, 407 
psychic disturbances, 407 
coronary disease direct cause of, 407 
arrhythmias accompanying, 410 
cardiac syphilis, 417 
coronary spasm in, 409 
diseases causing, 411 
endo-myocardial disease with general 
circulatory failure, 417 
gastric symptoms in, 410 
dyspnoea, 410 
epigastric pains, 410 
vomiting, 410 
gastro-intestinal paresis in, 411 
general considerations of, 408 
hypertension and myocardial insuffi- 
ciency, 412 
with labile vasomotor mechan- 
ism, 413 
uremic group, 414 
mottling of extremities or venous 
thrombosis in, 41 x 
myocardial insufficiency without hy- 
pertension, 414 
Precordial pain, coronary disease direct 
cause of, nephritis, transient, and 
dependent edema in, 411 
occlusion of smaller branches in, 408 
pains in, referred, 409 
in epigastrium, 409, 410 
in left shoulder, 409 
in precordium, 409 
premature arteriosclerosis, 417 
pulmonary edema in, acute, 411 
rheumatic endocarditis, acute, and 
exacerbations, 415 
in heart failure, 278 
sacculated aneurisms, 418 
senile arterio- and cardio-sclerosis, 418 
of extra-cardiac origin, 420 
accompanying vasomotor disturbances 
at menopause, 424 
cardiospasm with temporary hyperten- 
sion, 421 
cases, 422 
evidence for exclusion of organic 
disease in, 422 
mild, 421 
painful deglutition in, 421 
symptoms of, 421 
due to esophageal disease and spasms, 
423 
case, 423-424 
due to gastric disturbances, 420 
clinical picture of, 420 
treatment of, 421 
due to tobacco, 420 
case, 420 
character of pains, 420 
in crises of acute pulmonary affections, 
424 
case, 424 
differential diagnosis of, 424 
symptoms of, 424 
in syphilitic aortitis, case, 541 
in tobacco heart, 445 
intercostal neuralgia and myalgia, 425 
neuralgias of unknown origin, 425 
pericarditis, 425 
pleurisy, 425 
Pott’s disease, 425 
tumors, mediastinal and spinal, 425 
Precordial region, inspection of, in physi- 
cal examination of heart, 245 
Predicrotic wave of radial pulse, 89 
Pregnancy, heart disease and, 463 
cardiac strain and labor in, 466 694 
INDEX 
Pregnancy, induction of labor in, 467 
Caesarian operation in, 467-468 
case, 467 
cardiac neurosis in, 468 
cases, 468-469 
methods of ending labor in, 466 
summary of, 470 
symptoms of, 464 
in aortic lesions, 465 
in decompensated endocardial lesions, 
46S 
in mitral regurgitant lesions, simple, 
465 
in mitral stenosis and auricular fibrilla- 
tion, 465 
in rheumatic mitral stenosis, 464 
onset of, 464 
tachycardia and collapse at parturition, 
case, 595 
treatment of cardiac symptoms in, 469 
with cardiac disease and endocarditic 
recrudescence, case, 552 
with cardiac disease and neurotic symp- 
toms, cases, 553 
with cardiac neurosis, case, 578 
Premature contractions, 131. See Extra- 
, systoles. 
Pressure in cardiac chambers, 73 
Presystolic, definition of, 258 
Primary wave of radial pulse, 89 
Pulmonary affections, bradycardia in, 197 
Pulmonary artery, fetal beginnings of, 3, 4 
malposition of, 30 
pressure within, 74 
Pulmonary congestion in heart disease, 277 
Pulmonary edema, acute, in coronary dis- 
ease, 411 
in heart failure, 275 
Pulmonary reserve efficiency test of hear 
286 
Pulmonary stenosis, congenital, physical 
signs of, 354 
murmurs of, 261 
Pulmonary system, anatomy of, 17, t 
Pulse, jugular, 83. .See Jugular pulse, 
perpetually irregular, 202 
radial, 88. See Radial pulse, 
types of, 90 
alternating, 188 
anacrotic, 92 
bisferiens, 92 
collapsing, 92 
Corrigan, 92 
Pulse, types of, dicrotic, 92 
fast, 92 
hard, 90, 92 
hyperdicrotic, 92 
slow, 92 
soft, 90, 92 
strong, 90, 92 
water hammer, 92 
weak, 90, 92 
Pulse alternation, 188 
Pulse pressure, definition of, 89 
Pulsus alternans, 188 
digitalis in, 363 
in tachycardia, 190 
occurrence of, 190 
theory of, 190 
tracings, 189 
Pulsus bigeminus, 131 
Pulsus bisferiens, 92 
Pulsus celer, 92 
Pulsus durus, 90, 92 
Pulsus magnus, 92 
Pulsus mollis, 90, 92 
Pulsus paradoxus, 190 
palpation of, 249 
Pulsus tardus, 92 
Purkinje fibers in conductivity, 37 
Pyemia, coronary lesions in, 53 
Pyogenic abscesses, endocarditis due to, 
70 
Pyorrhoea alverolaris, cardio-vascular dis- 
ease due to, 68 
Q wave of electrocardiogram, 101, 102 
QRS complex, prolonged, due to abnormal 
ventricular mobility, 121, 122 
interpretation of, 127 
QRST deviations, 101 
Quinidine in heart disease, 371 
dangers of, from auricular thrombosis, 
37 2 
from tachycardia, 372 
from ventricular extrasystoles, 372 
dosage of, 373 
drug susceptibility to, 373 
effect of, neurogenic, upon vagus, 371- 
372 
upon auricular musculature, 371 
observation of, 374 
in auricular fibrillation, 372, 374 
cases, 641 
\permanent effects in, 373 
summary of, 375 INDEX 
695 
R wave, abnormally wide, significance of, 
491 
cases, 493, 494 
broadening of, due to abnormal ventri- 
cular mobility, 121 
interpretation of, 127 
in intraventricular block, 122 
cause of, 124 
electrocardiograms, 123 
deviation of, due to changes of position, 
106 
notching of, due to asynchronous ven- 
tricular activity, 120 
interpretation of, 127 
of electrocardiogram, 102 
splitting of, due to abnormal ventricular 
mobility, 119 
interpretation of, 127 
due to asynchronous activity of ven- 
tricles, 120 
interpretation of, 127 
thickening of, due to asynchronous ven- 
tricular activity, 120 
interpretation of, 127 
Radial artery, palpation of, 92 
Radial pulse, 88 
cause of, 89 
dicrotic notch in, 89 
dicrotic wave in, 89 
primary or percussion wave in, cause of, 89 
systolic wave (secondary tidal or pre- 
dicrotic wave) in, cause of, 89 
v. Recklinghausen method of estimation of 
venous blood pressure, 441 
Reduplicated apical impulse, 267 
Reduplicated heart sounds, 266 
first sounds, 267 
second sounds, 266 
Registration of heart sounds, graphic 
methods of, 482. See also Electrocardio- 
gram, and separate names. 
Renal involvement in heart failure, 278 
Resistance exercises, 383 
Respiration, Biot type of, 273 
periodic, 273 
Rheumatic aortic disease, orthodiascopy 
of, 227 
tracings, 228 
Rheumatic aortic lesion, double, beginning, 
case, 534 
Rheumatic aortic regurgitation, case, 283 
Rheumatic aortic stenosis and regurgita- 
tion, bovine heart, cases, 531 
Rheumatic aortitis, cases, 495 
Rheumatic endocarditis, 46 
acute simple, 290, 415 
cases of, 415-417, 513 
causes of, 415 
clinical phenomena in, 290 
arrhythmias in, 291 
endocarditic, 291 
myocardial, 291 
rheumatic, 290 
exacerbations and recurrences of, 293 
symptoms of, 291, 415 
anemia, 292 
fever, 291 
onset, 293 
physical signs, 292 
prodromal, 292 
pulse, 292 
subjective, 292 
treatment of, 415 
without decompensation, therapy of, 
300 
chronic, aortic regurgitation, decompen- 
sated, 299 
clinical syndromes of, 299 
dynamic considerations of, 299 
aortic stenosis in, 299 
clinical syndrome of heart failure in, 
299 
dynamic considerations of, 299 
decompensated mitral stenosis in, 297 
clinical syndrome of, 295 
auricular fibrillation in, 298 
embolism in, 298 
paroxysmal tachycardia in, 298 
dynamic considerations in, 295 
paralysis of vocal cord in, due to 
paralysis of left recurrent 
laryhgeal nerve, 295 
case, 296 
theories of, 295-296 
symptoms of, 293 
without decompensation, therapy of, 
301 
decompensated mitral regurgitation in, 
293 
clinical syndrome of, 294 
dynamic consideration of, 293 
in a syphilitic, case, 521 
prognosis of, 302 
in acute stage, 302 
in chronic stage, 303 
in quiescent stage, 302 696 
INDEX 
Rheumatic endocarditis, prognosis in 
subacute stage, 302 
valvular murmurs in, 257 
Rheumatic mitral stenosis in pregnancy, 464 
Rheumatic myocarditis, 55 
Rheumatic sore throat, tonsillectomy in, 
advisability of, 398 
Rheumatism, acute articular, Aschoff bodies 
in, 207 
automatic ventricular activity in, 207 
aneurismal dilatation due to, 322 
aortic aneurism due to, 322 
cardio-vascular disease due to, 67 
cause of heart disease, 397 
preventive measures in, 396 
Rhythm, cardiac, abnormal, in cardio- 
vascular examination of war recruits, 473 
Rhythm center of heart, 12 
anatomy of, 12 
Rhythmicity of heart musculature, 35 
Right lower interspaces, inspection of, in 
physical examination of heart, 246 
Ringer’s solution in heart experimentation, 
34 
Rokitansky on causes of deviations and 
transpositions of the arterial trunks, 30 
S wave of electrocardiogram, 101 
Sacculated aneurisms of the aorta, 318 
precordial pain in, 418 
Salicylate of soda, bradycardia due to, 170, 
197 
Scarlet fever, cause of heart disease, 396 
coronary lesions in, 53 
Secondary tidal wave of radial pulse, 89 
Semilunar valves, deformities of, 31 
fenestra in, 30 
Senile arteriosclerosis, high blood pressure 
in, 435 
precordial pain in, 418 
Senile cardio-sclerosis, cases, 542 
cause of symptoms in, case, 545 
precordial pain in, 418 
true bradycardia in, 196 
Senility, cardio-vascular disease and, 71 
Septal anomalies, 29 
Septal defects, congenital, 26. See under 
Congenital malformations, defects and 
anomalies of the heart. 
Septum aorta-pulmonale, embryonic, 3 
Septum primum, fetal, 2, 3 
Septum secundum, embryonic, 3 
Septum spurium, mal-development of, 29 
Seventh cervical vertebra, percussion over, 
for hypertension, 440 
Shock, surgical wound, 448 
cause of, theories of, 449 
abnormal production and absorption of 
poisonous proteids, 449 
acidosis, 450 
anoci-association, 450 
blood viscosity, 450 
capillary stasis, 450 
fat embolism, 449 
loss of blood, 449 
venous stasis in chest and abdomen, 449 
character of, 448 
clinical picture of, 448 
conclusions regarding theories of, 451 
definition of, 448 
dilated heart and, 451 
surgical conditions influencing, 448 
tachycardia and, 450 
treatment of circulatory failure in, 451 
Shortness of breath in life insurance exam- 
ination, 477 
Sino-auricular block, 175 
blocked auricular beat differentiated 
from, 176 
causes of, 175 
clinical etiology of, 193 
electrocardiograms, 175, 176 
incomplete heart block differentiated 
from, 188 
treatment of, 194 
Sino-auricular node, anatomy of, 12 
and cardiac nerve supply, 22 
center of rhythmicity, 35 
Sinus arrhythmia, 172 
and heart block, blood pressure in, 437 
causes of, 172 
clinical etiology of, 193 
clinical recognition of, 172 
description of, 172 
electrocardiograms, 172, 175 
non-respiratory type, tracing, 17a 
occurrence of, 193 
pathological, treatment of, 193 
respiratory type, electrocardiogram, 175 
tracings, 173, 174 
tracings, 173, 174 
Sinus venosus, as center of rhythmicity, 35 
Size of heart, 22 
in cardio-vascular examination of war 
recruits, 473 
in life insurance examination, 480 INDEX 
697 
Skin puncture, multiple, 381 
dangers of, 381 
“Smoker’s heart,” coronary spasm cause of 
precordial pains in, 409 
Smoking, auriculo-ventricular heart block 
due to, 199 
effect of, on ganglionic terminations of 
the vagus and accelerators, diagram, 
176 
heart disease due to, 65 
influence of, in arterial blood pressure, 
432 
sino-auricular block due to, 175, 194 
tachycardia, moderate, due to, 176 
Sodium acetate, 380 
Sodium salicylate, extrasystoles following 
use of, 196 
Soldier’s heart, etiology of, 342 
Spa treatment in hypertension, 440 
patients suitable for, 386 
Spalteholz, investigation of, on coronary 
circulation, 15 
Sparteine, 379 
Sphygmographs, 78 
capillary, 81 
early, 78 
Frank, 79 
Mackenzie ink polygraph, 81 
Marey, 79 
onychograph, 81 
polygraphs, 81 
sphygmopaleur, 81 
sphygmoscope, 81 
tachograph, 81 
Uskoff, 79 
Sphygmography, early studies in, by Marey 
and Chauveau, 78 
instruments used in. See Sphygmo- 
graphs. 
jugular pulse in, limitation of information 
from phlebogram in, 87 
normal, waves of, 83 
variations in phlebogram in, 86 
radial pulse in, 88 
Sphygmopaleur, 81 
Sphygmoscope, 81 
Spinal tumors, precordial pain in, 425 
Spleen complications in valvular lesions, 
277 
Splenic enlargement in acute bacterial 
endocarditis, 307 
■Squatty heart, effect of, on electrocardio- 
gram, 107 
Squills, tincture of, in heart disease, 371 
Stair-climbing test, 286 
“ Standard ” heart in life insurance examina- 
tion, 476 
Stannius, ligature experiment of, on sinus 
venosus as center of rhythmicity, 35 
Streptococcus viridans infection, 58 
cerebral lesions in, 59 
heart disease due to, 68 
kidney changes in, 58 
pathology of, 58 
String galvanometer, 95 
Strophanthus in heart disease, crystalline, 
37° 
tincture, 370 
Strychnine in heart disease, 378 
Stupor in heart failure, 279 
Submaxillary glands, infection of, indication 
of tonsillar disease, 397 
Superficial nerve plexus, 19 
Suprarenal extract, 379 
in extrasystoles, 196 
Surgery and the arrhythmic heart, 452 
electrocardiogram in, 453 
in cardio-vascular disease, 453 
in decompensation, 452 
in hypertensive cardio-renal disease, 
453 
in functional arrhythmias, 452 
in hypertensive cases, 452 
Surgical wound shock, 448. See Shock, 
surgical wound. 
Sympathetic nervous system, influence of, 
on heart, 19, 21 
Syphilis, cardiac, 57, 311, 396, 417 
aneurismal dilatation of aorta. See 
Aortic dilatation, aneurismal. 
aneurismal dilatation of descending 
thoracic aorta, 3x3 
aneurismal dilatation of first part and 
arch of aorta, 312 
aortitis in, 311 
presence of, characteristic, 311 
causes of precordial pain in, 417 
diagnosis of, 311 
Wassermann reaction in, 311 
parts attacked by, pathology of, 311 
sacculated aneurisms of aorta, 318. See 
Aortic aneurism, sacculated, 
treatment of, 321, 417 
Syphilis, cardio-vascular disease due to, 71 
cause of aneurismal dilatations of the 
aorta, 58 698 
INDEX 
Syphilitic aortitis, 311 
and myocarditis, case, 494 
aneurismal dilatation of aorta in. See 
Aortic dilatation, aneurismal. 
aneurismal dilatation of descending thor- 
acic aorta, 313 
aneurismal dilatation of first part and 
arch of aorta, 312 
diagnosis of, 311 
Wassermann reaction in, 311 
precordial pain, case, 541 
sacculated aneurisms of aorta, 318 
treatment of, 321 
of decompensation, 321 
digitalis in, 321 
of the pains, 321 
of underlying infection, 321 
mercury in, 321 
potassium iodide in, 321 
salvarsan in, 321 
typical, case, 536 
Syphilitic myocarditis, with tooth infec- 
tions, case, 537 
Systolic blood pressure. See Arterial blood 
pressure. 
Systolic blood pressure efficiency test of 
heart, 285 
Systolic murmur, loud rough, diagnostic of 
cardio-sclerosis, 328 
Systolic output of heart, 74 
Systolic wave of radial pulse, 89 
T wave, deviation of, in abnormal ventricu- 
lar motility, 124 
causes of, 124 
electrocardiograms, 125 
significance of, 125, 127 
effect of digitalis on, 125 
effect of exercise on, 126 
effect of nerve influences on, 126-127 
of electrocardiogram, 102 
Tachograph, 81 
Tachycardia, definition of, 139 
in life insurance examinations, 478 
in surgical wound shock, 450 
pulsus alternans in, 190 
with collapse at parturition, case, 595 
Tachycardia, paroxysmal, case, 204 
clinical etiology of, 203 
control of, by pressure over vagus, 40 
due to gastric neurosis at menopause, 
case, 619 
of auricular origin, 139 
Tachycardia, paroxysmal, of auricular 
origin, clinical recognition of, 141 
description of, 140 
electrocardiogram, 157 
origin of paroxysms in, 140 
of ventricular origin, description of, 167 
electrocardiogram, 166 
tracing, 140 
treatment of, 204 
without organic disease, cases, 614 
Tachycardia, simple, clinical etiology of, 
203 
clinical recognition of, 141 
treatment of, 203 
Tachycardia, true, 170 
Tachysystole, auricular, 153 
Tawara, node of, 8 
Tea in cardio-sclerosis, 389 
Teeth, as foci of infection, 398 
diseased, cardio-vascular disease and, 68 
valvular endocarditis in children, 69 
Teleroentgenography, 210 
procedure in, 2x0 
Theobromine sodium salicylate, in heart 
disease, 376 
as a diuretic, 376 
dosage of, 376 
method of administration of, 376-377 
in sino-auricular block, 176 
Thoracic pulsation, right lower, in physical 
examination of heart, 246 
Thorax, paracentesis of, 381 
Thrills, systolic, in life insurance examina- 
tion, 479 
Thyroid gland, cardio-vascular disease due 
to, 71 
Thyroid gland extract in heart block, 201 
Tobacco. See Smoking. 
effect of, on cardio-vascular system, 389 
arteriosclerosis and, 389 
precordial pains in, 389 
Tobacco heart, 64, 420 
cases, 581 
precordial pain in, 445 
rise of blood pressure in, 445 
selective action of nicotine in, 445 
symptoms of, 445 
Tobacco poisoning, heart disease due to, 
65 
Tonicity of heart musculature, 38 
Tonsillar affections, extrasystoles in, 195 
Tonsillectomy, cause of heart disease, 397 . 
in endocarditis, 397. See endocarditis. INDEX 
699 
Tonsillitis, auricular fibrillation in, 151 
cardio-vascular disease due to, 68, 397 
endocarditis caused by, 68 
Tonsils, portals of entry of endocardial 
injections, 397 
Tonus, cardiac, influence of, on volumetric 
ventricular curve, 75 
Tooth extraction in endocarditis, routine 
and radical, uncalled for, 399 
Tooth infection, cause of heart disease, 398 
Tricuspid valvular lesions, murmurs in, 260 
Truncus arteriosus, 29 
embryonic, 3 
Tuberculosis, pulmonary, tachycardia in, 
203 
Typhoid fever, cardio-vascular disease due 
to, 66 
coronary lesions in, 53 
U wave, 86 
in electrocardiogram, 102 
normal, cause of, 86 
variations in, 87 
Undefended space, aneurism of, 27 
Urea determination in cardio-renal disease, 
392 
Uric acid determination test, 394 
Urine, examination of, in cardio-renal dis- 
ease, 391 
elimination of lactose injected intra- 
venously in, 391 
iodide of potash excretion test in, 391 
nephritic test diet in, 392 
phenolsulphonepthalein test in, 391 
quantitative, for urea, salt and water 
output, 392 
Uskoff sphygmograph, 79 
Vaccines in heart disease, 382 
autogenous, 382 
stock, 382 
Vago-vasal attacks, bradycardia in, 197 
Vagus nerve, anatomy of, 19 
auriculo-ventricular heart block due to 
abnormal pressure on, 200 
effect of digitalis on, 361 
function of, 19 
influence of, on heart, 19, 21 
physiological influence and action of, 
39 
pressure over, for control of paroxysmal 
tachycardia, 40, 204, 205 
course of, 19 
Valve closure, mechanism of, 73 
Valves, cardiac, development of, 4 
position of, 23 
Valvula foraminis ovalis, embryonic, 3 
Valvula venosa, 4 
Valvular anomalies, 29 
Valvular disease of the heart, auricular 
fibrillation in, 151 
cardiac hypertrophy in, 61, 62 
chronic, prevalence of, 289 
cyanosis in, 276 
diet in, 360 
compensated, dietary in, 389 
digitalis in, 368 
due to bacterial infection, 70 
effect of, on cardiac mechanism, 76 
endocarditis and, 51 
in examination of war recruits, 472 
myocardial insufficiency and, high blood 
pressure in, with and without hyper- 
tension, 434 
orthodiascopy in, 223 
normal heart in size and contour in, 
tracings, 220 
renal involvement in, 278 
syphilis and, 57 
tobacco and, 389 
visceral congestion with, 277 
Valvular endocarditis in children, diseased 
teeth and, 69 
rheumatic, 67 
Valvular murmurs in pulmonary valve in- 
sufficiency, 261 
in rheumatic endocarditis, 257 
in tricuspid lesions, 260 
Valvular stenoses, 29 
Vasodilators in heart disease, 378 
Vasomotor instability and fainting attacks 
from so called weak heart, cases, 562 
Vasomotor neuroses, 338 
cases, 340 
causes of, 340 
clinical symptoms of, 338 
gastric complaints, 339 
in abnormal orthodiascopic signs, 339 
referrable to circulation, 338 
referred intercostal and precordial 
pains, 339 
treatment of, 341 
of gastric disturbances, 341 
Veins of heart, 15 
Venesection, 381 
in hypertension, 439 700 
INDEX 
Venous blood pressure, determination of, 
instruments for, 441 
methods of, 441 
Brown’s, 441 
Gaertner’s, 441 
v. Recklinghausen’s, 441 
influence of, upon volumetric ventricular 
curves 74 
Venous stasis, surgical wound shock due 
to, 449 
Venous system, factor in estimation of 
arterial blood pressure, 427 
Ventricles, pressure within, 73 
Ventricular activity, independent, case, 206 
clinical etiology of, 206, 207 
treatment of, 207 
Ventricular arrhythmias, 160 
idioventricular rate in, tracings, 183 
Ventricular complex in electrocardiogram, 
101 
Ventricular curves, volumetric, 74 
influence of cardiac tonus on, 75 
influence of venous pressure upon, 74 
Ventricular deviation, abnormally wide, 
clinical significance of, 491 
cases, 493, 494 
negative, in case of left ventricular hyper- 
trophy, electrocardiogram, 116 
Ventricular dilatation, effect of, on elec- 
trocardiogram, 117 
Ventricular escape, 163 
case, 206 
clinical etiology of, 206, 207 
description of, 163 
digitalis and, 164, 167 
electrocardiogram, 167 
nodal beats and, 164 
pulse retardation and, 164 
theory in, 164 
tracing, 166 
treatment of, 207 
Ventricular extrasystoles, description of, 
160 
electrocardiograms, 162, 163, 164, 165 
frustrane, tracings, 165 
interpolated, 161 
variations of, arising from ectopic foci, 
163 
schematic view 162 
tracing and electrocardiograms, 133, 134, 
136 
tracings, 160, 161 
Ventricular fibrillation, 168 
cause of, 168 
electrocardiogram, -i68 
in cardiac decompensation, 168 
Ventricular hypertrophy, 61, 62 
effect of, on electrocardiogram, 114 
electrocardiograms, 83, 84 
physical signs of, 268 
left, 269 
right, 269 
Ventricular mobility, abnormal, effect of, 
on electrocardiogram, 118 
M complex in, 119 
interpretation of, 127 
P wave in, notching of, 120 
splitting of, i2o 
QRS complex in, prolonged, 121, 122 
interpretation of, 127 
R wave in, broadening of, 122 
cause of, 124 
electrocardiogram, 123 
interpretation of, 127 
R wave in, notching of, 120 
interpretation of, 127 
R wave in, splitting of, 119 
interpretation of, 127 
R wave in, thickening of, 120 
interpretation of, 127 
T wave in, 124 
causes of, 124 
effect of digitalis on, 125 
of exercise, 126 
of nerve influences, 126-127 
electrocardiograms of, 125 
significance of, 125, 127 
W complex in, 119 
interpretation of, 127 
Ventricular rates, rapid, 187 
Ventricular tachycardia, paroxysmal, 167 
description of, 167 
differentiated from auricular tachycardia, 
168 
Ventricular wave, 86 
Veronal, 380 
Vocal cord, paralysis of, due to paralysis of 
left laryngeal nerve, 295 
Volumetric ventricular curves, 74 
influence of cardiac tonus on, 75 
influence of venous pressure upon, 74 
Vomiting in digitalis administration, 362, 
364 
atropin in, 364 
cases, 364 INDEX 
701 
W complex in abnormal ventricular mobil- 
ity, 119 
interpretation of, 127 
War recruits, cardio-vascular examination 
of, 47i . 
evident cardio-vascular disease in, 471 
hypertension, 472 
valvular disease, 471 
signs simulating cardio-vascular disease, 
472 
abnormal cardiac rhythm, 473 
abnormal cardiac sounds, 474 
dyspnea, 475 
War recruits, cardio-vascular examination 
of signs simulating cardio-vascular 
disease, size of heart, 473 
Wassermann reaction in cardiac syphilis, 
311 
Water hammer pulse, 92 
Weak heart, vasomotor instability and 
fainting from, cases, 562 
Weight of heart, 22 
Weight reduction, through diet, 390 
Weiss soap-film phonoscope, 484 
“Youthful irregularity,” 172