MANUAL 
f A^Rthe7 1881 
I PHY S DIA S 
OF 
DISEASES OF THE HEART 
INCLUDING THE USE OF THE 
SPHYGMOGRAPH AND CARDIOGRAPH 
BY 
ARTHUR ERNEST SANSOM, M.D. Lond. 
FELLOW OF THE ROYAL COLLEGE OF PHYSICIANS 
ASSISTANT PHYSICIAN TO THE LONDON HOSPITAL 
PHYSICIAN TO THE NORTH-EASTERN HOSPITAL FOR CHILDREN 
TOBMBRLY PHYSICIAN TO THE ROYAL HOSPITAL FOR DISEASES OF THE CHEST, CITY ROAD: 
HONORARY FELLOW OF THE MEDICAL SOCIETY, AND CORRESPONDING 
MEMBER OF THE THERAPEUTICAL SOCIETY OF NEW YORK 
PHILADELPHIA 
P R E S L E. Y BL A K ip TW 
1881 PREFACE 
TO 
THE THIRD EDITION. 
The favourable reception accorded to former editions 
has convinced me that my little work supplied a want. 
It was my aim to give in a concise form the essentials 
for the diagnosis of Diseases of the Heart according* 
to the most modern teachings of pathology, tested, 
confirmed, and extended, where possible, by personal 
investigation. I wished that my book should be a 
companion to the advanced student in the wards of 
the hospital, and an aide-memoire to the practi- 
tioner in his daily duties. Although the second 
edition became rapidly exhausted, cardiac pathology 
has made considerable progress since its publication; 
it has, therefore, been absolutely necessary to subject 
the whole to thorough revision. To my regret, nearly 
a twelvemonth has passed before I have been able to 
complete this third edition. 
The day has come when every educated practitioner 
should be familiar with the use of the sphygmograph 
and cardiograph. The difficulties in the use of these 
instruments, and especially the objection on account 
of the time which their application occupies, are van- 
ishing, owing to improvement in mechanism ■ whilst 
the value of the evidence which they afford is attested 
by daily experience. As regards the systematic inves- VI 
tigation of disease by such methods, much remains to 
be done, but, thanks to the labours of Drs. Galabin, 
Mahomed, Balthazar Foster, and others, as well as 
to the introduction by Dr. Pond of an instrument 
which can be employed readily and rapidly, data are 
rapidly accumulating. I have, therefore, endeavoured 
in this edition (though in the former I expressly 
excluded the subject as premature) to describe the 
methods of employment, and so far as observations 
warrant, the indications of the sphygmograph and 
cardiograph in cardiac diagnosis. The illustrations 
of this portion of the work are for the most part 
original, from tracings by myself or by my house- 
physicians and clinical assistants under my own 
direction. Among those who have rendered me efficient 
aid I would especially mention Drs. S. D. Clipping- 
dale and Needham, and Messrs. Major Greenwood, 
Basil W. Walker, Burry, and Sweeting. 
I indulge in a hope that I may be enabled to follow 
up this little work with another on the Treatment of 
Heart Disease, so arranged that the two volumes 
shall constitute a systematic work. 
PREFACE. SCHEMA. 
I.-Symptomatology. 
A. Symptoms referred to the Heart, (a.) Pain referred 
directly to the Heart-region in cardiac disease is rare. Or- 
ganic disease may progress without giving rise to Pain. The 
special pain of Heart Disease is A ngina Pectoris, characterized 
by paroxysmal recurrence, great distress, coldness, arrest of 
respiration. (A) Palpitation: A frequent symptom in Heart 
Disease, but common in dyspepsia and in emotional conditions, 
(c.) Intermission: Common in Heart Disease, but may be 
neurosal. (d.} Irregularity : Generally of grave import, but 
may also be neurosal. 
B. Symptoms referred to the Circulation, (a.) Pulsation: 
Excluding emotional causes, suspect Hypertrophy of Heart, 
and especially aortic regurgitation, (b.} Hcemorrhage: Common 
in Heart Disease : Not of dangerous import as in Phthisis: 
Note tendency thereto in mitral stenosis, (c.) Cyanosis : Vide 
Inspection, (d.) Dropsy: A late and dangerous symptom. 
C. Symptoms referred to the Lungs. Note that these 
symptoms are very frequent, (a.) Dyspncea, aggravated by 
exertion ; periodic or persistent, (b.) Cough. 
D. Symptoms referred to the Brain, (a.) Languor and 
powerlessness. (&.) Vertigo and symptoms of disturbance of 
cerebral circulation, (c.) Epilepsy, (d.) Chorea, (e.) Apo- 
plexy. (f.) Paralysis. 
Note.-In cases of cardiac hypertrophy co-existing with 
renal disease, there may be intra-cranial haemorrhage, some- 
times difficult to distinguish from uraemia. In sudden cerebral 
attacks in patients with valvular disease suspect Embolism. 
E. Symptoms referred to the Alimentary Canal, (a.) 
Dyspepsia, very common. (6.) Haemorrhoids. 
F. Symptoms referred to the Throat, (a.) Pain referred to 
the throat may be a variety of Angina. (b.) Aphonia 
occasional in pericarditis, (c.) Hoarseness. VIII 
SCHEMA. 
G. Symptoms referred to the Kidneys. (1.) Renal disease 
may be induced by the Heart-affection. (2.) Renal disease 
may induce hypertrophy of the Heart. (3.) Renal and cardiac 
disease may be the double effect of one cause. 
Note.-In cases of Cardiac Disease, always examine the 
urine, and especially record conditions of albuminuria. 
II.-Etiology. 
{a.} Rheumatism is the most frequent cause of valvular 
Disease of the Heart. Rheumatic Fever is in a large number of 
cases the starting-point, but in other cases the rheumatic 
symptoms may be very slight and obscure, and sometimes the 
rheumatic form of endocarditis may occur with no other 
manifestation of rheumatism. 
Note.-Examine the condition of the heart in the slight, as 
well as in the severe forms of Rheumatism. 
(&.) Scarlet Fever is also a cause of valvular disease and of 
pericarditis, probably because of the rheumatoid phenomena 
associated with it. Measles also may lie followed by heart- 
disease. (c.) The other most common causes of Heart Disease 
are muscular overstrain, alcoholism, syphilis, tuberculosis, the 
puerperal state, poisoning by phosphorus, mal-nutrition, 
disease contiguous to heart and pericardium, diseases of lung 
inducing venous engorgement. 
Note.-A satisfactory examination of any patient, what- 
ever his ailment, cannot be made unless the cardiac conditions 
are observed and recorded. 
A. Hue of the surface, (a.) Blueness. (1.) Congenital 
cyanosis indicates persistent foramen ovale, or imperfection of 
inter-ventricular septum, usually combined with obstruction 
of pulmonary artery. (2.) Intermittent cyanosis, common in 
cardiac dyspnoea. 
Note.-Chilling of iinger-tips with blueness and coldness 
common in Heart Disease. 
(6.) Pallor. (1.) When associated with oedema, suspect co- 
existence of renal disease. (2.) With exophthalmos, thyroid 
enlargement and irritability of Heart, Graves' Disease. 
III.-Physical Examination-Inspection. (c) Tinge of Jaundice. (1.) In passive congestion of liver 
in later stages of valvular disease. (2.) With arcus senilis in 
Patty Degeneration of Heart. 
B. Cardiac Dyspnoea. (1.) Characterized by gasping air- 
craving, aggravated by exertion-Orthopnoea; indicative of 
valvular diseases, or cardiac degenerations. 
(2.) Decubitus on right side, with expression of anxiety and 
apprehension. Suspect Pericarditis. 
C. (Edema: Commences in lower extremities, serous 
cavities affected last : Usually depends on valvular disease 
(especially mitral, or conjoined mitral disease and tricuspid 
insufficiency). 
Note.-Examine urine, and determine the question of co- 
existence of renal and cardiac disease. 
D. Pulsation, (a.) In veins of neck indicates tricuspid 
insufficiency. (6.) In arteries: Locomotive pulse indicates 
aortic regurgitation, (c.) Displacement outwards of visible 
apex-beat indicates hypertrophy or dilatation of left ventricle. 
Note.-Area of visible impulse maybe apparently increased 
at times in nervous palpitation. 
(d.) Retraction of intercostal spaces coincidently with 
systole indicates pericardial adhesions. 
(c.) Pulsation of the liver indicates tricuspid regurgitation. 
SCHEMA. 
IX 
A. Pulse, (a.) Rigid arteries, tortuous, with roughnesses 
felt in their walls, associated with hard pulse, indicate 
Atheroma. 
(b.) Slowness of pulse, with very weak impulse, may indi- 
cate Patty Degeneration. 
(c.) Sudden variation of pulse with great acceleration on 
movement may occur in Pericarditis. 
(d.) Jerking, collapsing pulse in aortic regurgitation. 
(e.) Feebleness of pulse, and (/.) Irregularity and inter- 
mission, increased by effort, in mitral disease and cardiac 
degeneration. 
B. Apex-beat. Displaced. (1.) Upwards by pericardial 
effusion. (2.) Downwards and outwards in hypertrophy and 
dilatation of heart. 
IV. -Physical Examination-Palpation. X 
SCHEMA. 
C. Forcible pulsation felt under false ribs to left of ensiform 
cartilage indicates hypertrophy of right ventricle. 
D. Visible pulsation of right auricle indicates hypertrophy 
and dilatation of right chambers. 
E. Visible pulsation of left auricle indicates mitral stenosis. 
Note that this pulsation may be rendered evident by 
vibrating levers. 
E. Special Cardiac Tactile Phenomena, (a.) Friction-fre- 
mitus denoting Pericarditis. (6.) Thrill. (1.) Occurring with 
systole over aortic valves denotes aortic stenosis or aneurism ; 
over pulmonary valves, pulmonary stenosis; at apex, mitral 
regurgitation. (2.) Occurring with diastole at base, denotes 
aortic regurgitation. (3.) Occurring at apex just before, and 
terminated by impulse, indicates mitral stenosis. 
Note that decided presystolic thrill at apex is pathogno- 
monic of mitral stenosis, and may occur without murmur. 
V.-Physical Examination-Percussion . 
A. Praecordial area over-resonant or tympanitic-in em- 
physema of lung, and in the very rare cases of pneumo-peri- 
cardium. 
B. Pnecordial dulness extended, (a.) Upwards ; outline of 
dull area being triangular or pyriform with apex at or above 
third costo-sternal articulation. There is probably Effusion 
into pericardium. (6.) Laterally. The heart is enlarged by 
hypertrophy or dilatation. 
I. Lateral dulness extends left of normal area. (1.) Area 
of dulness triangular, apex pointed, Hypertrophy of Left Ven- 
tricle. (2.) Area of dulness rhomboidal, apex rounded, Dila- 
tation of Left Ventricle. 
Note.-Compare position of apex and outline of left ven- 
tricle with evidences of force of apex-beat. If left side 
enlargement with forcible heaving impulse and long first 
sound, Hypertrophy. If enlargement with feeble impulse and 
short first sound, Dilatation. 
II. Lateral dulness extends right of normal area. There are 
Hypertrophy and Dilatation of Right Auricle and Ventricle. 
Note epigastric impulse and signs of tricuspid regurgitation, 
if present. SCHEMA. 
XI 
VI.-Physical Examination-Auscultation. 
Section I.-The normal heart-sounds are modified in degree. 
A. At the base of the heart:- 
(a.) The aortic second sound is intensified. There is Hyper- 
trophy of the Left Ventricle. 
{b.) The pulmonary second sound is intensified. There is 
heightened tension in the pulmonic circulation. 
Note.-A strong pulmonary, associated with a weak aortic 
second sound, is presumptive evidence of mitral obstruction or 
insufficiency. 
B. At the apex of the heart:- 
(a.) The first sound is increased in duration. There is 
Hypertrophy of Left Ventricle. 
Note.-When there are signs of Hypertrophy of Left Ven- 
tricle without other cardiac signs to account for it, suspect 
Chronic Renal Disease. 
(fi.) The first sound is short, resembling the second sound. 
There is feebleness, dilatation or degeneration of left ventricle. 
Note.-Reduplication of heart-sounds occasionally occurs 
in health ; when associated with fever or with grave debility, 
indicates myocarditis or cardiac degeneration ; if reduplication 
of second sound, suspect mitral stenosis. 
Section II. Abnormal sounds are heard over the heart- 
region. 
A. Generally over the prsecordial area. 
(a.) Friction sound indicates Acute Pericarditis-or Pericar- 
dial roughening, the result of a remote pericarditis. 
B. Localized in definite relation with the situations of the 
valves. 
(a.) First-sound murmur over site of aortic valves (amemia 
excluded) indicates aortic obstruction. 
Note.-The murmur may be localized or propagated in the 
course of the great arteries. 
(6.) Second-sound murmur over site of aortic valves indi- 
cates aortic regurgitation. 
Note.-This murmur may be localized, or propagated 
downwards in the line of the sternum. 
(c.) Double (first and second sound) murmur (a and b) de- 
notes combined aortic obstruction and insufficiency. XII 
SCHEMA. 
(d.) First-sound murmur over site of valves of pulmonary- 
artery denotes (ana>mia and pressure upon trunk of pulmonary 
artery excluded) obstruction of pulmonary artery. 
Note.-Pulmonary obstruction is nearly always congenital. 
(e.) First-sound murmur at base of ensiform cartilage indi- 
cates tricuspid regurgitation. 
Note.-This is most commonly found as secondary result of 
mitral disease. 
(/.) Before first-sound murmur at base of ensiform cartilage 
denotes tricuspid stenosis. 
(g.) First-sound murmur heard over situation of right 
ventricle may be due to myocarditis or anaemia with cardiac 
debility. 
Note.-These murmurs are not persistent. 
(h.) First-sound murmur localized in mitral area denotes 
mitral regurgitation. 
(i.) Before-first-sound murmur localized at apex, or just 
internal thereto, denotes mitral stenosis-ix., obstruction. PAW 7R 
THE ORDINARY METHODS OF PHYSICAL 
DIAGNOSIS. 
LECTURE I. 
INTRODUCTORY. 
Symptomatology-Importance of subjective symptoms in 
regard to treatment: of objective in diagnosis - Pain - 
Angina pectoris - Cardiac symptoms - Disturbances of 
circulation-Pulmonary symptoms-Cerebral phenomena- 
Embolism-Gastric symptoms-Signs referred to the throat 
-Kenai symptoms-Etiology-Rheumatism-Other causes 
of heart disease. 
A few words on the threshold of the subject-advice 
pertinent to investigation of disease in any form, but 
yet I think rather particularly so to the class of diseases 
which we shall presently examine. When a suffering- 
patient comes to you for examination, do not permit a 
diversity of purpose of intent to exist between you 
mind and his. His chief object is to get relief from 
his aches and pains ; yours, perhaps, is to find out- 
by a process similar to that employed by botanists to 
discover the name of a newly found Hower-the name 
of the disease which he suffers from. Remember that 
your duty is not chiefiy to find out what disease he is 
the subject of, but what his bufferings are, what his 
deviations from sound health. The plane of unhealt 2 
INTRODUCTORY. 
is divided into definite squares, which are called 
Diseases, and the nomenclature of these is very im- 
portant, because the mention of one of them displays 
before the medical mind a large picture, and a moving 
panorama of phenomena ; but your sole object is not 
to find out into what particular square your patient's 
aggregate of symptoms will fit. You must investigate 
his ailments as well as his diseases if you would do 
him good. I am very far from wishing to be a censor, 
but I do think that in these days of great and increas- 
ing precision in physical diagnosis, there is a real 
danger of students thinking too lightly of the uttered 
complaints of patients. It has been said that one 
objective sign is worth a dozen subjective symptoms, 
and this, so far as regards diagnosis, has a large 
amount of truth ; but we must recollect that pertur- 
bations, which greatly distress our patient, may exist 
independently of his chief disease, and it is the patient, 
not the disease, that we have to treat. Let me instance 
a hypothetical case. A. B. comes to you, and, under 
fire of cross-examination discloses that he has had 
rheumatic fever some years ago. You examine his 
heart and find something wrong with the mitral valve. 
You dose him, probably help his heart over its pre- 
sumed difficulties with digitalis, and order the inevit- 
able belladonna plaster to be applied. But your 
patient at his next visit is not a whit better. It was 
not his heart which troubled him-that was neither 
better nor worse than it had been for many years 
past, and was likely to be for many years to come; 
but he suffered from a trigeminal neuralgia, and would 
have showered blessings upon you had you relieved 
him. 
The moral I would point, then, is this : Always INTRODUCTORY. 
3 
commence your interrogatory of a patient by asking 
what he complains of, what are his troubles and 
distresses, and if you record his case, write on the 
first line, complaint, and give his expressions, as nearly 
as possible, with the necessary abbreviations, in his 
own words. 
Now we come more closely to our subject. The 
comprehensive view of what disturbs the equanimity 
of a patient, with a view to the alleviation of his 
troubles is one thing, the particular determination of 
the physical significance of his ailments, and the pre- 
cise diagnosis of his diseases is another. For this latter 
purpose, the details of pains and aches, though all due 
weight must be given to them, are very deceptive. 
How very common it is for a patient to fancy that he 
has disease of the heart because he experiences dis- 
comfort or pain in the heart-region, and to insist on 
being " sounded," so that his doubts may be set at 
rest. How rarely do we find that he really has organic 
heart disease ? Oftentimes the patient goes away ap- 
parently with a look of disappointment that his fears 
are not confirmed, and with a doubt probably of our 
skill, because his aches are so precise. 
In looking over the notes of a hundred cases of the 
coarse and decided forms of disease of the heart which 
have been under my own immediate care, I find that 
in just half the number, there was no complaint what- 
ever of any pain referred to any part of the chest. 
Seventeen referred the pain generally to the front of 
the chest, fifteen to the back of the chest, and especi- 
ally between the scapulte. Twelve referred the pain 
to the epigastrium; eleven suffered pain on the left 
side of the chest; whilst two referred their sufferings 
to the right side. Those who localised their suffer- 4 
INTRODUCTORY. 
ings to the exact area of the heart were but eight; 
and of these, two complained of it only on exertion ; 
one referred it to the base of the heart; one described 
it as a sense of extreme soreness at the apex; and in 
one, it partook of the character of neuralgia of the left 
breast. So far as the evidence derived from the above 
cases-which are, I believe, fair specimens of those 
presenting themselves at the public or the private 
consulting room-teaches only eight per cent., or less 
than one in a dozen, complain of pain directly referred 
to the situation of the organ which is diseased. This, 
though strange to the non-medical mind, can scarcely 
be surprising when we consider that the heart pos- 
sesses very little common sensation, and that its 
structure can be punctured, torn, or lacerated, with- 
out the direct infliction of pain. When we consider 
the vast number of patients who present themselves 
with symptoms referred to the region of the heart, 
but really caused by dyspepsia or pleurodynia, and 
then take into account the very small proportion of 
real undoubted heart cases presenting signs of local 
pain, we must estimate at a very low figure the value, 
in a diagnostic point of view, of pain in relation to 
heart disease. 
Looking on diseases of the heart in general from 
the point of view of symptomatology, we find that 
their origin and progress are oftentimes very insidious 
and obscure. Even the most pronounced and 
dangerous forms of the disease may, in some cases, 
go through their stages without betraying themselves 
by marked symptoms of distress. This fact was 
strongly impressed upon my mind by a case which 
was under my care at the North-Eastern Hospital for 
Children. A little girl, who had been treated pre- INTRODUCTORY. 
5 
viously for a valvular affection, was brought to me 
because the mother thought she seemed a little languid, 
though the child complained of no distress. On ex- 
amination, I found that there was effusion into the 
pericardium. She was admitted, and went through 
all the stages of pericarditis with extreme distension of 
the pericardium, exhibiting one of the most pro- 
nounced instances of pericardial friction that I have 
ever heard and an accompanying endocardial change, 
and yet throughout her whole illness the child com- 
plained neither of pain nor distress, and it was impos- 
sible to keep her in bed. 
There is one form of pain in heart disease, however, 
which is of terrible significance-I mean Angina 
Pectoris. It has the character of a grip: it shoots 
down the left arm and occasionally involves both 
arms, or radiates to the back.* This is the pain, sui 
generis, of cardiac origin, and if you have once seen a 
pronounced example of it, you will never forget it. 
The patient suddenly sits up in his bed, and with a 
cry of horror indicates his sense of pain at the prae- 
cordium. It has great intensity, but is of a cold and 
* " The pain of angina is distinctly located in or about the 
midsternum, whence it radiates. Eulenberg says this is due 
to the connection between the superior cardiac nerve and 
the anterior branches of the four upper cervical nerves; 
while the middle and inferior cardiac nerves are connected 
with the four lower cervical nerves, uniting in the brachial 
plexus and first dorsal nerve. The pain usually runs out at 
the peripheral endings of the ulnar nerve, especially the little 
finger. It is almost invariably found on the left side only. In 
a case where it was on the right side, the pulmonary artery 
was the seat of disease."-"Path. Soc. Trans.," 1878. "The 
Diseases of the Heart," Dr. Milner Fothergill. Second edition, 
London, 1879, p. 285. 6 
INTRODUCTORY. 
sickening character ; the chest is fixed, the breathing 
not quickened, and your hand, placed over the epigas- 
trium, finds that the heart's action is slow and 
laboured. The face wears a look of horror, the hue 
is pale or slightly leaden, and a cold sweat breaks out 
upon the forehead. Worse than the pain is the feel- 
ing of fearful sinking and depression ; the poor patient 
gasps, " I shall die I" and, sometimes, as in a case 
which it was once my lot to witness, his short, but 
concentrated sufferings in a few minutes end in death. 
From such a typical case of high diagnostic and prog- 
nostic import, there are many gradations of intensity, 
until, in some cases, it is difficult to differentiate the 
symptoms from those of dyspepsia or hysteria. In some 
cases the pain is absent though the other symptoms 
are present; such is the " angina sine dolore" of 
Gairdner. The points to be remembered are:-(1) 
The attacks are paroxysmal with long or short inter- 
vals. (fJ) There is always a sense of coldness experi- 
enced, and frequently a cold sweat. (3) The heart's 
action is not increased, and (4) The chest is fixed, the 
breathing slow. 
Few questions in the domain of medicine have presented 
greater difficulties than that of the nature and pathological 
significance of angina pectoris. Latham said of it: " We are 
sure of what it is as an assemblage of symptoms. We are not 
sure of what it is as a disease." In the fatal cases, the lesions 
which have been discovered have been various, and in some 
no morbid appearances have been demonstrated at all. The 
most commonly discovered conditions have been (a) degenera- 
tion and calcification of the coronary arteries ; (/>) atheromatous 
disease of the aorta ; (c) disease of the aortic valves; (d) fatty 
degeneration of the muscle of the heart. The affection is 
rare, though by no means unexampled, be foremiddle age, and 
is much more common in the male than in the female sex. It 
has proved fatal even in a first attack; Dr. Arnold, of INTRODUCTORY. 
7 
Rugby, died within three hours of the onset of an attack of 
angina pectoris. In the case of a young man, aged twenty- 
three (recorded by Dr. John Wilson, Edinburgh Medical 
Journal, September, 1874), who died the day after he had 
manifested heart-pang, no disease was found at the post- 
mortem examination. The heart was flaccid, the cavities 
empty, and the valves all healthy. The young man had been 
in perfect health until a sudden exposure to cold led up to the 
fatal attack. It is obvious, therefore, that we must not look 
alone to the post-mortem table for a solution of the difficulties 
which beset the pathology of angina pectoris. Fortunately, 
clinical investigation has succeeded in a large measure in 
dissipating those difficulties. Dr. Lauder Brunton demon- 
strated, in 1866, by means of the sphygmograph, that the 
arterial tension during an attach of angina pectoris is increased. 
Dr. Brunton, knowing that the effect of nitrite of amyl 
was to relax the arterioles and thus to relieve the tension, 
administered this drug by inhalation during the paroxysm of 
angina, with complete success ; the symptoms were imme- 
diately alleviated. Dr. L. Brunton's observations have been 
conclusively confirmed. More recently, Dr. Murrell has intro- 
duced for the treatment of angina pectoris another agent, 
which, like amyl nitrite, has the power of relaxing the 
arterioles-nitro-glycerine. The use of this drug, which is 
administered by the stomach, is also attended by most obvious 
relief of the symptoms. It may, therefore, be taken as 
proved, I consider, that angina pectoris is essentially a con- 
dition in which the arterioles are contracted, and in which 
there is high pressure in the arterial system, and that when 
the arterioles are made to dilate, and the intra-vascular 
pressure is relieved, the symptoms abate. You should remem- 
ber that angina pectoris is by no means a common affection. 
Dr. Hayden, in his large experience, states that he has met 
with only six genuine examples ("Diseases of Heart and 
Aorta,'.' p. 1043). It follows, therefore, that you must be 
careful, in any case which appears to you to present the 
characteristic symptoms, to discriminate between true angina 
and the many forms of pain which are sometimes called false 
angina, and which may be neuralgia, intercostal rheumatism, 
the consequences of dyspepsia, &c. You will make the 
diagnosis by observing whether the symptoms correspond 8 
INTRODUCTORY. 
with those I have before described, and especially also by 
ascertaining, if you have an opportunity of witnessing the 
phenomena of an attack, whether the arterial tension during 
the paroxysm is increased. On this point you should obtain 
the evidence of the sphygmograph if possible. Having recog- 
nized your case as one of true angina, supposing that you have 
opportunities of further investigation, you will find it, in my 
opinion, most practically useful to place it under one of 
two categories. A, in which the arterial tension is not increased 
in the intervals of attacks. B, in which there is persistently 
high arterial tension. The cases (A) in which normal tension is 
moderate or low, constitute the minority, and for the most part 
comprise the exceptional cases occurring in the earlier periods 
of life. In such there is an acute supervention of high pres- 
sure, the arterioles become contracted (perhaps in obedience 
to a direct external cause, such as exposure), the left ventricle 
struggles against the difficulty so imposed, and becomes over- 
distended. As I have said, such acute angina may be fatal. 
On the other hand, the paroxysm being relieved, the patient 
may go an unlimited time without recurrence. In such cases 
there may be no antecedent cardiac disease ; it is not common 
to meet with angina in the valvular diseases consequent on 
rheumatic endocarditis. I have seen, however, a single 
severe attack in a lady aged thirty-one, who presented the 
marked signs of mitral regurgitation; in this case, how- 
ever, the sphygmograph demonstrated high tension, a 
condition quite different to that usually obtaining in such 
pronounced mitral regurgitation. In resume, therefore, in 
Class A, the angina attack is a neurosis, the essential of which 
is the acute supervention of a contraction of the arterioles, 
with rise of blood pressure throughout the arterial system, 
and distension of the left ventricle from accumulation of blood 
therein. In Class B, which includes the majority of cases of 
angina pectoris, the arterial tension is persistently high, though 
it is still higher during the paroxysms. In these there is a 
special cause for the recurrence of attacks; such cause is 
disease of the coats of the aorta (aortitis deformans) or disease 
of the systemic arteries (arteritis) and especially of the 
coronary arteries. In such cases you will find the arterial 
pulse hard and incompressible, and there will be signs of 
hypertrophy of the left ventricle, and probably valvular disease, INTRODUCTORY. 
9 
which is usually aortic. When from any cause the already 
high arterial tension is increased, and the left ventricle is 
overtaxed in its struggle to propel the blood, angina may 
ensue. Undue exertion or effort are frequent exciting causes 
of an attack. In some cases, however, paroxysms occur with- 
out obvious disposing causes, and in such it seems highly 
probable that there is a direct interference with the nervous 
mechanism. Lancereaux has described a case which mani- 
fested attacks of angina pectoris wherein, at the autopsy, 
there was found aortitis, with a direct involvement, by the 
disease of some of the fibrils of the aortic and cardiac plexuses 
(Cf. Lancereaux, "Anatomie Pathologique," Paris, 1871, p. 
257, and Gazette Medicale, 1867, p, 432). Seeing the common 
association of the cases of angina which fall under this section, 
with disease of the arterial coats, it seems very reasonable to 
link the nerve-phenomena with an affection of the sympathetic 
filaments which are in such close relation to the coats of the 
vessel. If we accept this view, the calcification of the coro- 
nary arteries-heretofore supposed to induce the symptoms 
through the degeneration of the heart muscle, which, by 
impairing the blood-supply, it occasions-is the cause of the 
pain rather by the direct implication of the cardiac plexus. 
It is quite true that cardiac degeneration follows coronary 
obstruction; but this is a cause, not of the pain, but rather of 
the fatal issue. In a case recorded by Romberg, it was proved 
that not only the cardiac nerves were involved, but also the 
vagus. In his attacks, the patient, a man aged thirty-six, 
after a prodroma of apprehension and terror, felt his heart 
stand still-there was an intermission of from five to 
six beats-at the same time he experienced violent pain on 
both sides of the chest, extending to the neck and head. 
Here was a complex form of angina, the peculiarity of which 
was a long arrest of the heart's action. At the post-mortem 
examination the great cardiac nerve was found very distinctly 
diseased, and the left vagus as well as the phrenic were 
involved in diseased glands. The vagus is the inhibitory 
nerve of the heart, and there could be no doubt that an irrita- 
tion of its inhibitory fibres produced the long intermissions of 
the heart's action witnessed in the case. The high tension 
observed in these cases is nor necessarily associated with 
hypertrophy of the left ventricle. In the case of Dr. Arnold, 10 
INTRODUCTORY. 
the walls of the left ventricle were much thinner and softer 
than natural. The great John Hunter died after attacks of 
angina pectoris, and the heart in his case was found to be very- 
small and its tissue pale. Dr. W. T. Gairdner says : " Post- 
mortem examinations have generally shown that the heart is 
found flaccid rather than rigidly contracted, and the lesions 
found in the muscular substance of the heart itself are usually 
such as would confirm the idea t>f decidedly and permanently 
weakened energy, rather than a disposition to abnormal con- 
traction." The high tension, then, is due to vascular rather 
than to cardiac causes ; the left ventricle labours against the 
obstacle imposed by the firm contraction of the arterioles. In 
the large class of cases of angina pectoris associated with 
atheromatous disease of the great arteries, I consider that a 
strict analogy is established with those cases of epilepsy which 
are found to depend on local irritation of the nerve centres. 
In the former, owing to irritation of the nerve fibrils involved 
in the wall of the diseased artery, there are periodic explosions 
expressed by the tight contraction of the arterioles and the 
consecutive heart-struggles, whilst in the latter the expression 
of the maximum of central irritation is an epileptic fit. In 
any case manifesting angina pectoris, I counsel you strongly 
to obtain, by means of the sphygmograph, evidence of the con- 
dition of the vessels. I may mention a case in point. I saw, 
in conjunction with my friend Dr. John Brunton, an old lady 
of sixty-nine, who suffered from severe pain, referred to the 
epigastrium and abdomen. This pain might very easily be 
referred to visceral congestion, but it was to a considerable 
extent paroxysmal, and there was a marked look of anxiety 
upon the face with tendency to cold perspiration. The 
heart sounds betrayed nothing abnormal, but a tracing of the 
radial gave very important evidence. Not only was there 
extremely high tension, but the trace bore strongly the 
characters of aortic obstruction (see tracing of Aortic Obstruc- 
tion in Part II.). I had no hesitation in concluding that the 
vessels were extensively diseased, and it seemed to me very 
probable that the great suffering referred to the epigastric and 
umbilical regions might be ascribed to disease of the coats of 
the abdominal aorta. Nitro-glycerine gave relief, and the 
subsequent history of the case confirmed the diagnosis. Dr. 
Brunton wrote me : " The old lady has gone on tolerably well INTRODUCTORY. 
11 
till two days ago, when failure of pulse came on, only one 
decent beat in ten, but over the heart the sounds were quite 
normal in strength, rhythm, and note. . . . You will find the 
case a most interesting witness of the power of the sphygmo- 
graph." It is very probable that some of the recognized forms 
of abdominal pain are but varieties of angina. Whilst 
ascribing, however, to direct disease of the arterial tissues the 
causation of a large proportion of those cases of angina which 
are accompanied by persistently high vascular tension, I do 
not mean to assert that in some instances the attack may not 
be initiated by visceral causes. Bergson has narrated a case 
of angina, in which there was enlargement of the liver, the 
attacks ceasing after treatment directed to the hepatic 
disease. (On this as well as many points of interest as regards 
angina pectoris, see Dr. Milner Fothergill, "The Heart and 
its Diseases." Second edition, chap. xi. London: Lewis.) 
You have seen, then, that a large number of heart 
cases occur without the manifestation of any pain- 
that the special pain of heart disease, though of great 
diagnostic importance, is of comparatively rare oc- 
currence. You may be led to inquire what are the 
other symptoms that lead up to the suspicion of heart 
disease ; and although we cannot enter at all deeply 
into symptomatology, we may endeavour to give a 
brief answer to the question. 
In this review of symptoms, in order to give a 
rough idea of the relative frequency, I shall place 
between brackets the number of instances in which 
each has been observed in the hundred cases which 
I have taken as typical. The first class of symp- 
toms (A), excluding pain which we have already 
considered, includes palpitation and disturbances of 
the muscular structure of the heart. Palpitation is 
far from being a pathognomonic sign of heart disease. 
Its first cause resides often in the nervous system. It 
is not by any means a sign of heightened functional 12 
INTRODUCTORY. 
activity, but is rather the " spurt" of overtaxed and 
wearied muscle. Though occurring very often in 
conditions in which the heart is not structurally 
diseased, palpitation is a frequent sign and source of 
trouble in organic heart affections (28). It is 
specially called forth on exertion, often of the 
slightest degree, and it occasions much distress; in 
some cases, especially where the aortic valves cannot 
close perfectly, the patients complain that the heart 
beats like a hammer. Another sign of imperfect 
action of the muscle of the heart is ' Intermission. 
After a number of pulsations at regular intervals, the 
heart waits over the whole period necessary for a con- 
traction, and then resumes, to wait again after 
another interval. Intermittency, like palpitation, 
may be no sign of structural heart disease ; it is in 
many cases due to an incoordination of nervous 
actions, and is to be ascribed, not to cardiac, but to 
cerebro-spinal causes. When it does occur, however, 
in ascertained organic disease, it is of serious import. 
It often means that the contraction of the auricles 
is at certain times so imperfect that they do not fill the 
ventricles. The necessary stimulus to the ventricular 
contraction is a sufficient repletion of the cavities. 
Hence the ventricles wait until the auricles supply 
them with enough blood. A third trouble of heart- 
muscle is Irregularity. This, also, is due to a want of 
action, in accord, of the layers of muscular fibre of 
which the heart consists. The heart does not wait 
for a whole beat as in intermission, but alters its 
rhythm irregularly. Sometimes the left and right 
sides do not contract, or do not complete their con- 
traction, at one and the same moment; then the 
action may be reduplicate. Sometimes there is so much INTRODUCTORY. 
13 
disturbance that the periods of action and rest cannot 
be discriminated; the beats are tumultuous. Irre- 
gularity may, like the other disturbances of heart- 
muscle, exist independently of organic disease ; but 
when it reaches a high degree, it is one of the 
strongest evidences of such disease. Patients some- 
times describe the irregular action as like the flutter- 
ing of birds. One complained to me of a fluttering 
in his heart " like two pigeons." Such signs are of 
dangerous import. 
The symptoms, however, may be referred, not to 
the heart itself, but to the next portion of the system 
of blood-distribution-to the arteries. Patients com- 
plain of (B) Pulsation. This, we shall see, is very pro- 
nounced in the general arterial system when the aortic 
valves are incompetent to clcfse. It was complained 
of in my patients as a symptom of distress (3) in the 
ear whilst lying on the pillow, in the right temple, in 
the occipital region. Pulsation is, of course, a cha- 
racteristic sign of aneurism, but this condition we do 
not intend to discuss. Another arterial symptom in 
connection with heart disease, but rare and of no 
considerable diagnostic importance, is Flushing. A 
very important consequence is (C) Haemorrhage (22). 
This may occur from the lungs (12), when it must be 
remembered that it has not the dangerous signifi- 
cance of the haemoptysis of pulmonary phthisis. Con- 
siderable quantities of pure blood can be expectorated 
with the result of relieving the venous engorgement 
of the lung which is the result of some forms o 
heart disease. Of worse omen, in my opinion, is the 
frequent voiding of blood-stained sputa ; this occurs 
usually when the right side of the heart is dilated, 
and is one of the late consequences of valvular disease. 14 
INTRODUCTORY. 
Bleeding1 from the nose (5) is far from uncommon in 
heart disease; haemorrhage may occur also from the 
stomach (3), or from the uterus (metrorrhagia) (2). 
In all these cases the haemorrhage may occur from the 
direct rupture of capillaries by the shock of an unduly 
contracting left ventricle, but much more commonly it 
occurs from superinduced venous congestion. Occa- 
sionally the haemorrhage is not manifest outwardly, 
but occurs in the interior of organs. 
Other signs are referable to plethora of the venous 
system. The veins may sometimes be seen to be 
obviously distended, and in some cases, as we shall 
describe, the large veins pulsate. Patients with certain 
malformations of the heart exhibit a blueness of sur- 
face (D), Cyanosis, from the distribution of venous 
blood by the arterial dhannels or from venous con- 
gestion. A like blueness obtains intermittingly, on 
account of venous congestion, in the paroxysms of 
dyspnoea from which patients with heart disease occa- 
sionally suffer. A consequence of habitual venous 
plethora may be (E) Dropsy, of which it is well known 
that cardiac disease is one of the' great inducing- causes. 
Next in order to the obvious disturbances of the 
heart itself and the channels of blood-distribution, we 
come to consider the symptoms of disturbance of the 
functions of the lunys in heart diseases. These symp- 
toms are far more frequent than those referred to the 
heart itself. Nearly half the cases (45) complain of 
difficulty of breathing. Some (8) are obliged to sit 
upright (orthopnoea) in order to breathe. A very 
large proportion of patients with heart disease suffer 
from cough (45). 
A great characteristic of the dyspnoea of heart 
disease is, that it is produced or aggravated by slight INTRODUCTORY. 
15 
exertion. The heart may fairly accommodate itself to 
conditions of rest, hut let exertion call upon it for 
increased action, and it manifests its distress hy the 
imperfect pulmonary circulation, and the consequent 
dyspnoea. Or the dyspnoea may be periodic, and not 
induced by voluntary effort. Such attacks are called 
cardiac asthma. The induced conditions may, how- 
ever, be not temporary, but chronic. Persistently 
defective heart's action induces persistently defective 
pulmonary circulation. The blood tends to stagnate 
in the lungs. Chronic bronchitis, and, subsequently, 
emphysema follow, and the trouble may be augmented 
by oedema of the lungs. 
Next we will proceed to notice the Cerebral troubles 
which occur in heart disease. These are very com- 
mon. The patients complain of languor and extreme 
weakness (25). Often the muscular weakness is re- 
ferred especially to the arms; the patients cannot lift 
weights as they have been accustomed, and the 
muscles feel powerless. They suffer attacks of 
giddiness (vertigo) (8), or are subject to faintings 
(syncope) (6). There may be an undefined nervous- 
ness (7), with dread of a fit or some calamity, and 
lowness of spirits. Headache (5) is sometimes met 
with, but is not one of the commonest symptoms. 
Trembling of muscles and the irregular jactitations of 
chorea (3) are very important to notice. There may 
be fits epileptiform (2), or epileptic (2), or various 
forms of paralysis may be found. Lastly, there may 
be impaired memory and intellectual disturbance of 
various kinds. In all cases of heart diseases which 
present cerebral symptoms, the fundus of the eye 
should be examined by the ophthalmoscope. 
The cerebral phenomena observed in heart disease 16 
INTRODUCTORY. 
may, for the most part, be divided into three classes. 
The first embraces those due to the chronic distur- 
bance of balance between the arterial and venous 
systems which is the result of imperfection of the 
driving power in the great engine of the circulation. 
The brain may suffer from deficient supply of arterial 
blood, or from excess of venous blood, or from these 
causes variously combined. Arising from these con- 
ditions there may be increase of the fluids effused 
within the intra-cranial cavities, and degenerations of 
brain tissue, owing to the impaired nutrition. 
The second class of cerebral phenomena occurring 
in heart disease includes those due to intra-cranial 
haemorrhage. You must remember that apoplexy is 
to be feared in cases of hypertrophy of the left ven- 
tricle of the heart, the strong muscular contraction 
distending the arterioles and capillaries to the point 
of rupture. It is much more to be feared, however, 
when there are heart hypertrophy and kidney disease 
combined. In such cases there is not only excess of 
driving power, but the arterioles have suffered 
change-they have become brittle and prone to rup- 
ture. Out of twenty-two cases of apoplexy, Kirkes 
found thirteen accompanied by hypertrophy of left 
ventricle, and fourteen accompanied by renal disease ; 
and Eulenberg, in six cases of apoplexy, found five 
with contracted kidney and heart hypertrophy. 
The third class includes the interesting phenomena 
now known to be due to the sudden blocking of a 
cerebral artery by a morsel of coagulum detached 
from a diseased portion of endocardium, and swept 
onwards in the blood current until it happens to be 
arrested in an arterial channel which it is too large to 
pass through. INTRODUCTORY. 
17 
The straightest course which such a plug* can pursue 
is from aorta to middle cerebral artery of the left or 
the right side, and the symptoms produced are hemi- 
plegia, with coma, or aphasia. Sometimes, however, 
the effects are more chronic, the plugging of the cere- 
bral vessel, and hence the cutting off of nutrient 
supply, inducing softening of that portion of the 
brain supplied by the vessel. 
Instead of a large plug of this sort, we have reason 
to believe that small ones which are arrested in the 
cerebral arterioles occasionally occur, and may ac- 
count for symptoms for which no cause has been dis- 
covered. Thus in chorea, which has a notable con- 
nection with disease of the heart, it has been suggested 
by Dr. Hughlings Jackson that there are embolisms 
of the arterioles of the corpus striatum and the 
adjoining convolutions. 
Emboli may be carried in the blood current to other 
parts than the brain; the spleen, liver, and kidney can 
be thus affected. Capillary embolism of the kidney 
is probably by no means uncommon. It is suggestive 
that in two or three cases I have noted, in which 
chorea occurred in rheumatic endocarditis, frecpient 
micturition was a symptom complained of. Or 
from the right cavities plugs may be detached and 
carried into the pulmonary artery, plugging some of 
its branches in the lung. From this result the 
appearances which used to be called "pulmonary 
apoplexy." 
We turn now to another set of symptoms in heart 
affections, those of the stomach. Pain referable thereto 
we have already noticed. A large proportion of 
patients with heart disease complain of some of the 
symptoms of indigestion-gastric catarrh is common ; 18 
INTRODUCTORY. 
nausea, vomiting, pyrosis, and flatulence are frequent, 
and occur in a circle, the heart trouble occasioning 
them, and the symptoms reacting to cause palpitation 
and heart distress. The other abdominal viscera also 
partake of the venous plethora induced in heart 
disease. Haemorrhoids are frequently met with. 
Another set of symptoms in diseases of the heart 
comprises those referred to the throat. This subject 
presents, in my opinion, a wide and very promising 
field for observation. Pain beginning at the throat 
is referred to by some as a very dangerous sign in 
these affections. There are many instance on record 
in which a patient has grasped at his throat, evincing 
signs of acute pain, and has shortly afterwards ex- 
pired. The sudden throat pains in heart disease are, 
I believe, for the most part, varieties of angina, and 
may be discriminated by the rules, I have given. 
Other forms of pain of less laryngeal character and 
of less intensity are, however, met with, and these are 
usually accompanied by flatulence and dyspepsia. The 
a rising in the throat," unaccompanied by pain, is 
usually either dyspeptic or hysteric. Next to the 
throat-angina, the symptoms of greatest interest and 
importance are loss of voice (1) and hoarseness (4), 
The case of aphonia which I have noted, occurred 
during the progress of pericarditis-to what was it 
due ? A case which suggests an answer to this ques- 
tion is given by Dr. Morell Mackenzie in his book on 
" Hoarseness and Loss of Voice." In this instance 
pericardial effusion was accompanied by aphonia due 
to paralysis of the abductors of the vocal cords. 
After the cessation of the pericarditis, the mobility of 
the affected laryngeal muscles returned. The patho- 
logical process whereby such paralysis is brought INTRODUCTORY. 
19 
about is yet undiscovered. We find that hoarseness 
occurs as a symptom of aortic aneurism, the disposing- 
cause in such case being- pressure of the aneurismal 
sac on the left recurrent nerve, inducing- paralysis of 
certain of the laryngeal muscles. I have not found, 
as far as my own experience goes, that hoarseness is 
prone to occur in aortic valvular diseases.* The car- 
diac conditions accompanying hoarseness I have 
found to be disease of the mitral valve, with which 
broncho-pneumonia, or some other form of pulmo- 
nary mischief, co-exists. Unilateral paralysis of the 
intrinsic muscles of the larynx is frequently met 
with in local disease of the pulmonary texture. 
Disease of the kidneys may stand as to disease of 
the heart in a threefold relation. The latter may be 
cause, consequence, or concomitant. The renal dis- 
ease may be (a) directly caused by the heart-imper- 
fection. The kidneys, like the other viscera, suffer 
venous engorgement, and, if this be long continued, 
a low form of inff animation, attended with increased 
formation of fibrous tissue, may occur in them. In 
the earlier stages such a state of things is indicated 
by albuminuria, in the latter by the detection of 
kidney tube-casts in the urine by the microscope. 
But (&) the heart disease may be primarily caused by 
the renal disease. When, owing- to structural disease, 
the kidneys are unable to excrete from the blood the 
urinary solids, the natural consequence is the reten- 
tion in the circulation of effete material. It is sup- 
posed that this material perfunctorily retained, so 
irritates the arterioles, or the vaso-motor centre 
which governs them, as to cause them to contract. 
Such contraction (it seems to me that the term 
" spasm," which has been used in respect of this 20 
INTRODUCTORY. 
effect, is misapplied) being long kept up, the result is 
the same as occurs in overtaxed muscle-tissue gene- 
rally-viz., hypertrophy ; so there is induced a peri- 
pheral obstacle to the onward current of blood in the 
arteries. The heart struggles against such an ob- 
stacle, and its efforts produce hypertrophy of the left 
ventricle. Thus, hypertrophy of the left ventricle 
may even be induced subsequently to renal disease 
in children. Or it may be (c) that the heart disease 
and the kidney disease are both effects of one cause. 
The form of kidney disease which usually accom- 
panies cardiac hypertrophy is what is called " con- 
tracted kidney ; " this is for the most part associated 
with some gouty affection. We know that in gouty 
disease the blood is impure, and it is supposed that 
such condition gives rise to a disease of arteries and 
capillaries generally throughout the system leading 
to thickening of their walls, but not necessarily nor 
wholly of the muscular part thereof. The heart 
hypertrophies because it struggles against the ob- 
stacle, not of arterioles actively contracting, but of 
arterioles which have undergone degeneration, 
whereby their walls have become thickened and in- 
elastic. The capillary circulation is thus rendered 
slower, and the heart muscle becomes stronger to 
overcome the impediment so produced. The kidney 
is diseased because its vessels are involved in the 
general disease. The rules you can deduce from a 
consideration of the whole subject are : 1. In cases 
of cardiac disease carefully examine the condition of 
the urine. 2. When you find renal and cardiac 
disease co-existing, weigh carefully the facts of the 
previous history, and endeavour to find out which 
pathological condition preceded the other. INTRODUCTORY. 
21 
I turn now to another branch of the subject. I 
have said that the symptomatology of heart disease is 
often obscure. We find that its etiology is often 
obscure likewise. 
There are two errors, in my opinion, into which 
many are prone to fall. The first is that valvular 
disease of the heart is rarely found except as a conse- 
quence of rheumatic fever; the second that there is 
danger of heart-complications in the severer forms of 
rheumatism only. Let us turn to the records of 
actual cases. Taking seventy-seven of the hundred 
cases before cited, in which the early histories are 
sufficiently precise, I find that thirty-four occurred 
in those who had suffered one or more attacks of 
undoubted rheumatic fever ; but in thirteen there 
had been rheumatic pains only, not sufficient to keep 
the patients to their homes; and in fifteen there was 
no history of any rheumatic affection whatever, and 
only, if any symptoms at all, those of a lightly- 
regarded indigestion. Rheumatic gout had been 
suffered by two patients, scarlet fever by three, and 
typhoid, or " low " fever, by four. Typhoid fever is 
not attended by valvular disease, but by such an 
enfeeblement of the muscular walls that dilatation 
may ensue. In six cases the evidence pointed to the 
conclusion that the disease was congenital. You will 
conclude, therefore, that, though it is (1) pre- 
eminently necessary that you should carefully ex- 
amine the condition of the heart in any patient 
who is suffering from, or who has suffered from 
rheumatic fever, it is important to do so also in (2) 
those who have been subject to slight forms of 
rheumatic pain, and that (3) there is a large 
remnant requiring careful exploration whose diseases 22 
are not to be traced to any obviously rheumatic 
condition. 
Excluding, then, those I have mentioned, what are 
we to look for as the most common causes inducing 
heart disease ? I will briefly enumerate some of 
them : Over-exertion and muscular strain-alcoholic 
indulgence-syphilis-tuberculosis-the puer pe ral 
state-poisoning by phosphorus-lead poisoning- 
imperfect and improper nutrition-disease which 
involves the structures contiguous to the heart and 
pericardium-disease which induces venous engorge- 
ment of the lung, whence distension, dilatation, and 
hypertrophy of the right side of the heart. 
You may, from a general consideration of this in- 
troductory chapter, obtain in some degree an answer 
to the question which you will probably propound:- 
Under what circumstances of symptoms and previous 
history is it necessary for me to make a physical ex- 
amination of the heart-region ? There is one aphorism 
which I would impress on you, however, which covers 
the whole ground. It is this, that you have never made 
a complete examination of any patient, whatever be his ail- 
ment, unless you have estimated, as jar as possible, the con- 
dition of his heart. 
We shall now consider the mode of doing this. We 
pursue the investigation through our senses of sight, 
touch, and hearing. We do not grope for one sign 
which, when found, shall be conclusive to us; but 
after we have obtained all the evidence presented to 
our senses, our logical faculty must discriminate and 
lead us to the truth. We work by no single method, 
but by a combination of methods and modes of thought. 
INTRODUCTORY. 23 
LECTURE II. 
INSPECTION. 
Cyanosis temporary and permanent-Pathological causation- 
Chilling of finger-tips - Clubbing - Anaemia - Graves' 
Disease-Sub-icterus-Arcus senilis-Cardiac dyspnoea- 
Orthopnoea - Decubitus in pericarditis - Cheyne-Stokes' 
dyspnoea-(Edema-Venous turgescence-Venous pulsation 
-Visible arterial pulsation-Locomotive pulse-Apex-beat 
-Area of visible cardiac impulse. 
You may take it as an aphorism that you can never 
make a satisfactory examination in suspected heart 
disease, unless your patient be stripped to the waist. 
Very valuable evidence is afforded by inspection. 
The first point you will probably note is the general 
hue of the surface. 
We will suppose that there is (A) a marked blue- 
ness of the surface. You will elicit whether this is 
temporary, sometimes passing away altogether, or 
permanent, varying perhaps in intensity, but never 
quite disappearing. The temporary blueness will be 
associated, probably, with attacks of cardiac asthma, 
of which dyspnoea is the great feature. The perma- 
nent blueness may also depend on the same cause as 
the temporary-viz., undue fulness of the venous 
system. In such case you will find respiratory 
trouble-bronchitis or emphysema or both accom- 
panying it-and it affords strong presumptive 24 
INSPECTION 
evidence of dilatation of the right cavities of the 
heart. 
There is a form of blueness dependent on malfor- 
mation of the heart so special that it constitutes the 
chief sign of, and gives a name to, the affection. Such 
is blue disease, morbus caeruleus, or Cyanosis. Here 
you find a deep discoloration, in some cases approach- 
ing a black, involving all the surface, but especially 
manifest in the lips and the mucous membrane of the 
mouth. The colour is persistent, but is deepened 
when breathing and the heart's action are quickened, 
or when cough comes on. You will scarcely find any 
difficulty in recognising this condition-the hue is so 
characteristic; it is more pronounced and more 
general than that which obtains in ordinary venous 
congestion. Moreover, you will elicit perhaps that 
the affection dated from birth. If so, the evidence is 
nearly conclusive, but, if not, the diagnosis is by no 
means set aside, for the discoloration may not be 
obvious until periods remote from birth. Most pro- 
bably, however, your patient will be an infant or 
young child. Nearly half the cases of this affection 
die before they are a year old ; two-thirds before they 
are two years old ; and though a few instances are 
recorded in which adult life has been attained, they 
are very rare. 
We may now inquire, what is the pathological sig- 
nification of the phenomenon ? As a matter of fact, 
in a case of cyanosis the chances are rather more than 
ten to one that there is an abnormal communication 
between the right and left cavities of the heart, either 
between the auricles, owing to patency of the foramen 
ovale or between the ventricles, owing to imperfection 
of the inter-ventricular septum. Furthermore, the INSPECTION. 
25 
chances are about six to one that the pulmonary artery 
is obstructed. The cause of the blueness, according- to 
John Hunter, was the admixture of venous and arte- 
rial blood in the circulation. This explanation seemed 
simple enough. Owing to the structural defect in the 
heart, the dark-coloured venous blood mixed with the 
arterial, and the resulting darkened compound was 
propelled through the systemic arteries. This theory 
has been opposed in modern days, but it appears to me 
that its opponents try to prove too much. At any rate 
they hold that the explanation given above is not the 
true one of the cyanosis. According to them, cyanosis 
is due to congestion of the venous system, and this 
congestion is the resultofobstruction of the pulmonary 
artery, or of some other malformation which induces 
an obstacle to the return of blood from the systemic 
veins. Premising that, in my opinion, the truth lies 
between these two theories, we will examine each of 
them. 
The theory that the blueness results from direct 
mixture of venous with arterial blood, at first sight 
appears very plausible. Out of one hundred and 
ninety-five cases recorded by Stille and Peacock, one 
hundred and seventy-eight presented abnormal com- 
munication between the right and left sides of the 
heart; admixture of venous and arterial blood there- 
fore is possible and likely, and often inevitable. The 
hue of the patients is just that of those in whom venous 
blood is circulating : you see it in cases of impending 
suffocation; you may have many opportunities of 
witnessing it during the administration of nitrous oxide 
gas, when the blood is rendered of the venous colour 
by the excess of carbonic acid which it cannot get rid 
of. What are, then, the objections to the theory ? 26 
INSPECTION. 
The first objection is afforded by the anatomical excep- 
tions. Seventeen of the cases recorded presented no 
possibility of the arterial and venous currents abnor- 
mally commingling. This is sufficient to prove that 
the cyanotic tint cannot be always due to the arterio- 
venous anomaly. The second objection is that we can 
have communication between right and left heart with- 
out the appearance of cyanosis. This does not seem 
to me a fatal objection. The question is one of degree ; 
the tint of the arterial blood may mask that of the 
intermixed venous blood, or vice versa. Nay, more, a 
patient having this anomaly may present the peculiar 
coloration at one time and not at another. You may 
understand this by observing the differences in hue of 
a woman in health and in a state of anaemia and 
chlorosis. Let the blood corpuscles be numerous and 
healthy, and they would mask the coloration due to 
venous admixture, but let them be by any cause 
diminished in number or in colour, and the dark tint 
would declare itself. 
Now let us turn to the other theory-that the color- 
ation is alone due to venous congestion. The anato- 
mical argument weighing with those who uphold this 
theory is, that obstruction of the pulmonary artery is 
an important and frequently-observed condition in 
cyanosis even when there is communication between 
right and left heart. But by their own data it is 
shown that this sign is less constant than the arterio- 
venous communication, the chances of the first condi- 
tion being about six to one, the chances of the second 
more than ten to one. Moreover, it is an ascertained 
fact that there may be great obstruction of the pul- 
monary artery without cyanosis. A case under my 
care at the North-Eastern Hospital for Children INSPECTION. 
27 
showed this most positively. A little girl, aged eight 
years and a half, presented signs of extreme anaemia; 
there was no blueness, but great pallor ; all over the 
heart region was heard an extremely loud murmur 
with the first sound; it was loudest at the base of the 
heart. At the autopsy we found that there was 
obstruction by narrowing of the pulmonary artery. 
This was the only morbid condition to account for 
the murmur. It is evident, then, that there can be 
great obstruction of the pulmonary artery without 
cyanosis. It is, however, undoubtedly true that 
in some cases of blue disease, there has been found no 
communication between right and left heart, but only 
an obstruction upon the venous side which has given 
rise to a general congestion of the veins of the 
system. 
From these considerations I think we are justified 
in arriving at these conclusions-first, that in a large 
number of instances of congenital cyanosis there is 
abnormal communication between right and left 
heart, and it is scarcely reasonable to doubt that the 
circulation of venous blood with the arterial tends to 
produce the peculiar blue coloration; secondly, that 
in some cases the blueness is produced only by undue 
fulness of the superficial veins; We know that such 
blueness can be thus produced, because we see it 
during attacks of dyspnoea, which spring' from many 
causes, and we are familiar with it when severe cold 
affects the surface of the body. In this latter condi- 
tion the cold causes contraction of the arterioles, and 
the blood is retained in the capillaries and venous 
radicles. 
Having recognised your case as one of congenital 
cyanosis, you are by no means to stop here, but to 28 
INSPECTION. 
examine by all the methods which will be detailed 
hereafter, in order to determine, as far as possible, 
whether there be any cardiac malformation, and if so, 
what is its nature. For cyanosis may occur from 
causes which affect not the heart, but the lungs. 
Any cause which considerably impedes access of air 
to the lungs or seriously diminishes the extent of 
breathing surface, may induce cyanosis. You must, 
therefore, in these cases, carefully investigate the 
pulmonary as well as the cardiac conditions. 
There is one point in cases of venous obstruction 
from any cause which may be classed under minutiae, 
but which is of considerable diagnostic importance- 
the condition of the finger-ends. Notice if the 
finger-nails are blue in colour. If they are per- 
sistently blue, you may conclude that there is per- 
sistent fulness of the venous system. If they are 
occasionally blue, you will find the blueness coinci- 
dent with attacks of dyspnoea. Notice also the 
temperature of the finger-ends so far as it is manifest 
to touch. Coldness means great defect of circulating 
power. Blueness and coldness together constitute a 
measure of the danger of attacks of cardiac asthma, 
and when these signs are persistent in cardiac disease, 
they show that the end is not far off. Notice next 
the shape of the finger-ends. When the return of 
blood from the veins to the right heart is obstructed 
to a considerable degree and for a protracted period, 
the finger-ends become thickened at their extremity, 
or clubbed. Dr. Dobell considers that when there is 
symmetrical clubbing of the finger-ends, and the 
nails are of the normal shape, the chances are in 
favour of heart disease; when the clubbing is 
attended with curvature of the nails over the ball INSPECTION. 
29 
formed by the finger-tips, the chances are in favour 
of phthisis. The reason, probably, is that in the one 
case the adipose tissue exists in its normal quantity, 
and in the latter case it has wasted, just as in phthisis 
all the adipose structures waste. 
We will now turn to another branch, and suppose 
that our patient does not present blueness but (B) 
pallor. The skin, the mucous membrane of the lips, 
the gums, and the conjunctival surface of the eyelids 
are pale ; the sclerotic portion of the eyeball is of a 
pearly white. The patient, you say, is bloodless- 
anaemic. Anaemia may simulate heart disease, may 
be produced by heart disease, may aggravate heart 
disease. The method of differential diagnosis between 
the heart disturbances induced by anaemia and by 
organic heart disease respectively, we shall hereafter 
consider, but there are two conditions of anaemia 
which we may with advantage notice here. 
The first is the condition of pallor associated with 
renal disease. We have seen in our introductory 
lecture that there is an especial relation subsisting 
between cardiac and renal disease. It is most im- 
portant to discover such co-existence. If, in addition 
to pallor, you notice a " puffing " beneath the eyelids, 
or other signs of oedema about the face, you may 
suspect renal complication, and prepare (1) to ex- 
amine the urine, (2) to use the ophthalmoscope. You 
will determine the specific gravity of the urine, ascer- 
tain whether it is albuminous and examine its sedi- 
ment by the microscope. You will examine the 
fundus of the eye to ascertain whether certain changes 
which are known to co-exist with albuminuria are 
present. The red field of the fundus oculi presents 
in albuminuric retinitis irregular, or star-shaped 30 
INSPECTION. 
black and white patches, often glistening and pre- 
senting a metallic lustre, with, sometimes, dots of 
apoplectic extravasation. 
The next condition usually, if not always, asso- 
ciated with anaemia, which we shall consider, is known 
as Graves' or Basedow's disease. This peculiar 
affection, by a strange displacement of an adjective, 
has been called exophthalmic goitre. It is charac- 
terized by a triple sign; (1) prominence of the eye- 
balls ; (2) enlargement of the thyroid body; (3) 
irritable action of the heart. The affection is met 
with much more commonly in women, and between 
the ages of twenty and forty. The prominence of 
the eyeballs (exophthalmos or proptosis) is readily 
distinguished. The globe seems to be pushed for- 
ward in varying degrees from what seems merely an 
unusual size of the eyeball to a most unnatural pro- 
trusion-to such an extent that the eyelids cannot 
cover the globe, and the cornea becomes dimmed by 
inflammatory changes. The thyroid enlargement 
varies much in degree. In the cases I have seen, it 
has not been symmetrical; of three cases the en- 
largement was chiefly of the right lobe in two. The 
swelling is elastic to the touch, and pulsation of the 
arteries is readily felt. Care must be taken to dis- 
tinguish it from aneurism. Dr. Stokes has mentioned 
a case in which such a mistaken diagnosis was made, 
and a day actually fixed for the performance of the 
operation of deligation of the carotid artery. The 
beating of the heart is visible over a wide area ; 
the action is very rapid, excited by the least emo- 
tional provocation, and often exceeding 120 per 
minute. This affection does not rank as a heart 
disease, but it may lead to hypertrophy and dila- INSPECTION. 
31 
tation. It is really an affection of the sympathetic 
nerve. 
This strange disorder may be induced by causes operating 
on the nervous system. Trousseau has recorded a case in 
which its three symptoms were developed in a single night from 
excessive mental emotion. Milner Fothergill also has men- 
tioned an instance of its sudden occurrence after emotional 
shock. Dr. Lauder Brunton considers that the palpitation 
characteristic of the disease is due to direct stimulation of the 
accelerator cardiac nerves which proceed from the vaso-motor 
centre in the medulla oblongata, accompany the vertebral 
artery, and, after passing through the inferior cervical ganglion 
of the sympathetic, are supplied to the heart. Irritation of the 
inferior cervical ganglion would account for the cardiac excite- 
ment. The thyroid signs are explained by paralysis of the 
vaso-motor nerves of the thyroid, which are derived from the 
same ganglion. Such paralysis causes dilatation of the small 
arteries at the back of the eyeball; so the globe is pushed 
forwards, the degree of prominence varying with the amount 
of dilatation of the vessels. In some fatal cases, implication of 
the sympathetic nerve has been proved to demonstration. In 
one instance its ganglia in the neck were found atrophied 
almost to extinction. In another case, the middle and inferior 
cervical ganglia were enlarged, hardened, and infiltrated with 
granular matter, the sympathetic nerve itself being involved 
in the morbid change. (See "Diseases of the Heart," by Dr. 
Hayden, p. 1061.) More recently Dr. Shingleton Smith, of 
Bristol has described a very important case (Medical Times and 
Gazette, 1878), in which there was entire destruction, by disease, 
of the inferior cervical ganglion on the left side of the neck. 
The ganglion had become completely atrophied, " its place 
being occupied by an inert mass of calcareous matter and 
fibrous tissue." 
We will now suppose that our patient presents 
neither blueness nor pallor, but (C) a yellowish tinge of 
the surface. Deep jaundice is not frequent in heart 
disease, but a slightly icteric hue of the face, with a 
more deeply-tinged conjunctiva where it covers the 
sclerotic, is not uncommon in the later stages of 32 
INSPECTION. 
valvular disease when passive congestion of the liver 
is one of the troubles. When you find your patient 
past the prime of life, the victim perhaps of alco- 
holism, with a generally dusky yellowness of the 
skin, but without jaundice, the surface of the body 
somewhat greasy to the touch, the muscles felt to be 
flabby and found to be weak, patches of dilated capil- 
laries upon the face, and venous turgidity of the 
conjunctiva-when, moreover, you notice that breath- 
lessness or faintness is produced on exertion-you 
may fear fatty degeneration of the heart. For the 
diagnosis of this affection one sign has been ad- 
duced especially, and has perhaps sometimes been too 
strongly relied upon-the presence of an arcus senilis 
in the cornea. This requires careful scrutiny, for 
there are arcus and arcus. Near the junction of 
cornea and sclerotic, where the former should be clear 
and transparent, you may see a circle, a semicircle, or 
a crescent of opaque whiteness. If this be well 
defined, and the rest of the cornea bright and trans- 
lucent, it is, probably, no indication of serious in- 
ternal degenerative change. The corneal opacity is 
probably due to fibrous proliferation or calcareous 
infiltration. But if the ring be ill-defined, rather 
yellowish than white, the rest of the cornea being 
slightly cloudy, you may consider that the chances 
of cardiac degeneration are formidable. 
Having learnt the lessons to be deduced from the 
complexion and hue of our patient, we will next con- 
sider the points to be gained from observing his mode 
of breathing and the postures which he assumes. In 
this section we will consider first cardiac dyspnoea. 
As I have said in the introductory lecture, this symp- 
tom is especially provoked by exertion. Thus it differs INSPECTION. 
33 
from dyspnoea of pulmonary origin. You may find 
your patient breathe easily enough if he has been 
still for a short time previously to your examination, 
but if you call upon him to walk briskly for a few 
minutes, or especially if he ascend a few stairs, 
breathlessness comes on. This dyspnoea is peculiar- 
there is no real obstruction either to inspiration or 
expiration, but the patient gasps restlessly, there is 
an instinctive craving for more air to oxygenate the 
sluggish blood in the lung; there is air-hunger as the 
Germans expressively term it. Such is the dyspnoea 
of the earlier stages of valvular imperfection ; but in 
the later stages the symptoms may be far more dis- 
tressing. The sign which especially distinguishes 
the dyspnoea of the later stages of cardiac disease is 
orthopnoea-the patient cannot lie down; perhaps 
can scarcely recline from the perfectly upright posi- 
tion : the whole mental energies seem bent upon the 
one task of getting air into the chest. For a descrip- 
tion of the most extreme condition of cardiac dyspnoea, 
I will quote the graphic words of Hope. The 
patient, "incapable of lying down, is seen for weeks, 
and even for months together, either reclining in the 
semi-erect posture supported by pillows, or sitting 
with the trunk bent forwards and the elbows or fore- 
arms resting on the drawn-up knees. The latter 
position he assumes when attacked by a paroxysm of 
dyspnoea; sometimes, however, extending the arms 
against the bed on either side to afford a firmer 
fulcrum for the muscles of respiration. With eyes 
widely expanding and starting, eyebrows raised, nos- 
trils dilated, a ghastly and haggard countenance, and 
the head thrown back at every inspiration, he casts 
around a hurried distracted look of horror, of anouish. 
7 0 7 34 
INSPECTION. 
and of supplication; now imploring in plaintive 
moans or quick, broken accents and half-stifled voice, 
the assistance already often lavished in vain; now 
upbraiding the impotency of medicine, and now, in 
an agony of despair, drooping his head on his chest, 
and muttering a fervent invocation for death to put a 
period to his sufferings." When the conditions of 
cardiac dyspnoea have long continued, you may find 
a new condition established, more merciful, but of 
even more fatal augury - carbonic acid poisoning. 
The blood is deteriorated by the carbonic acid, of 
which the respiratory effort is powerless to disem- 
barrass it. The patient is in a constant state of drowsi- 
ness, with difficulty aroused, but waking in distress 
every now and then when the instinctive craving for 
more air asserts itself. In the end coma supervenes. 
Such are the modes of comportment in chronic 
diseases of the heart wherein dyspnoea is a feature. 
In some cases of acute pericarditis you observe no re- 
spiratory trouble. Your patient usually lies upon 
his back, sometimes desiring that his head and 
shoulders should be raised; if he turns, he prefers to 
lie upon his right side, because when on his left side 
there is not only more direct pressure upon the peri- 
cardium, but the liver tends by its weight in this 
position to press upon the heart. It is usual in peri- 
carditis for a patient to be very unwilling to change 
his position; syncope may be easily induced by rough 
movements, and it is to be remembered that such 
syncope may be fatal. The expression of counte- 
nance in pericarditis is often that of anxiety and appre- 
hension, and wandering of the mind is common. 
Dyspnoea, such, as we have described in relation with 
chronic heart disease, may occur in pericarditis, but 35 
you must not look for it as a common symptom. It 
occurs when the fluid effused into the pericardial sac 
mechanically obstructs the action of the heart, or in 
cases where a less amount of effusion weakens an 
already weak heart. 
The " reason why" of all the forms of cardiac 
dyspnoea is not very easy to trace. In some cases 
the desire for the upright position is probably due to 
the relief from the pressure that the diaphragm, im- 
pelled by the abdominal viscera, occasions upon the 
right ventricle which such position induces. In 
others, where there is fluid in the pericardium, this 
relief is enhanced by the gravitation of this fluid to 
the most dependent parts of the pericardial sac, and 
thus the easing of the heart-muscle from pressure. 
A characteristic form of rhythmical dyspnoea is occasionally, 
though rarely, observed. In such cases there are alternating 
periods of arrest, and of excitement of respiration. In the 
former period the thorax is absolutely motionless, and the 
patient appears almost as if dead. Then a faint wave of inspi- 
ration is noticed, followed by other respiratory efforts shallow 
and slow. The succeeding respirations become gradually 
deeper and quicker, until the chest is agitated with severe 
dyspnoea ; then, arrived at its maximum, the paroxysm abates, 
the retrocession being as gradual as the onset, and at the end 
there is a period during which breathing is in complete arrest. 
This form of dyspnoea has been called after those v'ho first 
observed and described it Cheyne-Stokes1 respiration. 
Dr. Stokes termed it "respiration of ascending and descend- 
ing rhythm." The periods during which respiration is sus- 
pended usually last from a quarter of a minute to half-a- 
minute, whilst the periods of rise and fall of respiration are 
of about the same (or rather longer) duration. In some cases 
arrest has been for only ten seconds, and respiration for 
seventy-five. The greatest duration of periods which I have 
found recorded is in a Memoir by Prof. Sacchi (" Riv. Clin, di 
Bologna," Feb. 1877, pp. 33-47). Here the respiratory arrest 
INSPECTION. 36 
INSPECTION. 
and the dyspnoea each lasted for two minutes. When this 
peculiar symptom was first observed, it was supposed to 
directly indicate a condition of disease of the he irt, especially' 
fatty degeneration; further observation showed, however, 
that such disease was by no means necessary for its produc- 
tion. Then it was thought to be causally' associated with 
dilatation and loss of elasticity in the aorta. Now that atten- 
tion has been more fully called to the symptom, how'ever, a 
numerous array of cases shows that this association also can- 
not be upheld. The symptom has been observed in cases which 
at first sight seem very diverse, but which can, I think, be 
conveniently divided into three categories. 1. Cases attended 
with cerebral lesions-viz., cerebral hemorrhage, tumours, 
urtemia, shock from surgical injury, alcoholism, acute renal 
disease, tubercular meningitis. 2. Cases attended with lesions 
of heart and great vessels-viz., fatty degeneration, pericar 
ditis, atheromatous disease of aorta, aortic aneurism, valvular 
disease (double aortic with mitral insufficiency, mitral stenosis 
dilated aorta co-existing, aortic regurgitation and obstruction), 
sclerosis of coronary arteries. 3. Cases of certain acute 
febrile diseases-viz., diphtheria (Hiitterbrenner), typhoid 
fever (Wharry). A large majority of the cases occur in the 
male sex ; for the most part the age is over fifty, when dege- 
nerative diseases are common, the exceptions being in the 
acute diseases which I have noted. The sign is one of extreme 
danger ; the cases, with very few exceptions, have been fatal. 
The question as to the causation of this peculiar rhythmical 
dyspnoea is a very difficult one. -The most plausible theory' 
was first propounded by Traube. He considered that the 
conditions giving rest to the symptom have one feature in 
common-they impair the due arterialization of the blood 
supply to the nerve centres. You w'ill realize that this would 
be the effect either of the direct impairment of the heait- 
muscle, or more indirectly of the cerebral lesions. As regards 
the latter, it is to be noted that the symptom seems to be 
allied with causes that induce compression in the neighbour- 
hood of the medulla oblongata (Cf. Guttmann " Handbook of 
Physical Diagnosis," Sydenham Society's Translation, p. 55). 
According to Traube's theory, then, the inadequate arteriali- 
zation of the blood lowers the irritability of the cerebral centre 
which presides over the respiratory movements. In physiological INSPECTION. 
37 
conditions this centre is called into activity by the accumu- 
lation of carbonic acid in the blood; when, owing to condi- 
tions of disease, the irritability of the centre is materially 
lessened, it follows that a much greater than normal accumu- 
lation of carbonic-acid is necessary to rouse it to action. In 
a case, therefore, which manifests Cheyne-Stokes' respiration, 
the first thing which occurs is the establishment of a condition 
of impaired irritability of the respiratory centre (this by 
Traube's theory through mal-oxygenation); the long respi- 
ratory arrest gives time for the accumulation of carbonic-acid 
in excess in the blood; arrived at a certain maximum, this 
begins to stimulate, slowly and imperfectly at first, and after- 
wards in increasing degrees, the centre, so that it develops 
the respiratory efforts till they culminate in dyspnoea. Then, 
as the centre ceases to be stimulated, or becomes exhausted, 
dyspnoea again supervenes. To this theory Filehne has 
instituted objections, but these rather go to modify 
and amplify than to destroy it. He would ascribe the 
phenomena to impaired coordination between the respiratory 
and the vaso-motor centres, the former must be less excitable 
than the latter. His theory is thus expressed by Gutt- 
mann At the end of the respiratory pause there is a large 
disappearance of oxygen from the blood, carbonic acid has 
accumulated, the vaso-motor centre is thereby stimulated, and 
the arteries (the cerebral arteries amongst the rest) at once con- 
tract; this produces a gradually-increasing anaemia of the respi- 
ratory centre, and inspiration becomes more and more deep; this, 
however, supplies the wonted oxygen to the blood, the arterial 
spasm is relieved, the anaemia of the respiratory centre passes' 
off, and with it the exaggerated impulse to respiration, and 
breathing once more becomes superficial. When the arterial 
spasm has entirely subsided, so that the respiratory centre is 
abundantly provided with decarbonized blood, the stage of 
apncea, the pause, is reached, and lasts till, by the abstrac- 
tion of oxygen from the blood, the irritation of the vaso- 
motor nervous centre is renewed, and the whole series of 
operations again gone through. That the arteries are strongly 
contracted is proved by the increase of the arterial tension and 
of the blood pressure, while the amende condition of the brain 
is demonstrated by the fact that in young children, at the end 
of each respiratory pause, immediately before the recommence- 38 
INSPECTION. 
ment of respiration, and also while inspiration is gaining in 
depth, the great fontanelle is depressed. And, further, this 
form of dyspnoea may invariably be arrested at the very com- 
mencement of each seizure by the inhalation of nitrite of amyl, 
which dilates the vessels (loc. cit., p. 56). The occurrence 
under my care of a typical case has given me close opportunities 
of studying the phenomena which wre are discussing. In my 
case the symptoms developed simultaneously with an attack 
of right hemiplegia and aphasia. The attack wras proved to be 
due to disease of many branches of the cerebral arteries, espe- 
cially the middle cerebral of the left side, and there was much 
disorganization of brain-tissue, the morbid changes approach- 
ing close to the medulla oblongata. The heart and aorta were 
perfectly healthy. In the first case recorded (by Dr. Cheyne) 
there was, in like manner, right hemiplegia and aphasia. Dr. 
Broadbent has recorded a case in which there were the same 
paralytic lesions due to cerebral haemorrhage. Mr. Frederick 
Treves has described a case in which the phenomenon super- 
vened on the shock of an injury-comminuted fracture of the 
leg, amputation : iu this instance, also, there was no cardiac 
lesion. It can scarcely be doubted, that at least in certain cases 
the symptoms can be developed by cerebral and not cardiac 
causes. The theory, therefore, which ascribes its cause to an 
induced ana?mia of, or a defective circulation in, the respiratory 
nerve-centre, necessarily fails. In my case, the sphygmograph 
showed that both volume and tension in the arteries were good 
and above the noimal (see Part II.). There is, however, but 
little difficulty in concluding that in these cases the respiratory 
nerve centre is directly influenced-that it suffers a paralytic 
lesion, and so its irritability is impaired. This could be 
accomplished by the contiguity of disease or by shock. The 
acute diseases-typhoid fever and diphtheria-in which the 
phenomenon has been noted, are both occasionally attended 
with cerebral implication and paralysis-in such cases where 
the symptom supervenes, it may not unreasonably be ascribed 
to a paresis of the respiratory centre. Still, it may be doubted 
whether, in some cases, the symptom may not be initiated by 
disease of the heartmuscle itself. A review' of the recorded 
cases seems to afford no positive evidence that it can be so 
initiated, for those in which degeneration of heart has been 
described have been almost invariably associated with disease INSPECTION. 
39 
of the great vessels. Dr. Bradbury has recorded a case asso- 
ciated with fatty degeneration of the heart, but here the 
occurrence of syncopal convulsions showed the implication of 
he central nervous system. It is evident that the phenomenon 
is by no means to be interpreted as a sign of fatty degeneration 
of the heart; and it is even improbable that such affection of 
the heart, apart from cerebral complications, can in any case 
induce the symptom. It may be questioned whether the 
rhythmic dyspnoea can be induced by reflex causes. Its occur- 
rence in aortic disease (certainly its most frequent association), 
as well as in aortic aneurism, would render this probable. It 
is possible, however, that the aortic diseases is not causal: it 
may but be the indication of arterial disease elsewhere, and the 
vera causa of the phenomenon may be found in disease of the 
walls of the cerebral arterioles. As a practical point, in any 
case which manifests Cheyne-Stokes' respiration, you will bear 
in mind the probability of disease of the vascular walls, or of 
cerebral affection. I consider that the initial lesion is paresis 
of the respiratory centre, and though this paresis may be pro- 
duced by reflex nerve influence, it is usually a direct exhaus- 
tion from cerebral causes. Once initiated, the explanation of 
the phenomena on the theory of Traube is complete. In my 
case the interesting fact was established that not only the 
respiratory, but the cardiac centre was interfered with. The 
sphygmograph gave a remarkable tracing, showing a rhyth- 
mical irregularity in volume, an ample cardiac revolution being 
always succeeded by one of about half its amplitude. It has 
frequently been urged that in Cheyne-Stokes' respiration the 
pulse is uninfluenced, but it is obvious that in the absence of 
sphygmographic evidence the observation is of little value. 
In my case the peculiarity was not detected by the finger. 
Having observed the general hue, posture, and 
mode of breathing-, you will notice whether there are 
dropsical swellings of the surface of the body, pitting 
with the pressure of the finger, or whether there is 
evidence of fluid in the abdomen. Particularly in- 
quire in what situation the oedema first manifested 
itself. It is an almost invariable rule that the dropsy, 
which depends upon cardiac disease, commences at 40 
the feet and gradually extends over the the lower ex- 
tremities. Thus it is distinguished from dropsy 
dependent upon renal disease, which commences in 
the face. Let me urge you, however, to receive the 
evidence of patients, when interrogated as to the 
locality in which the swelling first appeared, with 
considerable caution. The swelling of the face may 
have been transient, and even entirely overlooked. 
I must reiterate the rule which I have given you 
before-always examine the urine for albumen. If 
you find albumen present, you must still proceed 
with your examination of the heart, for a cardiac 
complication may exist with the renal disease. If 
you do not find it, you must hesitate before coming 
to the conclusion that the dropsy is cardiac, for it 
may be due simply to debility and anaemia. When 
the patient presents the concurrence of dyspnoea on 
exertion with a swelling of the feet which pits upon 
pressure, there is a strong presumption of cardiac 
disease. Cardiac dropsy proceeds upwards from the 
more depending parts, involving, after the legs and 
thighs, the scrotum and the general areolar tissue of 
the body (anasarca). The serous cavities, the peri- 
toneal or the pleural, are usually the last to be af- 
fected. In renal dropsy the face is generally pallid ; 
in cardiac it is dusky, and the surface of the skin 
is often marked by ecchymosed patches. In this 
latter condition slight wounds may become serious 
sores, and the sores sometimes gangrenous. The 
most common cause of dropsy in heart disease is 
imperfection of the valves. Of such, the most cer- 
tain and most direct is disease of the valve of the 
right side of the heart-the tricuspid. This disease, 
however, is comparatively rare; the most common 
INSPECTION. INSPECTION. 
41 
valvular imperfection which gives rise to dropsy is 
disease of the mitral valve. Aortic lesions, however, 
sometimes induce the complication. It may also 
occur in fatty degeneration of the heart when there 
is no valvular imperfection. 
We now turn from the more general to the more 
particular points of observation. Of these, first 
notice the condition of the veins, especially of those 
at the root of the neck-the internal jugular and the 
external jugular. Notice if the veins are distended. 
We have already noticed venous turgescence in the 
consideration of Cyanosis, and have seen that it is a 
sign of distension of the right side of the heart. You 
observe this fulness of veins in conditions of asphyxia 
-you can produce it temporarily by holding your 
breath-you observe it in those who play forcibly 
upon wind instruments, or in patients during the 
efforts of paroxysmal couo-h. In these cases there 
are stasis of blood in the lung, accumulations in the 
venous channels, and retention in the right cardiac 
chambers. In a chronic form you may see the same 
thing in patients affected with emphysema of the lung ; 
in these the rmht chambers, being in. a lasting state 
of distension, become dilated. Turgescence of the 
superficial veins may be due, however, to valvular 
lesion of the right side-to disease of the tricuspid 
or the pulmonary valves. In cases of venous dis- 
tension you may often note that the positions of the 
valves within the vessel are marked by a slight ring 
or knot; sometimes the veins of the neck may be 
seen to be varicose. Closely observe the veins to 
ascertain whether they pulsate. The phenomena of 
venous pulsation, though not very common, are of great 
interest and importance. A very slight pulsation at 42 
INSPECTION. 
the root of the neck may be no more than natural: a 
slight wave of pulsation in a more distended jugular, 
synchronous with the systole of the heart, is a sign that 
the right auricle is distended, and that the contracting 
ventricle communicates to it its impulse. Be careful 
to note that the pulsation which appears to be in the 
vein is really so. The impulse may be conveyed by 
the artery beneath. To determine this, place your 
finger on the vein and press the blood upwards for a 
short distance so as to empty a portion of the vessel; 
retain your finger thus for a short period ; then, if 
there is distinct venous pulsation, you will see the 
vein fill from below by jets synchronous with the 
beats of the heart. In the case of arterial pulsation 
beneath the vein, the latter does not fill by jets, and 
you readily feel the strong pulsation of the artery. 
In some cases you may observe that the pulsation is 
double, at first slight, being followed by a second 
stronger impulse. This is caused by the contraction 
of a hypertrophied auricle communicated backwards 
upon the column of blood in the vein, the closely 
succeeding pulsation being due to the reflux current 
impelled through the imperfectly-closed orifice by the 
right ventricle. Venous pulse is more common and 
more marked on the right side, the communication 
through the innominate vein with the vena cava beinsr 
in a more direct line than obtains in the case of the 
great veins of the left side. If you satisfy yourself 
that there exists venous pulsation, the observation is 
of high diagnostic import-it means that the tricuspid 
valve is faulty, and permits regurgitation into the 
right auricle. 
But, perhaps, you perceive not venous, but visible 
arterial pulsation. You notice, we will suppose, that INSPECTION. 
43 
the carotids pulsate forcibly. There may be a vibra- 
tion ovei- the sternal notch due to the pulse in the aorta. 
If you look at the situation of the brachial artery in 
the upper arm, along- the inner border of the biceps 
muscle, you will notice a jerking- movement of the 
vessel at each impulse of the heart. On causing- your 
patient to ilex the arm, the movement of the artery is 
rendered still more pronounced. The vessel is seen to 
curve outwards from the centre line of the arm with 
the contraction of the heart, and then quickly return 
to its first position. Such is the locomotive pulse de- 
scribed, in association with the lesion which causes it, 
by Sir D. Corrig-an, and often called Corrigan's pulse. 
This phenomenon is of g-reat importance, for it is sig- 
nificant of one of the most grave of valvular lesions; 
incompetency of the semilunar valves of the aorta per- 
mitting reflux of blood into the left ventricle. The 
ventricle, which in these cases is hypertrophied, con- 
tracts with an exalted force and drives the jet of blood 
into the arteries with a sharp and sudden stroke, but, 
immediately on the subsequent dilatation of the ven- 
tricle, the arterial current flows back, leaking through 
the imperfect valve, and the arteries become abnor- 
mally empty. The natural result of the forcible filling 
of the partially emptied tube is the jerking pulse. 
I ou may observe visible pulsation of arteries in cases 
of aneurism of hypertrophy of the left ventricle, and 
especially when the vessels are tortuous and hardened 
from atheroma, but this peculiar jerking pulse is 
characteristic of aortic regurgitation.* 
We will now narrow our area of observation to 
the neighbourhood of the heart itself. First notice 
* Vide subsequent Lecture on " Palpation." 44 
whether the beating of the heart causes vibration at 
any part of the chest-wall or not. The heart-impulse 
may not be visible for many causes-a thick layer of 
subcutaneous fat in your patient, an encroachment 
over the normal situation of the heart by a portion of 
emphysematous lung, any cause which displaces the 
heart from the thoracic parietes, or an enfeebled con- 
dition of the heart itself. The absence of apex-beat 
is only of value when taken with other signs, but it is 
to be noted. Suppose that the beating is visible in 
one of the intercostal spaces, it is advisable not only 
to take a mental note of its position, but to mark it 
upon the cuticular surface with a soft pencil, a 
spot of ink, or tincture of iodine, or, if you wish a more 
permanent record, the stain of a moistened point of 
nitrate of silver. 
The apex, under normal conditions, beats between 
the fifth and sixth ribs. To determine the spot at which 
it ought to be evident, you can make one or two obser- 
vations. (1) Draw a vertical line rather more than an 
inch internally to the nipple. Where this line inter- 
sects, the fifth intercostal space is the spot where the 
apex, in the average of healthy hearts, is evident. The 
nipple can be taken as a fixed point in cases of men; 
but not so in cases of women. Then (2) draw your 
vertical line* two inches from the left edge of the 
sternum ; where this intersects, the fifth intercostal 
space is the spot required. Slight variations from this 
point may be, however, not abnormal. In adult life 
the apex may approach within a quarter of an inch of 
the nipple-line, or may recede to two inches nearer 
the sternum. 1 think you may take it that in adults, 
an apex-beat, which is either in the nipple-line or 
outside it, is abnormal. In the case of children, I 
INSPECTION. INSPECTION. 
45 
am accustomed to draw my vertical line midway 
between the left edge of the sternum, and a line 
dropped from the anterior border of the axilla, an apex 
beat outside this line indicates an abnormality. Any 
deviation, however, from the transverse line of the 
fifth intercostal space is irregular or abnormal. 
Many causes may produce displacement of the apex 
from its normal position, but such displacement is not 
usually discoverable by mere inspection. We shall, 
therefore, briefly consider most of these causes here- 
after. The displacement chiefly obvious to inspection 
is where the apex heats helow and externally to the normal 
position. This indicates hypertrophy or dilatation, or 
both combined, of the left ventricle. In hypertrophy 
the beating may be observed as far as the eighth in- 
tercostal space, or even lower, and it is distinct, strong, 
and defined. In dilatation it does not usually reach 
quite so low, and is more diffused and more obvious 
in the lateral direction. In hypertrophy of the right 
side of the heart there is sometimes marked visible 
pulsation in the space between the 'situation of the 
normal apex and the ensiform cartilage. Note par- 
ticularly the area over which the visible pulsation is 
manifest. Usually it is simply a tap in the fifth inter- 
space. In hypertrophy this area is enormously in- 
creased, especially in children, before 'the ribs have 
fully ossified and the cartilages have become firm. I 
have observed the vibration in an extreme case of 
cardiac hypertrophy to extend outwards as far as a 
line depending from the anterior border of the axilla 
downwards, to half way between ensiform cartilage 
and umbilicus, and to the right to a considerable dis- 
tance beyond the right border of the sternum. In 
young people hypertrophy of the heart gives rise to a 46 
INSPECTION. 
distinct prominence of the superincumbent thoracic 
wall. In cases of considerable dilatation and hyper- 
trophy, the movement of the chest-wall caused by the 
cardiac contractions may be seen to be undulatory. 
It is obvious that the motions of the muscles which 
contribute to form the heart are not synchronous. 
Pulsations may be seen over the situation of a dilated 
auricle right or left. We shall learn in the next lec- 
ture that enlarged and hypertrophied auricles can give 
rise to pulsations which differ in point of time from 
the ventricular contractions. This is one cause of the 
apparent undulation. Adhesions of the pericardium 
may increase the irregularity of the movement. 
The area of visible impulse may, however, be con- 
siderably increased, although there be no hyper- 
trophy ; in nervous palpitation, in some cases of 
anaemia, in Graves' disease or in chorea, pulsation 
may be observed over a space the size of the palm of 
the hand. You will note, however, that in such 
cases, the apex-beat is not displaced from its normal 
position, nor is the chest-wall bulged outwards. 
You will notice particularly whether the praecordial 
region is rendered unduly prominent. The bony 
chest may be made thus prominent by rickets. You 
will recognize this condition by the fact that other 
portions of the thorax present nodosities, bulgings, or 
irregularities. Carefully observe whether there is 
any spinal curvature, for this, by causing depression 
of the thorax posteriorly, may induce bulging in 
front. If you are satisfied that there is distinct 
prominence of the heart region you will notice 
whether there is pulsation over the area-if so, you 
have obtained another evidence of hypertrophy. If, 
however, pulsation is feeble or absent, and the inter- INSPECTION. 
47 
costal spaces are rendered convex, the presumption is 
strong- that there is effusion into the pericardium. If 
the intercostal spaces are retracted so as to be ren- 
dered concave when the heart contracts, there is a 
probability that pericarditis has at one time existed, 
and has resulted in adhesions of the pericardium. In 
some cases this retraction with the cardiac systole is 
manifest in the epigastrium to the left of the ensiform 
cartilag-e. This is due to the attachment of the base 
of the pericardium to the central tendon of the 
diaphragm. 
We may now recapitulate briefly the evidence 
which we have obtained by inspection in relation to 
its diagnostic value. We have obtained evidence 
which indicates the highest point of probability in 
cases of (1) cardiac malformation, producing cyanosis, 
(2) Graves' disease, (3) distension of the right cavi- 
ties, (4) incompetency of the auriculo-ventricular 
valve of the right side (tricuspid), (5) incompetency 
of the semilunar valves of the aorta, (6) hypertrophy 
of the heart, (7) dilatation of the chambers of the 
heart. We have gained a considerable amount of in- 
formation leading to the diagnosis of (8) acute 
pericarditis in cases when effusion has taken place in 
sufficient amount to obviously distend the pericardium, 
and of (9) a past pericarditis when pericardial adhe- 
sions have taken place in any considerable degree. 
We have obtained valuable evidence, though in less 
degree, of (10) conjunction of renal with cardiac 
disease, (11) fatty degeneration of the heart, and (12) 
valvular lesions where they have given rise to 
symptoms of dyspnoea. 
We next propose to exercise the sense of touch to 
form or confirm our diagnosis. 48 
LECTURE III. 
PALPATION. 
The pulse-radial compared with cardiac-Rhythm-Effect 
of effort - Position of apex-beat - Displacement-Topo- 
graphy of heart-Mechanism of auricles and ventricles- 
Chronometry of cardiac pulsations-Presystolic, epigastric, 
and hepatic pulsation-Pericardial friction-fremitus-Thrill. 
We have now to cause our perceptions to enter by 
the tips of the fingers; we gain our knowledge 
through the sense of touch. 
We will first examine the pulse. It is better to do 
so now that the chest, neck, and upper extremities 
are exposed, in order that we may consider the radial 
beats in relation with any obvious pulsations in 
arteries elsewhere. 
(a.) Notice whether there be peculiarity in the 
radial artery. It may be rigid, unyielding, present- 
ing irregular hard plates, as it were, embedded in 
its wall. This indicates atheroma, a degeneration or 
calcification of the coats of the vessel. Your patient, 
in this case, will be past the prime of life, for the 
condition is essentially senile. The pulse will be felt 
to be hard and strong, the left ventricle having be- 
come hypertrophied, and contracting forcibly to 
overcome the obstruction created by the inelastic 
arteries. The changes of the radial are indicative of 
like changes in many other arteries of the body. 
You may probably observe the temporal artery PALPATION. 
49 
tortuous to the eye, and rigid to the feel, its pulsations 
visible. Frequently there is a semblance of strength 
in the pulse without reality, the shock being- created 
by a feeble wave of blood in a rigid tube ; in such 
case you will find that the impulse at the apex of the 
heart is feeble ; this indicates that the atheromatous 
condition of the arteries is associated with fatty de- 
generation of the heart. 
(b.) Observe in the next place whether there is a 
difference in volume and force between the pulsations 
of the two radials. If so, examine the brachials ; if 
these are equal, the difference is merely one of ir- 
regular distribution. If there is a decided difference 
in the pulses of the upper extremities, there is a 
probability of aneurism of one of the great vessels. 
(c.) Eliminating the above conditions, we now 
examine the pulse in relation to rapidity, regularity, 
strength, and volume. 
(1.) Notable slowness of the pulse is generally due 
rather to neurosal than to cardiac causes; it may 
occur, however, in a heart extremely weak from fatty 
degeneration. It may also accompany atheroma of 
the aorta, probably from mechanical irritation of the 
branches of the vagus. The pulse has been noted as 
low as 20-30, and even 8-9 per minute. 
(2.) Rapidity of pulse is much more common. It 
may be found associated with pyrexial conditions in 
the early stage of pericarditis, before effusion to any 
amount has taken place in the sac. Very frequently, 
however, abnormal quickness of pulse is not noticed 
at any stage of pericarditis. Of very far greater 
significance, is a point noticed by Dr. Walshe- 
sudden variation of the rate of the pulse. In a case of 
pericarditis, a very slight movement of the body may 50 
PALPATION. 
increase the pulse from 80-90 to 120-140. Unusual 
quickness of the pulse occurs in many emotional 
conditions, and you must not rely upon it, except in 
connexion with other signs. In lesions of the mitral 
valve the pulse is usually quicker than in those of the 
aortic. 
(3.) Force of the pulse.-This is a point of great 
moment. The apparent force of the pulse is notably 
increased in two conditions-hypertrophy of the heart 
and regurgitation through the aortic valves. It is 
diminished in degeneration of the muscular fibre of the 
heart, in dilatation of the cavities, and in most of the 
valvular affections. 
In hypertrophy we find the pulse strong, full, and 
incompressible. As you feel the radial pulse with 
one hand, place the other upon the thorax over the 
heart-region, and you will find a strong, hfeaving, 
prolonged cardiac impulse as an accompaniment. 
There is an expression of power, both about pulse 
and apex-beat, which is quite wanting in simply 
functional excitement of the heart. In the latter 
case the stroke is not sustained, but abrupt and 
brief. 
The other cause of exalted force of pulse, aortic 
regurgitation, has already been indicated to us by 
signs which we have considered under " Inspection." 
The pulse is first jerking, then collapsing; the artery 
strikes the finger with a sudden blow. 
Suppose now that, on the other hand, you find the 
pulse small and feeble, it is a good rule to elevate the 
patient's arm vertically above his head, and observe the 
characters of the pulse in this position. This will enable 
you to eliminate doubtful cases of aortic regurgitation 
in which the pulse has become temporarily feeble; PALPATION. 
51 
in the aortic regurgitant lesion the pulse will become 
intensified instead of enfeebled, its hammer-like cha- 
racter exalted, and the patient may complain of dis- 
comfort. In most of the other valvular lesions, aortic 
obstructive disease excepted, in which no influence 
probably will be detected, the pulse is enfeebled by 
the vertical position of the arm. In some cases of 
mitral disease, and in conditions wherein the heart- 
muscle is feeble, the radial pulse in this position 
may be quite extinguished. The same occurs,' how- 
ever, equally in antemia. The pulse being per- 
ceptible, notice whether the vertical position in- 
duces irregularity, especially irregularity of volume. 
If so, there is a probability of disease of the mitral 
valve. 
You snould now, while still keeping the finger 
upon the radial pulse, examine with your other hand 
the situation of the heart's impulse. It is very im- 
portant if you note that, though the heart's con- 
traction is strong, the pulse at the wrist is small and 
weak. This suggests imperfection of the mitral 
valve, inducing either regurgitation or obstruction. 
In mitral regurgitation the current of blood which 
should, by the contraction of the ventricle, be forced 
into the aorta, and thence to the systemic arteries, is, 
by the leak in the mitral valve, in part diverted to 
the left auricle. The pulse, therefore, is not pro- 
portionate to the strength of the heart's contraction, 
but is enfeebled in ratio to the amount of blood lost to 
the arteries by regurgitation. In mitral obstruction, 
the pulse is weak because the blood reaches the left 
ventricle with difficulty, and the latter contracts on 
an insufficient amount. It is not often possible by 
mere observation of the pulse to differentiate between 52 
PALPATION. 
obstructive and regurgitant lesions at the mitral 
orifice. The irregularity so often attributed to the 
pulse of mitral regurgitation I consider to indicate 
engorgement or dilatation of the right chambers 
of the heart. For arguments see Part II. In 
many cases of mitral regurgitation the pulse appears 
to be quite normal. This indicates either that only a 
small quantity of blood is lost to the systemic arteries 
by such regurgitation, or else that the left ventricle 
has become hypertrophi'ed sufficiently, and contracts 
with adequate force, to compensate for the obstruc- 
tion caused by the reflux into the auricle. If you 
notice the pulse to be persistently weak, the contrac- 
tions of the heart feeble, and yet by examination you 
find no evidence of valvular disease, there is a strong 
probability that the heart-muscle is enfeebled by 
degeneration. 
If you find that the pulse is feeble, although the 
hand, placed over the praecordium, detects tolerably 
strong pulsation, and yet evidence of valvular disease 
is absent, then it is very probable that the hyper- 
trophy of the heart causing the strength of systole is 
in the right ventricle, and not in the left. 
In all cases in which there is a morbid condition of the 
right chambers of the heart, the radial pulse tends to be weak. 
The supply to the left ventricle is from the lungs; if, from 
any defect in the right heart, the lungs are ill supplied with 
blood, the left ventricle is also insufficiently supplied, and 
thus the systemic arteries are imperfectly filled. 
Occasionally you may find that the hand on the 
prtecordial region is sensible of a contraction, which 
does not make itself evident by a pulse at the wrist- 
there is an ineffectual systole. The ventricular con- 
traction is at such times too feeble to produce a sen- 53 
sible pulse in the remote arteries. It may be found, 
however, that, though lost in the radial, the pulsation 
can be detected in the larger arteries nearer the heart, 
such as the carotids. This is but a less significant 
expression of the conditions we are about to consider 
-viz., irregularity and intermittency. 
(4.) Rhythm of the pulse.-Carefully distinguish 
between irregularity of volume and irregularity in time. 
In the former case the pulse is felt to occur at equal 
intervals, but is fuller at one beat than at another. 
You are sensible that varying volumes of blood are 
transmitted by the various contractions of the ven- 
tricle. This condition is rendered more evident by 
elevation of the arm, and the observation may give 
you an important aid to diagnosis. It is almost 
pathognomonic of mitral regurgitation with yielding 
of the right chambers. 
We will suppose that the pulsations are irregular 
in time. Irregularity and intermittency are condi- 
tions which differ only in degree, so we will here con- 
sider them together. In intermittency, the pause 
between the pulses is longer, there being an interval 
equal to that occupied by a pulsation. The first 
thing I have to urge upon you is to be very careful 
in giving this phenomenon its due weight in a dia- 
gnostic sense, and nomore. I am afraid that mischief 
has been done many times by a hasty opinion to the 
effect that a patient has heart-mischief, when this 
sign has been too exclusively relied on. Remember 
that irregularity or intermittency of heart's action, 
and consequently of pulse, may coincide with organic 
integrity of heart, and even with good health. The 
first question I would ask you to propound to your- 
selves is :-Does this irregularity co-exist with a fair 
PALPATION. 54 
strength of impulse, as felt over the praecordium or 
otherwise ? 
Intermittency maybe merely a constitutional pecu- 
liarity. It may be due, as Dr. B. W. Richardson has 
shown, to causes operating upon the general nervous 
system. It may be superinduced by strong emotions, 
by terror, anxiety, grief, pain, fatigue ; it may occur 
in organic diseases of the brain. It may be tem- 
porarily caused by attacks of indigestion. In the 
absence, therefore, of a notable feebleness of heart- 
beat, and excluding other diagnostic signs, you are 
not to conclude from mere intermission of heart and 
pulse that organic cardiac disease exists. 
If, however, notable feebleness of impulse co-exists 
with irregularity, and especially ineffectual systole, it 
is of serious diagnostic import. It is the sign, the 
very early sign it may be, of a strike on the part of 
the left ventricle. Too languid to contract from the 
ordinary stimulus of the blood with which the 
auricle by its single contraction supplies it, it waits 
until a second, or even a third, contraction of the 
auricle has supplied it with more. This is the condi- 
tion which obtains in mitral regurgitation and in 
dilatation of the ventricle. It is pathognomonic of 
dilatation of the left ventricle, and indicates that the 
muscular fibres have become degenerated, and have 
lost their tonicity. Most commonly it is associated 
with mitral regurgitation, which is the frequent in- 
ducing' cause of such dilatation. When you observe 
in a case of mitral disease that the heart's action 
assumes this character, note it as a sign of prognostic 
import. In the absence of signs of valvular disease, 
the observation is of importance, both from a dia- 
gnostic and a prognostic point of view. When you 
PALPATION. PALPATION. 
55 
find it in conjunction with senile changes-with 
feeble but diffused impulse, with atheromatous vessels, 
" arcus senilis " of cornea, &c., you may know that 
a heart at one time hypertrophied has become de- 
generated, that it will never recover its power, and 
that the patient trembles on the verge of life. 
A further question I would ask you to propound 
to yourselves when you notice in any patient irregu- 
larity or intermittency of heart's action is :-What is 
the effect of effort upon this heart ? 
An irregularity which is merely neurosal is scarcely 
affected by effort; the ptdse is quickened of course, 
but its irregularity is often diminished .rather than 
increased. When the irregularity is due to cardiac 
imperfection, however, very slight effort, such as 
making your patient walk briskly for a minute or 
two up and down the room, notably increases such 
irregularity. When there is dilatation, palpitation 
usually precedes the more pronounced irregularity; 
but when degeneration has proceeded far, the halting 
action takes place without notable quickening. 
Notice also whether effort on the part of your 
patient causes distress, and what is the form of such 
distress. Little or no discomfort occurs in neurosal 
irregularity. In dilatation you find palpitation and 
dyspnoea; in degeneration, faintness and dyspnoea; 
in certain rare cases the ventricular halt is accom- 
panied.by horrible sensations, and a fear of impending 
death. Such was noticed by Romberg- in a case in 
which a tumoui- involved the vagus nerve. 
W e turn from the consideration of the pulse* to that 
of the cardiac area itself. 
* For further particulars as to the signs afforded by the 
pulse, see Part II. 56 
PALPATION. 
We have noted in our inspection of the chest 
where the impulse of the apex of the heart should be 
manifest. We proceed to confirm or enlarge our 
observation by placing the hand over this region. 
Suppose that 
(a.) The apex-heat is feeble or indistinguishable. Be- 
fore recording this as a positive observation, let your 
patient sit up and lean well forward; an apex-beat 
may then become evident which was before unde- 
tected. If notable feebleness of the beat be associated 
with weakness of the pulse and the signs we have 
before recorded as pertaining to the affection, you 
have gone yery far towards the diagnosis of fatty de- 
generation of the heart In rare instances, such 
feebleness may be found to be due to pericardial 
effusion ; in such case the postural change just noted 
will serve you in good stead as an additional means of 
diagnosis, for the tilting forwards of the body may 
render evident the apex pulsation in a situation above 
the normal, probably in the fourth intercostal space, 
the fluid in the pericardium having tilted the apex 
upwards to this level. Palpation, is of high im- 
portance in thediagnosis of pericarditis with effusion. 
In the earlier stages of the affection you may find 
excited, diffused, and, sometimes, tumultuous action 
of the heart with the general signs of pyrexia; as 
effusion takes place the apex-beat is enfeebled and 
carried upwards and to the left of its normal posi- 
tion ; then, if distension be extreme, the beat is no 
longer to be felt. You must, however, draw no hasty 
conclusion from the observation that the apex-beat is 
feeble or imperceptible to the touch. It may be thus 
because the heart is overlapped by emphysematous 
lung, or on account of a thick layer of subcutaneous 57 
fat in your patient, or, even in health, in persons with 
deep chests. You may readily understand that in 
women with full breasts the apex-beat may not be 
perceptible to the touch. It is a fundamental rule, 
however, that you should always observe in cardiac 
diagnosis-to fix the exact spot of the apex-heat. If in- 
spection and palpation fail to do this, you will 
proceed to determine it by auscultation, as we shall 
hereafter consider. 
We will now suppose that you have been able to 
feel the apex-beat, and have compared its position with 
that which it should normally occupy, as we have 
determined in the Lecture on Inspection. You will 
find that 
(J.) The apex-heat is displaced from its normal position. 
Such displacement may take place from disease of the 
neighbouring textures and organs. Pleuritic effusion 
in the left cavity of the thorax may push the heart 
completely to the right side, so that the impulse which 
is wanting on the left side is felt right of the sternum ; 
effusion in the right thoracic cavity, on the other hand, 
may push the apex left of its normal position. Em- 
physema of the lung pushes the heart downwards and 
towards the epigastrium, and oftentimes in this disease 
you find an impulse below the ensiform cartilage ; 
you must examine further, however, before concluding- 
that this is the apex-beat, for in emphysema the right 
side of the heart is usually enlarged, and the impulse 
which you feel is caused by the contraction of the 
right ventricle, the tip of the left ventricle being out- 
side the point of obvious pulsation. Another disease 
of the lung which may give rise to a singular displace- 
ment of the apex-beat is fibroid phthisis; in such 
condition, w-hen it affects the left lung, you may find 
PALPATION. 58 
PALPATION. 
the chest-wall drawn inwards and the heart so dis- 
placed that its apex beats at or above the fourth rib. 
Tumours, aneurism, or cancer occupying the thoracic 
cavity may also cause displacement of the heart: 
enlargement of the left lobe of the liver, cysts, abdomi- 
nal tumours, and dropsy, may produce a like residt. 
We have already said that pericardial effusion tilts the 
apex upwards. All these causes must be eliminated 
by careful examination. 
In the rare cases of transposition of the viscera, the apex of 
the heart is found to beat under the right, instead of under the 
left, nipple. The liver dulness then occurs on the left, and not 
on the right, side, whilst the stomach is to be recognized on the 
right. 
We come now to causes of displacement intrinsic to 
the heart itself. 
When the heart-apex is found to beat below and to 
the left of its normal position (fifth interspace and 
two inches from left border of sternum, or about an 
inch right of a vertical line through the nipple), 
you may diagnose hypertrophy of the muscular wall 
of the left ventricle or dilatation of the ventricular 
cavity. The sensations communicated to your fingers 
aid you to differentiate those two conditions. Remem- 
ber that hypertrophy means power, and dilatation weak- 
ness, but the phenomena and their causes may be 
variously combined. A full, long, and heaving stroke 
is characteristic of hypertrophy; an excited, short, 
diffused, struggling beat indicates dilatation. Action 
with power is shown in the one case, excitement with- 
out power in the other. In hypertrophy and dilatation, 
the apex may be felt two or three inches, or even 
more, outside the nipple-line, and as low as the 
seventh or eighth intercostal space. If the apex 
happen to beat against a rib the shock is, of course, PALPATION. 
59 
subdued; it is necessary to recollect this, otherwise 
you might put down as feeble, an impulse which is 
really strong. 
We now consider not only the situation of the tactile 
pulsation, but the extent of area over which it is mani- 
fest. Normally, as I have said, only a tap in the fifth 
interspace is felt; pulsation may be evident, however, 
over a superficial inch in strictly normal conditions. 
Pulsations in other positions may possibly be evident 
in health. Such may be felt in slight degree in the 
fourth intercostal space ; or, and this more commonly, 
in the epigastrium to the left of the ensiform cartilage. 
By pushing the fingers upwards beneath the false ribs 
on the left side, you may sometimes feel the throb of 
the right ventricle. You must give these contingencies 
due weight, but, as a general rule, any pulsation 
manifest in other situations than the neighbourhood 
of the normal apex, is evidence of disease of the heart 
or the great vessels. We proceed to consider the 
conditions wherein 
(c.) Pulsations, apart from the apex-heat, are mani- 
fested over the cardiac area. To appreciate these we 
shoidd endeavour to obtain an idea of the normal 
Topography of the Heart. The area occupied by 
the healthy heart may be thus roughly illustrated on 
the thoracic wall:-Draw a line, a little externally to 
the right border of the sternum from the second inter- 
costal space to a point just below the fifth sterno-costal 
articulation. Draw a second line from a point just 
below the second sterno-costal articulation on the left 
side to the situation of the normal apex. Unite the 
extremities of these lines respectively above and below, 
so as to describe a quadrilateral figure. Of this super- 
ficies (which will be bounded above by the aorta which 60 
PALPATION. 
crosses from right to left, and below by the diaphragm) 
about four-fifths are occupied by the right ventricle, 
which lies immediately behind the sternum and the 
third, fotlrth, and fifth costal cartilages of the left 
side, and culminates in the pulmonary artery at the 
second (left) interspace close to the sternum. The 
left ventricle is chiefly posterior ; but it borders the 
right ventricle to the left from the third sterno-costal 
articulation to the apex, which itself constitutes. The 
right auricle is in the third interspace (right) and 
behind the third and fourth cartilages. The left 
auricle is for the most part overlapped by the pul- 
monary artery, but a small part of it is situated 
superficially in the second interspace left of the 
sternum. 
If you find a forcible impulse of the heart towards 
the left of the border we have sketched as the normal 
left boundary of the cardiac area, the apex strongly 
defined in its beat and manifest below and to the left 
of its usual place, the pulse being full and strong, you 
may conclude that there is hypertrophy of the left 
ventricle. If you find a strong impulse in the epigas- 
trium extending from the normal apex to the right of 
the ensiform cartilage and sternum, and yet a much 
weaker pulse than you would think such a systole 
would produce, you probably have hypertrophy of the 
right ventricle. Tuck your fingers under the false 
ribs to the left, of the ensiform cartilage, and you will 
feel the contraction of the ventricular wall. We shall 
return hereafter to epigastric pulsations. 
As I have before said, hypertrophy and dilatation 
are often combined. When the left ventricle is 
dilated as well as hypertrophied, palpation gives you 
a less locab'zed and less firm and strong impression. PALPATION. 
61 
The impulse is more diffuse, the apex feels less 
pointed, and more rounded or globular to the finger. 
When the left ventricle is dilated, but not hyper- 
trophied, you feel its impulse over a wide area in the 
situation indicated, but it is felt as a short excited 
" slap." 
Hypertrophy of the right ventricle scarcely ever 
exists without dilatation. 
It has been supposed that auricular hypertrophy is 
not to be demonstrated by physical signs. I shall 
presently show you that this is not the case, for I 
have in many instances been able to demonstrate 
upon the surface of the chest-wall the contraction 
both of the right and of the left auricle. 
When you have a general dilatation, or hypertrophy 
and dilatation combined, of all the cavities of the 
heart, the hand and the eye both perceive a fluctua- 
tion-or, as Dr. Walshe has expressed it, a seeming 
undulation-over the extended area over which the 
contractions of the cardiac chambers are manifest. 
This is obviously due to the fact that the contractions 
of the muscular walls of the various chambers are 
occurring not simultaneously, but in successive 
moments of time. 
We will briefly consider the mechanism of the 
muscular walls of the heart. We should remember 
that the auricles and ventricles possess the double 
function of reservoirs and propellers. Such function is 
exercised in alternation-at rest they are reservoirs, 
in action they are propellers. You know that the 
rhythm of the heart comprises a period of contraction 
(systole), and a period of rest and dilatation (diastole). 
The latter occupies much the longer time : as a rule, 
the systole occupies one-fifth of the period; the 62 
PALPATION. 
diastole, of course, the remaining four-fifths. During 
the period of repose, what is taking place ? On the 
right side of the heart, the great veins of the body, 
the superior vena cava, and the inferior vena cava, are 
pouring their impure venous blood into the right 
auricle, which is gradually filling; the ventricle is 
becoming filled at the same time, for, the auriculo- 
ventricular valves being now flaccid, auricle and ven- 
tricle form one cavity. On the left side of the heart, 
the pulmonary veins are carrying the pure blood, 
which has been aerated in the lungs, to the left 
auricle, and hence to the ventricle, these cavities 
becoming filled simultaneously w'ith the right. 
During all this period, the muscle of auricles and 
ventricles is receiving its nutrient supply, for the 
heart differs from all the other structures of the body 
in that, whilst the latter are supplied with blood by 
the heart's contraction, itself receives its arterial 
supply during its own period of repose. The muscle 
of the heart is supplied with blood through the 
coronary arteries, which arise from the aorta (pouches 
of Valsalva) just above the semi-lunar valves. The 
open mouths of these arteries had just been occluded 
by the flaps of the valves whilst the aortic orifice was 
open, but now in diastole, the valves falling back 
from the weight of the superincumbent column of 
blood and closing the aortic aperture, the channels 
are opened for the sudden in-rush of the stream of 
arterial blood into the tissue of the heart. 
The cavities having become replete, the contraction 
of the heart, the systole, begins. The important point 
to notice is, that this contraction is not synchronous 
throughouut all the muscular cavities of the heart; 
but that the auricles always contract before the ventricles. PALPATION. 
63 
You are aware that the fibres which constitute the 
muscle of the heart are under the control of the 
minute ganglia of the sympathetic nerve; the action 
of these ganglia is, however, controlled and co-ordi- 
nated by the vagus nerve, which restrains contraction 
until the movement shall be uniform and regular. 
The necessary stimulus to the contraction of the 
auricle is distension; until it is sufficiently filled with 
blood, its systole does not occur. Distension, then, 
provokes auricular contraction, and the ventricle 
which has already been filling by the passive flow of 
blood into it, is now more completely gorged by the 
additional blood forced into it by the auricle. In the 
normal heart, this precedence in action of the auricle 
is only momentary, the wave of contraction speedily 
ensuing in the ventricle. Still, it is of high impor- 
tance to realize this priority of auricular contraction. 
Though the arrangement of the muscular fibres of the. 
heart is such, that many of the fibres are common to 
all the .cavities, yet the auricles are much more inde- 
pendent of the ventricles than the ventricles are of 
each other. Extremely early in foetal life there is a 
mark of differentiation of the then single auricle 
from the single ventricle, but the right ventricle is 
formed by' a doubling over of a part of the original 
(left) ventricle. 
The necessary stimulus, then, for the contraction 
of the ventricles, is the extra repletion induced by 
the immediately preceding contraction of the auricles. 
The ventricular contraction, though strictly speaking- 
vermicular, occurs in such a brief moment of time, that 
it is indistinguishable save as* one movement in syn- 
chronism. The simultaneous contraction of the ven- 
tricles driving the blood into the aorta on the one 64 
PALPATION. 
side, and the pulmonary artery on the other, the apex- 
beat, the pulse in the aorta, and the pulse in the pul- 
monary artery, are practically coincident in time. 
I have said that in the normal state of the heart 
the pulsation of the auricles causes no apparent vibra- 
tion of the thoracic wall; it is not so in disease, how- 
ever ; hypertrophy and dilatation of right or of left 
auricle may give rise to a visible pulse. As regards 
the right auricle, this has been generally admitted. 
The right side of the heart becomes dilated, and often 
hypertrophied, under all the circumstances which 
induce an undue repletion of the venous system. We 
have already alluded to these conditions, and we shall 
again briefly consider them in the next lecture. The 
right auricle is never hypertrophied and dilated with- 
out the right ventricle being in like condition. Under 
such circumstances you feel a heaving impulse, which 
seems to be very near the surface, extending from the 
normal apex across the epigastrium to the right side 
of the sternum; this is caused by the right ventricle, 
and you may feel a pulsation in the second or third 
intercostal space just right of the sternum, which is 
caused by the auricle. How to determine this we shall 
presently consider. 
We turn to the left auricle. Undoubtedly, in certain 
cases, you may observe a pulsation in the second, third, 
or fourth intercostal space left of the sternum, but is 
this caused by the auricle ? On this point there has 
been difference of opinion. Some writers have stated 
that inasmuch as the greater part of the auricle is 
covered by the great arteries emerging from the heart, 
and the muscular walls of the auricle are comparatively 
thin and feeble, its power of contracting with sufficient 
force to produce an impulse is improbable. These PALPATION. 
65 
observations are undoubtedly correct in reference to 
the left auricle when in a state of health. It is a very 
different matter, however, when it is in a state of 
disease. There is one condition of disease or malforma- 
tion, which gives rise to great hypertrophy and dilata- 
tion of the left auricle-narrowing (stenosis) of the 
auriculo-ventricular orifice of the left side (mitral). The 
causation of this hypertrophy and dilatation is easy to 
understand. I have explained that the contraction of 
the auricles is necessary to produce that perfect reple- 
tion (that additional supply to the already partially 
filled ventricle) which is required to call forth the 
ventricular systole. When the aperture between 
auricle and ventricle is so narrowed as to become an 
obstruction, the auricle has perforce to contract with 
enhanced power to overcome it. The auricle thus 
called upon for abnormal force of contraction becomes 
hypertrophied, and, from being in a state of preter- 
natural distension, dilated. In the case of a boy of 
nine, who had constriction of the mitral orifice, I 
found at the post-mortem examination that the mus- 
cular wall of the left auricle was from | to | inch in 
thickness.* The normal thickness of the left auricle 
in adult life is somewhat more than inch.f Ac- 
cording to Bouillaud, it is inch. Here was an 
auricle, the thickness of the muscular wall of which 
was in great part thicker than the thickest part of the 
normal adult right ventricle. Who could doubt the 
ability of such an auricle to communicate a distinct 
pulsation to the thoracic wall ? 
The foregoing considerations will point us to a plan 
* Medical Times and Gazette, January 10, 1874, p. 35. 
t Flint, "Diseases of the Heart," 2nd edition, p. 21. 66 
PALPATION. 
of demonstrating such pulsations as are caused by the 
auricles. A pulsation left of the sternum may be due 
to the contraction of the left ventricle, the pulse in 
the pulmonary artery, or the contraction of the auricle. 
A pulsation right of the sternum may be due to the 
contraction of the right ventricle or the right auricle, 
to the pulse in the aorta, or some aneurismal dilata- 
tion of that vessel. To determine whether the pulsa- 
tions are, or are not auricular, we may adopt a simple 
plan of CHRONOMETRY OF PULSATIONS OCCURRING 
over the cardiac area. It has been recommended 
that the movements of two doubtful points of pulsa- 
tion should be compared by attaching to each, by 
means of a pellet of beeswax, a bristle carrying a 
small paper Hag. The variation in time of the two 
movements is observed by the vibrations of the flag. 
The modification of this valuable plan which 1 adopt, 
is the following :-Cut two small circles of sticking 
plaster, about the size of fourpenny-pieces; transfix 
the centre of each by a pin, so that the head is in 
contact with the adhesive side of the plaster. Attach 
the one adhesive circle over the site of pulsation sup- 
posed to be auricular, and the other over the situation 
of the apex of the heart. The shafts and points of 
the pins projecting forwards, you have two levers 
which vibrate with the movements communicated to 
them by the several pulsations; these levers you 
elongate by attaching to them rolled " spills" of tissue 
paper. A still simpler plan, which I now generally 
adopt, is to pull out a small piece of cotton wool into 
the form of a tall cone and attach it by its base to the 
pulsating portion of chest-wall by means of a little 
ointment. Any number of these can be applied 
over points of pulsation, and the relation of their 
vibrations be thus compared. PALPATION'. 
67 
If you have to do with an auricular pulsation you 
will see that the movement of its lever invariably 
precedes that of the lever adapted over the heart's 
apex. The movement is presystolic, and must be due 
to the contraction of the auricle. If the two con- 
tractions occur simultaneously they must be produced 
by the ventricle or in the pulmonary artery or aorta. 
Pulsation of the pulmonary artery, which may be 
felt between the second and third ribs, close to the 
left border of the sternum, is only manifest when 
from any cause the left lung is retracted from the 
base of the heart. You feel that such pulsation is 
very superficial; it is said that even the click of the 
pulmonary semilunar valves may be felt as a little 
shock to the finger. It is interesting to note the 
relation of this phenomenon to respiration. If the 
lung be only partially retracted from the pulmonary 
artery, you will observe the pulsation to become more 
and more visible during expiration, whereas, during 
inspiration, as the lungs, becoming more and more filled 
with air, encroach over the heart, the pulsation becomes 
less and less evident till it ceases, reappearing at the 
next inspiration. 
Pulsations of the aorta, which, of course, occur on 
the opposite-the right-side of the sternum, may be 
due to aneurism, or to displacement of the vessel which 
occasionally occurs in rickety chests. 
It remains for us to considerprulsationfelt at the epigas- 
trium. We have already noticed the pulsation due to 
a displaced or hypertrophied and dilated right ventricle. 
Any considerable enlargement of the right side of the 
heart will give rise to a pulsation felt at the epigas- 
trium. An impulse is sometimes communicated to the 
edge of the left lobe of the liver, which is to be felt 68 
PALPATION. 
below the ensiform cartilage. Occasionally, but very 
rarely, the impulse is reversed ; the integuments at the 
epigastrium are felt to be retracted, instead of propelled 
at each systole of the heart. In such cases there has 
been an extensive pericarditis, which has resulted in 
adhesion of the heart to the diaphragm and the liver. 
But we have to consider pulsations felt at the epigas- 
trium, which may be due to other causes, with a view 
to differential diagnosis. We will suppose that: 
(J.) The pulsation is felt in the median line, that is, 
the line joining the ensiform cartilage and the umbili- 
cus. It will probably occur to you that such pulsation 
may be due to aneurism of the abdominal aorta. The 
suggestion readily occurs, but though you feel a for- 
cible pulsation over the vessel, you must hesitate very 
considerably before committing yourself to the opinion 
that it is due to an aneurism. Abdominal aneurism is 
rare. " So," as Sir William Jenner has said, " instead 
of being your first, it should be your last idea, that an 
abdominal pulsation is due to aneurism."* If there be 
an aneurism, you will feel a localized swelling of the 
vessel, which with, or just after, the systole of the 
heart expands equally in all directions, above, below, 
and laterally. A tumour, superficial to the aorta, may 
pulsate from the communicated impulse of the vessel; 
but then you will feel no lateral pulsation. You may 
find assistance in the diagnosis, by causing your patient 
to bend forward on the hands and knees ; a tumour 
isolated from the vessel then recedes from it, and you 
no longer feel the pulsation, ■which in aneurism is 
unaffected by this position. Having eliminated abdo- 
* Clinical Lecture on Tumours of Abdomen: British Medical 
Journal, 1869, p. 42. PALPATION. 
69 
minal aneurism and tumours to which the abdominal 
aorta may communicate its impulse, we will suppose 
that you yet find a pulsation in the central line, below 
the ensiform cartilage, which you have convinced your- 
self, by palpation under the false ribs, is not due to the 
impulse of the right ventricle. You will find such a 
pulsation very commonly ; it is the pulse of the abdo- 
minal aorta. In the vast majority of abdominal pul- 
sations there is no structural alteration to account for 
them ; they are palpitations due to neurotic conditions. 
The abdominal aorta shows the excited pulse that the 
other great arteries of the body manifest. This pheno- 
menon is, of course, most evident in spare people ; you 
will find it in cases of anaemia, in dyspepsia, and spe- 
cially the dyspepsia of old people whose arteries have 
commenced to de-generate. We will consider in the 
next place that: 
(B.) The pulsation is felt to the right of the median 
line. I have said that the beating ventricle may propel 
the edge of the left lobe of the liver; an aneurism may 
do the same still more extensively; but in some cases 
it may be observed that the whole liver pulsates. This 
phenomenon is of rare occurrence, but it is of great dia- 
gnostic importance : it indicates regurgitation through 
the tricuspid orifice. The liver, in this condition, is 
like an erectile tumour; it pulsates with the systole 
of the heart. The right ventricle, by its contraction, 
instead of driving all the blood it contains into the 
pulmonary artery, on account of the imperfection of 
the tricuspid valve, forces some of its contents back 
again into the right auricle. Consequently, an impulse 
is given to the blood contained in the vessels opening 
into the auricle-i.e., the great systemic veins and 
their tributaries. Hence the rhythmical injection of 70 
PALPATION. 
the hepatic veins, and the consequent pulsation of the 
liver.* You will see that this phenomenon is exactly 
analogous to the venous pulse in the jugulars which 
we have before noticed. Both indicate the same 
morbid condition of the heart, tricuspid insufficiency. 
Suppose, now, that : 
(C.) The pulsation is felt to the left of the median line. 
This may be due to an aneurism of the abdominal aorta, 
especially when it involves also the superior mesen- 
teric artery. I once met with a case in which there 
was pulsation felt to the left of the middle line, midway 
between ensiform cartilage and umbilicus. The pul- 
sation gave rise to distress, and was associated with a 
fulness at the epigastrium. The case had been diag- 
nosed as one of cancer of the liver. Whilst, however, 
it was evident that the left edge of the liver encroached 
over the epigastrium, I could find no signs leading- to 
the conclusion that there was any malignant disease. 
The left side pulsation was very difficult of explanation. 
I had the opportunity, however, of seeing the case 
several times, and I found (1) that the pulsation always 
became pronounced just previously to the cata- 
menial period (the patient, a woman of full habit, was 
nearing the climacteric), and that it diminished almost 
to extinction, after the period was passed; (2) that it 
was always controlled, even to almost extinction, by 
large doses of quinine. The view that I took of the 
case was, that the pulsation was in the splenic artery. 
The patient completely recovered. 
We have hitherto considered the evidence afforded 
by the well-known phenomenon, pulsation, as detected 
* Aided perhaps by the pulsation of the inferior cava which 
lies behind the liver. PALPATION. 
71 
over the cardiac area. Now we have to consider other 
peculiar diagnostic signs recognizable to the touch. 
The Special tactile phenomena manifest 
over the cardiac region are briefly, («) friction, 
(b) thrill. 
(a.) On placing the hand over the praecordium, you 
may, in certain cases, detect a sensation of rubbing 
accompanying the systole and diastole of the heart. 
You should cause the patient to hold his breath so as 
to convince yourself that the sensation is not com- 
municated by any part of the respiratory mechanism. 
If you feel that the periods of contraction and dilata- 
tion of the heart are accompanied by this feeling of 
friction, you may be sure that your patient is suffering 
from pericarditis. The phenomenon is termed peri' 
cardial friction-fremitus; itis not common; in a very large 
proportion of cases of pericarditis it is not observed. 
There must be the concurrence of certain conditions 
to produce it. The pericarditis must be in an early 
stage ; it occurs only at the commencement of effusion 
into the pericardial sac: the fluid effused must be 
thick or rich in fibrine; at autopsies in some cases of 
pericarditis, you may see' the surface of the heart 
covered by a layer of material like soft butter, this is 
the kind of effusion which gives rise to the feeling of 
friction : the amount of fluid must be limited ; as the 
pericardial sac becomes distended the exudation is less 
viscid, the heart is separated from the thoracic wall, 
and the systole is enfeebled-all these causes concur 
to prevent the sensation of pericardial fremitus : lastly, 
the heart must contract with sufficient force; a feeble 
heart does not produce it. This sign never occurs 
without the friction being recognizable by the ear, as 
we shall hereafter describe. You will find a great 72 
PALPATION. 
number of cases of pericarditis occurring without this 
sign, but, where you observe it, it is of great import- 
ance ; for it renders certain the diagnosis of pericar- 
ditis, and it enables you to state that the pericardial 
surfaces are roughened, or that the effused material 
is of a viscid character. 
We come now to an interesting- phenomenon, which 
will well repay careful investigation. This is : 
(b.) Thrill. On placing the hand over the praecor- 
dium you are sensible of a peculiar vibration occurring 
over a certain area and at a certain period of the heart's 
action. The vibration is quite characteristic ; a sense 
of trembling is communicated to the fingers-rapidly 
as if the finger touched the twanged string of a violin, 
or comparatively slowly as if the vibration had pro- 
ceeded from the bass string of a violoncello. The 
French observers aptly compared the sensation to 
that experienced when one places the hand on the 
back of a purring cat or kitten; they gave to the 
phenomenon the name of fremissement cataire. It is 
characterized also by the terms purring tremor, and in 
German, Katzenschnurren. It is not sufficient, how- 
ever, merely to note the existence of this sign. You 
must especially establish, (1) its position; (2) its 
rhythm. 
You may feel it over the base of the heart, about 
the second intercostal space and right of the sternal 
border. Placing the tips of the fingers over the 
situation where the thrill is felt, now touch with the 
fingers of your other hand the spot where the heart's 
apex beats. This will enable you to determine the 
rhythm of the thrill. You find, we will say, that the 
thrill coincides in time with the apex-beat. Then you 
have either contraction (stenosis) of the aortic orifice PALPATION. 
73 
or aortic aneurism. You will notice whether the latter 
condition is indicated by a pulsatile swelling or the 
concurrent signs of aneurismal dilatation of the aorta. 
If not, you will proceed to confirm your diagnosis of 
aortic stenosis by auscultation and the means we shall 
hereafter describe. In rare cases the purring tremor 
may be felt over the situation of the pulmonary artery; 
it indicates obstruction of that vessel. Perhaps, how- 
ever, you find that the thrill does -not coincide with 
the beat of the apex but occurs during the diastole of 
the heart. A diastolic thrill is rare ; it is character- 
istic of regurgitation through the aortic orifice. It 
signifies that the aortic valves cannot perfectly close, 
that they permit reflux of blood. So you may find 
this sign in conjunction with the phenomena we have 
noted as occurring in a like condition-forcible apex- 
beat and locomotive (Corrigan's) or water-hammer 
pulse. 
Suppose, however, that you feel a thrill at or near 
the apex of the heart. In this position it is of the 
utmost importance to establish the rhythm of the 
thrill. I always advise that for this purpose you 
employ the fingers of each hand, as in the case of 
aortic thrill. First determine the spot at which the 
apex beats. You may find that this is also the point 
of greatest intensity of the thrill; to assure yourself 
of this, however, place a finger of your other hand a 
little externally. You will then convince yourself 
whether thrill and impulse occur together ; in other 
words, whether the thrill is systolic. If so, if thrill= 
impulse, it is caused by regurgitation through the 
mitral orifice. Such a thrill is not common. You 
may find, however, and much more commonly, that 
the thrill felt in the neighbourhood of the apex 74 
PALPATION. 
is not exactly simultaneous with the systole. You 
distinctly recognize that the finger which receives 
the impression of the thrill does so just before the 
finger of the other hand receives the impression of the 
impulse of the ventricle. The thrill is abruptly ter- 
minated by the ventricular systole-it is presystolic. 
Moreover, you may find that it is felt not just at the 
apex, but slightly internal to it, and at a higher level. 
This separation of thrill from apex-beat renders the 
detection of the rhythm of the former more easy by 
the rule which I have laid down. Always investigate 
the phenomenon of thrill by using both hands, examining 
the site of the thrill by the finger or fingers of the one hand, 
and noting the apex-beat by the finger or fingers of the other. 
It will be found that of thrills about the apex, that 
which is presystolic in rhythm is by far the more 
common. To recognize it is of very great importance. 
It is pathognomonic of contraction (stenosis) of the 
mitral orifice, and is due to the vibration caused by 
the forcible contraction of the auricle urging the blood 
through the obstructed outlet into the ventricle. We 
shall return to this subject when we come to auscul- 
tation, and consider the relation of thrill to murmur, 
but it is necessary to premise that both thrill and 
murmur are due to a like cause, but that we may have 
thrill without murmur and murmur without thrill. 
Vibration produces both phenomena ; if the vibrations 
be insufficiently rapid they cannot be perceived by the 
ear, whilst they are obvious to touch ; again, they 
may be so rapid as to be undetected by touch but 
detected by the ear ; or the material which conducts 
the vibrations may be more suitable to convey impres- 
sions of touch in the one case, and of sound in the 
other. I wish strongly to insist that you shall give 75 
due prominence to investigation by the sense of touch, 
and not fall into the error of esteeming auscultation 
the be-all and end-all of cardiac diagnosis. I have 
had cases in which the existence of thrill, presystolic 
in rhythm, led me to the diagnosis of mitral stenosis, 
though, in the one case, there was no murmur at all, 
and in the other it was so short as to be scarcely dis- 
tinguishable. You must by no means draw any con- 
clusion from the absence of thrill, but where you find 
a well-marked thrill before the impulse, you have, in 
my opinion, ascertain sign of constriction of the mitral 
orifice. 
We may thus summarize the diagnostic evidence to 
be obtained from the purring- tremor. Felt over («) 
the base of the heart its rhythm may be (1) systolic 
oi- (2) diastolic. If (1) systolic, it indicates (exclu- 
ding aneurismal thrills, which are outside our subject, 
and the rare thrill denoting obstruction of the pul- 
monary artery) a morbid condition of the aortic 
valves which has resulted in a narrowing of the outlet 
from the ventricle. If (2) diastolic, it indicates 
regurgitation into the left ventricle, owing to imper- 
fect aortic valves. Felt over (b) the apex of the heart, 
the thrill may be (1) systolic, or (2) presystolic.* 
Systolic thrill indicates regurgitation from the left 
ventricle through an imperfect mitral valve. Pre- 
systolic thrill indicates obstruction afforded by a 
narro-wed mitral orifice to the current of blood issuing 
from the left auricle. 
We will conclude the subject of palpation by a 
brief retrospect of the evidence which we have ob- 
PALPATION. 
* German observers call this presystolic thrill, diastolic. 76 
PALPATION. 
tained. Excluding1 negative and doubtful evidence, 
you will observe that the sense of touch has given us 
signs of great and positive value in the following 
morbid conditions-atheromatous changes in the 
arterial vessels-hypertrophy of the left or the right 
ventricle; dilatation of either of the ventricles ; peri- 
carditis, in which it may have afforded evidence 
as to the stage of the disease, whether there is 
liquid effusion, whether the pericardium is rough- 
ened, or whether old disease has resulted in ad- 
hesions. Concerning valvular diseases of the heart 
and their effects, we may have received evidence of 
aortic obstruction from thrill; of aortic regurgitation 
from the locomotive pulsation of arteries, and, per- 
haps, from diastolic thrill; of mitral obstruction from 
presystolic thrill, as well as from pulsation of the 
left auricle; possibly of mitral regurgitation from 
systolic thrill; of tricuspid regurgitation from hepatic 
pulsation. 
We shall next consider the evidence to be derived 
from percussion. 77 
LECTURE IV. 
PERCUSSION. 
Increased resonance over heart-Increased dulness-Relations 
of areas of partial and complete dulness-Pericardial effu- 
sion-Cardiac hypertrophy and dilatation-Differential 
diagnosis of the two conditions. 
The object of percussion is to determine the size and 
shape of the heart and its relation to the neighbour- 
ing' structures. In my own opinion the best plan of 
percussing the heart region is to use the fingers only. 
Place the fore and middle fingers of the left hand 
closely upon the surface of the chest, and tap with a 
short, decided, but not violent stroke, and in no 
hurried manner, with the ends of the fore and middle 
fingers of the right hand. I consider that the fing ers 
of the left hand constitute the best pleximeter, and 
the fingers of the right the best plessor, Thus we 
obtain at the same time information by two distinct 
routes: the ear obtains evidence of sound at the 
moment that the tactile apparatus receives impressions 
of vibration'. 
Proceeding by the method of exclusion we will 
suppose that : 
(«.) The prcecordial area is resonant-that is to say, 
the percussion sound is clear and the vibration unim- 
paired-there is no dulness. The most common cause 
of this condition is emphysema of the lung. The 
morbidly dilated pulmonary air-cells encroach over 78 
PERCUSSIOX. 
the area which, under ordinary circumstances, is 
occupied by the walls of the heart. Moreover, the 
heart may be pushed downwards by the too bulky lung. 
You may have been able, as I have indicated under 
" Palpation," to feel the beating of the right ventricle 
at the epigastrium. 
A far less common cause of resonance over the 
heart-region is the presence of air in the cavity of 
the left pleura (pneumo-thorax). The tympanitic re- 
sonance in this condition exists, of course, over the 
whole of the affected side of the thorax. 
In extremely rare cases, tympanitic resonance has 
been found only over the situation of the heart and 
pericardium ; it indicates the presence of air or gas 
in the pericardium (pneumo-pericardium), a condition 
which may be induced by fistulous communication with 
the lung, the oesophagus, or the stomach, or by the 
decomposition of effused products of inflammation 
within the pericardial sac. 
We will now suppose that: 
(Z>.) The preecordial area is dull.- We shall have to 
exclude, first, cases wherein the dulness is not to be 
distinguished from that existing over the contiguous 
thorax. Pleuritic effusion in, or empyema of, the left 
side causes such dulness that the area of the heart 
cannot be mapped out by percussion. If such liquid 
effusion be in considerable amount, the heart may be 
pushed completely to the right side, so that its apex 
may be felt to beat under the right instead of under 
the left nipple. Condensations of the left lung, 
cancer, and abnormal growths in the thoracic cavity 
also may make it impossible for us to determine by 
percussion the outline of the heart. Assuming that 
these interfering circumstances have been eliminated, PERCUSSION. 
79 
we have now to consider the modifications of the 
percussion-note induced by the heart itself. 
We have already considered the normal topography 
of the heart. We have now to remember that only a 
certain portion of the heart, covered by its pericar- 
dium, approaches close to the thoracic wall-a con- 
siderable part being overlapped by the borders of the 
lung. The portion of the heart which is uncovered 
by lung in conditions of health may be demonstrated 
with sufficient precision in the following manner:- 
Draw a vertical line through the centre of the ster- 
num. Mark a point A, on this midsternal line at the 
level of the fourth left costal articulation. Note the 
point B, where the apex of the heart is felt to beat. 
Join A and B by an oblique line. Complete the right- 
angled triangle by drawing a line from the heart- 
apex, B, to the midsternal line at a point, C, just 
above the ensiform cartilage, at the lower part of the 
sixth costal articulation. The area enclosed by this 
triangle will be the portion of heart which, in con- 
ditions of health, is uncovered by lung. You should 
compare it with the area on the thoracic wall occupied 
by the whole heart as we have before described. 
Now to percuss the heart-region. Begin by adapt- 
ing the two fingers of your left hand held vertically, 
nails upwards (we are, of course, still supposing our 
patient to be in the vertical position, sitting or stand- 
ino-\ to the thoracic surface, a little to the right of 
the right border of the sternum. After percussing 
in this situation, advance the fingers nearer to the 
midsternal line until the elicited sound is dull. Mark 
the vertical line where dulness commences by a soft 
pencil or by ink. In the next place commence to deter- 
mine the left border of the dull area by percussing out- 80 
PERCUSSION. 
side the point of the apex-beat. It is more convenient 
now to incline the fingers which are adapted to the 
chest-wall obliquely, pointing towards the sternum, 
as the left line of dulness will be oblique. Mark the 
line as previously. The upper limit of the dull area 
is determined by percussing from above downwards, 
the fingers adapted to the chest-wall being held hori- 
zontally. You have now obtained the upper and the 
two lateral limits. The lower limit is not so easily 
determined, because the cardiac merges into the 
hepatic dulness. The heart and pericardium are close 
to the left lobe of the liver, separated only by the 
diaphragm, and I hold that the dulness over these 
two organs cannot be discriminated. A line of dul- 
ness, however, can be determined between the apex 
on the left, and the commencement of liver-dulness 
on the right, and you should join these points by a 
line. For all practical purposes this procedure will 
indicate to you the area of complete dulness over the 
heart-region, the superficial cardiac region as it has 
been tailed, and it demonstrates the portion of the 
heart which is uncovered by lung. 
But this is not all that is necessary. You should 
now reverse the order of your procedure, and starting 
from the line of dulness, make percussion farther and 
farther outwards until the sound has the perfectly 
clear character which it possesses over healthy lung. 
I do not think it necessary to overburden you with 
acoustic terms. To understand all that has been 
written about percussion-sonoriety, pitch, clang, 
timbre, intensity, tones, overtones, fundamentals, har- 
monics, &c.-one ought to be able at any moment to 
conduct an orchestra, tune a harp, read music at 
sight, and be equally versed in acoustics and prac- PERCUSSION. 
81 
tical medicine. Some observers have made assertions 
as regards the diagnostic power of percussion, that 
others cannot help thinking extravagant; thus, it 
has been said that it is possible to ascertain from the 
percussion-note alone whether a heart has under- 
gone any fatty degeneration. It used to be told of 
Piorry, when I attended his class, that he was able, 
by knocking at the front door, to find out who was in 
the drawing-room, but such a critical ear is not given 
to everybody. Suffice it that the sound elicited by 
percussion over the heart in the situations where the 
lung overlaps it is modified by two causes-first, by 
the nearness of a dense body (the heart) to the point 
percussed, and secondly, by the existence between 
the point percussed and this dense body of an air- 
containing structure, the lung-i.e., an arrangement 
capable of transmitting sonorous vibrations. As one 
proceeds outwards the sound becomes less muffled, 
and the vibration more manifest; but there is no 
abrupt line of demarcation to indicate the outline of 
the heart. Nevertheless, you should learn carefully 
to note where the sound and vibration are uncom- 
plicated (that is, where there is lung vibration only), 
and where they commence to be modified. In esti- 
mating the curves of this area, I think it is best to 
employ as your pleximeter the little finger of the left 
hand, placed laterally against the thorax, instead of 
the fore and middle fingers. You should outline the 
area with ink or pencil; you will now have two con- 
centric figures, the internal being the superficial 
cardiac area which we have before noted, the external 
the so-called " deep cardiac area " corresponding, if 
it be carefully, and, I think I may add, fortunately, 
ascertained, to the actual outline of the heart. For 82 
PERCUSSION. 
practical purposes I would advise you to realize these 
two areas as, (1) the area of dulness, (2) the area of defi- 
cient resonance, and it is the mutual relations of these 
that you will find of diagnostic importance. The 
breadth of (1) the area of dulness in health and in 
adult life scarcely exceeds three inches transversely. 
As regards (2), the sound in percussing from above 
downwards begins to be impaired about the third rib ; 
a curved outline can be mapped out at this level to- 
wards the right of the sternum, which indicates the 
aorta, but you cannot separate the aorta from the 
heart by percussion. 
We will now assume that: 
(c) The preecordial dulness is extended upwards, and its 
outline is of pyramidal or pyriform shape. Whenever 
you find that dulness extends upwards above the third 
rib, you have strong presumptive evidence of effusion 
into the pericardial sac. If the sac is distended with 
fluid you will find that the area of dulness extends 
from the articulation of the first or second costal 
cartilage, above to the sixth rib, or sixth intercostal 
space below. 
Here let me insist on the great value of charts or 
diagrams as records of the physical signs of heart 
diseases. These may be roughly drawn in a few 
minutes, for sternum, clavicle, and ribs constitute 
almost all the outlines that it is necessary to depict. 
Be careful always to number the ribs as you outline 
them. Blank chest-charts have been prepared by 
many observers, and are extremely useful. You may 
procure one in a few seconds by a rubbing from the 
cover of this book. 
Inspection and palpation have already indicated 
points which should be recorded on the chart. The area of visible impulse should be outlined, the position 
of the apex-beat and the locality of thrill or tactile 
friction, if these exist, should be marked. Chalks, 
or pencils of different colours, may be used with 
advantage. 
I have often found it of the greatest value to obtain graphic 
records from the chest-wall itself; for this purpose I use one 
of Perry's copying-ink pencils, which I have found most con- 
venient. The plan is valuable as an aide-memoire in all cases in 
which a physical examination of the heart is made. You first 
mark with the point of the pencil the spot of visible apex-beat; 
if this be extended, you denote the area of impulse by a dotted 
outline. Then you mark, in like manner, any other points of 
pulsation over the cardiac area, and proceed to further define 
the outline by palpation ; afterwards the limits of praecordial 
dulness are traced out, and the positions and lines of con- 
duction of murmurs, &c. The picture thus formed on the 
chest-wall itself gives you a vivid summary of the evidence 
which your physical examination has elicited. If you desire 
to preserve a tracing, you should also make a dotted 
outline of the position of certain of the costal cartilages, the 
ensiform cartilage, and any other fixed points that you 
may think necessary ; you then apply over the portion of the 
chest thus marked, a piece of moistened tissue-paper. The 
paper, of course, takes the markings made by the copying- 
pencil, and you can thus preserve a permanent and exact record 
of the physical signs in the case, and can compare it at 
future times with tracings taken in like manner. 
Now you will proceed to record the area of prsecor- 
dial dulness. If this area be pyriform or pyramidal in 
shape, with apex upwards, the probability is strong 
that the case is one of pericarditis with effusion. We 
will consider the signs that are confirmatory of this 
view. 
In the first place, the transition from dulness to 
lung resonance is abrupt. As I have said, the normal 
area of cardiac dulness widens gradually into pul- 
PERCUSSION. 
83 84 
PERCUSSION. 
monary resonance. The same occurs in many con- 
ditions of disease, but where you have the pericardial 
sac filled with fluid, the edge of lung, which normally 
overlaps the cardiac area, is pushed aside, and the 
area of deficient resonance (as opposed to dulness) is 
done away with. The line between pulmonary reso- 
nance and priecordial dulness is well defined, more- 
over the sense of resistance to the fingers on percus- 
sion is increased; vibrations are lessened. 
In the second place, there may be noted a peculiar 
relation between the area of dulness and the position 
of the apex-beat. You may readily understand that 
if the area of dulness which you have mapped out be 
due not to liquid effusion but to enlargement of the 
heart, you will feel the apex-beat at the lowest limit 
of the dull area. Not so, however, when there is 
effusion into the sac of the pericardium. Then the 
apex-beat is tilted or floated upwards, and you get a 
certain breadth of dulness between the apex above 
and the stomach resonance below. 
In the third place, you may observe that the extent 
of dulness varies within comparatively short periods of 
time. Effusion into the pericardium often takes place 
rapidly, and you may find that the dull area which you 
have mapped out previously, has, in a few hours, very 
considerably increased. From day to day there may 
be advances or recessions of dulness. 
Again, in effusion into the pericardial sac the 
dulness varies with the position of the patient. On 
his lying down flat, the fluid subsides, then the apex- 
beat again becomes evident, and the percussion note 
becomes clearer, the lungs now returning to the 
position whence they were displaced by the fluid. 
These signs, then, assure us that there is fluid in PERCUSSION. 
85 
the pericardium, whether due to pericarditis (the 
other signs of which you will search for) or to passive 
dropsy of the pericardium, which occurs, as I have 
Fig. 1. 
Showing the triangular area of normal cardiac dulness 
and its relation to the hepatic dulness. The shading 
indicates the area of deficient resonance-i.e., the deep 
cardiac region. 
said, with the manifestations of dropsy in other 
situations. 
The foregoing points may, perhaps, be better under- 
stood by reference to the accompanying diagrams, 
for drawing which I have to thank Dr. Stephen 
Mackenzie. 
Suppose now that: 
(d.) The pr(ecordial areas of dulness and deficient re- 
sonance are extended laterally. The impairment of 
resonance may be extended in either lateral direction. 86 
PERCUSSION. 
Assume (1) that it continues to the left of the border 
of the normal triangle of cardiac dulness depicted in 
Fig. 2. 
Showing the pyramidal outline of dulness due to the 
effusion into the pericardium, and the relation of the 
heart to the distended sac. 
Fig. 1. This extension of dulness must be due either 
to hypertrophy or to dilatation, or to both combined, 
of the left ventricle. In hypertrophy you will have 
already found that the apex beats below and perhaps 
outside its normal position. The area of dulness will 
be sharply defined, but it is only the extreme left of it 
which will be much changed in outline. The base 
line will be prolonged to the left of a line vertically 
drawn from the nipple, and it will incline downwards 
and towards the left instead of preserving its horizontal 
position. PERCUSSION. 
87 
In hypertrophy of the left ventricle, you will note 
that the prsecordial dulness preserves its triangular 
form, but is prolonged towards the left side. You 
will of course notice the expression of power in the 
ventricular contraction, as evidenced to the eye, the 
hand, and the ear. 
When the extension of dulness left of the normal 
area is due to dilatation of the left ventricle, the out- 
line is less angular and more rounded than it is in the 
case of hypertrophy. The apex is less pointed and 
more globular. The left border of the region also is 
less defined; the area of deficient resonance is ex- 
tended towards the left, and you will find the apex- 
beat less powerful and less sustained, with the cha- 
racter rather of a short and feeble slap. 
As I have said before, hypertrophy and dilatation 
often co-exist. As a rule, the more obtuse the outline 
of the apex as obtained by percussion, the greater 
the probability of dilatation, but the further discrimi- 
nation between these conditions we shall consider 
under " Auscultation." 
We will suppose now the case that (2) the praecor- 
dial deficiency of resonance extends to the riyht of 
the normal area. We have not, in this case, to de- 
termine between hypertrophy and dilatation of the 
right chambers of the heart, because practically the 
two conditions always occur together. 
You may («) have no difficulty in discovering such 
right side hypertrophy. You may find that the area 
of absolute dulness extends beyond the right border 
of the sternum over the cartilages of the third, fourth, 
and fifth ribs, and when the right auricle is consider- 
ably dilated, you may find dulness extend from the 
second rib to the third intercostal space. In this case 88 
PERCUSSION. 
the enlarged heart has displaced the lung which under 
other conditions overlaps it. 
Often, however, (b) the determination by percussion 
of the outline of the right chambers is not easy. 
Sometimes percussion over the praecordial area elicits 
no dulness at all. In such case the heart is over- 
lapped by emphysematous lung, and it is precisely in 
emphysema that dilatation of the right chambers is 
apt to occur. Disorders of the pulmonary circulation, 
involving as they do turgescence of the general venous 
system, lead up to dilatation of the right (the venous) 
chambers of the heart. Out of forty-five such cases 
of secondary dilatation of the right heart, Lancereaux 
observed twenty-four due to emphysema and chronic 
bronchitis, and six due to respiratory trouble induced 
by a malformation of the chest through rickets. 
Though the area of absolute dulness may be abolished 
in such cases, percussion, nevertheless, affords valu- 
able data. You will be able to map out an area of 
deficient resonance. Commencing well to the right of 
the sternum, where the sound over the emphysema- 
tous lung is uncomplicated, you will advance nearer 
to the middle line of the sternum until you find that 
the sound, though not dull, is impaired. Thu§ you 
may obtain the outline of the deep cardiac area, and 
closely approximate to that of the heart, covered as it 
is by lung. You will, of course, observe the con- 
current signs-pulsation of the right ventricle at the 
epigastrium, venous turgescence, perhaps venous 
pulse, and, if the symptoms are advanced, oedema 
spreading from the feet upwards. 
We have now considered the evidence afforded by 
percussion of dilatation and hypertrophy of the left 
and right chambers respectively. You must, of course, PERCUSSION. 
89 
be aware that the condition of enlargement may affect 
both sides. In fact, dilatation of the right chambers 
may follow from impairment of the propulsive force 
of the left ventricle as consequence from cause. We 
shall see this especially when we come to consider 
valvular incompetence of the left heart. Suppose the 
left ventricle to be dilated and enfeebled, it is obvious 
that the first effect is a deficient propulsion of blood 
through the aorta-the general circulation is impaired 
owing to the reduced vis a tergo-the next result is 
engorgement of the venous channels; the right 
chambers of the heart may be considered as part and 
parcel of these venous channels-like the rest of the 
venous system, they are in a state of habitual plethora, 
so they become distended and enlarged, and their 
muscle becomes hypertrophied. 
Having learnt the chief lessons to be derived from 
percussion of the preecordial area, we shall in the next 
lecture proceed to "Auscultation." 90 
LECTURE V. 
AUSCULTATION. 
PART I. 
Immediate and intermediate auscultation - Stethoscopes- 
Normal heart sounds-Auscultation of voice to determine 
area occupied by heart-Topography of the valves-Modi- 
fication of normal heart sounds-Accent-Exalted second 
sound, aortic and pulmonary-Strong pulmonary with weak 
aortic second sound-Skoda's sign of mitral lesion-Strong 
aortic second sound in renal disease-Prolonged first sound 
-Short loud first sound-Reduplication of sounds-Ineffec- 
tual systole. 
I do not think it necessary to call your attention to 
the importance of Auscultation. In the present day 
this is fully recognized. I am not sure that there is 
not a slight tendency towards an opposite danger-I 
mean a too exclusive reliance upon the signs offered 
to the sense of hearing. When the suggestion has 
come that the heart-region shall be examined, I have 
often observed that the stethoscope has been at once 
flourished, and the listening over the prsecordium 
finished, the diagnosis has been supposed to be mature. 
I hope to have convinced you by the preceding lectures 
that precious aids to diagnosis are neglected if auscul- 
tation is alone relied upon. 
On the other hand, the method of diagnosis cannot 
be complete without auscultation. 
Auscultation may be direct and immediate, or in- 
direct and mediate. AUSCULTATION. 
91 
(A.) Immediate Auscultation.-You may obtain some 
general lessons by applying the ear directly to the 
heart-region, the chest being covered only by a fold of 
linen. By this you will learn whether the heart is dis- 
placed from its normal situation, and whether the sound 
of its contraction is strong or feeble. If prolonged 
and heaving you have corroborative evidence to add 
to the signs of hypertrophy, which have been deduced 
from previous examination. If feeble, you must hesi- 
tate before concluding that the heart-muscle is weak, 
for it is very probable that fatty tissue or emphyse- 
matous lung may intervene between the heart and 
your ear, and so occasion the feebleness of sound. If 
loud and heard over a wide area-a wider area than 
your examination by percussion of the space occupied 
by the heart -would lead you to suppose-it is very 
probable that you have to deal only with functional 
palpitation. 
(5.) Intermediate Auscultation.-Immediate auscul- 
tation is a useful preliminary; it gives you certain 
broad general impressions-but intermediate ausculta- 
tion is absolutely indispensable. You have to dif- 
ferentiate sounds coming- from situations very close 
one to the other. The valves of the heart all lie 
within a square half-inch of surface; if the tricuspid 
be excluded, portions of all may be covered by a 
superficial quarter of an inch. Practically, a sound 
obvious enough at a given point, may cease to be 
perceptible one-third of an inch therefrom. It is 
obvious, therefore, that the unaided ear cannot be 
relied upon, but that some means must be adopted 
for collecting and localizing sounds. The stethoscope 
must be used. 
A few words as to the form of stethoscope most 92 
AUSCULTATION. 
suitable. The ordinary wooden stethoscope is the 
most generally useful; the thoracic end should be 
small enough to be adaptable to the intercostal spaces 
in thin subjects. As a rule, I think the metallic stetho- 
scopes are inferior. 
The binaural stethoscope is extremely valuable. 
For the cardiac auscultation of infants and children, 
it is indispensable. Not only does it shut off from the 
ears external sounds and allow the impressions to 
come only from the part at which its cup is applied, 
but its flexible collecting tubes allow each movement 
of the patient to be followed. Otherwise, children 
and infants may elude all your attempts at ausculta- 
tion. Moreover, the sounds obtained through the 
double tube of this stethoscope, transmitted as they 
are to both ears, are perceived very intensely : sounds 
may be heard which otherwise would be inaudible. 
Still, I fully recognize that there is a danger-the 
sound may be too intense, so that if two occur near 
together, one may be drowned. The practical con- 
clusion is, use both forms of stethoscope, the ordinary 
and the binaural. I have my own stethoscope so con- 
structed that the same cup and stalk can be screwed 
into the ordinary wooden ear-piece, or into the 
junction of the tubes of the binaural arrangement.* 
So I examine successively with each form of instru- 
ment. 
I have now for some time been accustomed to use 
a form of binaural stethoscope, introduced, I believe, 
by Professor Stern of Vienna. In this instrument 
the spring which keeps the terminal cups applied to 
* This has been made for me by Messrs. Maw, Son, and 
Thompson. AUSCULTATION. 
93 
the ears (and often when auscultation is long-continued, 
causes inconvenient oi* even painful pressure) is dis- 
pensed with. Each of the two india-rubber conducting 
tubes has a vulcanite extremity, which " plugs " into 
the auditory meatus, and with a little practice is easily 
retained. The distal extremity of each india-rubber 
tube plugs into a vulcanite cup, which is applied to 
the chest. Messrs. Maw and Son have made for me 
a modification of this instrument, with these advan- 
tages :-(1) the distal extremities fit into a short 
stethoscope made of vulcanite or wood, which, by 
adapting an ear-piece can be used as an ordinary 
stethoscope ; (2) the india-rubber tubing is graduated 
in inches, so that the stethoscope serves also as a 
cyrtometer, or chest measure. 
Now it is necessary briefly to consider the Normal 
Sounds of the Heart. The mere application of 
the ear to the prmcordium will convince you that the 
noise of the heart in action can be resolved into two 
sounds, which can be imitated by the syllables, lubb- 
dup. A little consideration will show you that the 
first, the longer sound of lower pitch, is separated 
from the shorter, sharper sound, by a short but dis- 
tinctly appreciable interval of silence, and that, again, 
a longer pause or silence intervenes between the 
second sound and the recurrence of the first. Listen- 
ing near the situation of the apex, you will find that 
the first sound co-exists with the impulse of the heart 
against the walls of the chest-that is to say, the 
contraction of the ventricles, the systole. 
Without entering in the spirit of criticism upon the 
much-debated question of the exact mode of causation 
of these sounds of the heart, we shall find it sufficient 
for our present purpose to consider what is taking 94 
AUSCULTATION. 
place at the exact time at which these sounds respec- 
tively are occurring. 
At the time of the production of the Jirst sound, the 
following are the conditions. The ventricles are full 
of blood. The auricles have just contracted, impel- 
ling their contents through the auriculo-ventricular 
openings, and completing the replenishment of the 
ventricles. Then the muscle of the ventricular walls 
contracts-the tension of the enclosed blood forcing 
upwards the curtains of the auriculo-ventricular valves, 
putting them suddenly upon the stretch, and thus 
closing the orifices which they guard-driving the 
blood contained in the ventricles through the only now 
pervious openings-viz., the aorta on the left side, and 
pulmonary artery on the right. 
At the time of the production of the second sound 
the conditions are these. The aorta, and through it 
the arterial channels of the whole body, as well as the 
pulmonary artery and its branches which carry venous 
blood to the lungs, have just been filled with a gush 
of blood. A momentary interval has occurred whilst 
these onward currents have passed, and during which 
the ventricles have commenced to become relaxed. 
The blood has been forced by the systole not into 
rigid tubes or into inert canals, but into the elastic 
arteries. When, therefore, the ventricles have ceased 
their contraction, and an appreciable pause has oc- 
curred during which the impetus of the blood-current 
has been unresisted, the semilunar valves of the aorta 
and pulmonary artery respectively are suddenly closed. 
The cause of such closure is twofold. First-the 
mere weight of the superincumbent column of blood in 
these great vessels ; secondly-the elastic recoil of 
the previously stretched coats of the vessels of distri- AUSCULTATION. 
95 
bution. In the case of the aorta, the elastic recoil 
comes not only from itself, but from every artery and 
arteriole in the whole system-in the case of the 
pulmonary artery, from the narrower limits of the 
distributing channels within the lungs. The second 
sound, then, is short, sharp, and sudden, and there is 
no doubt that it is due to the sudden closure of the 
semilunar valves of the pulmonary artery and the 
aorta. 
During the pause following the second sound, the 
heart muscle is flaccid, and the cavities are becoming 
refilled. 
The first sound, then, is coincident with the con- 
traction of the ventricles ; it is systolic. The second 
occurs at the moment of closure of the semilunar 
valves; it is called diastolic, but it is obvious that it 
occupies only a portion of the diastole. The diastole 
of the heart embraces all that period which is not 
occupied by systole. 
Supposing the period of rhythm to be divided into 
ten equal parts, the following expresses, according to 
Dr. Walshe, the relative duration of sounds and 
silences: 
First sound = *4 
First silence = T 
Second sound = '2 
Second silence = '3 
In commencing the auscultation of the heart's area, 
you may have a duty as yet unfulfilled. Your former 
investigation may have failed to have indicated the 
situation of the heart's apex. This you must now de- 
termine by means of the stethoscope; observe and 
mark the extreme left of the situation at which the 96 
AUSCULTATION. 
impulse is heard at its maximum ; that will corre- 
spond to the apex. 
It may be necessary also to employ auscultation as 
a corroborative means of determining the area occu- 
pied by the heart, or by distended pericardium. You 
do this by auscultating the voice. The lines where 
vocal resonance terminates or becomes greatly dimi- 
nished, indicate the border of the area. 
We have now considered the necessary prelimi- 
naries for Auscultation of the Heart. The apex has 
been indicated, and the area occupied by the various 
chambers has been mapped out. We have already 
described the topography of the heart; we have now 
to consider the Topography of the Valves. The 
aortic, pulmonary, and tricuspid valves all are situated 
near the surface of thoracic wall-not so the mitral- 
this only approaches the surface at the point of the 
apex-beat, where the left ventricle comes towards 
the thoracic surface. 
For the purposes of clinical investigation, the exact 
anatomical delimitation of the valves is of less impor- 
tance than the determination of the areas on the 
thoracic surface to which the sounds proceeding from 
them are conducted. There are four centres where 
the sounds proceeding from the heart are determined 
to the thoracic surface :- 
At the heart's apex are heard the sounds produced 
at the mitral valve. 
At the lower end of the sternum, the base of the ensi- 
form cartilage, the sound emanating from the tricuspid 
valve. 
At the second left intercostal space close to the sternum 
the sound proceeding from the pulmonary artery. 
At the junction of the second right costal cartilage AUSCULTATION. 
97 
with the sternum and the contiguous second right 
intercostal space, the sound generated in the aorta. 
As I have said, the area, as indicated by the sound, 
is not the absolute anatomical area. 
1. 11 Sounds emanating from the mitral valve are not 
looked for directly over the valve (in the second left 
intercostal space, close to the sternal insertion of the 
third left costal cartilage), as here the latter lies be- 
hind air-containing lung tissue, a bad conductor of 
sound; they are auscultated rather at the apex of the 
heart, which is free of lung, and in immediate contact 
with the chest-wall, and towards which experience 
shows that sonorous vibrations coming from the mitral 
valve are transmitted with greatest intensity. 
2. 11 In the same way the sounds of the tricuspid 
valve are not to be sought for exactly over their point 
of origin (behind the sternum at the level of a line 
drawn obliquely from the sternal insertion of the third 
left rib to the fifth right costo-sternal articulation), 
but somewhat lower down on the lower portion of the 
sternum." * 
3. The sounds from the pulmonary artery are heard 
best over its exact anatomical position : from its origin 
in the right ventricle it rises to the lower border of 
the second left cartilage, where it divides into its 
ris-ht and left branches. The sounds from the vessel 
are, therefore, best heard in the second left interspace, 
where it is close to the thoracic wall. 
4. u Sounds developed in the aorta are loudest, not 
just over the orifice of the vessel (in the second left 
intercostal space), but in the second right intercostal 
* Guttmann, "Handbook of Physical Diagnosis New 
Sydenham Society's Translation. London, 1879. 98 
AUSCULTATION. 
space, in the direction of the ascending aorta. As the 
aorta at its origin completely covers the root of the 
pulmonary artery, the sounds produced in these ves- 
sels are necessarily intermingled, and would be indis- 
tinguishable from each other, were it not for the fact 
that those generated at the aortic valves are propa- 
gated most energetically in the direction taken by the 
current of blood in the ascending aorta, along the 
course of the vessel towards the second right inter- 
space ; at the latter point, therefore, aortic sounds 
should be auscultated."* 
Deferring for a time any consideration of abnormal 
sounds heard over the heart's area, we will consider: 
(a.) That the heart-sounds are modified 
IN DEGREE. 
A few words as regards accent. If you listen over 
the apex of the heart, you will find that the more pro- 
nounced of the two sounds is the first or systolic one. 
The accent falls on the sound produced by the con- 
traction of the ventricles, such sound more readily 
reaching the ear. It would be expressed by the 
syllables, lubb-dup. At the base, however, the accent 
is reversed. The semilunar valves are nearer to the 
ear, the accent falls on the shorter second sound and 
the expression would be dvp-lubb. This may give rise 
in some cases to a little perplexity : you may take 
the second sound for the first, and vice versa. The 
difficulties may be obviated, however, by a very simple 
rule. When you are auscultating the base of the 
heart, place the finger over the spot of the apex-beat, 
or, if this be too feeble to be distinguished, over the 
* Guttmann, loc. cit. p. 262. AUSCULTATION. 
99 
situation of the great vessels at the root of the neck. 
The impulse or the pulse will thus tell you which is 
the first sound: of course if the sound you hear be 
synchronous with the systole or pulse, it is the first 
sound, if not it is the second. 
It is well, in my opinion, to commence by auscul- 
tating at the base of the heart, because the situations 
of the aorta and pulmonary valves are fixed points, 
whilst the apex is variable. 
At the base, in the absence of abnormal sounds, it is to 
the second sound that you must pay attention. The qua- 
lity of the first sound will be investigated at the apex. 
You will place your stethoscope over the second 
right costo-sternal articulation, then carry it across 
the sternum to the second left interspace and the articu- 
lation of the sternum with the third costal cartilage on 
the left side. You will observe and compare the 
qualities of the second sound in these right and left 
situations respectively. The aortic second sound is 
normally more pronounced than the pulmonary. It 
is the closure of the aortic valves which gives, for the 
most part, the character to the second sound which is 
heard over the general area of the heart-that is to say, 
the aortic overpowers the pulmonary second sound. 
Suppose now that (a) the aortic second sound is intensified. 
It is obvious that you must train your ear by observing 
the second sound in cases of health. When you have 
recognized its normal intensity only are you in a posi- 
tion to judge of its exaggeration. If on placing your 
stethoscope over the second right costo-sternal articu- 
lation you hear a sharp and loud flap coming closely 
to the ear, your inference must be that an abnormal 
amount of blood, which has been forced into the aorta 
by the contraction of the left ventricle, has, by the 100 
AUSCULTATION. 
energy of its reflux, closed and put on the stretch the 
semilunar valves. Carrying your inference further, 
you will find that you must have a strong, muscular, 
in other words, hypertrophied left ventricle, and an aorta 
capable of containing an unusual amount of blood, in 
other words, a dilated aorta. In conjunction, therefore, 
with other signs, you will find persisted exaggeration 
of the aortic second sound a valuable evidence of hyper- 
trophy of the left ventricle. Conversely, if you find 
that (b) the aortic second sound is feeble, you may infer 
that there is a deficiency of arterial blood supplied to 
the aorta by the ventricle. This observation is some- 
times valuable as a means of prognosis when the blood 
has been diminished in quantity by haemorrhage, or 
when the tone of the heart has been enfeebled by disease. 
In fevers a very weak second sound is a bad prognostic. 
There are certain circumstances, however, which mar 
or modify such absolute deductions from the observed 
force or feebleness of the second sound. There may 
be a sharp and loud second sound when the aortic 
valves are unusually thin. Or it may have a dull or 
leathery character when the valves are thickened. You 
must, therefore, remember to record the observation, 
but to make no absolute deduction without comparison 
with other physical signs. 
Suppose now that (c) the pulmonary second sound is 
intensified. This is a sign of more absolute importance. 
I have said that the great cause of intensification of 
the aortic second sound is an increase above the 
normal quantity of blood in the aorta. In case of the 
pulmonary second sound another cause is present to 
augment it. The pulmonary is a smaller circuit, and 
the blood contained in it, like the water in a Bramah 
press, exerts equal pressure in all directions. The AUSCULTATION. 
101 
blood-pressure in the general systemic circulation is 
modified in various ways, by subsidiary circulations, 
as the portal, and by many special conditions in the 
various tissues. The pulmonary circulation may be 
looked on as if conducted by a single flexible and con- 
tractile tube from right ventricle to left auricle. If, 
from any cause, therefore, there is any obstruction to 
the flow of blood within the pulmonary circuit, the 
result is not only congestion of the lungs, but also "a 
uniform increase of the tension throughout the whole 
of the pulmonary circulation, often accompanied, if 
long continued, by slight dilatation of the pulmonary 
artery, and always by a closure of the semilunar valves 
with an exaggerated force proportionate to the hin- 
drance it has met with."* 
Of still greater importance than the estimation of the 
absolute strength or weakness of the aortic and pul- 
monic second sound, is the observation of the relative 
force of the sound in the two situations. 
Suppose that you find that (<7) the pulmonary second 
sound is intensified whilst the aortic is enfeebled. Your 
first inference will be, as I have just indicated, that 
there is exaggerated tension in the pulmonic circula- 
tion-that is the cause which must produce the exalted 
second sound. This may occur, however, in any con- 
dition of respiratory trouble when there is congestion 
of the lungs, but then the second sound over the aortic 
valves need not be perceptibly or persistently enfeebled. 
The co-existence of a strong pulmonary with a weak 
aortic second sound is a sign that whilst the pulmonary 
artery receives too much blood, the aorta receives too 
little. It is valuable evidence, as Skoda first pointed 
* Balfour. 102 
AUSCULTATION. 
out, of a diseased condition of the mitral orifice either 
permitting regurgitation, or inducing obstruction of the 
blood-stream. In the case of the former, the expla- 
nation of the phenomenon is easy: the arterial current, 
urged into the aorta by the contraction of the left ven- 
tricle, is diminished by the amount which regurgitates 
through the imperfectly-closed mitral orifice; the aorta, 
therefore, is insufficiently supplied with blood, and the 
sound caused by the reflux against its semilunar valves 
is consequently weak. In the case of mitral obstruction 
(stenosis) the effect is the same, though the cause is 
different. Here the blood reaches the ventricle with 
difficulty on account of the narrowing of the outlet from 
the auricle, systole takes place upon an insufficient 
amount, and the aorta is ill supplied. The case is just 
otherwise with regard to the pulmonary artery ; as a 
consequence of the deficient arterial supply, induced by 
both the above conditions, there has been a reduction 
of the rate of venous return, and engorgement of the 
venous system, a secondary dilatation of the right side 
of the heart. In regurgitation, a backward current is 
created by the systole of the ventricle ; in obstruction, 
the contraction of the auricle tends to cause reflux A1J 
these causes, therefore, produce high tension in the pul- 
monary circuit. So, with the arterial anaemia there is 
venous and pulmonic hyperaemia, and hence exaltation 
of the shock of recoil of the semilunar valves pertaining 
to the right heart. This observation of the comparative 
intensification of the pulmonary second sound is valu- 
able, not only as a sign of the existence of the conditions 
I have just mentioned, but as an indication of their 
degree-so it is of great importance in prognosis. In 
proportion to the comparative feebleness of the aortic 
second sound is the failure of the ventricle ; in propor- AUSCULTATION. 
103 
tion to its strength is the power of the ventricle, by its 
compensatory hypertrophy, to overcome the obstacles 
imposed. 
If you find the opposite condition when (e) the aortic 
second sound is relatively intensified, it is evidence, of 
course, of hyperaemia on the arterial side of the circu- 
lation. I have already spoken of this as suggesting 
hypertrophy of the left ventricle, but it is only to be 
relied on in concurrence with other signs. There may 
be much hypertrophy of left ventricle concurrent with 
mitral regurgitation, when, as we have just seen, the 
aortic second sound is enfeebled. In such case the 
hypertrophy is insufficient to compensate for the loss 
by regurgitation through the mitral orifice. Again, 
though the left ventricle may be hypertrophied and 
the aorta dilated, the coats of the latter (through 
atheroma for instance) may be so inelastic that the 
second sound may evidence no exaltation. There is one 
condition of disease, however, in which accentuation 
of the aortic second sound is a sign of considerable 
importance-this is Chronic Bright's Disease. I have 
called your attention already to the conditions which 
exist in this disorder. There is a peripheral obstruc- 
tion to the circulation of the blood through the ter- 
minal arterioles, coincidently there is heightened 
power of left ventricle; the necessary consequence is 
an abnormal excess of tension in the arterial system, 
and this state of tension occasions the sharp and pro- 
nounced aortic second sound. 
It is important to note the relative predominance of the first 
and second sounds at the base of the heart. You may find 
that the first sound is nearly or quite inaudible, the only sound 
is the diastolic. In such case there is strong presumptive 
evidence of hypertrophy of the left ventricle. 
We turn now from the base to the apex ; and our 104 
consideration will be devoted to the first instead of 
the second sound. Suppose we find that (/) the first 
sound is abnormally prolonged. We have then evidence 
of hypertrophy of the left ventricle. In auscultating 
at the apex I advise you to keep distinct in your 
minds the element of sound and the element of dura- 
tion. You see that as evidence of hypertrophy I have 
called especial attention to the latter. The first sound 
is constituted by two factors, the contraction of the 
ventricular walls, and the tension of the auriculo- 
ventricular valves. The muscular sound of the con- 
tracting ventricles is dull and prolonged, whilst the 
sound of the stretching of the curtains of the valve 
is (as you know it to be in the case of the semilunar 
valves) sharp, short, and sudden. In proportion as 
the muscular element of the first sound preponderates 
over the valvular, so the first sound will be dull and 
prolonged. 
In hypertrophy the first sound is dull, partly because the 
flap of the valve-curtains is less easily conducted to the ear 
through the thick muscle of the ventricular wall, partly 
because the contraction of the ventricle itself produces a dull 
(muscular) sound. It is prolonged, because the thicker the 
muscle, the longer its period of contraction. (For a review of 
the numerous theories as to the causation of the sounds of the 
heart, see Hayden's " Diseases of Heart and Aorta," 1875, 
pp. 93 et seq.) An able investigation on the question has been 
made by Guttmann (see "Handbook of Physical Diseases," 
translated by Dr. Napier: New Sydenham Society, 1879, 
p. 265, et seq.), who concludes thus :-"Although the whole 
question in dispute cannot yet be said to be definitely settled, 
the conclusion to which the present state of our knowledge 
seems to point is, that the first sound is essentially of valvular 
origin, and only to a slight extent muscular." 
If on the other hand (^) thefirst sound is shortened, 
it is evidence that the ventricle is weak. In this rela- 
AUSCULTATION. AUSCULTATION. 
105 
tion we may have several conditions. The first sound, 
though short, may be loud. It is rather a frequent 
mistake to interpret loudness of the first sound as a 
sign of increased power of the ventricle ; as a rule it 
is the opposite. A loud, sharp, short, flapping first 
sound at the apex indicates dilatation, and consequent 
feebleness of the ventricular walls.* In such case 
the muscular sound is reduced to a minimum, and the 
ear appreciates in the greatest degree the valvular 
element of the first sound. Then the first sound 
approaches the second sound in character and dura- 
tion. You may even be puzzled to discern the one 
from the other. The following rule will easily guide 
you: whilst you are listening by means of your 
stethoscope, place your finger over the spot nearest 
the heart apex, at which a decided pulsation is to be 
felt. If the apex-beat is evident, place your finger 
over its situation, if not, observe the carotid pulse 
(not the radial, for that is fallacious, because it is not 
always coincident with the cardiac systole). You 
thus have a certain indication of the time of the systole, 
and you will be able at once to know whether the 
sound which you hear is synchronous with it-i.e., 
the first sound-or intermediate between pulse and 
pulse, when it will, of course, be the second sound. 
But the first sound may be short and yet feeble, and 
this is evidence of a still graver condition of heart- 
debility. You then have, not only an impaired mus- 
cular sound, but a weak valve sound, for the enfeebled 
muscle cannot create sufficient tension to produce the 
pronounced flap of the valvular curtains. In such 
* Such a first sound is met with in Graves' Disease. See 
p. 30. 106 
AUSCULTATION. 
case you must look for the other signs and symptoms 
of degeneration of the muscular walls of the heart. 
In extreme cases of fatty degeneration, the first sound 
mav he lost altogether. 
We will next consider briefly a condition which is 
sometimes more interesting than important, but which 
must always be noted and deciphered where it exists- 
(A) the sounds of the heart are reduplicate. I nstead of the 
single sound of the normal rhythm you hear two 
sounds following as if the syllables tah-ta were uttered. 
This may occur at the base or at the apex, or in both 
situations. It may be heard as a permanent sign in 
conditions of health, as a transient occurrence in such 
conditions, as a permanent sign in disease, and lastly, 
as a phenomenon, continuing definitely during a 
morbid condition of the heart, and vanishing when 
health becomes restored. On what does it depend ? 
The inquiry is interesting, but the answer is not easy. 
We will first take the case in which the phenomenon 
is manifest at the apex and not at the base. Now I must 
ask you carefully to discriminate between reduplica- 
tion and ineffectual systole. I have already said that 
in some cases contraction of the ventricles may be 
repeated without producing a pulse to be felt at the 
wrist; so if you count the pulse at the wrist and 
compare with the rate of pulsations as determined by 
auscultating the apex, you find that the two records 
do not exactly correspond. 
Many cases and observations have been recorded 
which illustrate this ineffectual working of the ven- 
tricle, notably by Von Dusch, Potain, Hayem, and 
Flint. This is not reduplication, however; in re- 
duplication there is a repetition only of a portion 
(the systolic or diastolic sound as the case may be) AUSCULTATION. 
107 
of the cardiac revolution, whilst in ineffectual systole 
the whole cardiac revolution is repeated once, twice, 
thrice, or even four times, until sufficient arterial ten- 
sion is attained to produce the pulse. In such case 
the pulse may be sometimes felt in the larger vessels, 
as the carotids, before it is manifest in the radials. 
You may, perhaps, understand this better if I indicate 
it graphically. Let the syllables tah-ta express the 
cardiac sounds, tah being the first sound and ta the 
second. Then Ineffectual Systole is thus re- 
presented :- 
tah ta tah-ta = Pulse: or 
tah ta tah-ta : tah-ta = Pulse : or 
tah ta tah-ta: tah-ta tah-ta = Pulse, 
the latter indicating varying expressions of strength 
of the sounds. 
Reduplication of the First Sound is repre- 
sented by 
tah tah ta = Pulse : tah tah ta - Pulse, or 
tah tah ta = Pulse : tah tah ta = Pulse. 
A doubling of the first sound may be heard in health 
at that period of the respiratory rhythm when expira- 
tion has just been completed and inspiration is com- 
mencing. 
According to Dr. Hayden the phenomenon may 
be associated (1) with simple functional derange- 
ment of the heart, such as nervous palpitation and 
fluttering, usually accompanied by anaemia ; (2) with 
attenuation and weakness of the ventricles in persons 
of middle age of nervous temperament; (3) with a 
weak degenerating heart, and dilated atheromatous 
arteries; (4) with simple hypertrophy of the ventricle. 
According to Guttmann it may occur temporarily in 
perfectly healthy persons; it may be noted at times 108 
AUSCULTATION. 
in diseases of the heart-sometimes connected with 
mitral, sometimes with tricuspid disorder-but cannot 
be said to be characteristic of any particular affection. 
As far as regards clinical diagnosis, therefore, you 
may conclude that the sign is of but little importance. 
Of course you will in every case which comes before 
you be careful to note it, because, as we shall see, its 
investigation may have a strong bearing upon the 
interpretation of some unsolved cardiac phenomena. 
We will now consider reduplication of the second 
sound, which is much more commonly observed. This 
may be expressed by 
tah ta ta = Pulse : tah ta ta = Pulse, &c. 
Potain noted that reduplication of the second sound 
occurred in health at the end of inspiration and begin- 
ning of expiration. 
It may take place in conditions of debility of the 
muscular structure of the heart, and is often observed 
in the course of typhoid fever, commencing usually in 
the second week. In such cases M. Hayem has shown 
that there is an inflammation of heart muscle. The 
reduplication ceases as health is regained. 
There is no doubt, however, that there is one con- 
dition in which the phenomena occurs most frequently 
and in its most pronounced degree-that is, in obstruc- 
tion at the mitral orifice. Guttmann says it is heard in 
almost a third of the cases of mitral stenosis, and Dr. 
Hayden found it in thirty out of eighty-one. This 
accords with my own experience. Of twenty- 
seven instances of reduplicated second sound noted by 
Dr. Hayden, twenty-six were cases of mitral obstruc- 
tion ; you will conclude, therefore, that doubling of 
the second sound is a sign not only of physiological 
but of clinical and diagnostic importance ; you will AUSCULTATION. 
109 
consider it as presumptive evidence of mitral stenosis. 
Doubling- of the second sound is also heard in cases of 
adherent pericardium (Friedreich) occasionally, and 
passim in engorgement of the right side of the heart, 
in fatty degeneration, and in some cases of pulmonary 
emphysema and of pulmonary tubercle; and accom- 
panied by murmur, occasionally in disease at the 
aortic orifice. When you meet with it, note carefully 
the area over which it is heard, and determine which 
of its elements has the preponderance in given areas. 
Dr. Hayden says : " In every example of this anomaly 
which has come under my notice, the double character 
of the sound was exhibited only in the area over which 
the sounds of the aorta and the pulmonary artery were 
both audible; whereas when the stethoscope was shifted 
a short distance to the right or left of this region, a 
single second sound only was heard." * This does 
not accord with Guttmann, who says : " The broken 
diastolic sound is (so far as I have observed) certainly 
not loudest over the large vessels, but at the lower 
part of the sternum and near the apex of the heart."! 
My own observations accord with those of Guttmann. 
There are few questions in cardiac pathology more difficult 
than that of the mode of causation of reduplication of the 
heart-sounds. This can scarcely be surprising when it is 
considered that observers are by no means agreed as to the 
causes of the normal, uncomplicated sounds of the heart. As 
regards reduplication of the first sound, the theory of which long 
seemed with greatest probability to be correct, ascribed it to 
non-synchronous contraction of the two ventricles. Thus, 
a right ventricular systole is followed by a left ventricular 
* " Diseases of Heart and Aorta," p. 165. 
+ " Handbook of Physical Diagnosis Sydenham Society's 
Translation, p. 278. 110 
AUSCULTATION. 
systole, or vice versA. Many observers have, however, found 
it difficult to accept this theory on account of the structural 
unity of the ventricles, and the observed consentaneousness 
of their action. That such derangement of synchronism is pos- 
sible is, however, some observers consider, well proved by 
physiological research. 
Dr. J. Barr, of Liverpool, considers that each side of 
the heart has, to a certain extent, its own nerve-supply, and 
can accomplish its own peristaltic action, and, though both 
sides are set to the same time and have a complex interlace- 
ment of fibres, "it is an experimental fact that one side can 
begin or end contraction before the other."* In some rare 
cases, too, this want of synchronism on the part of the ven- 
tricles can be clinically demonstrated. Dr. Barr has described 
to me a case in which the impulse of the left ventricle could be 
first felt, and then that of the right ventricle, and this suc- 
ceeded by a weak impulse of the left. On auscultation there 
were heard a loud systolic (mitral) murmur, then a sharp, clear 
first sound, followed by a short murmur (mitral). The proxi- 
mate cause of the reduplication then, as advanced by those 
who first adopted the theory of asynchronous systole of the 
ventricles was the retarded closure of the tricuspid valve, 
owing to the excess of blood-pressure in the right cavities. 
Dr. Barr, however, whose investigation of the subject is a very 
careful one, whilst adopting the theory of asynchronism of the 
ventricles, gives an opposite explanation of the proximate 
cause. He considers that the excess of blood pressure in 
the right heart (such as occurs in the normal heart during 
deep expiration, when physiological reduplication of the first 
sound is heard) stimulates the right ventricle to commence 
contraction before the left, so the tense closure of the tricuspid 
valves occurs before that of the mitral. One of the chief 
objections urged against the theory of ventricular asyn- 
chronism has been that the disturbance in systole ought in the 
nature of things to be accompanied by disturbance in diastole, 
that the non-simultaneous impletion of the aorta and pul- 
monary artery respectively should be followed by non- 
* Vide a Paper on Reduplication of the Heart-Sounds, 
Medical Times and Gazette, 1877. AUSCULTATION. 
111 
simultaneous closure, by reflux of the aortic and the pulmonary 
semilunar valves ; that, therefore, doubling of the first sound, 
should invariably be accompanied by doubling of the second, 
which is not the case. Dr. Barr meets this difficulty by ad- 
vancing the view " that though the right ventricle commences 
its systole before the left, it is longer in emptying itself, 
owing to its overloading, and to the increased obstruction in 
the pulmonary circuit, hence, although it had the start of 
the left, it has not completed its contraction before it, so there 
is no reduplication of the second sound under these circum- 
stances." Of other theories which have been advanced to 
explain reduplication of the first sound, may be mentioned 
that of Guttmann, which ascribes it to non-synchronous 
tension of the individual segments of the auriculo-ventricular 
valves owing to absence of perfect uniformity in the con- 
traction of the papillary muscles. This hypothesis appears to 
me in the highest degree improbable; it would seem much more 
likely that such irregularities on the part of the papillary 
muscles could produce, not reduplications, but murmurs. Dr. 
Hayden's view is, that the doubling is equivalent to the resolu- 
tion of the first sound into its two constituent elements-viz , 
the ventricular impulse and the click of valvular tension. 
According to this, the click of valve tension should occur at 
the very latest period of systole, the " thud " of muscular 
impulse always preceding it. This cannot, however, be sus - 
tained, for cardiographic evidence abundantly shows that the 
closure of the auriculo-ventricular valves occurs early in the 
systole, and that the first sound is prolonged subsequently to 
their closure. The "click " therefore ought always to precede 
the "thud," whereas Dr. Hayden says that, in his experience, 
without exception, " the first element of the double sound has 
been dull and muffled, and the second sharp and clear."* 
Dr. George Johnson has advanced a theory totally distinct 
from the others. He considers that the so-called reduplicated 
first sound consists of really the rapidly following sounds of first 
an auricular and then a ventricular, systole. The contraction of 
a dilated, and especially of a hypertrophied auricle becomes 
audible, and the first division of the double first sound is the result 
* "Diseases of Heart and Aorta," p. 118. 112 
AUSCULTATION. 
of the auricular systole. That the sound can be the direct effect 
of the systole of the auricle is very difficult to believe. As 
well as other observers I have had opportunities of auscultating 
the auricle in very many conditions of dilatation and hyper- 
trophy, and when it has been through pulmonary disease 
totally uncovered by lung, but in no case has there been a 
particle of evidence that its muscular contraction is accom- 
panied by sound. Nor does it seem probable, when we 
consider how feeble is the muscular sound of the ventricle, 
even in conditions of the greatest hypertrophy. Whilst 
denying that the sound is the direct effect of the auricular 
systole, I would by no means assert that it may not be the 
indirect effect thereof. It is quite conceivable that in some 
cases the energetic systole of the auricle suddenly floating up 
the curtains of the mitral valve, may so put them on the stretch 
as to cause a sound-the click of valve-tension. Potain noticed 
a form of seeming reduplication of the first sound, which he 
termed "bruit de galop" in cases of hypertrophy of the heart 
associated with granular kidneys. He considered that the 
first element of the apparent reduplication was presystolic. 
Guttmann also has observed such presystolic sound in a 
number of cases of cardiac hypertrophy; he considers that the 
auriculo-ventricular valves are to a certain extent rendered 
tense at the end of diastole-that is in the presystole ; but this 
tension is so feeble that no sound results; when, however, 
from hypertrophy of the auricle the tension is increased, it is 
quite possible that sound may be occasioned. 
As I have said, reduplication of the first sound is a pheno- 
menon of comparative rarity. Many good observers have 
never met with a case. Dr. Hayden has noted twelve 
examples-eight in cases of females, four in males. Of 
these, six were considered nervous; three associated with 
menstrual disturbance; one with gout; another with Graves' 
disease. Hypertrophy of the left ventricle existed in three 
cases ; dilatation (in connection with cirrhosis of the liver) in 
one case ; and fatty degeneration in two cases. Mitral 
stenosis existed in one case; in this both sounds were 
double.* Dr. Hayden says: " Reduplication of the first 
sound is so intimately associated with simple or eccentric 
* " Diseases of Heart and Aorta," p. 164. AUSCULTATION". 
113 
hypertrophy that, if carefully sought, it will be found in every 
such case anterior to consecutive degeneration of tissue." I 
have already said that I can by no means accept Dr. Hayden's 
theory of a splitting-up of the normal first-sound into its two 
component elements of muscular susurrus and valve tension. 
It appears to me that either (a) the reduplication is real and 
caused by non-synchronous tension of the auriculo-ventricular 
valves of the right and left sides, or (6) it is only apparent and 
due to a presystolic being closely followed by a normal first 
sound, the presystolic sound being produced by the sudden 
floating upwards of the mitral curtains, occasioned by the 
auricular systole. I have met with reduplication, or apparent 
reduplication of the first sound in eleven cases. Of these the 
conditions were various, but classification could, in my opinion, 
be made as follows:-(ci) cases (four) in which there was 
evidence of prolonged ventricular systole, with rough first 
sound or murmur (in one case double murmur) at the base of 
the heart, and a pulse of decidedly high tension ; (b) cases 
(three) in which there was a disturbance of respiration and 
evidence of, at least temporary, distension of the right chambers 
of the heart; (c) cases of mitral stenosis (three); (d) one case of 
myocarditis in course of typhoid fever; here both first and 
second sounds were doubled. The positions of audibility of 
the reduplication were over the apex, five cases; over the base, 
two cases ; generally over the praecordium, one case ; over the 
right cavities, one case ; and in two cases its audibility varied 
from apex to base. In a, b, and d, it would seem quite pro- 
bable that the theory of asynchronism of the pulmonary and 
aortic second sounds might be justified ; but in group c, it 
appears to me that there are strong probabilities that the 
apparent reduplication is really a presystolic succeeded by a 
systolic sound. This view may be best illustrated by the 
following brief abstract of a case:-Female, aged thirty, 
admitted under my care at the London Hospital, for epilepsy. 
Subacute rheumatism occasionally from age of six. Pregnant. 
The physical signs as regards the heart showed briefly the 
apex in normal position ; first sound subdued but accompanied 
by murmur conveyed towards axilla. At base, Second sound 
pronounced, but no other abnormality. On the day follow- 
ing admission, I found that the first sound was reduplicated, 
the reduplication was heard in a line leading from the fourth 114 
AUSCULTATION, 
interspace to the anterior border of the axilla. Two days 
afterwards the patient aborted. The reduplication persisted 
but changed in certain characters, at the end of a fortnight it 
was heard from the third interspace to the apex ; a little 
internal to the apex reduplication was distinct and sounds 
uncomplicated. On nearing the apex a soft systolic murmur 
tailed off from the second element of the reduplication, and at 
the apex, reduplication was lost, a first-sound murmur only 
being heard. Sphygmographic tracings gave evidence of hyper- 
trophy of the left ventricle ; there was an ample tidal wave 
and the dicrotic was high in the tracing. The trace also 
showed occasional disturbance of rhythm (double pulse), and 
the diastolic periods were unequal in time. Cardiographic 
evidence confirmed this diagnosis of hypertrophy. In some 
tracings there was evidence of the point of closure of the 
auriculo-ventricular valves; the summit of the systolic portion 
was broad, and the terminal swelling marked. In the diastolic 
portion, the auricular eminence was chiefly remarkable for the 
breadth of its base. This case tells in favour of the view that 
the second element of the reduplication was the voice of the left 
ventricle. This is shown by the fact that the murmur which 
started from it was mitral systolic. To what then was due the 
first element ? It seems scarcely likely that it could be the voice 
of the right ventricle-of the tricuspid valve-for reduplica- 
tion was at first not even audible over the right ventricle. It 
would seem to me more probable that it was due to the 
presystolic flap of the mitral valve in the manner I have before 
mentioned. This view was, I think, confirmed by the progress 
of the case ; for, after losing sight of the patient during the 
interval, I had an opportunity of examining her again eight 
months subsequently, then there was no reduplication of the 
first sound but a presystolic murmur, typical and distinct. I 
am convinced that in certain cases of mitral stenosis a phe- 
nomenon closely or exactly simulating reduplication of the 
first sound may be observed. (See Part II.) In one case 
of mitral stenosis, in which I noted this close resemblance to 
reduplication of the first sound, the cardiographic tracing 
showed a very broad, pronounced eminence, indicating the 
auricular systole; the inference was plain that there was much 
hypertrophy of the auricle and the degree of stenosis slight, so 
that the auricular contraction gave a distinct impulse to the AUSCULTATION. 
115 
apex. The mechanism of production of such sound seems to 
me by no means difficult to realize. During the interval imme- 
diately succeeding the relaxation of the ventricle, the blood, 
subject to the tension in the left auricle and pulmonary veins 
has been pouring into the ventricular cavity; the fluid 
naturally finds its way in the direction of least resistance, that 
is, its course, when impelled towards the apex, is round the 
walls of the ventricle, thus coming behind the curtains of the 
mitral valve, and bellying them out (so to speak) as the sails of 
a ship are bulged by the force of the wind. At the moment of 
auricular systole, the ventricle, as yet only partially full, is 
rapidly distended, the force of contraction of the auricle 
giving an impulse to the apex of the ventricle, and, as may of 
course be inferred, giving a contre-coup to the already 
partially-strained mitral curtains. In normal conditions such 
contre-coup is inaudible, but when the auricle is more than 
ordinarily powerful, or when the mitral valve is so changed as 
to give rise to the sound of membranous tension, it becomes 
perceptible closely preceding the sound produced by the ven- 
tricular systole-that is, the sound of complete closure of the 
valves guarding both auriculo-ventricular orifices plus the 
muscular sounds of the ventricles. The sharp, short, first 
sound so common in mitral stenosis I believe to be chiefly due 
to sudden tension of the tricuspid valve. In this I know other 
observers, especially Dr. Barr, agree with me. I would by no 
means urge, however, that such must be the universal inter- 
pretation of cases of reduplication of the first sound. Infre- 
quent as are the instances, their very incongruity teaches that 
each case must be judged for itself. For cases of physiological 
reduplication, Dr. Barr's theory offers, to my mind, a plausible 
explanation. So also it may explain others connected with 
neurotic disturbance. I find it difficult, however, to associate 
reduplicate first sound in any causal way with differences 
of intra-ventricular pressure, seeing that long-persisting varia- 
tions in such pressure and disturbances of balance must be so 
common, whilst the phenomenon itself is so rare. As regards 
its probable auricular origin, in some cases we may get 
more evidence in our consideration of reduplication of the 
second sound. A reference to A. B. Fig. 3 will show the 
mutual relations of these reduplications. Now supposing it 
were granted that the sound-producing tension of the mitral 116 
AUSCULTATION. 
curtains might be effected in some cases early in diastole, and 
not only always late in diastole-that is, in presystole-we 
Fig. 3. 
Diagram showing positions in the cardiac rhythm oi apparent 
reduplications of A the second, B the first sound. 
might have in some instances a semblance of reduplication of 
the first, in others of the second, sound. If the tension 
happened to be effected late, or in presystole, it would be 
represented by B, in the diagram-apparent reduplication of 
the first sound ; if early, by A, apparent reduplication of the 
second sound. 
So-called reduplication of the second sound is a phenome- 
non which observers agree to be much more frequent than that 
we have just considered. It is undoubted that by far the most 
common condition in which double-second sound is heard 
is mitral stenosis. Next in point of frequency, according 
to Dr. Hayden, is aortic insufficiency. With considerable 
unanimity the phenomenon has been ascribed to a want of 
synchronism in the closure of the valves of the aorta, and of the 
pulmonary artery respectively. The sequence of closure may 
vary. In cases of aortic insufficiency, Dr. Hayden is satisfied 
that the second element is aortic, because the murmur of 
aortic regurgitation accompanies it. He believes that in such 
cases the left ventricle is dilated, and so is slower to become 
emptied in systole; consequently the aortic reflux is post- 
poned. On the other hand, in mitral stenosis the derange- 
ment is chiefly in the pulmonary artery, "the entire pul- 
monary system and the right chambers being engorged by 
obstruction at the mitral orifice. In the effort to overcome 
this obstruction, the systole of the right ventricle is pro- 
tracted, and the reaction of the pulmonary artery proportion- AUSCULTATION. 
117 
ately postponed. The reaction of the aorta is, on the other 
hand, in mitral stenosis most probably anticipated, where the 
left ventricle is reduced in capacity, as always is the case 
where mitral or aortic reflux does not co-exist. Hence it is 
likely that in simple mitral stenosis two causes of doubling of 
the second sound are in operation-viz., diminished capacity 
of the left, and dilatation of the right, ventricle " (" Diseases 
of Heart and Aorta," p. 128). It seems a truism to assert 
that conditions of blood-pressure in the two great vessels 
respectively, cannot be the ver a causa of such reduplication ; 
for until the occurrence of diastole, there can be no reflux, 
and consequently no second sound. The causation of redu- 
plication, as of the first so of the second sound under the 
theory we are now discussing, must revert to the ventricles. 
When their systole is simultaneous, the second sound, pro- 
duced by reflux against the semilunar valves of the two great 
vessels, at the moment of their relaxation, must be simul- 
taneous also. When their systole is not simultaneous, or does 
not last through equal periods, the diastolic reflux cannot be 
simultaneous; if the discrepancy be such as can be appre- 
ciated by the ear, the second sound is doubled. The following 
is Dr. Barr's view :-"As I have ascribed reduplication of 
the first sound to asynchronism in the initial stage of ventri- 
cular contraction, so I believe reduplication of the second 
sound to be due to asynchronism at the end of contraction, 
and in the consecutive reaction of the aorta and pulmonary 
artery, with the tension of their respective valves." The 
comparative rarity of cases of reduplication Qf the first sound 
is explained, by Dr. Barr, by the much greater length of time 
occupied by the first than by the second sound, whence is 
required a correspondingly greater want of synchronism 
between the closure of the tricuspid and mitral valves than 
between the pulmonic and aortic, to produce a reduplication. 
Physiological reduplication at the end of inspiration is 
accounted for by the fact that the capacity of the pulmonic 
system being increased, the obstructive burden upon the right 
ventricle is lessened, consequently the systole of the latter 
is shortened. The lessening of the duration of the systole of 
the right ventricle implies anticipation of the diastolic closure 
of the pulmonary semilunar valves-so there is a reduplicate 
second sound, the primary element being pulmonic, In 118 
AUSCULTATION. 
pathological reduplication, the origin may be in either the 
right or the left ventricle. If from any cause the systole of 
one of the ventricles be protracted, the diastolic closure of 
the valves of its great vessel of exit will be delayed also, and 
so the second sound will be double. Guttmann supports the 
view of non-simultaneous closure of the aortic and pulmonary 
valves, without giving reasons for the proximate cause. He 
says, however, that it is not unreasonable to explain the phe- 
nomenon by a change in a single set of the semilunar valves, 
causing their tension to take place in two distinct moments. 
This hypothesis appears to me impossible to accept; such 
change would surely be likely to produce murmur rather than 
reduplication. But Guttmann says that reduplication of the 
second sound in mitral stenosis is difficult to account for satis- 
factorily, and in this I quite agree with him. He adds: 
" The broken diastolic sound is (so far as I have observed) 
certainly not loudest over the large vessels, but at the 
lower part of the sternum, and near the apex of the heart, 
and is further absent in those more marked cases of mitral 
contraction, precisely in the cases in which the conditions 
most favourable to the postponement of the closure of the 
pulmonary valve are present in their highest degree." Redu- 
plication, moreover, does not occur in mitral regurgitation 
where the conditions of relative blood-pressure are profoundly 
altered. Guttmann considers it probable that the redupli- 
cation may arise at the narrowed mitral orifice itself; that it 
may be a component part of a presystolic (or, as he terms it, 
diastolic) murmur, and adds that it has been conjectured that 
the first element of the reduplication is the diastolic pulmonary 
sound, and the second is produced towards the end of diastole 
by the contraction of the hypertrophied left auricle (" Physical 
Diagnosis," p. 279). In fact, the hypothesis reverts to the 
last I have mentioned as probably explaining some cases of 
reduplication of the first sound. I consider then that there 
is a theory of auricular causation of reduplication of the 
second sound which is well worth considering and that we 
have before us two plausible explanations of the pheno- 
menon :- 
A. That it is due to non-simultaneous closure of the semi- 
lunar valves in the aorta and the pulmonary artery respec- 
tively. AUSCULTATION. 
119 
B. That it is the effect of a sudden tension of the mitral 
curtains after the normal second sound. 
I now proceed to discuss the evidence on this question, 
which my own cases have afforded me. As I have said, I 
have observed reduplication of the second to be far more fre- 
quent than that of the first sound, and in a vastly prepon- 
derating number of cases the phenomenon is associated with 
■mitral stenosis. It has occurred in about a third of the cases 
of mitral stenosis which I hbve examined ;* it would therefore 
appear d priori probable that in this form of valve-tension 
there should be some special reason for its occurrence. I will 
consider first the evidence of my cases of reduplication of 
second sound in conjunction with mitral stenosis. 
The following case is illustrative:-A lady of fifty was fre- 
quently under my care for symptoms of dyspepsia ; there was 
no history of rheumatism nor development at any time of 
articular phenomena. I had frequent opportunities of ex- 
amining the heart, but found no lesion. After a few months, 
however, during which no special symptoms had manifested 
themselves, the patient complained of fluttering of the heart, 
and I then found a rough presystolic murmur just internal to 
the apex, with a short systolic murmur heard at and outside 
the apex. There was distinct reduplication of the second sound 
heard at the aortic cartilage and down the left border of the 
sternum, but ceasing at the point internal to the apex, where 
the presystolic murmur became audible. At the next exami- 
nation the reduplication was heard as far as the apex. A sub- 
sequent note states, "reduplication very marked, but no 
presystolic murmur heard." Afterwards, " no reduplication 
heard at any part of base ; commences well below the region 
of the pulmonary valves, and is certainly loudest at or even a 
little outside the apex." A subsequent note : " Reduplication 
still very pronounced ; not heard at left base nor anywhere 
left of the sternum until the level of the fourth costal car- 
tilage ; it is well heard at the apex, and marked in the axilla/' 
Afterwards it was audible at the left seapula. 
We will ask now whether these phenomena can be explained 
by the theory which postulates want of synchronism between 
the aortic and the pulmonary second sounds. Supposing this 
* Strictly speaking, eleven cases in 37. 120 
AUSCULTATION. 
theory to be correct, it would be the aortic that would be the 
first element of the reduplication ; because, as the aortic 
region was receded from, the second element of the reduplica- 
tion undoubtedly became more and more pronounced. But 
to accept this theory even under the conditions first noted, we 
must agree that the aortic second sound was very loud, not 
only over its normal area, but as far as the apex. We had in 
this case, however, abundant reason for knowing that the 
aortic tension instead of being above was far below the 
normal. A reference to the record of one of Dr. Hayden's 
cases points to the same difficulty. Here " the second sound 
was double, and heard all over the praecordium." Under the 
accepted theory, therefore, the aortic second sound, its first 
element, must of course have been audible all over the 
praecordium, that is, over a wider area than often the normal 
aortic second sound is heard. But the case was well 
observed and diagnosis confirmed by post-mortem exami- 
nation, and Dr. Hayden adds : " The quantity of blood, which 
in this case, passed into the aorta at each systole of the 
left ventricle must have been very small, owing to the twofold 
lesion of mitral obstruction and incompetency." Moreover, 
the aortic orifice was reduced to the diameter of the point of 
the little finger, and its valves thick, and therefore less dis- 
posed to give the " click " of closure. The difficulty of accept- 
ing the asynchronism theory is further greatly increased by 
consideration of the subsequent areas of audibility, for 
the reduplication was not even audible in the aortic area. 
On the other hand its area of audibility became nearer to 
the apex, and afterwards included, not only the apex, but 
the region of the axilla external to it and even the back. 
Seeing, therefore, that the reduplication was manifest in areas 
in which even the normal aortic second sound is often 
inaudible, I conclude that, in this case, the latter could have 
had no share in producing the phenomenon of reduplication. 
In not more than half the cases of reduplicated second sound 
in mitral stenosis which I have observed, has such reduplica- 
tion been audible in the aortic region. It is almost invariably 
heard best down the left border of the sternum up to the 
point at which the presystolic murmur becomes manifest. 
It seems to me, therefore, that reduplication of the second 
sound in cases of mitral stenosis can be best explained thus : AUSCULTATION. 
121 
The first element of the reduplication is the normal second 
sound ; the tension in the aorta being feeble, it is the pulmonic 
element which has the chief share in the production of such 
second sound. The second element of the reduplication is the 
sudden tension of the abnormal mitral-curtains produced after 
the relaxation of the left ventricle. I am not prepared to say 
that systole of the auricle is essential to produce this sudden 
tension ; it may be quite possible that the reaction of the dis- 
tended pulmonary veins and left auricle may be sufficient to 
cause it. So it may occur previously to the auricular contrac- 
tion, the latter occasioning or reinforcing the presystolic 
murmur, separated by a slight interval from the second element 
of the reduplication. 
I will now consider the evidence in the cases of reduplica- 
tion of the second sound, which I have met with not in asso- 
ciation with mitral stenosis. Of such there were eleven 
examples, which I consider could be ranged under two cate- 
gories. I. Cases in which there were troubles of respiration 
(broncho-pneumonia, phthisis, dilatation and signs of failure 
of the left ventricle, and especially dilatation of the right 
chambers of the heart). In this class were eight cases. It 
is noteworthy that in all in which the area of audibility of the 
reduplication was noted, this -was either that of the origin of 
the pulmonary artery or else of the apex of the right ventricle. 
In this respect, therefore, the cases were strikingly dissimilar 
from those in which the reduplication was associated with 
mitral stenosis. I am quite disposed to think that the theory 
of asynchronism of the two second sounds would best explain 
them, and that Dr. James Barr's view as applietl to explain 
the physiological doubling of the second sound-i.e., the 
assumption that the systole of the right ventricle is shortened- 
is in these particular pathological conditions probably correct. 
The other class in which I have found doubling of the second 
sound in the absence of mitral stenosis is:-II. Cases in which 
there was hypertrophy of the left ventricle, with high tension 
in the arteries. In these it is to be noted that the area of 
audibility of the reduplication was more variable, more exten- 
sive, and especially approached the apex more closely than in 
those of the former group. In the case of a female, aged 
fifty, with chronic renal disease and hypertrophy of the left 
ventricle, the reduplication, as observed at different periods 122 
auscultation. 
was, (1) the heart's apex ; (2) base as well as apex ; (3) base 
only and maximum in aortic area. Post-mortem examination 
showed great hypertrophy and dilatation of left and right 
chambers. In the three cases in this category it would be 
quite legitimate to infer that there was protracted systole of 
the left ventricle, and that the right ventricle having more 
quickly accomplished its contraction, reflux against the pul- 
monary valves took place at an earlier period in diastole than 
reflux against the aortic. Such would accord with Dr. Barr's 
theory, and a case which I had an opportunity of closely 
observing, convinced me that if there were such asynchronism, 
the pulmonary second sound was the first element of the 
double sound. Whilst the probabilities are here also in favour 
of the theory of asynchronism, I think it not impossible that 
the phenomena may be explained by my theory of diastolic 
tension of the mitral curtains as in the cases of mitral 
stenosis. On this point we require more evidence. As prac- 
tical points I would urge that in any case which seems to 
present reduplication of the sounds of the heart, you should 
endeavour with care to establish whether such reduplication 
is real or apparent. Remember that reduplication of the first 
sound may be simulated by a presystolic sound occasioned 
(as I have described) by the systole of the left auricle. In 
apparent reduplication of the second sound, remember that 
there is presumptive evidence of mitral obstruction; in a 
minority there is a disturbance of rhythm owing to comparative 
feebleness of the right ventricle, or to hypertrophy with slow 
contraction of the left. 
You will meet with many instances of disturbed 
rhythm of the heart which are exceedingly puzzling, 
but by attention and repeated examinations you will 
be able to resolve them in most cases. A tumultuous 
and irregular succession of sounds, which at first seem 
chaotic, may frequently be analysed, and found due to 
a definite association of morbid and normal heart- 
sounds. 123 
LECTURE VI. 
AUSCULTATION. 
Abnormal sounds-Pericardial friction-sound-Relations be- 
tween pericarditis, rheumatism and renal disease- 
Influence of posture on friction-sound-Exocardial friction 
-First sound murmur over aortic valves-Anaemic mur- 
murs-Murmurs in chorea-Aortic stenosis- Ulceration of 
aortic valve-segments-Aortic second sound murmur-Evi- 
dence from ophthalmoscopic examination-Aortic insuffi- 
ciency-Physical cause of murmurs-Conduction and con- 
vection of murmurs-Double aortic murmur. 
PART II. 
Having considered the modifications of the normal 
sounds, we will now turn to our second subdivision 
and assume:- 
(b.) That abnormal sounds are heard over 
THE HEART REGION. 
Abnormal sounds, heard at, or close to, the situa- 
tion of the heart, acompanying the cardiac movements 
and apparently mingling with some of the normal 
sounds, may have their origin (1) in the structures ex- 
ternal to the heart and pericardium; (2) in the peri- 
cardial sac; (3) in the muscular tissues of the heart; 
(4) in the endocardium and the valves of the heart; 
(5) in the blood transmitted by the heart. 
As regards the first-mentioned cause of abnormal 
sound, it is of course assumed that you have carefully 
estimated the pulmonary conditions, especially of the 124 
AUSCULTATION. 
left cavity of the thorax and the lung which borders 
on the heart region. The diseases which you have 
chiefly to consider as inducing sounds which resemble 
those due to intrinsic diseases of the heart, or as modi- 
fying and irregularly conducting the sounds due to 
intrinsic diseases, are pleurisy with viscid effusion, 
cavities in the pulmonary substance near the heart, 
and condensation of the lung. The differential dia- 
gnosis of these conditions we shall consider as occa- 
sion arises. 
We will assume that: 
(1.) A rubbing or creaking sound, accompanying 
both movements of the heart, is heard superficially 
over the cardiac region, but is not intensified at apex 
or base. 
This indicates a diseased condition of the pericar- 
dium in which the visceral and parietal layers are 
separated by a viscid or fibrinous effusion, or in which 
the pericardium itself has become thickened or rough- 
ened. Your previous examination may have given 
a clue to your diagnosis. You may have con- 
cluded that the pericardial sac is more or less dis- 
tended, and the symptoms may have assured you that 
there is in existence a pyrexial disease accompanied by 
cardiac, pulmonary, and, perhaps, cerebral phenomena. 
You may even have had the more positive evidence of 
pericardial friction fremitus. Moreover, you may have 
heard the friction-sound by direct application of your 
ear to the chest before commencing to use your stetho- 
scope. If you suspect pericarditis you should, in my 
opinion, never omit the method of direct auscultation. 
But you may have none of these signs to guide you, 
■and let me insist strongly on this. Your patient may 
have pain referred to some of the joints; these pains AUSCULTATION. 
125 
may be very trivial in character, may, indeed, be 
absent; pyrexia may be very slight or inappreciable. 
I mentioned in an early Lecture a case of pericarditis 
in the most pronounced degree which went through 
its course without a single symptom of distress. I 
have lately had under my care, at the North-Eastern 
Hospital for Children, a boy who manifested the 
disease with its grave progressive course and compli- 
cations, but with the occurrence of so few subjective 
symptoms that it was impossible for me to persuade 
the parents to leave the child as an in-patient, and he 
was brought to me bi-weekly as an out-patient. In 
this case there was loud pericardial friction, which, as 
it faded away, gave place to the murmur of mitral 
regurgitation, indicating that endocarditis had at- 
tacked and spoiled the mitral valve; at the next con- 
sultation it was evident that the disease had spread to 
the aortic valves, for there was a murmur of aortic 
obstruction, and at the following there was, in addi- 
tion, a murmur of aortic regurgitation, showing that 
the endocarditis had rapidly destroyed the integrity of 
the aortic valves and induced their most dangerous 
lesion. You will remember, then, that you are not 
to look for pronounced symptoms to suggest to you 
the occurrence of pericardial friction. 
I have said that your patient may complain of pain 
in one or more of the joints. This rule you are most 
strongly to observe-carefully to examine the heart 
and to suspect pericarditis in any case manifesting 
acute or subacute rheumatism. By far the most com- 
mon form of pericarditis is that which is associated 
with rheumatism. Many circumstances govern the 
frequency of the manifestation of pericarditis in rheu- 
matic fever, and authors vary in their estimate of such 126 
AUSCULTATION. 
liability even from 16 to 37 per cent. I have com- 
pared the figures recorded by Fuller, Von Bamberger, 
Roth, Leudet, Duchek, and Chambers, and I find 
that they give about 24 per cent, as the ratio of cases 
of pericarditis occurring in acute rheumatism.* Of 
50 cases of recent pericarditis, Flint observed that 19 
were manifestly rheumatic. Even this high figure, 
however, does not represent the prevalence of the 
rheumatic form of pericarditis; for I have already 
drawn your attention to the fact that pericarditis 
occurs in the subacute form of rheumatism, and in 
cases where the articular phenomena are very slightly 
developed. In some rare cases the process of rheu- 
matic fever commences by pericarditis. 
Another condition of disease in which you must 
recollect that pericarditis is probable, is renal disease. 
In all cases of pericarditis, but especially in cases 
occurring after adult age, you should examine the 
urine for albumen. This is highly important from 
the point of view of prognosis, for whilst rheumatic 
pericarditis generally ends in recovery, pericarditis 
occurring with renal disease is generally fatal. The 
disease may also develop in morbid conditions of the 
blood as scurvy, and, though rarely, in the course of 
scarlatina or variola. 
Your previous examination will, in most cases, have 
indicated that the pericardium contains some liquid 
effusion ; but this is not invariable. Pericarditis, with 
friction-sound, may occur, when the exudation is in- 
appreciable (pericarditis sicca), or you may examine 
* The results of the following observers approach very 
closely and are probably nearest the truth : Fuller, 16'7; 
Duchek, 16 : Chambers, 18 per cent. AUSCULTATION. 
127 
the case at a period when most of the effusion has 
disappeared by absorption. 
The importance of the observation of the sound of 
pericardial friction is very great. This is one of the 
very few great points that we have gained since the 
time of Laennec. In most cases it is marvellous to 
see how close and complete were the observations of 
this great master. Our advances in physical diagnosis 
since his day, until lately, have been neither great nor 
rapid; but in this case there is an exception. Laennec 
says :-" There are few diseases more difficult to 
recognize than pericarditis, or more variable in their 
symptoms. ... I must acknowledge that mediate 
auscultation does not afford much more certain signs 
of pericarditis than the study of the general and local 
symptoms." Thanks to the subsequent observations 
of Stokes, Watson, and Bouillaud, we now know that 
the existence and course of pericarditis can be traced 
with precision as in the case of other cardiac diseases. 
It is very rare indeed that a friction murmur fails 
to be developed at some time during- the evolution of 
the pericarditis. It appears early in the disease. 
Sometimes it disappears also early. Walshe has known 
it appear and disappear within six hours. Sometimes 
it appears, then disappears for a time during a period 
of greater abundance of liquid effusion, then reap- 
pears, to vanish gradually. Most frequently it lasts 
for many days, varying in character and intensity, and 
is heard over a less and less extended area as the 
disease terminates. 
The characteristics of the pericardial friction-sound 
are chiefly-(1) Its quality; it is a "rubbing" or 
" creaking " sound, resembling- that produced by the 
attrition of two surfaces of cloth or leather. It accom- 128 
AUSCULTATION. 
panies both movements of the ventricles, and is 
admirably indicated by the expression of Sir Thomas 
Watson-a "to-and-fro" sound. This rule is subject 
to very rare exception when the rub is heard only 
with the systole. We must postpone consideration of 
this till we come to the differential diagnosis of val- 
vular murmurs. 
It is by no means uncommon to find that the rub of peri- 
carditis has a triple rhythm. This was shown by the late Dr. 
Hyde Salter to be due to the fact that roughening occurred 
not only over the ventricles but over the auricles. The sound 
over the auricles is presystolic, then follows the friction-sound 
produced by the systole of the ventricles, and the third 
portion is produced by the diastole of the ventricles. 
(2) Its limitation. It is heard only over the superficial 
cardiac region. This is very important. The sound is 
not conveyed in certain directions from the heart-area, 
as we shall find to be the case in regard to endocardial 
murmurs. It is situated over the heart-muscle, and is 
associated more with the movement than with the normal 
sounds of the heart. At apex and base these normal 
sounds may be heard-distant and feeble if there be 
much effusion. On applying the stethoscope over the 
intervening area occupied by the heart-muscle (chiefly 
the right ventricle), the rubbing sound becomes mani- 
fest. Pericardial friction appears earliest, and most fre- 
quently, at the base of the heart, near the great vessels. 
(3) Its superficiality. It seems to be generated near 
the ear. If you withdraw your ear slightly from the 
chest, you may still hear the sound. Dr. King 
Chambers calls attention to the following plan, as 
affording valuable evidence :-Having observed the 
sound with the ear, as usual, close to the stethoscope, 
gradually withdraw your ear, the stethoscope remain- 
ing applied to the chest, the sound of pericardial AUSCULTATION. 
129 
friction will still, with great probability, be recogniz- 
able. This nearness of sound to the surface is valuable 
in the differential diagnosis between exocardial and 
endocardial murmurs. 
The friction-sound, however, may be very slight 
and faint. In such case you should make your patient 
change posture ; the friction may then become more 
manifest. The intensity may be increased by a change 
from the vertical to the recumbent position, or vice 
versa, or by inclining the body backwards or forwards. 
In some cases a friction murmur is only heard when 
a particular position is assumed by the patient. When, 
therefore, your examination has led you to suspect 
pericarditis, especially when you are satisfied that 
there is effusion into the pericardial sac, and you are 
anxious to discover evidence that the exudation is 
fibrinous and tending to absorption, you should care- 
fully auscultate in various positions, and note the 
presence or absence of friction-sound. 
Attention to the points I have mentioned will 
generally enable you to recognize the existence of a 
pericardial friction-sound; but there is one condition 
in which the diagnosis may be difficult. This is when 
the friction is produced, not within the pericardial 
sac, but outside, in the pleura. 
You will remember the rule I adduced-to examine 
carefully for disease in the left side of the chest. Sup- 
pose that your examination has led you to conclude 
that there is pleurisy with effusion, or pneumonia, or 
that the lung- abutting on the heart-region has under- 
gone any of the changes occurring in the course of 
pulmonary phthisis. If, in such conditions, you hear 
a "to-and-fro" sound over the prsecordium, remember 
that this may be a pleural friction, modified by the 130 
AUSCULTATION. 
movements of the neighbouring heart, and so made to 
resemble the pericardial rub. The pleural surface 
may be locally roughened by recent exudation, or 
thickened by more remote, or by progressive inflam- 
matory changes. If you have such a sound under 
such conditions, and there is no other evidence of the 
existence of pericarditis, the balance of probability 
will be in favour of its exocardial origin. To further 
the differential diagnosis, observe whether the sound 
varies in character, and what are its relations with the 
rhythm of respiration. Does it alter in intensity in 
an irregular manner ? Does it become imperceptible 
in some of the cardiac revolutions ? Is it more pro- 
nounced at the end of a full inspiration ? Observation 
of these points will help you to a correct conclusion. 
A pericardial friction-sound is less liable to varia- 
tion than a pleuro-pericardial: the latter is most 
evident when the lung is inflated, and thus the roue'll 
pleural surface more closely adapted to the peri- 
cardium, whilst the pericardial sound is most pro- 
nounced when the heart is least covered by lung-that 
is to say, at the end of expiration. 
Having excluded the sounds which take their 
origin in the structures superficial to the heart, we 
come now to a wide field of inquiry-that which 
includes the morbid sounds intrinsic to a diseased 
heart. The subdivision of abnormal sounds which we 
now consider is that wherein : 
(2.) Abnormal sounds, occurring with or replacing 
the normal sounds are heard only, or with a maximum 
intensity, over the various situations of the valves, 
or in definite relation with such situations. 
You have applied your stethoscope over the aortic 
cartilage (the point where the second right costal AUSCULTATION. 
131 
cartilage joins the sternum), and you hear a soft 
blowing sound ; placing the tip of your finger over 
the apex of the heart, or over the carotid artery, you 
are convinced that the murmur coincides in time with 
the pulse-that is to say, with the first sound of the 
heart. Moving your stethoscope so as to auscultate 
in a direction upwards beneath the right clavicle or 
downwards over the heart, you find that the sound is 
lost. It is, in fact, a first sound murmur localized over 
the situation of the aortic valves, and it indicates an 
alteration of the segments of these valves or a change 
in the normal aortic orifice: the form and nature of 
such change we shall consider presently. 
Suppose, however, that you are satisfied that whilst 
the sound which I have just mentioned is not propagated 
downwards towards the heart, it is conveyed in a line 
extending towards the right clavicle. This may possibly 
be due to an aneurism of the ascending part of the 
arch of the aorta, or of the innominate artery. To 
establish or eliminate this hypothesis, you must 
examine carefully for the concurrent signs of such 
condition-a local prominence, pulsatory to the touch, 
and perhaps communicating a thrill, a localized area 
of dulness over the affected vessel, signs of alteration 
of circulation in the distal branches of the diseased 
vessel, and effects of the progressive pressure on 
neighbouring structures, caused by the growth of the 
aneurismal tumour. 
You must remember, however, that whilst the 
occurrence of aneurism may explain the existence of 
the murmur, the hearing of this murmur is by no 
means necessary to establish the existence of aneurism. 
A systolic murmur is absent in a large number of 
cases of aneurism. 132 
AUSCULTATION. 
Aneurism eliminated, you have next to consider 
whether the murmur may be anaemic. Here let me 
say that you may find the differential diagnosis not 
at all easy. Carrying your stethoscope in the direc- 
tion of the right subclavian artery, the right carotid, 
the left subclavian and the left carotid, note the points 
where the murmur disappears, and, if this happens, 
where it reappears. In the great majority of cases 
an anaemic murmur is a soft murmur ; it is heard in 
the course of the great arterial vessels, not with 
a diminishing intensity, as one recedes from the 
heart, but often with reinforcement over the arteries ; 
a slight increase of pressure made by the stethoscope 
increases the loudness of the murmur or develops it 
when it is not heard. There is one observation which 
will give you positive aid in the differentiation. 
Having caused your patient to turn the head towards 
the left, apply your stethoscope above the right 
clavicle in the hollow behind the sterno-cleido-mastoid 
muscle : you may now hear a continuous musical 
hum, the origin of which is in the great veins. You 
can at once distinguish it from the murmur which 
you have just heard in the arteries, because, whilst 
the latter is systolic, occurring only with the 
arterial pulse, the former is an uninterrupted sound, a 
sound called by French observers the bruit de diable, 
" humming-top sound." By making pressure with 
the finger over the veins above the stethoscope, the 
murmur will be made to cease-a sufficient proof of 
its venous origin. You should auscultate in like 
manner on the left side of the neck. If you hear the 
venous hum in either or both of these situations, you 
have strong evidence that the murmur which you 
have heard at the base and up the vessels is a so-called 133 
hcemic or anaemic murmur. But you obtain very 
valuable collateral evidence from the general condition 
of your patient. If there are the pallor and usual 
signs of antemia; if your patient is a female of an 
age when the catamenia are commencing, or of a 
later age, when there are troubles due to excess or 
deficiency of the menstrual function or leucorrhoea, or 
of a still later age, when there has been much loss of 
blood-or if the case is one of a male, who has 
suffered from haemorrhage or some potent debilitating 
cause, or presents the signs of early phthisis, the 
probability of the murmur being anaemic is rendered 
very great.* I have seen it stated- that anaemic 
murmurs are seldom or never met with in young 
children. I can only say, that at the North-Eastern 
Hospital for Children, where we do not admit patients 
above the age of twelve years, I have had many 
opportunities of demonstrating this form of murmur. 
' ' Cardiac murmurs of haemic origin are invariably basic, 
they are loudest at midsternum or in the anatomical site of 
the orifices of the aorta and pulmonary artery. With this 
point as centre they have a diffusion area of three to four 
AUSCULTATION. 
* I find, from notes taken by myself, of 57 cases under my 
own care where I discovered uncomplicated anfemtc murmurs, 
that 15 only were males. The ages were, under sixteen, 
7 cases ; from sixteen to twenty-four, 18 cases; from twenty- 
four to thirty-two, 15 cases ; from thirty-two to forty, 6 cases ; 
from forty to sixty-six, 4 cases. The arterial anaemic bruit 
was heard at the base as well as in the carotids and subclavians 
of both sides, in 8 cases ; in both carotids in 11 cases ; in left 
carotid and subclavian, in 6 cases; in right carotid and sub- 
clavian, in 4 cases ; in right carotid only, 1 case ; in both sub- 
clavians, 2 cases; in left subclavian, 6 cases; at limited area 
over base not propagated up vessels, 16 cases. 134 
AUSCULTATION. 
inches in diameter, according to the intensity of the murmur 
and the conducting qualities of the chest-wall; but they 
never exhibit a definite line of propagation, as is the case with 
organic murmurs in this situation."-Hayden, "Diseases of 
Heart and Aorta," p. 252. 
These murmurs, according to Guttmann, occur most fre- 
quently at the pulmonary orifice, and very seldom at the 
aortic. 
I have said that you may find difficulties in deter- 
mining whether a murmur be inorganic-i.e., haemic, 
due to the causes just considered; or organic-i.e., 
due to structural change of the aortic valves. This 
difficulty occurs especially when the murmur is local- 
ized at the aortic cartilage, and when, as is some- 
times the case, a general condition of anaemia develops 
or reinforces a murmur, due to structural disease. 
We shall lessen the difficulty when we have contrasted 
the organic with the inorganic basic murmur. 
In the case of the soft murmur, which we are still 
considering (for we shall hereafter notice the loud 
basic murmur), the difficulties in diagnosing between 
the anemic and the structural may be great. 
I have occasionally found murmurs in anaemic subjects 
closely to resemble a double aortic-i.e, systolic and diastolic. 
In such cases you will find that the systolic is the haemic 
souffle heard at the aortic base, and generated either in the 
aorta, the subclavian artery, or in the pulmonary artery ; and 
the seeming diastolic is really a continuous venous hum 
generated in the great veins of the neck. This continuous 
hum is overpowered during the systolic period by the arterial 
murmur, but it is audible during the diastole :-so the murmur 
appears to be to and fro. 
The cases wherein the chances are in favour of its 
being structural will be, as I consider, in two classes 
-one in young subjects, where there has been a his- AUSCULTATION. 
135 
tory of rheumatism, and especially where there is, or 
has been, chorea; the other in patients past middle 
life, where there is a probability of atheroma. In 
these cases there may be but slight impediment to the 
onward course of the blood in the aorta. It is very 
seldom that the aortic valve is much affected by the 
ordinary form of rheumatic endocarditis without the 
mitral valve being affected first or coincidentally. 
Bear in mind that we are now considering a soft 
murmur, heard alone over the aortic valves, without 
discoverable alteration of the other valves. There is 
a condition of the aortic valve in which the edges of 
its segments are fringed by little villosities, so-called 
vegetations ; these may give rise to a very soft aortic 
murmur with the first sound. This condition is not 
necessarily an accompaniment of rheumatism, but 
where a valve is diseased by rheumatism or by athe- 
roma, it is more apt to occur. In chorea, as we shall 
consider hereafter, the vegetations are more fre- 
quently found fringing the mitral valve, but they do 
occur on the aortic segments. In patients after 
middle life, such vegetations may be detached from 
the valve by the force of the current of blood, and 
being carried into the arteries, may plug one of the 
arterial branches. Such may occur in various parts 
of the system, but especially in the brain. Occurring 
in the small terminal arteries of certain parts of the 
brain, it is considered with great probability to be 
often the cause of chorea ; when blocking a larger 
trunk, it causes various forms of paralysis, or attacks 
which are ascribed to apoplexy. Remember, there- 
fore, the possibility of arterial embolism when you 
hear a soft murmur localized at the aortic cartilage 
in cases at the predisposing ages I have just alluded 136 
AUSCULTATION. 
to, and wherein you do not find anaemia to be a direct 
explanation of the phenomenon. 
So also you may turn the argument round and con- 
clude that when, with these predispositions and under 
these circumstances you hear a soft first sound murmur 
localized over the aortic cartilage, such murmur is 
probably due to a slight obstruction of the aortic 
orifice, and that vegetations may fringe the valves. 
We will now suppose that instead of the soft 
murmur we have been considering, there is a loud 
bruit heard over a wide area, but having its maximum in- 
tensity over the aortic cartilage. When you commence 
to auscultate the heart region, you are at once cogni- 
zant of a loud rough systolic murmur ; over the 
second right costal cartilage this is very intense ; as 
the stethoscope is carried towards the apex, the sound 
is found to become less loud, and probably at the apex 
itself it ceases to be audible. On auscultating in the 
reverse direction the bruit is loudly heard in the 
direction of the aorta and the carotid arteries. In 
some cases it may be heard at the back, but then only 
about the level of the spines of the scapulae. 
Flint considers that an aortic systolic murmur is loudest at 
the second right intercostal space close to the sternum. 
Hayden considers that its maximum is at midsternum ; 
exceptionally it is audible at the back in the left interscapular 
space. Guttmann says that it is essential "in investigating 
any case of aortic disease, that the whole of the sternum 
should be carefully auscultated, as the murmur presents its 
greatest intensity sometimes at one spot, sometimes at 
another, on the surface of the bone."-" Physical Diagnosis," 
Sydenham Society's Translation, p. 291. 
In case of a murmur having these characters, if you 
have eliminated the probability of an anaemic causation, AUSCULTATION. 
137 
you will have no difficulty in diagnosing- obstruction 
(stenosis) of the aortic outlet due to a diseased condition 
of the valves. The concurrent signs will be hypertrophy, 
without dilatation, of the left ventricle, with small 
hard arterial pulse. The pathological changes which 
give rise to this form of murmur consist in thickening-, 
rigidity, and fusion of the segments of the semilunar 
valves of the aorta, so that the orifice of exit of the 
blood from the left ventricle is narrowed. This may 
occur to such extent that the orifice will barely admit 
a probe. Sometimes the valves are hardened from 
atheroma and calcareous deposit, sometimes fringed 
and obstructed by fibrinous vegetations or warty 
excrescences, sometimes roughened by ulceration. 
It is important, even from a diagnostic point of view, 
to attempt to define under what conditions these 
various causes of obstruction of the aortic orifice 
arise. A significant and somewhat strange argument 
meets us at the very commencement of the investiga- 
tion. Taking the positive evidence of post-mortem 
examinations, lesions affecting the aortic valves alone 
are of very common occurrence. Dr. King Chambers, 
in analysing 367 cases in which valvular lesions of the 
heart were discovered at the autopsies, found that the 
aortic valves were solely affected in 107, the mitral only 
in ninety-six. The general experience of observers 
has been that the frequency of disease in the mitral 
valve alone, and at the aortic orifice alone respectively, 
is about equal, but that the proneness of the mitral 
is slightly the greater. Compare this observation 
with clinical experience; I think you will find all 
physicians concur in saying that mitral lesions per se 
are diagnosed far more frequently than aortic. Of 
the hundred cases of heart disease which I mentioned 138 
AUSCULTATION. 
in an early part of these Lectures, as observed by 
myself, only fifteen were declared by the physical 
signs to be solely due to morbid changes at the aortic 
orifice, whilst no less than fifty-eight were mitral. It 
seems fair to conclude from these facts that aortic 
lesions are often present during life, but are only dis- 
covered after death. The regurgitant lesions which 
we shall soon consider, are much more baneful in their 
obvious effects than the obstructive lesions of the 
aortic valves. It is very probable, therefore, that 
obstructive lesions are more frequently present than 
detected. Positive experience confirms this view in 
many cases, especially of sudden and alarming symp- 
toms in old people with cerebral or visceral, disease ; 
patients who are sometimes brought moribund to the 
hospital are found to present obstruction of the aortic 
outlet. Now as to the forms of disease which pro- 
duce aortic obstruction. Of twenty-four cases ob- 
served by myself in which the physical signs indicated 
aortic obstruction, ten were obviously rheumatic, 
nearly all having suffered well-defined rheumatic 
fever. Flint records that of thirty cases of aortic 
lesions, rheumatism had occurred in sixteen. We 
shall see, however, that the aortic valves are less 
prone to be attacked by rheumatic endocarditis than 
the mitral. Rheumatic endocarditis attacks first the 
mitral valve, then extends upwards involving the 
endocardium lining the ventricle, till it includes the 
aortic valves in the morbid change. In the majority 
of cases in which we hear an aortic obstructive 
murmur without evidence of impairment of the mitral 
valve, endocarditis has not been limited to the aortic 
valves, but has begun in the mitral, though its effects 
have not been sufficient to destroy the integrity of 
the latter. AUSCULTATION. 
139 
Besides the alteration of the valves from rheumatic 
endocarditis, there is another cause which is very- 
common in inducing obstruction-atheroma. In this 
the valves are often incrusted with calcareous deposit. 
This form of alteration is exclusively met with after 
middle age, and is by far the most common cause of 
aortic obstruction in patients past the prime of life. 
The most common cause of mechanical impediment at the 
aortic orifice is not primary disease of the heart or of its valves, 
but of the aorta adjacent to the valves. The latter become 
implicated by extension of the disease. The morbid process 
{aortitis; endarteritis) commences by swellings, localized in 
patches, in the internal coat of the vessel, with infiltration of 
the layer next to the endothelium by cellular elements ; sub- 
sequently such infiltration extends outwards to the muscular 
coat. In the later stages degeneration occurs, so that the 
elements become yellowish and softened from fatty change, or 
undergo calcareous transformation, giving rise to hard stony 
plates in the wall of the vessel. This stage of degeneration, 
fatty or calcareous, is the condition known as atheroma. 
Occurring in the neighbourhood of the aortic semilunar valves, 
these are involved in the thickening ; so they may become of 
fibro-cartilaginous consistence, or hard and bony from calcareous 
transformation. The conditions leading up to such morbid 
change in the arteries are probably (a) alcoholism. Dr. Hay- 
den believes that amongst the humble classes alcoholism is the 
chief cause of the diseases of the aortic valves-that is, it 
induces the lesion of the aorta, which involves the valves; (b) 
gout or the lithic acid diathesis. This, according to the same 
authority, is the most frequent disposing cause amongst the 
rich. The acute and sub-acute forms of rheumatism do not 
predispose to the affection, whilst the gouty forms, such as 
chronic rheumatic arthritis, are distinctly associated with the 
arterial disease; (c) syphilis. I have had abundant evidence, to 
my mind conclusive, that endarteritis and aortitis can be the 
direct result of the action of the syphilitic poison; (d) muscular 
strain. This has been strongly insisted upon by Dr. Clifford 
Allbutt, who has pointed out the proclivity to aortic disease of 
persons whose avocations subject them to severe or sustained 140 
AUSCULTATION. 
effort, such as soldiers, strikers, lifters, &c. I confess I am not 
convinced that mere muscular effort can induce the disease in 
^previously healthy aorta. In the cases I have observed, when the 
affection existed in the classes mentioned by Dr. Allbutt, there 
has been a strong suspicion that a concurring cause might have 
been alcohol or syphilis, or both combined. At all events, effort 
is a proximate cause, and with it may be classed constriction 
of the chest by tight clothing, &c. ; (e) a condition of per- 
sistently high tension in the general arterial system. This is 
most typicallj- expressed in chronic renal disease, where there 
are tight arteries and hypertrophy of the left ventricle. I 
entirely agree with Dr. F. A. Mahomed, who has called 
attention to the fact that this tendency to high arterial tension 
may be manifested in the early ages of life, and when there is 
no renal implication whatever. It is, therefore, of the highest 
practical importance to recognize it, to caution the subjects of 
it against any possible overstrain, and so to ward off the 
actual disease of the arterial coats, to which it tends. In these 
cases the pulse may be recognized as hard and full by the finger, 
and there may be signs of some hypertrophy of the left 
ventricle, with heightened tension in the aorta, as shown by 
accentuation of the aortic second sound ; but there is no 
evidence comparable in value with that obtained by the 
sphygmograph (see Part II.) If at any age a condition 
of high tension in the arteries is demonstrated, the danger 
of disease in the arterial coats should be recognized. 
For the differential diagnosis of the rheumatic and the 
atheromatous forms of disease occasioning obstruction at the 
aortic outlet, the evidence afforded by the sphygmograph is of 
great value. The tension in the atheromatous form is much 
greater than that which usually obtains in the rheumatic; in 
the former is found the typical trace of aortic obstruction. 
See typical tracing ot aortic obstruction in Part II. 
By both these forms of disease (rheumatic endo- 
carditis and atheroma) the narrowing' of the aortic 
orifice may be extreme, and yet the signs of subjective 
and objective may not be pronounced. In two cases, 
one mentioned by Stokes and another occurring in AUSCULTATION. 
141 
America, the orifice left in the fused and hardened 
valves was so small as only to admit a small prohe, 
and yet disease of the heart was not suspected till the 
occurrence of acute disease of the lungs which proved 
fatal. If the signs in such extreme obstructions are 
obscure, they are still more so in the form of endo- 
carditis characterized only by vegetations upon the 
valves. According' to French observers, these lesions 
have nothing to do with rheumatism, but are associ- 
ated with various maladies (Lancereaux, " Anatomie 
Pathologicpe," p. 220). It is this form of endocarditis 
which is especially associated with chorea in young- 
subjects, and with the accidents of cerebral embolism 
in the old. There is yet much obscurity as to its 
pathogenesis; it is characterized by hyperplasia of the 
superficial layer of the endocardium, giving- rise to 
little excrescences forming groups upon the ventri- 
cular surface of the valves, sometimes fringing their 
free borders. These vegetations are often attached 
to the surface of the valve by slender pedicles 
easily detached; their size is frequently augmented 
by the attachment of fibrine derived from the blood 
current. It differs in histological characters from the 
rheumatic form of endocarditis which affects the deeper 
fibrous structures of the valves and involves their 
whole substance. It seems very probable that the 
French observers are correct in differentiating this 
form pathogenetic ally. Lancereaux says that it may 
occur under various obscure conditions, but especially 
in alcoholism, the puerperal state, and, perhaps in 
intermittent fever. Whether isolable or not, we must 
admit that this form of endocarditis may accompany 
other forms-in fact that, though it may probably 
arise per se in certain as yet untraced conditions, it 142 
AUSCULTATION. 
frequently occurs upon any valve which has under- 
gone morbid change from other causes. 
Another form of disease affecting the aortic valves, 
which, though rare, must be borne in mind as affecting 
diagnosis, is that in which the valves are ulcerated. 
Under certain circumstances of depressed vitality, the 
valve already diseased tends to ulcerate ; the patient 
is seized with rigors and symptoms of septic poison- 
ing. The debris of the ulcerated portions of the 
valves form plugs which, being carried by the current 
of blood, cause embolism of many arteries through- 
out the system as well as general blood-poisoning. 
In eleven cases recorded by M. Lancereaux, the aortic 
valves alone were affected by the ulceration in six. 
The disease may arise in various adynamic conditions ; 
several cases have been recorded as occurring in the 
puerperal state. You may conclude that when in a 
case of aortic obstructive disease (mitral conditions we 
shall consider hereafter) your patient is seized with 
severe rigors, with pyaemic symptoms, with vomiting 
and diarrhoea, with alternations of very high with low 
temperatures, and especially with signs of cerebral 
embolism, there is present an ulcerative endocarditis. 
The disease is uniformly fatal. 
To resume, concerning aortic obstructions in ge- 
neral, especially as regards prognosis. When you have 
a loud obstructive murmur with a history of rheu- 
matism or of senile change, with some cardiac hyper- 
trophy, the lesion, compensated as it is by increased 
force of the heart, need not give occasion to a grave 
prognosis. The patient may with considerable proba- 
bility live long in spite of the obstruction. In the 
case of the soft murmur you should be guarded in 
your prognosis. Examine your patient with great AUSCULTATION. 
143 
care, for these cases are often overlooked. Remember 
in children the proclivity to chorea ; in advanced age, 
in puerperal conditions, in alcoholism, and in Bright's 
disease, the danger of embolism. When you are called 
to a case of so-called apoplexy where the symptoms 
occur very suddenly, always carefully auscultate the 
heart, remembering the great probability that there 
has been cerebral embolism by detachment of a vege- 
tation from a diseased valve. 
We return now to the aortic cartilage. Suppose 
that we find the first sound to be unaccompanied by 
murmur but not so the second or diastolic sound. 
The latter, which should consist only of the click occa- 
sioned by the closure of the semilunar valves, is com- 
plicated by a murmur. Like the systolic, which we 
have just considered, this may be soft and short, or 
loud and pronounced. If soft, you will notice first, 
its point of greatest intensity. You will probably 
hear it at the aortic cartilage, but on carrying your 
stethoscope to the left side of the sternum and auscul- 
tating- over the cartilage of the third or fourth rib, it 
will be yet louder. The reason of this we shall pre- 
sently see. Notice in the next place whether some of 
the clicking sound of the closure of the aortic semilunar 
valves is heard with it-i.e., whether it accompanies 
and not replaces the aortic second sound; if this occurs, 
it is evidence that some of the segments of the valve 
are capable of performing their functions-that the 
lesion does not involve them all. 
This second sound murmur, instead of being soft 
and local, may be loud and prolongedj in quality it 
may be rough, or musical, and it may be heard over 
a wide area. You may not hear it over the right or 
left base, or up the great vessels, but by carrying 144 
AUSCULTATION. 
your stethoscope downwards along the centre-line of 
the sternum you arrive at a spot where the murmur 
with the second sound is distinctly heard. Excep- 
tionally it is heard only as you get near the apex of the 
heart. You have many collateral signs to guide you 
in the diagnosis : the visible throbbing of the arteries, 
the heaving of the praecordial region, the signs of 
hypertrophy and dilatation of the left ventricle. In 
no condition is the probability greater of enlargement 
of the heart; in some cases there is enormous increase 
of mass and weight, the so-called " cor bovinum." 
There is another objective sign which I take to be 
of great value. On making an ophthalmoscopic examina- 
tion of the retinal vessels by means of the erect image, 
you observe pulsation of the veins or arteries, or of both. 
Dr. Stephen Mackenzie has done great service in 
drawing attention to this sign. I have made ophthal- 
moscopic examinations in a large number of cases in 
which an aortic second sound murmur existed, and I 
I have rarely failed to find visible pulsation of 
the retinal vessels. Such pulsation is found most 
commonly in the veins, but both arteries and veins 
pulsate in many cases. This sign may have great 
value, especially when other signs are masked-for 
example, when the lungs are affected, and the loud 
rhonchi and rales of bronchitis render it difficult to 
hear the sounds of the heart. 
Suppose that you have heard a second sound 
murmur, and that by its position and by the existence 
of collateral signs you have located its production in 
the aortic outlet, what is its pathological significance 1 
It means that there is regurgitation of the blood- 
stream into the left ventricle when the heart is in 
diastole, on account of the imperfect closure of the AUSCULTATION. 
145 
valves which guard the aortic outlet. In the case of 
the systolic murmur, we had obstruction afforded to 
the onward stream of blood through the aortic orifice; 
in the case of this diastolic murmur we have in- 
sufficiency of the valves to close the orifice after the 
systolic gush is over. 
Imperfection of the valves, permitting regurgitation 
into the left ventricle, is brought about by patho- 
logical processes similar to those which induce 
obstruction. In the rheumatic form of endocarditis 
the valves, after having become thickened by hyper- 
trophy of their connective tissue, undergo a slow and 
gradual process of contraction, so that the free edges 
of the valves are retracted from the centre, and a gap 
of necessity results. Or, in the villous form of 
endocarditis, a bunch of vegetations may depend 
from the segments of the valve on their ventricular 
aspect, and so weigh down such segments as to pre- 
vent their apposition in diastole. These masses of 
vegetations may vary in size from a pin's head to 
a walnut. Again, such imperfection of the valves as 
may induce regurgitation, may be caused by the 
rigidity of segments which have undergone athero- 
matous change. In rare cases the valves may be- 
come ruptured through violence or perforated by 
ulceration. 
In all these pathological conditions, the mechanical 
effect is reflux of blood, in diastole, through the 
abnormal gap in the valves. The secondary effects 
are, first, that there is a deficiency of supply of blood 
to the general arterial system ; secondly, that the left 
ventricle contains always too much blood. The 
further consequences are, that the ventricle under- 
goes compensatory hypertrophy, thus making up for 146 
AUSCULTATION. 
the loss to general arterial system induced by the 
reflux, and that, from its over-repletion (for you will 
understand that it contains blood early in diastole 
when it ought to be empty, and the normal amount 
of aerated blood is superadded to the amount which 
has regurgitated through the imperfectly-closed aortic 
orifice) the ventricle becomes dilated. You will thus 
comprehend why, in the case of aortic obstruction, we 
have hypertrophy only of the left ventricle, whilst in 
aortic regurgitation we have hypertrophy and dilata- 
tion. In obstruction there is enhanced power of the 
ventricle to overcome the difficulty, but no distension 
of the ventricle by an abnormal content of blood. 
You are now in a position to understand the 
mechanism of the murmur of aortic regurgitation-it 
is the murmur caused by the backward rush of blood 
through the partially-closed and imperfect aortic 
orifice. Remember that this is not a merely passive 
reflux-it is not simply by the w'eight of the column 
of blood that the murmur is occasioned. The ven- 
tricular systole drives the blood into arterial channels 
which are both elastic and muscular. There is a 
recoil, therefore, of all the arteries which have been 
distended by the ventricular systole, and the blood is 
forcibly urged backwards into the ventricle. Thus 
you may understand how prolonged and loud the 
murmur is in some cases. 
Aortic regurgitation is most commonly met with at 
or after the prime of life (of fifty cases noted by Von 
Bamberger, only fifteen occurred before the age of 
thirty), and in the male sex, the proportion in recorded 
cases being three males to one female. The pro- 
gnosis is generally bad ; in the rare cases of youthful 
patients, compensation by hypertrophy of the ventricle AUSCULTATION. 
147 
may be such that but little trouble is experienced,* 
but when adult life is attained the lesion is one of the 
g-ravest that can affect the heart. This is one of the 
conditions in which sudden death may occur, and the 
subjects should be cautioned against excitement and 
over-exertion. 
Suppose, now, that you hear two sounds at the 
aortic cartilage, the one with the systole and the other 
in the diastole. There is a double murmur. Or over 
certain spots whereto, as I have described, an obstruc- 
tive a bruit" may be carried by conduction or convec- 
tion, you may hear a first sound murmur, and over 
other spots in the direction of the retrograde current 
you may hear a second sound murmur. You may 
conclude in such cases that there is a combination of 
the two lesions which we have just considered-that 
there is aortic obstruction as well as aortic regurgita- 
tion. This is not uncommon. The semilunar valves, 
roughened on their ventricular aspect, or rigid and 
offering an obstructed orifice of exit for the blood, are 
also imperfectly opposed in diastole. 
We have now considered three forms of heart- 
murmur-the aortic direct, or obstructive; the haemic 
or anaemic, and the aortic regurgitant or murmur of 
aortic insufficiency. It will be well to make a short 
digression and endeavour to understand the physical 
cause of these abnormal sounds. 
There are few subjects which have been more 
voluminously debated than the physical causes of 
cardiac murmurs, and few concerning which there is 
less accord. It would appear that each observer has 
taken infinite pains to elaborately convey his impres- 
* I have met with several instances of the affection in 
children, who nevertheless evinced little or no cardiac distress. 148 
AUSCULTATION. 
sions, with the result of convincing no one but him- 
self. No two observers seem to be in complete 
agreement. It will serve, I think, no good end to 
make a critical examination of the various theories 
which have been propounded; I purpose, therefore, 
to express my own views on the subject in a way 
which I conceive to be the most simple, the most 
practically useful, and the most in accord with the 
present teachings of science. 
1. Sound is the effect of vibrations transmitted to 
the organ of hearing. The sounds of the heart, 
normal and morbid, are due to vibrations conveyed 
from the surface of the thorax to the ear. If the ear 
be applied closely to the chest (immediate ausculta- 
tion), the vibrations of the thoracic wall are commu- 
nicated to the intervening layer of air, and then to 
the external ear. If the stethoscope be used (inter- 
mediate auscultation), the vibrations are transmitted 
to its walls, and by these to the air intervening 
between the ear-piece and the tympanum. The tube 
of the stethoscope does not perceptibly weaken the 
sound. " The law that the intensity of sound 
increases in inverse proportion to the square of the 
distance, does not apply to the case of tubes, espe- 
cially if they are straight and cylindrical."* Many 
vibrations are communicated to the chest-wall, from 
the movements of the heart, and the fluids and 
structures in relation with it, which are not capable 
of giving rise to impressions of sound. Such are im- 
pulse and thrill. To be perceived by the auditory 
centre, vibrations must have a certain rapidity and a 
certain amplitude or intensity. The tactile faculty 
* Ganot's " Elementary Physics," translated by Atkinson. 
Eighth edition, p. 177. London: Longmans. AUSCULTATION. 
149 
can appreciate vibrations which are too slow for the 
auditory, and the auditory those which are too rapid 
for the tactile ; but the areas of perceptibility by the 
two faculties overlap, so that vibrations may in some 
cases be detected by both and in others tactile im- 
pressions may be supplementary in duration to audi- 
tory or vice versd. Thrill may precede, accompany, 
or succeed murmur. It is to the thoracic surface, 
then, whereto vibrations are conducted, some of which 
are sonorous, or capable of exciting- auditory percep- 
tion. It is at the thoracic surface alone that the con- 
ditions obtain for the production of sound, for it is 
here only that the vibrations are given to the air. 
2. The sounds heard are produced by vibrations 
communicated to the air by the thoracic wall, irre- 
spectively of the mechanical means by which such 
vibrations are produced. This proposition is proved 
by the telephone. By it sounds are not transmitted, 
but vibrations similar to those of the sounds are pro- 
duced, and the effect on the organ of hearing is the 
same in the one case as in the other. It is further 
demonstrated by the phonograph, by which sonorous 
vibrations are made to record themselves as motion- 
vibrations upon the surface of a soft metal; 
these being by mechanical means recommunicated 
to the air, the original effect on the organ of 
hearing is reproduced. There is synthesis of sound 
from the mechanical vibrations. It appears to me, 
therefore, that the qu&stio vexata of the site and 
mode of production of sounds in the heart, the vessels, 
or the fluids, is a barren controversy. Sounds are 
not produced, save at the thoracic wall, where the air 
receives its undulations. In the heart and its sur- 
roundings are produced vibrations, which at the sur- 150 
AUSCULTATION 
face may, or may not, give rise to impressions of 
sound. 
3. The normal sounds of the heart partake rather 
of the character of noise than of music; they are 
either sudden and abrupt, or dull and muffled. 
The second sound is the uncomplicated sound of 
valve-tension, such as one imitates by suddenly 
stretching a previously lax piece of membrane. The 
sound is of too short a duration to be capable of 
musical determination ; the auditory faculty receives 
it as a shock. The first sound is for the most part 
similar to the second-that is, it is chiefly due to 
valve-tension occurring over a larger area (in propor- 
tion, as the mitral and tricuspid valves combined 
exceed in extent the aortic and pulmonary), but mo- 
dified first, because the intervening walls of the 
ventricles subdue the sound in proportion to their 
thickness ; secondly, because the (muscular) sound of 
the contracting ventricles supplements and pro- 
longs the valve-sound. The muscular sound is dull, 
because the fibres mutually interfere to arrest their 
own vibrations. 
4. The morbid sounds which are heard in relation 
with the heart and vessels, partake, on the other hand, 
rather of the character of music than of noise. They 
are not abrupt, but, varying in intensity and pitch, 
commence at one end of the scale as a scarcely per- 
ceptible blowing (aspirate), and become rough and 
grating, or else occur in many varieties of pitch up 
to the production of a distinct musical note. 
5. The organic conditions giving rise to such mur- 
murs as have their origin in disease or abnormality 
of the valves or orifices of the heart may be for the 
most part referred to two types : first, in which the 
orifice which originates the vibrations occasioning the AUSCULTATION. 
151 
murmur is converted into a ring ; secondly, in which 
across the orifice and in the blood-stream there is a 
vibrating tongue. In these conditions a strict analogy 
obtains with musical instruments. In one case the 
fluid which is the intermediate agent of vibration is 
the blood, in the other it is air. The first type is 
exemplified by the flute, the cornet, or other usual 
form of wind instrument; in these, vibrations are pro- 
duced by the forcing of air, under compression, 
against the wooden or metallic walls of the instru- 
ment. More familiarly still, it is illustrated by 
whistling produced by the mouth with the lips pursed 
up so as to make a circular aperture, the pitch of 
the note produced being heightened in propor- 
tion to the decrease in size of the aperture, and 
the intensity or loudness varying in proportion to 
the force of expiration. It seems to me a popular 
error to ascribe too much of the sound-producing 
agency to currents of air forced through the aper- 
ture. The air is rather the intermediate than the 
immediate agent-that is, the force of expiration 
sets the solid boundaries of the orifice vibrating, 
these vibrating solids communicate their vibrations to 
the air, and the stream which issues from the orifice 
has little to do with the production of sound-vibra- 
tions. This can be easily proved. Produce with the 
mouth an audible " whistle," then apply the fingers 
to the pursed-up lips so as to stop their vibrations, 
but in such manner that the exit of air from the 
orifice is unimpeded. You will find that though the 
air issues just as before, the " whistling " sound is 
arrested by the arrest of vibration of the -walls of the 
orifice of exit. A similar experiment with a metallic 
■whistle has the same result. So I think we may infer 
that the vibrations which give rise to sound in the 152 
AUSCULTATION. 
case of the intra-cardiac murmur start from the solid 
structures rather than from the fluid blood, though 
this latter is an agent for the communication of vibra- 
tions to the solid structures. Savart's fluid veins are 
agents for the production and communication of 
vibrations, which imparted to solids give rise ulti- 
mately to sonorous vibrations. The second type of 
murmur is illustrated by the Jew's harp or accordion, 
in which a tongue of metal is set in vibration. At 
the aortic orifice it is exemplified when a shred of 
fibrin, a prolongation of fibro-cartilaginous material 
or the debris of a ruptured valve stretches across and 
vibrates in the blood-stream. When so originating, 
the murmur often has a markedly musical quality ; it 
usually is diastolic, but may be systolic, and is not 
unfrequently double. 
5. We have already seen (p. 96) that the sounds 
heard over the heart-region are not immediately 
superficial to the positions whence they originate- 
that is, the vibrations which give rise to sonorous 
impressions are conveyed from their sources to cer- 
tain areas of the thoracic surface. Such transmission 
occurs in two modes (1) by conduction, so termed 
when the vibrations are conveyed by still media or 
solid structures. The normal lung, filled as it is with 
air, is a very bad conductor of vibrations ; when, 
however, there are condensations of the pulmonary 
tissue, exudations or solid growths, these may act 
the part of conductors, and the heart sounds, normal 
or abnormal, may be heard in unusual situations. In 
the case of the diastolic aortic murmur, the sternum, 
which is comparatively a good conductor, causes the 
sound to be heard in a direction down its central- 
line or along its left border. (2) There is, however, AUSCULTATION. 
153 
another way by which vibrations are transmitted, 
that is, by media in motion. A murmur is best 
heard in the direction of the current of blood. This 
was called by the late Dr. Hyde Salter the law 
of convection of murmurs, and explains away many 
difficulties. This also may be illustrated by analogy 
with the air. On a still day everything may be 
silent, but let a breeze spring up, and the sounds 
-of distant bells, for instance-are wafted to the 
ear. The sound is heard only in the direction of 
the current of air ; if the wind change it will be no 
longer audible. In like manner, a cardiac murmur 
is heard in the direction of the current of blood. In 
the murmur of aortic obstruction, the vibrations gene- 
rated at the time of the systole are carried by the 
blood-stream into the aorta and up the great vessels. 
In the murmur of aortic regurgitation, the direction 
of the current of blood at the time of occurrence of 
the sound is exactly the reverse of the former; the 
stream is gushing back into the left ventricle, and 
the line of convection is downwards from the aortic 
cartilage to the apex of the heart. In some excep- 
tional cases the regurgitant murmur is only heard at 
or near the apex. 
The late Dr. Hyde Salter called attention to the fact that adias- 
tolic murmur generated at the aortic outlet was in exceptional 
cases audible only at the apex of the heart. Two illustrative cases 
were quoted {Lancet, August 14,1869, p. 225). In one of these there 
had been, no doubt, rheumatic endocarditis :-"It was quite 
certain that the murmur so plain at the apex and inaudible at 
the base, was due to aortic regurgitation-that is, that the 
stream of blood flowing down towards the apex carried thither 
the sonorous vibrations of which conduction failed to give any 
evidence in the immediate neighbourhood of their production." 
In the second case there was " a very distinct diastolic mur- 154 
AUSCULTATION. 
mur" heard at the left apex in the case of a female in whom it 
was extremely probable that there had been rupture of the 
aortic valves. These observations have been confirmed, ampli- 
fied, and rendered of great practical importance by Dr. Baltha- 
zar Foster (see "Clinical Medicine," p. 112 et seq. London, 
Churchill, 1874). Dr. Foster's observations were also in cases 
of rupture of the aortic valves, and the experience of one case 
dictated a precise diagnosis in another. When a diastolic 
murmur of aortic origin is conducted to the left apex, "it 
depends on the regurgitation taking place through incom- 
petency of the posterior aortic segment, either at its right angle 
or through perforation of its curtain." In such pathological 
conditions the regurgitant blood-column falls upon the upper 
segment of the mitral valve ; this was proved, not only by ex- 
periment after death, but by inference from the thickening of 
the segment which had probably taken place on account of the 
stream which had been projected against it during life. The 
vibration produced, notwithstanding that the lesion is aortic, 
being of the mitral valve, is heard in the mitral area-that is, 
at the apex. Dr. B. Foster adds :-"I believe we may also 
say that a similar murmur propagated towards the ensiform 
cartilage indicates incompetency of either the left or the right 
coronary segment, by which the regurgitant current is thrown 
more upon the septum of the ventricles. " 
The diagnosis of rupture which may occur in the case of 
previously healthy aortic valves is to be made from the history 
of the onset of symptoms:-sudden pain at the precordium, 
palpitation and dyspnoea arising in direct relation with violent 
strain, effort, or after a blow upon the sternum, in the absence 
of a history of rheumatism, but attended with the physical 
signs of aortic regurgitation, or of aortic obstruction and 
regurgitation combined. Dr. Hayden adduces also the exist- 
ence of systolic arterial thrill as an important sign for the 
physical diagnosis of such cases. 
Supposing Dr. Foster's experience to be confirmed, it becomes 
possible to determine in cases of aortic regurgitatiou which seg- 
ment is affected, and this may be of high importance as regards 
prognosis. "Two of the segments have above them each 
a coronary artery which is filled by the blood-column as it 
rebounds from their curtains. When these segments are torn 
down and retroverted, the regurgitant blood-column running AUSCULTATION. 
155 
past the mouths of the coronary vessels must to some extent 
diminish the amount of diastolic blood-wave which they receive, 
and consequently impair the heart-nutrition. . . . That seg- 
ment of the aortic valves by whose incompetency, we believe, 
a murmur is specially carried to the left apex, has no coronary 
artery above it, and therefore when it is affected, we should 
expect the coronary circulation to suffer less than when either 
of the other segments is imperfect." Death usually follows 
rupture of the aortic valves within three months, the maximum 
duration of life has been four years and a half. In the case of 
injury to the non-coronary segment recorded by Dr. Foster, 
life was prolonged to nearly three months ; whilst the duration 
was eighteen months, and three months in the other cases. It 
would appear, therefore, that when in a case of aortic regurgi- 
tation a diastolic murmur is localized at the apex of the heart, 
it is probable that the posterior segment of the aortic valve is 
affected, and that the chances of duration of life are greater 
than when the murmur is heard at the usual situation over 
the sternum. 
6. Vascular murmurs-the so-called haemic mur- 
murs-are due to vibrations produced in the walls of 
vessels. The murmur heard over the site of the 
aortic valves is the effect of vibration of the initial 
portion of the aorta; sounds of similar character 
heard over the carotid and subclavian arteries are due 
to vibrations of the arterial walls occurring in cer- 
tain areas. It is characteristic of these murmurs 
that they are not transmitted along the vessel in un- 
broken continuity, but are heard over certain portions 
of it; they are much intensified by a little pressure 
with the stethoscope. Murmurs closely resembling 
these may be produced by such pressure even in con- 
ditions of health. Vascular murmurs may be heard 
in acute febrile diseases, but they are especially asso- 
ciated with anaemia and chlorosis. It has been proved, 
both by Marshall Hall and by Hope, that such 
murmurs can be induced in animals by copious bleed- 156 
AUSCULTATION. 
ings, and we are familiar with the fact that they 
appear in the human subject after sudden and copious 
haemorrhage. That they are not due to the mere ab- 
straction of quantity of blood, however, is proved by 
the experiments of Richardson, who found that the 
" bruits " were produced in dogs after injection of 
large quantities of water into the veins. Moreover, 
in common with other observers, I have noted them 
in cases where there was good volume of blood in 
the arteries. There can be little doubt that a watery 
condition of the blood aids to the production of such 
murmurs; and this is only probable, for a mobile 
fluid can oscillate much more readily than a viscid 
one. Neither decrease in quantity nor deterioration 
of quality in the blood can, however, be the only and 
absolute cause of the murmur, for the latter is not 
constant in conditions of anaemia, nor is it heard 
throughout the great arterial vessels. The localiza- 
tion of the murmur points to a local cause, and this 
cause I take to be a modification of tension in the 
arteries in certain areas, whereby the walls of the 
artery in these portions are rendered prone to vibrate. 
These murmurs are particularly marked when there 
is any cause for the abnormal conduction of vibrations 
to the surface of the chest. This is especially the 
case in subclavian murmur, which is thus of dia- 
gnostic importance in the early stages of disease in 
the apices of the lungs. The venous hum-bruit de 
diable-has its origin in the internal jugular vein. It 
is due to the vibration of the coats and valves of the 
vein, just as the arterial murmur is due to the vibra- 
tion of the walls of the artery, such vibration being 
communicated by the whirling movement of the 
blood. " The blood flows from the relatively narrow AUSCULTATION. 
157 
jugular vein into the relatively wide bulb (the part at 
which the vessel debouches into the innominate vein), 
and is thus caused to sweep in a somewhat spiral 
course round the walls of the chamber, so that the 
mode of origination of the venous hum may be re- 
garded as strictly analogous to that of murmurs in 
the arteries. This dilatation at the end of the vessel 
remains permanently wider than the upper part of 
the vein, as its sides are held apart by the tense cer- 
vical fascia."* The venous hum is intensified when 
the patient turns the head Jrom the side which is 
auscultated; thus, the superficial structures of the 
neck being put upon the stretch, the jugular vein is 
compressed and narrowed. It is obscured or extin- 
guished when the patient resumes the recumbent 
position, the aid to the force of the current afforded 
by gravity being thus removed. The hum is gene- 
rally louder on the right side of the neck. 
Chauveau and Corrigan have both demonstrated 
experimentally that " when a liquid current is hurried 
past a constriction in its passage into a wider space 
b eyond, a ripple or perturbation in the current is 
created, giving rise to vibration and murmur."! 
This I consider to be the key to the explanation of 
vascular murmurs, both venous and arterial, only I 
do not attribute the sound-producing vibrations to 
the liquids, but to the solids, to which the ver- 
tiginous movements of the fluids impart motion. In 
the case of the basic aortic murmur, there is a condi- 
tion of impaired tension at the origin of the vessel, 
so that its walls vibrate. In the case of arterial 
* Guttmann's " Handbook of Physical Diagnosis,'' p. 308. 
t Hayden's " Diseases of Heart and Aorta," p. 250. 158 
AUSCULTATION. 
murmurs there is non-equable tension of the vascular 
wall, and at the portions where tension is impaired, 
eddies are produced which set these portions vibrating. 
The venous hum is the effect of deficient impletion or 
defective muscular tone in the jugular, whose walls 
vibrate owing to the eddies developed in its fluid 
contents. 159 
LECTURE VII. 
AUSCULTATION. 
PART in. 
Haemic pulmonary murmur-Pulmonary stenosis-Relation to 
cyanosis-Tricuspid, regurgitation-Ventricular murmurs- 
Murmurs in chorea-Myocarditis-Arguments concerning 
cause of non-valvular murmurs-Cardiac phenomena of 
typhoid fever-Organic mitral murmurs-Causes of mitral 
lesions-Varieties of lesion-Mitral insufficiency-Mitral 
stenosis. 
We now leave altogether the region of the aortic 
valves and cross the sternum to the second left inter- 
space and the sternal end of the third cartilage-the 
area of the valves of the pulmonary artery. 
Suppose that you hear a soft murmur with the first 
sound localized in the pulmonic area. The chances 
are enormously in favour of this being- inorganic- 
vascular. Observe all the rules as regards differential 
diagnosis which I have given you, for the discrimina- 
tion of anaemic murmurs when heard at the aortic 
base. Especially notice whether the sound is carried 
along the left subclavian. If it be strictly localized, 
the haemic murmur may be generated in the pul- 
monary artery. Dr. Flint considers that an inorganic 
murmur emanates as frequently from the pulmonic 
orifice as from the aortic. I must say that I have not 
observed this in my own experience. I have found 
the soft murmur heard at the left base in the 
majority of cases, to be distinctly traceable to the left 160 
AUSCULTATION. 
subclavian artery. I would say of a soft systolic 
murmur localized in the pulmonary area, always 
assume it to be inorganic or independent of structural 
change, unless there is strong collateral evidence in 
favour of its being organic. 
Assuming that you have eliminated anaemia as a 
possible explanation of the murmur, you have yet to 
consider whether the sound may be produced by the 
pressure of a tumour upon the trunk of the pulmonary 
artery. It has been said that tuberculous lung can 
give rise to such pressure. I should explain the mur- 
mur heard in these cases as due to the conduction by 
the tubercular consolidations of a haemic murmur 
generated in the pulmonary artery. Tumours in the 
mediastinum, enlarged bronchial glands, cancerous 
and other growths in the lung may undoubtedly 
cause pressure against the trunk of the pulmonary 
artery, and give rise to a systolic murmur. All 
such probabilities of extra-cardial causation you must 
eliminate by careful examination. 
We will imagine that you have eliminated anaemia 
and pressure on the pulmonary artery as probable 
causes, and yet you hear a localized murmur over the 
situation of the pulmonary semilunar valves. This 
murmur with the first sound may be soft, and heard 
only at the spot indicated, or it may be loud, and 
heard over a wide area, but distinctly most intense 
about the third left cartilage. You may be sensible 
that it is very superficial-generated very close to the 
ear. A murmur with these characteristics will, with 
much probability, be due to obstruction of the pulmonary 
artery, but before completing the diagnosis we will 
briefly consider the pathological causation and clinical 
concomitants of such a condition. AUSCULTATION. 
161 
In considering aortic disease, I made no mention of 
congenital defects, because these so rarely affect the 
aortic orifice that they do not practically influence 
diagnosis. Aortic defects are not congenital, but ac- 
quired. It is quite otherwise with pulmonary lesions. 
Intra-uterine malformations are far more likely to 
involve the pulmonary artery; moreover, when 
endocarditis attacks the " foetus in utero" it is the 
right chambers of the heart that are much more fre- 
quently affected. The rule in after-life is exactly 
reversed. 
The pathological causes which give rise to obstruc- 
tion of the pulmonary orifice operate chiefly in fcetal 
life. Through faulty development, the pulmonary 
artery itself may be contracted in varying degree, 
even to complete obliteration, a blind extremity or 
rudimentary cord only remaining. Or the semilunar 
valves may be fused together, and may form a mem- 
branous, cartilaginiform or cretaceous septum with a 
circular or slit-like opening. Or the contraction may 
be below the valves at the apex of the right ventricle 
-the conus arteriosus dexter-the cause being the 
shrinking of the muscular tissue, subsequent to inflam- 
mation (myocarditis). In one or two cases vegetations 
like those described in case of aortic disease have been 
found about the valves. In the rare cases met with 
as originating at or after adult life atheroma may be 
a cause, or an inflammation due to direct violence, to 
which the right ventricle and pulmonary artery, by 
their superficial position, would seem to be more liable.* 
For convenience in clinical diagnosis, I think it best 
to group the cases according to age. 
* Von Dusch, " Lehrbuch der Herzkrankheiten. " Leipzig, 
1868, p. 248. 162 
AUSCULTATION. 
In infancy the patient will probably be the subject 
of cyanosis, presenting the characteristics which we 
have already considered. You will hear the murmur 
loudly at the base, though in the small area of chest 
presented in infancy you may not be able precisely to 
locate it in the pulmonary region. The blueness of 
surface, however, the venous distension, and the ex- 
treme improbability of aortic disease at this period of 
life, will leave little doubt as to the diagnosis. You 
may safely infer that a patent foramen ovale, or an 
aperture in the interventricular septum, co-exists with 
the pulmonary obstruction, for such is the case almost 
invariably. 
In later childhood you will have more chance of 
localizing the murmur, unless it be exceptionally loud. 
You must bear in mind, however, that aortic disease 
may possibly have been developed by rheumatic endo- 
carditis subsequently to birth; therefore the differential 
diagnosis between aortic and pulmonary obstruction is 
now necessary. If the bruit be pulmonary, you will 
probably observe a condition of cyanosis, at least in- 
termittingly, and venous turgescence increased by 
exertion and by coughing. Moreover, you may be 
able to ascertain that the right side of the heart is 
hypertrophied and dilated. There may be venous 
pulsation. The following case, which occurred 
under my own. observation, affords many points of 
interest:- 
A little girl (L. S.), aged eight and a half, was ad- 
mitted under my care at the North-Eastern Hospital 
for children, on January 12, 1873; she seemed weak, 
and was excessively pale, but presented no blueness nor 
obvious dyspnoea. On auscultating the heart-region 
a very loud rough first sound murmur was heard at AUSCULTATION. 
163 
the base, quite as intense at the aortic as at the pul- 
monary point. The child had been ailing- occasionally 
ever since birth, but there was no obvious symptom 
except weakness. She was one of seven children, of 
those, four were living-, one had been stillborn, and 
one died during dentition. The mother was healthy, 
and could give no account of il maternal impression." 
I could not help giving a very doubtful diagnosis-it 
appeared to me that it was quite as probable, from 
the physical and general signs, that the obstruction 
was seated at the aortic orifice as at the pul- 
monary. As the case progressed, the next observed 
phenomenon was diarrhoea, which began on January 
13, and became very persistent and uncontrollable. 
On February 1, hremorrhoids were noticed. Progres- 
sive enfeeblement occurred, the radial pulse became 
scarcely perceptible, the hands very cold, while the 
feet were fairly warm. A week afterwards delirium 
was manifested; the diarrhoea persisted, and there 
was much abdominal pain ; emaciation continued, the 
pallor increased, but throughout there was no cya- 
nosis. The child died on March 10. At the autopsy 
we found the lowest lobe of the right lung thickly 
studded with masses of soft tubercle, varying in size 
from a small pea to a large bean. The left lung also 
was tuberculous at the apex. The large intestine was 
ulcerated throughout its whole length, and the mesen- 
teric glands were a complete mass of hard tubercle. 
We found about an ounce of pale yellow serous fluid 
in the cavity of the pericardium, and the heart itself 
very small, pale, and contracted. The aorta and its 
valves were quite normal, but the pulmonary artery 
was very small in calibre (diameter four-tenths of an 
inch), its walls firm and inflexible, so that it resembled 164 
AUSCULTATION. 
the aorta or a systemic artery. It was a pulmonary 
artery in miniature, with valves minute but perfect. 
The area of a section across the aorta compared with that 
of a section across the pulmonary artery was in the pro- 
portion of three to one. The wall of the right ventricle 
was greatly hypertrophied, so that it was thicker at 
its thickest part than any portion of the left ventricle. 
The foramen ovale was patent, the aperture being 
circular, with rounded edges, the communication 
between the auricles quite unimpeded. There was no 
imperfection of the septum between the ventricles ; 
the valves were all healthy. 
This case shows that we may have a loud murmur 
of obstruction at the pulmonary orifice without 
cyanosis. The signs strongly suggested aortic con- 
striction, but there was one chain of circumstances 
that led up to the diagnosis of pulmonary lesion-the 
occurrence of general tuberculosis. The persistent 
uncontrolled diarrhoea and wasting seemed to indicate 
tubercular ulceration ; the post-mortem examination 
showed tubercle abundantly scattered throughout 
the body. Now tubercular changes in valvular 
diseases of the heart, are, for a reason which I 
will not stay to discuss for it is yet very obscure, 
very rare. The great exception to this immunity 
is in pulmonary obstructive disease. That con- 
genital pulmonary construction predisposes to tubercle 
has been noticed, especially by Lebert and Pea- 
cock ; the observation is valuable as an element of 
diagnosis.* 
* I have discussed the subject of Pulmonic Murmurs in 
Children more at length in " Clinical Lectures on Diseases 
of the Heart in Children."-Vide " Medical Timesand Gazette, 
September 6, 1879, p. 255. AUSCULTATION. 
165 
When adult life is attained, patients who present 
signs of obstruction at the pulmonary orifice rarely 
come under our notice. Besides the si^ns I have 
already given you, enlargement of the right chambers 
of the heart may now be more decided, or more readily 
detected; in addition, a pronounced superficial systolic 
thrill may be felt over the pulmonary area. There 
may be considerable difficulty in determining whether 
the pulmonary' stenosis be congenital or acquired. 
Though the congenital malformation is so fatal that 
only about fifteen per cent, of the subjects reach the 
age of twenty, some cases attain to a considerable 
age. Instances are recorded, where the defect was 
undoubtedly congenital, in which the subjects lived to 
the age of forty (Kussmaul), fifty-seven (Peacock), 
and sixty-five (Stblker), respectively. In nearly all 
cases, however, inquiry will elicit the fact that there 
has been some respiratory trouble, or some tendencyr 
to lividity from infancy or early childhood. On the 
other hand, in acquired obstruction there may be 
a history of comparatively recent development of 
symptoms ; a blow may have been received upon the 
praecordial region -which has set up myocarditis, or in 
a patient past the prime of life you may observe such 
evidence of degeneration of the systemic arteries 
as would suggest the probability of atheromatous 
change in the pulmonary artery. 
Murmur with the second sound in the pulmonary area, 
due to incompetency of the pulmonic valves, may be 
dismissed in very few words. It is very improbable 
that you will meet with an instance. I only know of 
one, recorded by Hope ; in this, the pulmonary artery 
was dilated, and the apposition of the segments of the 
valve thus prevented. 166 
AUSCULTATION. 
Double murmur-that is, murmur both with first and 
second sounds-has been recorded in a few instances, 
but is very rare. Of course it indicates obstruction, 
combined with incompetence. 
Having- finished the exploration of the pulmonary 
valves, we now complete the investigation of the 
right side of the heart by auscultating the tricuspid 
area. 
You may hear a soft blowing murmur with the 
first sound limited to the triangular surface occupied 
by the right ventricle, but most evident at the base of 
the ensiform cartilage. If you have made this observa- 
tion with care, and have excluded the probabilities of 
extra-cardiac causation, you will conclude that the 
murmur is due to regurgitation through a defective 
tricuspid valve. 
Remember that the conditions in regard to the 
production of murmur are now exactly the reverse of 
those which we have hitherto considered. A murmur 
with the first sound, the site of which is the aorta or 
pulmonary artery, indicates obstruction in one of these 
vessels, the systole urging the blood through the 
obstructed orifice. A murmur with the first sound at 
either of the auriculo-ventricular apertures indicates 
regurgitation through such aperture; the contraction 
of the ventricle whilst impelling, in the usual way, a 
portion of the content of blood into the vessel of exit, 
at the same time forces backwards, on account of the 
gap left by the imperfectly apposed valve, another 
portion into the auricle. 
As regards the right side of the heart, the patho- 
logical causes which bring about this result are dilata- 
tion of the right ventricle and morbid changes in the 
valves themselves. Of these the more common is the AUSCULTATION. 
167 
former. When from any cause there is considerable 
and continued venous congestion, the right ventricle 
becomes distended and dilated. Emphysema of the 
lung may dispose to this condition, but the most 
common cause of all is disease of the left side of the 
heart. Dilatation of the right ventricle follows disease 
of the mitral valve when there is deficient propulsive 
power in the left ventricle as consequence from cause. 
The last result of such dilatation of the right ventricle, 
is, that the curtains of the tricuspid valve, which under 
normal conditions were competent to close the auricu- 
lo-ventricular aperture during systole, are by the 
circumferential traction of the walls of the widened 
ventricle, withdrawn from the centre, so that their 
edges do not perfectly meet. In systole, therefore, 
blood regurgitates into the right auricle. The same 
condition may result from a contracted state of the 
papillary muscles to which are attached the ten- 
dinous cords of any of the curtains of the valve. 
The valve may have been altered by rheumatic en- 
docarditis, though this disease very rarely attacks the 
right side. It is very improbable that you will meet 
with a case of tricuspid murmur with a history of 
rheumatic origin without there being concurrent signs 
of disease of the mitral or aortic valves. There may, 
however, be a congenital affection of the tricuspid 
due to endocarditis in foetal life, when disease of the 
left chambers is almost unknown. Rupture of the 
valve has also been recorded. 
You must particularly note the concurrent sig'ns of 
tricuspid regurgitation. These are, first, the evidences 
of hypertrophy and dilatation of the right side which 
we have already discussed-the pulsation of the right 
auricle may be obvious in the second right intercostal 168 
AUSCULTATION. 
space; secondly, turgescence of the veins of the 
surface and often cyanosis ; thirdly, in some cases, 
venous pulsation evidenced in the jugulars or in the 
liver. The symptoms of tricuspid regurgitation are 
dyspnoea, dropsy, and the distresses of heart-disease 
in their gravest forms. For a very good account of 
the secondary consequences of tricuspid insufficiency, 
consult Dr. Milner Fothergill, on " The Heart and 
its Diseases."* It is very important for you to call 
to your aid these concurrent signs, for whilst they 
will assist you when you hear a murmur soft and ill- 
defined as it often is, they will lead you to a diagnosis 
when there is no murmur at all. Tricuspid regurgita- 
tion without murmur is far from uncommon; thus 
differing from mitral regurgitation, the reason being 
the comparative feebleness of the right ventricle. 
If you have arrived at the diagnosis of tricuspid 
regurgitation, the prognosis is very unfavourable. 
There is in this condition no chance of compensating 
change to overcome the difficulty, such as exists in 
most other morbid conditions of heart. Enhanced 
power of the right ventricle but serves the more to 
engorge the venous system by the greater regurgita- 
tion ; greater strength of left ventricle, if attained, 
would but increase by vis a tergo the tension in the 
venous system, but it is not attained because the arte- 
rial supply to the ventricle is diminished by the 
existing conditions, t 
You may possibly hear in the tricuspid area a 
murmur which does not occur with the first sound, 
but immediately before it. It is a prcsystolic murmur, 
and indicates obstruction of the tricuspid orifice. 
* London : Lewis, 3rd edition, p. 85. 
+ Cf. Von Dusch, loc. cit. p. 230. AUSCULTATION. 
169 
This lesion, however, in the absence of disease of 
the other valves of the heart is almost unknown, 
and its consideration may be conveniently deferred 
until after the exploration of the mitral area. 
Before proceeding to auscultate the mitral area, I 
shall ask you to consider certain sounds which are 
heard in the interval between base and apex, and 
even over the apex itself-sounds which are not due 
to any organic disease of the valves. 
I can show you many examples in which the first 
sound of the heart, heard on auscultating between 
base and apex-that is, oVer the right ventricle-is 
rough in its character. The sound is not pronounced 
enough to be designated a murmur, but the quality 
of the contraction is not pure like that of the healthy 
ventricle. I have found this to be distinctly the 
case in some instances of dilatation of the right 
ventricle, such as one meets with in chronic pulmonary 
complaints. It occurs also in some cases of anaemia, 
and is, in my opinion, evidence of a weak right 
ventricle. 
The sound may, however, be more than a mere 
roughness: it may be termed a soft first-sound 
murmur. This also may be due to anaemia, especially 
when the condition of corpuscle-deficiency is associ- 
ated with dilated right ventricle. That anaemic mur- 
murs are occasionally generated over the right ven- 
tricle, I have no doubt whatever. In these cases the 
soft murmur may be heard only as far as the base, 
or, and this much more commonly, it may disappear 
at the aortic cartilage, and reappear with reinforce- 
ment over the great arteries of the neck, in the 
manner I have already described; it is lost, how- 
ever, at the apex of the heart. You may find such 170 
AUSCULTATION. 
murmurs in cases of any profound alteration of the 
blood in advanced stages of tuberculosis and in 
carcinoma. 
But, going one step farther in degree, we may find 
a blowing murmur heard as far as the apex, and even 
localized at the apex-a murmur which, from its 
quality and characters, is absolutely indistinguishable 
from that of valvular disease. The great point, how- 
ever, which differentiates it from the organic murmur 
is its temporary or evanescent character; its occur- 
rence corresponds with a definite period in the history 
of a disease, it fades away and ceases entirely when 
the disease enters upon a new phase. 
Murmurs having these characters have been de- 
scribed as occurring (1) in chorea, (2) in the early 
stages of certain acute febrile affections. 
We will consider the explanations which have been 
given of their occurrence-first in chorea. Every one 
will agree that in a certain proportion of patients 
suffering from chorea there is manifest a cardiac 
murmur, sometimes at the base, but more commonly 
at the apex. I have already said that this murmur 
is in many cases very soft, often difficult to find, and 
I think it is a fair inference that it is often overlooked. 
I know I have often overlooked it myself in the early 
examinations of a patient. Yet, when once it is 
manifested, it may be observed to be persistent in 
some cases, whilst in others it may completely disap- 
pear, and leave no trace of heart-affection. What 
is the pathology of this condition ? To begin with a 
matter concerning which there is no doubt-in a con- 
siderable proportion of the cases of chorea which 
have proved fatal, vegetations have been found in 
greater or less degree fringing the cardiac valves. AUSCULTATION. 
171 
Organic disease of the valves will undoubtedly, 
therefore, explain a certain proportion of the cases. 
Happily, however, chorea is rarely a fatal disease. 
Will the existence of structural changes in the valves 
explain the murmur which, unlike that in other 
valvular affections, entirely disappears ? Many ob- 
servers say no. How, then, do they explain the 
occurrence of the murmur which is heard over the 
mitral area ? By assuming that there is in these 
cases a peculiar contraction of the papillary muscles 
of the ventricle, to which are attached the cords 
which control the curtains of the valve, or else a 
peculiar condition of the muscular walls of the ven- 
tricle, whereby the apposition of the valvular curtains 
is prevented, and consequently regurgitation takes 
place into the auricle. You will understand that this 
is mere hypothesis, and it seems to me very difficult 
to acc.ept it. That in chorea the muscle of the heart 
should in some degree partake of the muscular per- 
turbation which characterizes the disease is not im- 
possible to realize, but whilst this would explain 
irregularities in the time and quality of contraction 
which undoubtedly do occur, it appears to me in- 
capable of explaining the murmur. If the cardiac 
muscle behaved in any spasmodic manner, surely the 
murmur wTould present strange variations of site and 
character; sometimes it would be present and some- 
times absent, sometimes soft, sometimes loud ; where- 
as it often presents no considerable variations from 
hour to hour, day to day, or week to week. Spasm 
of the papillary muscles I cannot help but reject; 
disease of their muscular elements is out of the 
question ; and any constant or consentaneous action 
on their part, whereby they keep open the orifice 172 
AUSCULTATION. 
they are intended to close, seems also to impose a too 
great demand upon our credulity. Parietal debility 
of the ventricle seems to me equally difficult to accept: 
it is quite unproved in these cases. 
If we exclude the probability of a muscular causa- 
tion, how shall we explain the non-persistent murmur 
of chorea ? My answer is, that I see no difficulty in 
concluding that such murmurs are always due to some 
change in or on the valves. The objections taken to 
this view may be thus stated:-The endocarditis 
which produces these changes of the valves is a 
rheumatic endocarditis ; only a small proportion of 
the sufferers from chorea are demonstrably rheumatic; 
therefore a changed condition of the heart-valves is 
unlikely. The second objection is the formidable one 
that endocardial changes of the valves do not pass 
away, and the murmur which they occasion is per- 
manent. As regards the first of these objections, 
however, I have already shown how insidious may 
be the advent and course of the endocarditis, even in 
the form known as rheumatic, and that especially in 
children, the articular symptoms may be. trivial or 
entirely absent. Moreover, there is no reason to be- 
lieve that the form of endocarditis occurring in chorea 
is of necessity rheumatic. It is the endocarditis 
characterized by the presence of vegetations on the 
endothelial surface which is met with in chorea; 
this is prone to occur on valves already altered by 
rheumatic disease, but it can occur in the absence of 
rheumatism. It is a mere hyperplasia of the endo- 
thelium which may exist in very slight degree, but 
when it does occur the fibrine of the blood tends to 
adhere to the thickened spot. The obstruction caused 
by such a vegetation may readily occasion the mur AUSCULTATION. 
173 
mur; but under the repeated washings of the current 
of blood, the pedicle itself and the attached fibrine 
may be washed away suddenly or gradually, and the 
valve subsequently may present no trace of lesion. 
I think that there is a very high probability that 
fragments thus derived may block some of the 
arterioles supplying the corpora striata or other por- 
tions of the cerebro-spinal motor tract, and that thus 
is produced that form of chorea which is associated 
with cardiac change. You must not misunderstand 
me, however, and conclude that in my opinion this is 
the exclusive pathogeny of chorea. It is to me highly 
probable that just as epilepsy is induced in some in- 
stances by actual disease of the brain and in others 
by reflex irritations, so chorea may be the result, in - 
some cases of direct physical interference with the 
arterial supply of the motor tract, in others of the 
peripheral irritations (such as intestinal worms), and 
probably in others of psychical stimuli such as fright 
or emotional shock. 
I shall teach you, therefore, that when in a case of 
chorea you hear a murmur distinctly located at apex 
or base you are to conclude that there is an org'anic 
lesion of the mitral or aortic valves. 
We turn now to the consideration of the temporary 
systolic murmur which mav be heard over the apex 
during the course of certain acute febrile affections. 
A murmur with the first sound, heard over the 
apex of the heart but disappearing entirely with con- 
valescence, has been observed in the course of small- 
pox, erysipelas, and typhoid fever. The phenomenon 
has been best investigated in the case of the last- 
mentioned disease. In certain of the cases of typhoid, 
about the end of the second week from the onset, a 174 
AUSCULTATION. 
first-sound murmur may be heard over the right ven- 
tricle or just confined to the situation of the apex. 
When localized at the apex the sound may have pre- 
cisely the characters of an endocardial murmur, yet 
as convalescence approaches it entirely disappears. 
Certain other cardiac phenomena accompany it. The 
impulse of the heart may be felt to be very feeble or 
undulatory: the radial pulse may become inter- 
mittent ; the second sound of heart may be heard to 
be reduplicate. The signs show great enfeeblement 
of the heart; this is so obvious that it does not need 
discussion, and it is well known that some of the 
subjects die suddenly in syncope. 
We come to the inquiry-to what is the first-sound 
murmur which is heard at the apex in these cases 
due ? We may at once exclude any organic disease 
of the valves, for it is known to be extremely rare 
and almost unexampled for endocarditis to develop in 
the course of typhoid, and the cases which have-died 
in syncope have shown no trace of structural altera- 
tion of the valves. There is evidence, however, of a 
decided change in the muscular structure of the heart. 
M. Hayem, who has deeply studied this question, has 
found evidence of myocarditis-an inflammation of 
the muscular fibrillae-with granular and fatty de- 
generation and a special form known as a vitreous " 
change. Undoubtedly, therefore, there is structural 
enfeeblement of the muscular walls of the heart. 
We have again to encounter the question: How 
can such enfeeblement induce the murmur ? And 
first, is there a veritable regurgitation in such cases ? 
M. Hayem considers that there is-the weakened 
muscle can but imperfectly fulfil its functions, the 
auriculo-ventricular orifice, powerless to resist the AUSCULTATION. 
175 
force of the blood-current, allows itself to be passively 
distended, or else the enfeebled papillary muscles can 
no longer sufficiently restrain the valvular curtains. 
Hence a practical, though a functional, insufficiency 
of the valves. 
The difficulty in accepting this explanation is far 
less than that which besets the " dynamic" hypothesis 
in the case of chorea. It seemed to me impossible to 
admit that a neurosis, the special phenomenon of 
which is spasm, should give rise to a long-lasting and 
little-varying condition of patency of the auriculo- 
ventricular aperture ; I even found it difficult to allow 
that mere passive weakness of the ventricle without 
dilatation could permit of regurgitation. In the case 
of typhoid, however, we have to deal not only with 
general weakness but also with localized lesions. M. 
Hayem says that in histo-pathological examinations 
he has found patches of disease in the muscular 
fibrillae disseminated here and there in a most irre- 
gular manner.* It is not difficult to assume, there- 
fore, that there is a paralysis of certain of the papil- 
lary muscles, and of necessity a condition of incom- 
petence of the valves permitting regurgitation. 
Let us consider the lessons derived from a case 
under my own care. A young lady, aged nineteen, 
whom I saw on the 10th day of well-marked typhoid, 
manifested no cardiac murmur whatever. On the 
ll'th day there was a very soft murmur with the first 
sound, localized at the third left costal cartilag-e. On 
the 13th day the bruit reached almost as far as the 
apex of the heart; it had all the characters of a blow- 
ing endocardial murmur; in fact, had I heard it under 
* See "Le Progrbs Medical," 24 Juillet, 1875, p. 416. 176 
AUSCULTATION. 
other circumstances, I am sure I should not have hesi- 
tated to ascribe it to valvular disease, for it was heard 
well within the mitral area, though careful ausculta- 
tion showed that its maximum was a little right of 
the apex. On the 15th day it was still heard as far 
as the apex, but its maximum was at the third left 
costal cartilage. On the 17th day of the fever, the 
bruit was only heard in the last-mentioned situation, 
but there was a distinct reduplication of both the first 
and the second sounds of the heart. On the 21st day 
there was reduplication of the first sound only, the 
bruit still audible as before. Convalescence went on 
most satisfactorily, in a few days all trace of redupli- 
cation had ceased, the basic murmur passed away, and 
slight amemic murmurs were manifest over the arteries 
of the neck. On the 38th day the patient called at 
my house in perfect convalescence, and presenting no 
signs of cardiac trouble. 
r This case was one of typhoid of not more than the 
average severity ; the intestinal symptoms were well 
marked, and the diarrhoea continued during the second 
week in considerable degree ; the pulmonary signs 
were a slight general bronchitis with condensation 
about the base of the left lung which soon passed 
through resolution; the temperature taken in the 
axilla never exceeded 104'2° F., nor the pulse 128, 
and defervescence, commencing on the nineteenth day, 
proceeded with almost perfect regularity. The cardiac 
troubles seemed to be the most grave of those which 
surrounded the case, and yet the course of the disease 
appeared in nowise to be injuriously complicated by 
them. 
Let us review the circumstances of this case with 
the view of explaining the murmur. In the first AUSCULTATION. 
177 
place we have positive signs of enfeeblement of the 
heart-muscle. A like weakness existed in marked 
degree in the voluntary muscles; the " subsultus" 
characteristic of typhoid was a prominent symptom. 
It is found that in these cases the changes which occur 
in the muscles of the heart occur also in the muscles 
of the body. M. Hayem concludes from his able 
researches that the cardiac fibrillae are diseased in like 
manner and in like degree with the fibrillae of the 
voluntary muscles. The existence of reduplication of 
both of the heart sounds was a very pronounced sign 
of cardiac implication. Let us consider the concurrent 
conditions. No one could doubt that in a case of this 
sort there was a profound deterioration of the qualify 
of the blood due to the septic influences at work and 
to the G ensemble'' of adynamic conditions. But, 
furthermore, there must have been a notable diminu- 
tion of the normal quantity of the blood on which the 
heart could contract, for a part of its volume had 
drained away (and was still draining) from the 
alimentary canal, and another part remained stagnant 
in the congested lung. Such conditions were just 
tantamount to a notable abstraction of blood. 
Cardiac debility and deterioration of blood in quality 
and quantity, therefore, are positive indications in our 
case. Moreover, we have signs similar to those ob- 
served in anaemia. The murmur first noticed could 
have been taken for an anaemic murmur localized at 
the commencement of the pulmonary artery. Soon it 
became heard over the right ventricle; in convales- 
cence it was gradually lost, and anaemic murmurs 
were heard over the arteries. M. Hayem, speaking- 
from other experiences, says of the murmur, " After 
having been localized just at the apex near the nipple, 178 
AUSCULTATION. 
it deviates to the right near the sternum, and tends 
little by little to ascend towards the base. At the 
same time the bruit becomes softer, and takes in a 
more and more decided manner the character of an 
anaemic murmur."* We have here just the factors 
which induce the anaemic murmurs which are heard 
over the aorta and the great arteries. 
I have long hesitated to adopt the theory of so-called 
dynamic mitral murmurs, which I prefer to term adynamic 
valvular murmurs. As I have just said, I feel bound to reject 
the hypothesis in regard to the murmurs of the subjects of 
chorea. In the case of the mitral systolic bruit, heard in 
the acute fevers and in profound amemia-a bruit which so 
closely resembles that which is undoubtedly due to disease of 
the valve, but which is nevertheless non-persistent-I am 
now convinced, from personal experience, that there is tem- 
porary mitral regurgitation. Dr. Hayden has published cases 
illustrating such murmurs in the subjects of anaemia and 
purpura, and of induced nervous prostration caused in one 
instance by habits of masturbation, and in another by exces- 
sive tobacco-smoking. In the case of the acute fevers it is 
not difficult to accept with M. Hayem, the view that the papil- 
lary muscles share in the disease which involves in various 
portions the muscular structure of the heart, that thus their 
co-ordinate action upon the curtains of the valve is impaired, 
and leakage takes place through the imperfectly closed orifice. 
In the cases of amemia, &c., it is probable also that the papillary 
muscles are enfeebled. Guttmann says, " Inorganic mur- 
murs at the mitral orifice are caused by the unequal tension of 
the segments of the valve," which "is chiefly the result of 
slight fatty metamorphosis of the muscular structure of the 
heart, more especially of the papillary muscles, which takes 
place whenever amemia becomes profound" (cf. "Hand- 
book of Physical Diagnosis," p. 287). Perl has stated that in 
animals fatty degeneration of the heart may be experimentally 
produced by repeated and copious venesection. Usually in 
* " Le Progres Medical," 24 Juillet, 1875, p. 415. AUSCULTATION. 
179 
cases presenting the adynamic murmur in the mitral 
area the symptoms of grave mitral regurgitation are absent 
-it is probable that the amount of blood gushing back 
into the auricle and occasioning the murmur is small. When 
the papillary muscles sufficiently recover their strength the 
mitral curtains become properly apposed, and the murmur dis- 
appears. Dr. Cuming, of Belfast, has described a case in 
which there was a mitral murmur with the usual signs of 
advanced organic disease-pulmonary engorgement, haemo- 
ptysis, anasarca, &c.-and yet dissection demonstrated the 
absence of anomaly or disease in the cavities, walls, or valves 
of the heart. Dr. Hayden adds that he has also met with 
two such cases. In Part II. I have quoted a case of profound 
anaemia in which there were the usual signs of advanced 
organic valvular disease, and yet recovery and total disappear- 
ance of the murmur. In this case, relying on the evidence of 
the sphygmograph, I made the diagnosis that the murmur was 
adynamic (see Part II.). In the apex-murmurs, therefore, 
occurring in typhoid and other acute fevers as well as in pro- 
nounced anaemia and conditions of nervous shock, I think, 
with Hayein, Hayden, Guttmann, Cuming, Bamberger, Hare, 
and others, that there is veritable regurgitation due to en- 
feeblement of the muscle, chiefly of the papillary muscles, of the 
heart. 
You will remember, therefore, whenever you hear 
a first-sound murmur localized at or near the apex in 
a case of pronounced amemia, to consider the pro- 
bability of its occurring1 independently of actual 
disease of the mitral valve ; and, in the absence of a 
history of rheumatic causation, to give a hopeful 
prognosis, if only the condition of general anaemia 
can be satisfactorily recovered from. And especially 
if you hear such a murmur in a patient manifesting 
typhoid fever (if there be evidence that no mitral 
lesion has taken place previously to the occurrence 
of the fever) you may predict with the highest pro- 
bability that the sound will disappear, and that the 
valves will not be affected. 180 
Fugitive murmurs excluded, we now suppose that 
a murmur is heard in the mitral area. You have deter- 
mined the situation of the apex-beat, and you observe 
that there is a bruit localized within, or having- a 
maximum intensity within, the circumference of a circle 
extending- an inch around the apex. The phenomenon 
indicates a morbid condition of the mitral orifice. 
A murmur indicative of mitral lesion is met with as 
probably the most common of all the signs of heart- 
disease. Of the hundred cases of the various clinical 
forms of disease which I have cited, fifty-eight mani- 
fested the murmur indicating morbid change at the 
mitral orifice. 
By far the most common cause of mitral lesions is 
rheumatic endocarditis. Of the fifty-eight cases just 
mentioned thirty-two had suffered from rheumatism, 
and of these twenty-three had been the subjects of 
rheumatic fever; two, in addition, had suffered from 
rheumatoid symptoms which occurred subsequently to 
scarlatina. In seventy cases of mitral lesions noted by 
Dr. Flint, rheumatism had occurred in fifty-five. 
You will remember that I called your attention to the 
frequency of pericarditis in acute rheumatism; a like 
frequency exists as regards endocarditis-in fact, the 
latter probably occurs rather more frequently than 
the former. Whilst Hasse, Bamberger, and Lebert 
give twenty-two, twenty, and seventeen per cent, re- 
spectively as the proportion of cases of endocarditis 
occurring in the course of rheumatic fever, Fuller and 
others have fixed the percentage much higher. Not 
at all infrequently the two diseases, endocarditis and 
pericarditis, occur together during acute rheumatism. 
1 have already hinted that endocarditis, like pericar- 
ditis, can arise and run its course in subacute rheu- 
AUSCULTATION. AUSCULTATION. 
181 
matism, where the articular symptoms are very slight 
indeed-in fact, that in some cases objective symptoms 
may be entirely absent. We must conclude, there- 
fore, that endocarditis of the rheumatic form may 
occasionally occur very insidiously, so that its origin 
and course may be entirely overlooked. 
Rheumatic endocarditis commonly starts from the 
mitral valve; in many cases the disease does not 
extend further. It is an obvious corollary that the 
mitral is the most frequent site of valvular deterio- 
ration. Combining the figures of Willigk, Flint, and 
Cockle, it would appear that the mitral is affected in 
one hundred and sixty-six cases to one hundred and 
thirty in which the aortic valves are diseased. The dis- 
ease spreads from the mitral valve to the endocardium 
lining auricle and ventricle ; its effects may often be 
traced by the appearance of a milky patch of thick- 
ened endocardium, stretching' in a direct path across 
the ventricle from the mitral to the aortic valves. The 
pathological changes occurring in rheumatic endocar- 
ditis consist, first, in a swelling and thickening of the 
serous membrane and the substance of the valve, the 
microscope showing an increase in the number of con- 
nective tissue nuclei; subsequently there is much de- 
velopment of fibrous tissue; lastly, there is a gradual 
process of retraction of the newly-formed tissue just 
as occurs in cicatrices. The morbid process may in- 
volve the muscular structures immediately subjacent- 
there may be myocarditis, with the result of shorten- 
ing of the papillary muscles and consequent retraction 
of the cords and curtains of the valve. 
Other causes besides rheumatic endocarditis may 
produce lesion of the mitral valve and orifice. These 
are identical with those which we have already con- 182 
AUSCULTATION. 
sidered as affecting the aortic valves-atheroma and 
endocarditis of the villous (i.e., accompanied by vege- 
tations) and the ulcerative forms. The valve may be 
incrusted by calcareous salts, and rendered hard as 
bone. Endocarditis may be induced by renal disease. 
Lancereaux has recorded a very interesting case, in 
which, with a condition of contracted kidney, there 
was disease of the mitral valve characterized by 
thickening and the appearance of vegetations which, 
under the microscope, were seen to be studded with 
granules, distinctly proved to be deposits of urates. 
The probabilities are very great that rheumatic endo- 
carditis is due to the presence or excess in the blood 
of the acid products of tissue disintegration, and that 
the endocarditis met with in renal disease is due to 
retention of the products which the kidneys are 
unable to excrete. In the villous form of endocar- 
ditis little excrescences may be seen fringing the 
margin of the mitral orifice, especially on the auricular 
side; these have been often observed after death in 
cases of chorea. The indications of ulcerative endo- 
carditis we have briefly considered in connection with 
the aortic valves; remember that it may in like 
manner attack the mitral ; recent observations have 
shown that it may occur as one of the sequela? of par- 
turition. Another cause of lesion of the mitral orifice 
is rupture of the tendinous cords connecting the 
curtains of the valve with the papillary muscles. 
This is not very uncommon ; Flint found it in four out 
of thirty-nine cases of mitral defect; it may occur 
from violent action of the heart. Again, the mitral 
orifice may be rendered imperfect on account of 
dilatation of the ventricle, whereby approximation of 
the curtains of the valves is prevented. Lastly, but AUSCULTATION. 
183 
very rarely, fusion together, or perforations, of the 
mitral valve may be congenital. 
When we come to review these various patholo- 
gical causes in relation to their effect upon the 
auriculo-ventricular orifice, we find that they can pro- 
duce two well-marked varieties of lesion, as well as 
a third variety, which is a compound of both the 
others. Thus the orifice may be patent, the valve 
imperfectly closing it; or it may be obstructed, the 
outlet from the auricle being narrowed; or it may be 
both obstructed and patent, an impediment existing to 
the outflow from the auricle, as well as an imperfec- 
tion of the valve whereby it is prevented from closing 
the orifice. 
The first of these conditions is the most common. 
By thickening and shrinking of the curtains of the 
valve, by the presence of vegetations distorting them 
or weighing them down, by their " pouching" with 
aneurismal dilatations, by their perforation or ulcera- 
tion, by swelling and shortening- of the tendinous 
cords attached to the curtains, by deformity or rup- 
ture of the musculi papillares, by disease and retrac- 
tion of the muscular wall of the ventricle, or by such 
dilatation of it that the edges of the valves cannot 
meet-by these and some other causes the mitral 
orifice is prevented from closure at the time of the 
systole of the heart. There is then said to be a con- 
dition of mitral insufficiency; that is, the valve is 
insufficient to close the auriculo-ventricular aperture. 
The consecpience is that at each contraction of the 
ventricle a portion of the content of blood gushes 
backwards, through the space left by the imperfect 
apposition of the valve, into the left auricle. There is 
said to be mitral regurgitation. One consequence of 184 
AUSCULTATION. 
this condition is that the auricle is always abnormally 
full; the continuance of this leads to dilatation of the 
auricle, and the amount of such dilatation affords an 
index of the amount of regurgitation. Furthermore, 
the ventricle is of necessity incompletely emptied ; 
from containing habitually too much blood it also 
becomes dilated, and, in obedience to the law which 
enables involuntary muscle to increase in bulk and 
strength in order to overcome obstacles, it becomes 
hypertrophied. This condition of hypertrophy with 
dilatation has been called eccentric hypertrophy. 
The consequences on the general system arising from 
the leakage through the mitral orifice are, unless the 
condition of hypertrophy exactly compensate for the 
evils, insufficient supply of blood through the aorta, 
whence diminished blood-pressure in the arteries, 
sluggishness of flow in the capillaries from impaired 
vis d tergo, and undue repletion of the venous radicles 
and the general venous system. And when we come 
to the right heart we find a condition of distension 
(the pulmonary second sound is intensified, owing to 
the heightened blood-pressure, as I have before 
pointed out), and thus the right cavities may become 
dilated. In the majority of cases the cause inducing 
the condition of mitral regurgitation is rheumatic endo- 
carditis. Mitral regurgitation occurred in forty-eight 
out of my hundred cases of heart disease. Of these 
twenty-six had suffered rheumatism, nineteen having 
had rheumatic fever; besides, two had suffered scar- 
latina, wherein you know there are rheumatoid phe- 
momena. Chorea existed in two cases, gout occurred 
in one. 
A quite different set of conditions obtains when the 
mitral orifice is obstructed. The average circumference AUSCULTATION. 
185 
of the normal orifice, according- to Bizot,is four inches; 
its form is oval, the long- diameter being- one inch. 
These dimensions are greatly modified by disease. 
The cords, curtains, and muscles of the valve may be 
stiffened into a rig-id mass, or the edges of the orifice 
may be obstructed by vegetations, in some cases very 
small and insignificant, in others assuming the dimen- 
sions of large polypi. In many cases the form of the 
valve curtains and the shape of the outlet are singu- 
larly altered. The curtains are, as it were, fused 
tog-ether into an even tube, more or less conical, with 
its smaller extremity downwards opening into the 
ventricle: sometimes this extremity is circular and 
may be extremely small; it may admit only the 
thumb or the little finger, or be so minute as scarcely 
to allow a small catheter or even a crow's quill to pass 
through it. This variety is known as the " funnel- 
mitral." Or the free extremity, instead of being cir- 
cular, maybe slit-like. Dr. Hilton Fagge has recorded 
a case in which the slit was so narrow that it would 
not admit a three-pennypiece edgewise. This is called 
the "button-hole" mitral. The septum formed by 
the adherent valve-curtains may be incrusted with 
calcareous salts so as to be of bony hardness. In 
many cases, however, it is perfectly smooth and so 
uniform in its conformation as a hollow cone, that it 
seems to suggest that it must be a congenital anomaly ; 
its perfect regularity appearing to contradict the 
probability that it is the product of disease. 
The effect of these conditions upon the auriculo- 
ventricular aperture is the reverse of that produced 
by the conditions which permit regurgitation. The 
aperture guarded by the mitral valve, instead of being 
widened, is narrowed-there is said to be mitral stenosis. 186 
AUSCULTATION. 
There exists an impediment to the flow from the 
auricle into the ventricle-there is mitral obstruction. 
Such an occurrence is not uncommon. Flint found 
stenosis in sixteen cases out of thirty-nine instances 
of mitral lesion. Of my forty-eight cases of mitral 
disease, stenosis was declared by the physical signs to 
exist in ten. 
As I have before said, the regularity of form in the 
case of the fused mitral valve has suggested the pro- 
bability of a congenital causation. Dr. Hilton Fagge 
inclines to this view in some cases, and thinks that a 
rheumatic origin is comparatively rare. For my own 
part, however, I am disposed to the view that nearly 
all the cases are the result of rheumatic endocarditis 
of a very chronic form. Of the ten cases I have 
mentioned, four had suffered from rheumatic fever, 
and two from subacute rheumatism ; in the remaining 
four the causation was hypothetical. In undoubtedly 
rheumatic cases, however, I have seen the funnel 
mitral of the precisely regular conformation suggestive 
of the congenital anpmaly, and I think it must be ex- 
plained by the involvement of the whole texture of 
the valve by one or successive attacks of endocarditis 
(which attacks, as I have before said, may occur with 
little or no subjective sign), and by slow and regular 
development of fibrous tissue with quasi-cicatricial 
change. The great rarity of the positive evidence of 
congenital anomaly of the mitral valve is in favour of 
this view. 
The secondary effects of mitral obstruction are quite 
different from those of mitral regurgitation. The 
most constant and most pronounced effect is upon the 
left auricle, the wall of which becomes hyinrtrophicd. AUSCULTATION. 
187 
I have already cited a case under my own care illus- 
trative of this point in considering the chronometry 
of pulsations. It is quite clear that the hypertrophy 
occurs in obedience to the usual rule-there is an 
impediment to the outflow from the auricle to the 
ventricle, and the muscle of the auricle becomes 
hypertrophied to overcome the obstruction. Whilst 
dilatation of the left auricle without hypertrophy is 
characteristic of mitral regurgitation, dilatation with 
hypertrophy is characteristic of mitral obstruction. 
The left ventricle in mitral obstruction is found not 
to be dilated. In some cases it has been observed 
to be smaller than normal, its muscular wall has rarely 
been found hypertrophied. When it has been thus 
found the condition has been that formerly known as 
concentric hypertrophy, which simply means hyper- 
trophy without dilatation. In the great majority of 
cases the left ventricle in mitral obstruction is found 
not obviously abnormal, the condition thus differing 
from that in mitral regurgitation wherein dilatation 
and hypertrophy are the rule. 
The consecutive changes in the right heart are alike 
in regurgitation and obstruction, though the initial 
causes are different. In both conditions there is im- 
paired vis a tergo, and hence venous congestion and dila- 
tation of the cavities of the right heart, but this is due 
in the case of stenosis to the imperfection of supply 
from the auricle to the ventricle with retention in the 
auricle, wrhilst in regurgitation it is due to the retro- 
grade diversion of the blood-stream through the mitral 
aperture. 
The subjoined diagrammatic sketches may aid you 
to comprehend the conditions in mitral stenosis, as 188 
AUSCULTATION. 
distinguished from those in mitral regurgitation. They 
are intended to represent vertical sections through the 
left auricle and ventricle. 
FlO. 4. 
Fig. 5. 
Mitral Stenosis 
(Obstruction). 
a Hypertrophied muscu- 
lar wall of left auricle. 
, Section of wall of left 
ventricle. 
c, Narrowed auriculo- 
ventricular orifice. 
Mitral Insufficiency 
(Regurgitation). 
a, Dilated left auricle 
b, Section of hypertrophied 
and dilated left ventricle. 
c, Patent auriculo-ventri- 
cular orifice. 
(The arrow shows the direction of the current of blood at the 
time of the production of the murmur.) 189 
LECTURE VIII. 
AUSCULTATION. 
Difl'erential diagnosis of mitral lesions-Rhythm-Chrono- 
metry of murmurs-Vocal representation of murmurs- 
Graphic representation of murmurs-Area of audibility- 
Signs of mitral stenosis-Signs of mitral insufficiency- 
Double mitral murmur-Combined murmurs-Diagnosis of 
complex lesions. 
PART IV. 
Seeing that there are these well-marked varieties of 
lesion of the mitral orifice, the question now occurs- 
can they be detected and differentiated during life ? 
The answer is undoubtedly in the affirmative. 
The previous examination of the patient has given 
many data. We must exclude the evidence of any 
departure from the normal as regards the right cham- 
bers of the heart, for consecutive changes in these 
can occur from either of the abnormal conditions of 
the mitral orifice. Our examination of the left 
chambers, however, may have afforded valuable evi- 
dence. If we have found from the physical signs 
that the left ventricle is dilated or dilated and hyper- 
trophied, the probability is great that if there be any 
mitral lesion at all it will be one of regurgitation. 
Palpation may strengthen this probability by evi- 
dencing a systolic thrill ; remember, however, to 
time it carefully, for systolic thrill is rare and 
presystolic thrill by far the more common. Suppos- 190 
AUSCULTATION. 
ing, on the other hand, that we find little or no 
evidence of displacement of the apex, but a thrill 
communicated to the finger distinctly antecedently to 
the impulse of the heart-in this case the diagnosis of 
mitral obstruction may be positively made. In some 
such cases as I have before shown, the pulsation of 
the hypertrophied left auricle may be visible in 
vibration of the chest-wall, and its movement im- 
mediately before the ventricular systole can be de- 
monstrated. 
It is but a small proportion only, however, of the 
cases of obstruction of the mitral orifice that can be 
thus diagnosed. The question now becomes narrower: 
can the conditions be differentiated by auscultation ? 
Twenty years ago it would have been declared 
impossible. Contraction of the mitral orifice was 
revealed by post-mortem examinations in a large 
number of cases then as now. The diseased con- 
dition of the valve was not overlooked, but obstructive 
and regurgitant lesions were no doubt mingled to- 
gether in clinical diagnosis. A murmur was heard 
in both classes of cases, but the rhythm of such 
murmur was not recognized. Although some steps 
had been taken in this direction by French observers, 
Fauvel and others, it was not till Dr. W. T. Gairdner, 
in 1861, by careful clinical observation and philo- 
sophical demonstration showed the characters, the 
import and the causation of the murmur dependent 
upon mitral constriction, that the diagnosis in any 
considerable number of cases was affected. Further 
observations, especially those of the late Dr. Hyde 
Salter and Dr. Hilton Fagge, have contributed to 
spread the knowlege of the methods of discriminating 
the two conditions, but there is not the least doubt AUSCULTATION. 
191 
that even now the condition of mitral stenosis in a 
large number of cases is not differentiated from the 
regurgitant lesion. As to the ease with which this 
diagnosis can be effected the opinions of good 
observers vary; some say, with Dr. Hyde Salter, 
that any one who should fail to recognize the mur- 
mur of mitral obstruction " could hardly be con- 
sidered a decently informed member of our pro- 
fession;" others, with abundant opportunities of 
observation, have failed to discover the murmur, and 
have written papers to prove that it has no existence. 
The truth lies probably between these two extremes. 
The typical presystolic murmur any instructed clinical 
observer who takes the necessary time and trouble 
cannot fail to recognize, but there are some murmurs 
so short, so slight, and so obscure that their re- 
cognition and the determination of their rhythm are 
matters of very great difficulty. Such obscurities are, 
however, quite exceptional, and in the great majority 
of cases it will be your own fault if you fail to 
diagnose mitral stenosis when it exists. 
We must first inquire : what is the rhythm of the 
murmurs heard at the apex of the heart ? At the 
base we know that the rhythm is very simple. Of 
the murmurs there localized one is heard with the 
first sound (systolic), the other commences with the 
second sound (diastolic). At the apex we may have, 
as at the base, a murmur coincident with the first 
sound-systolic murmurs may occur both at the base 
and apex-but, as a matter of fact, a murmur whose 
origin is at the mitral orifice scarcely ever commences 
at the same period of the heart's rhythm as the 
diastolic murmur heard at the base. Such mitral 
murmur occurs not with the second sound, but after 192 
AUSCULTATION. 
it. Careful observation will show that a mitral 
murmur is not diastolic in the sense of being abso- 
lutely coincident with the diastolic or second sound 
of the heart, but that it occurs after the second sound 
and before the first sound. It is now well known as 
the presystolic murmur. A strictly diastolic murmur 
of mitral origin-that is, a murmur commencing at 
the time of the second sound with a pause before the 
first sound-although extremely rare, is not un- 
known. Its mechanism will be considered hereafter. 
It is unfortunate that the German authorities describe 
all those murmurs generated at the mitral orifice 
which are not systolic as diastolic. Under this term 
they include the presystolic murmur-in fact, all 
sounds that occur between the second sound and the 
succeeding first sound. (Cf. Guttmann, " Handbook 
of Physical Diagnosis," p. 289.) I have already 
described to you the mechanism of presystolic thrill 
and presystolic pulsation. The murmur which we 
are now considering is produced by the same cause- 
the forcing of the blood through the narrowed auriculo- 
ventricular orifice. 
The term presystolic is not wholly devoid of objec- 
tion. It is obvious that the systole of the heart 
means the systole both of auricles and ventricles-the 
presystolic murmur is presystolic only as regards the 
ventricular systole, it is coincident with the auricular 
systole. Nevertheless, the term has been so useful 
that we cannot wholly discard it. Dr. Gairdner pro- 
posed the term auricular-systolic, and this is for the 
njost part expressive of its physiological causation. 
The propriety of the termswill, I consider, necessarily 
vary as these are employed for the expression of the 
clinical or the pathological conditions. For the latter AUSCULTATION. 
193 
purpose, Dr. Gairdner's term is usually appropriate; 
but for clinical record it is better, in my opinion, to 
use a term which shall fix the period of the murmur 
in the heart's rhythm without even the semblance of 
hypothesis. I do not think that the use of the words 
systolic" and " diastolic," for the purpose of timing- 
murmurs, is without reproach: but these, as well as 
" presystolic," have become incorporate with our 
notions, and we cannot well do without them. We 
use them, however, on the principle expressed by the 
phrase : If you know what I mean, what does it 
matter what I say ? For precision, it would be much 
better, in my humble opinion, if heart murmurs were 
expressed in plain English and indicated by the 
periods of the obvious and precise sounds of the 
normal heart. Thus, a systolic should be expressed 
as a first-sound murmur, a diastolic as a second-sound 
murmur, a presystolic as a before-first-sound murmur. 
From this preface let us turn to the practical 
methods of discriminating- the rhythm of the mur- 
murs heard over the mitral area and dependent upon 
disease of the mitral valve. Here let me say, that 
you must give full and long attention; for the dia- 
gnosis is easy if you take sufficient care, confused and 
obscure otherwise. 
First.-Endeavour to determine the exact position 
of the murmur in the heart's rhythm. We may call 
'this the method of Chronometry of Murmurs. 
The principles of it I have already applied in the cases 
of pulsations occurring over the cardiac area and the 
phenomena of thrill. At the risk of frequent repeti- 
tion I will again state the rule :-Apply your stetho- 
scope over the point of maximum loudness of the 
murmur, and place the tips of the fingers on any 194 
AUSCULTATION. 
point of the chest where you can feel the impulse of 
the ventricles or over the site of the pulse of the 
carotids. You auscultate at the same time that you 
feel the pulsation of the heart or of one of the great 
arteries near it. The question which you have to ask 
yourself is this : Is the murmur which I hear coin- 
cident with the first sound of the heart, or is it 
previous to it and directly terminated by it ? Do not 
run away with the notion that without all this care 
you can determine the question : you may not be able 
even to distinguish the first sound from the second 
sound. What said one of the greatest authorities, 
the late Dr. Stokes ?-" So great is the difficulty, that 
we cannot resist altering our opinions from day to day 
as to which is the first and which is the second 
sound."* There can, 1 think, be no doubt that the 
great reasons why in times past the condition of 
mitral stenosis remained undistinguished from that of 
regurgitation, was that the murmur was judged to be 
systolic, and the first sound was taken for the second 
sound. Incases of stenosis, the mistake is peculiarly 
easy, for the first sound is usually very short, sharp, 
and sudden, much resembling the second sound. 
These considerations are quite enough to inculcate 
lessons of care in observation, and the absolute 
necessity of timing the murmurs. If the murmur be 
systolic you will hear it commence at the same instant 
that the finger is sensible of the cardiac pulsation. 
It is produced, as you know, by the reflux current 
forced into the left auricle by the ventricular contrac- 
tion. It is a truism, therefore, to say that its period 
of production is the period of its cause-i.e., the 
* "A Practical Treatise on Diseases of the Heart," 3rd 
edition, 18G2, quoted by Dr, Fagge, loc. cit. AUSCULTATION. 
195 
ventricular systole. Commencing' immediately with 
t lie full force of the contraction, it may last through- 
out the whole systole, or it may become feebler and 
inaudible as the ventricle becomes emptied. In other 
words, it may be short or long ; commencing with the. 
systole, its duration may be the whole or a part there- 
of. Such is the first-sound murmur,-the murmur of 
mitral regurgitation. 
Suppose now that the murmur which you hear be 
not coincident with the systole. A.t the moment that 
your finger becomes sensible of the impulse of the 
heart against the wall of the chest, the flap or thud 
of the first sound is audible. Preceding this, how- 
ever, and soon after the second sound, a rough murmur 
is heard. This murmur also may be either short or 
long; it may commence immediately after the second 
sound, or it may occur momentarily before the first 
sound, but the latter always terminates it as with a 
sudden full stop. The mechanism I have before ex- 
plained-it is the sound produced by the effort of a 
hypertrophied auricle in urging the blood through a 
narrowed mitral orifice. This presystolic, before- 
first-sound murmur, is absolutely diagnostic of mitral 
stenosis. 
Secondly.-In order to help you to realize the dis- 
tinctive characters of these sounds, I would call your 
attention to a method of Vocal Representation 
of Murmurs. The " bruits" heard over the heart- 
region have received since the time of Laennec many 
names according to their nature and quality. Thus 
we have bellows' sounds, filing-, grating, rasping, 
croaking, crowing', whining, caterwauling-, and blub- 
bering sounds, or musical or sibilant sounds. Bouil- 
laud imitated the character and pitch of the sounds 196 
by letters, the pronunciation of S expressing the ex- 
treme of sibilant murmurs of high pitch, It represent- 
ing those of low pitch. These illustrations are all of 
some value, as enabling one to note the variations in 
character of any given murmur from time to time, 
and thus indicating changes favourable or unfavour- 
able, or the persistency of the lesion. Any of the 
illustrations just given may be applied to the mur- 
murs produced by the valvular conditions we have as 
yet considered; the sounds, therefore, cannot be con- 
sidered diagnostic. Valuable help, however, may be 
derived from a consideration of the sound in the 
differential diagnosis of murmurs heard over the 
mitral area. The murmur of regurgitation may have 
almost any of the characters just described, but not 
so the murmur of obstruction. This latter is almost 
invariably rough ; it has been called a " churning,'' 
" grinding," or " blubbering" murmur. In my own 
opinion, in typical cases, it may be best illustrated as 
" rolling," or " bubbling," resembling the sound of 
air rising through water. You may easily realize its 
distinctiveness from the systolic murmur by these 
simple considerations-the systolic fades off but never 
terminates abruptly, the presystolic always stops sud- 
denly. I have frequently illustrated this by the sub- 
joined vocal illustration, the sound of " p" indicating 
the abrupt termination of the presystolic murmur. 
AUSCULTATION. 
Sound of Systolic 
Murmur. 
Hook-ko of- r uff. 
Sound of Presystolic 
Murmur. 
Up-rup-rr. rr. rvp. 
Thirdly.-We come to a plan which we owe to- 
Dr. Gairdner, and I know of none which is more 
valuable to fix upon the mind the phenomena of the AUSCULTATION. 
197 
murmur, and to serve as a method of record. We 
may term this the method of Graphic Represen- 
tation of Murmurs. To represent all the facts 
and conditions, I have combined Dr. Gairdner's plan 
with a chart which I have modified from Dr. Salter. 
The upper portion of this diagram represents the 
conditions of the auricle and ventricle during three 
'cardiac pulsations. Each such pulsation or cycle is 
divided into six equal parts, which are denoted by the 
squares. The squares which are shaded denote that 
the chamber (auricle or ventricle) contains blood, 
whilst the black squares indicate that it is replete- 
i.e., at its maximum of distension. The squares 
marked C denote contraction or systole. The upper 
line of squares A pertain to the auricle, the lower V 
to the ventricle. Taking the auricle first and pro- 
ceeding from left to right, we see that it is receiving 
Fig. 6. 
I PAUSE. I PAUSE I PAUSE 
THE NORMAL CARDIAC RHYTHM. 
blood during the period indicated by the first four 
squares, and that at the fifth it has arrived at its 
maximum distension. Then follows C, its systole or 
emptying through muscular contraction. Looking at 
the ventricular line V, we see that the systole lasts 
■during the first two squares, or two-sixths of the 198 
AUSCULTATION. 
<-ycle, that during- the following three it is in diastole 
or receiving blood, and at the sixth it has arrived at 
its maximum distension. Then the cycle is in each 
case repeated. Now, we are enabled by a glance at 
the diagram to note the relative condition of auricle 
and ventricle at any given moment of the heart's 
action ; we have only to compare the upper sections 
with the lower. Thus we see that whilst the ventricle 
V is in systole, the auricle A is in diastole : that A, 
having at last become distended, contracts, while A is 
yet in diastole, and completes the repletion of V, which 
recommences the cycle by contraction. Again, by a 
horizontal line below, we have a means of comparing* 
these conditions with the sounds of the normal heart, 
the vertical lines 1 and 2 denoting the first and the 
second sounds respectively. You will see that the 
latter occurs very soon (about half a square) after the 
ventricular contraction, the first sound lasting during 
two squares. 
We have thus a very simple and concise method of 
registering murmurs, their position in the cardiac 
Fra. 7. 
SYSTOLIC OR FIRST-SOUND 
MURMUR 
DIASTOLIC GR SECOND-SOUND MURMUR 
rhythm and their duration. Taking- the horizontal 
lino to express the duration of the cycle, and the ver- 
tical lines to denote the first and second sounds, we 
have merely to indicate by shading- the place and AUSCULTATION. 
199 
estimated length of the murmur. Thus, the simple 
systolic and diastolic murmurs heard at the base of the 
heart, would be indicated by the diagram (fig. 7). 
The one commences with the first, the other with the 
second sound. 
The rhythm of the first-sound murmur heard at 
base and apex is precisely similar. The upper line of 
this diagram would alike express the sounds of aortic 
obstruction and mitral regurgitation. Of course a 
note of the area of audibility and maximum intensity 
would at once indicate the diagnosis. 
We will now consider how this method illustrates 
the differential diagnosis between the murmurs of 
mitral res'uro'itation and mitral stenosis. The sub- 
o n 
joined diagram you will readily understand from the 
Fig. 8. 
SYSTOLIC OR FIRST SOUND MURMUR. 
PRESYSTOL1C 08 BEFORE-FIRST SOUND MURMUR 
explanation I have already given. It shows how the 
systolic murmur starts with the first sound, and the 
prcsystolic leads up to the first sound; whilst a glance 200 
AUSCULTATION. 
at the upper section of the diagram indicates the 
cardiac conditions at the time of the production of 
the murmurs. The first-sound murmur occurs with 
V C C, the ventricular contraction ; the presystolic 
with A C, the auricular contraction. It is possible 
that, as the diagram shows, the presystolic murmur 
may commence during the distension of the auricle, 
and previously to its actual systole. 
Having considered the rhythm of the murmur, we 
have yet another aid towards the differentiation of 
mitral stenosis from mitral regurgitation in the deter- 
mination of the area of audibility. 
It is rare for the murmur of stenosis to be heard 
to any considerable degree below or outside the situa- 
tion of the normal apex. As I have before said, the 
conditions of hypertrophy and dilatation of the left 
ventricle, which cause the apex-beat to be discernible 
externally and inferiorly to the normal position, 
seldom coexist with mitral stenosis. A murmur, 
therefore, heard left of the cardiac area in conjunc- 
tion with the signs of ventricular enlargement is 
unlikely to be a murmur of mitral obstruction. Ex- 
ceptions to this rule occur when hypertrophy of the 
ventricle from other causes coexists with mitral 
stenosis. 1 have recorded a case in point in which 
there had been repeated attacks of pericarditis with 
numerous adhesions.* Observers have agreed that 
the murmur of obstruction is a localized murmur-it 
is seldom audible far from the apex. Again it is 
said to have its maximum intensity at the apex. To 
this last conclusion, however, I shall have to demur ; 
it has been an almost invariable experience with me 
* Vide Medical Times and Gazette, June 10th, 1874. p. 34. AUSCULTATION. 
201 
that the presystolic murmur is loudest at a point in- 
ternal to (i.e., right of) the apex-beat. It is usually 
audible over a portion of the normal area of the right 
ventricle, but seldom as far on the pulmonary car- 
tilage, but is suddenly cut off at the left apex and is 
inaudible, or scarcely audible, left of the apex. 
Let us contrast this with the murmur of mitral re- 
gurgitation. This systolic murmur may have a very 
small area of audibility around the apex, but its 
maximum is never just internal to this point. On the 
contrary, in a large majority of cases it is louder a 
short distance outside the apex than at the apex itself. 
When it is of considerable intensity, the sound of the 
murmur may be carried towards the axilla and may 
be audible over the axillary part of the chest-wall : 
it will probably disappear as the stethoscope is carried 
to the back, but may again become evident between 
the scapulae, especially in the interval between the 
angle and the spine of the left scapula. 
In exceptional cases both the systolic and the presystolic mur- 
murs, generated at the mitral orifice, may be conducted towards 
the right instead of to the left apex. In these there is an unusual 
conduction of the murmur, due, accordingto my observation and 
experience, to the fact that the disease of the valve has involved 
that portion whose papillary muscles and cords are connected 
with the inter-ventricular septum. So the vibrations are con- 
ducted by the dense material through the septum to the sternum 
and the right apex, and the maximum of the murmur is in the 
tricuspid area. In like manner a tactile thrill of systolic rhythm 
may be abnormally conducted towards the right. I have also 
found the presystolic murmur under like circumstances con- 
ducted to the tricuspid region. Where the bruit is loud and 
musical or whistling, I consider that we may infer that the 
diseased portions of the valve have undergone calcareous trans- 
formation. Guided by this experience, I made, in a case which 
presented a presystolic murmur having these characters (but 
■which ceased at the later stages of the disease), as well as a 202 
AUSCULTATION. 
systolic mitral murmur, the following diagnosis :-That there 
was mitral constriction, the characteristic presystolic murmur 
of which had been conducted by dense material to the inter- 
ventricular septum and thence towards the right apex ; that 
the valve-aperture was probably a calcareous ring; that the 
murmur had ceased to be audible because the left auricle had 
become dilated and its muscle enfeebled; that there was, in 
addition, incompetency both of mitral and tricuspid valves, 
with hypertrophy and dilatation of each ventricle. At the 
autopsy, in which I was kindly assisted by Dr.Hamilton of Canon - 
bury, who had had daily charge of the patient, the diagnosis 
was exactly confirmed. The left auricle was very large and its 
walls extremely thin. Seen from the auricular aspect, the 
mitral orifice was of button-hole shape, with rigid borders, and 
allowing abundant regurgitation ; the right boundary was con- 
verted into a dense calcareous mass with numerous hard and 
rough projections. The tricuspid orifice was moderately in- 
competent, but its valves normal. It thus appears that in 
certain cases of murmurs heard in the tricuspid area we may 
be able not only to infer that the morbid change is at the mitral 
orifice, but to diagnose the nature of the deposit. (Cf. "Pro- 
ceedings of the Medical Society of London," vol. iii., p. 145. 
and Medical Examiner, Jan. 25, 1877, p. 65.) Guttmann, fol- 
lowing Naunyn. says that in very exceptional cases a mitral 
systolic murmur is of greatest intensity in the second left inter- 
costal space. Naunyn believes this to indicate hypertrophy of 
the left auricular appendix:-"That, as in every case of 
mitral insufficiency the systolic regurgitant current of blood, 
rushing from the left ventricle, enters not only the corre- 
sponding auricle, but penetrates also to its appendix (the cavities 
<>f both parts being continuous), the further the latter passes 
round the pulmonary artery, and the nearer its apex comes to 
the anterior chest-wall, the more favourable are the conditions 
presented for the propagation of the mitral murmur through 
the left auricle into the. appendix and thence to the thoracic 
parietes (Guttmann, "Hand-book of Physical Diagnosis," 
Sydenham Society's translation, p. 289). This seems to me 
a far-fetched theory : it is far more likely that the murmur, as 
in the instances I have quoted, is abnormally conducted by 
the diseased structures at the insertion of the right curtain of 
the mitral valve. AUSCULTATION. 
203 
A little consideration will, I think, enable yon to 
realize the physiological causes of the differences in 
site of the two murmurs. A reference to the diagram 
illustrating the conditions in mitral stenosis (p. 188) 
will remind you that the direction of the current-i.e., 
the line of convection of the murmur-is from tho 
auricle to the apex of the heart. It would seem, 
therefore, primd j'acic that the " bruit" should be most 
audible at the apex. We must recollect, however, 
that at the time of production of the murmur the 
apex is not close to the wall of the chest; its position 
is slightly internal to that which it occupies when the 
ventricle strikes the chest-wall, and a space inter- 
venes. These considerations to my mind explain the 
position and the limitation of the murmur. In re- 
f/wpitation, on the other hand (see fig. 5), the direc- 
tion of convection is contrariwise ; you might say 
that the sound ought to be carried to the region of 
the left auricle. Why is it not so ? Surely because 
the walls of the left ventricle conduct the sound in a 
direct line to the apex, and thence to the ear. At the 
moment of production of the first sound the apex is 
in direct contact with the chest-wall, and occupies a 
position left of that which it occupied previously. 
The muscular ventricle, the thoracic parietes and the 
stethoscope, being in close apposition, constitute one 
solid conductor through which the sonorous vibrations 
travel in uninterrupted course to the ear. Both these 
murmurs maybe intensified by causing the patient to 
use muscular exertion; but especially the presystolic. 
The latter is apt to vary in intensity and audibility : it 
may be absolutely inaudible till the patient is put 
through a little walking exercise. 
We will now sum up our auscultatory evidence. 204 
AUSCULTATION. 
A rough murmur is heard antecedently to thcjirst sound, 
■and abruptly terminated by it: its maximum intensity 
being slightly internal to the normal apex. The condition 
is one of Mitral Stenosis. 
We will devote a short time to the clinical history 
•of these cases, and the phenomena which you may 
observe during your observation of their progress. 
The late Dr. Hyde Salter noticed the remarkable 
proclivity of the subjects of mitral stenosis to hamo- 
ptysis. He recorded this as occurring in six out of 
•eight cases. I have no doubt, however, that this was 
an exceptional frequency; for out of sixteen cases 
recorded by Dr. Fagge, J find haemoptysis noted only 
in three, and in seventeen cases under my own care it 
occurred also in three. Though these figures modify 
those of Dr. Salter, they support his conclusion that 
haemoptysis is a frequent symptom in mitral obstruc- 
tion. The cause is no doubt the backward pressure 
•exerted by the contraction of the auricle (opposed as 
it is by the obstruction at the auriculo-ventricular 
outlet) upon the pulmonary veins; hence there is 
congestion of the pulmonary capillaries to the point 
of rupture. In mitral obstruction the capillaries 
suffer the direct pressure of the contracting auricle, 
whilst in regurgitation the auricle intervenes as a 
•dilatable cavity between the contracting ventricle and 
the pulmonary veins. 
The next point of interest in the clinical history or 
these cases is the proneness to embolism of one of the 
cerebral arteries, or of some artery of the lower limb. 
Remember, therefore, to inquire carefully into the 
-cerebral conditions of all patients whom you find to 
manifest the signs of mitral stenosis, and conversely 
in cases of sudden paralysis, apparently of cerebral AUSCULTATION. 
205 
origin, be mindful to explore the mitral region. You 
will readily understand how the contraction of the 
auricle may detach a pellet of fibrine or a pediculated 
vegetation from the endocardial surface, or from the 
margin of the auriculo-ventricular orifice, and trans- 
mit it into the direct current of blood urged by the 
ventricle into the arteries. 
With regard to other symptoms, the subjects of 
stenosis are in most respects affected in like manner 
with the subjects of insufficiency. As I have said 
before, the secondary effects upon the right chambers 
of the heart are alike in both cases. So we have in 
both cough, dyspnoea, and the evidences of congestion, 
pulmonary and general, and in the end, dropsy, &c. 
In one point, in my experience, the cases are slightly 
different-the subjects of stenosis are more liable to 
variable symptoms and spasmodic troubles. 
Mitral stenosis excluded, we -turn to the other 
condition. 
A murmur is heard with the first sound, or entirely 
occupying the place of the first sound in the cardiac 
rhythm : its maximum, at, or external to, the position of 
the apex-heat. The condition is that of Mitral In- 
sufficiency. 
Tn these cases of mitral regurgitation, when the 
lesion is not compensated by exactly sufficient hyper- 
trophy of the ventricle, the symptoms may be any of 
those which wo have already considered early in these 
lectures. It is unnecessary to revert to them. 
With regard to Prognosis'^ stenosis and insufficiency 
respectively, opinions are divided. For my own part, 
whilst agreeing that in stenosis there are certain special 
dangers, I am inclined to the belief that on the whole 
compensation is more certain and more persistent. 206 
AUSCULTATION. 
We come now to consider the case wherein the 
conditions we have just discussed coexist. 
J murmur is heard antecedently to th/ first sound, and 
in addition a, murmur is heard supplanting, or occurring 
with, the Ji rst sound. The condition is one of combined 
Mitral Obstruction and Mitral Regurgita- 
tion. 
In a very small minority of cases the sound is 
distinctly double. At the situation of the apex-beat 
you hear a murmur with the systole, then a pause, 
then a murmur which seems to be diastolic, and then 
a short pause before the recurrence of the first-sound 
murmur. You can convince yourself, by carefully 
timing-, that the murmur which appears to be diastolic 
is really subsequent to the click of the semilunar valves. 
I am aware that in saying; that there may be a pause 
between a presystolic and a systolic murmur, I am 
diverging- from the teaching of some who have deeply 
studied the question, but I do not speak without prac- 
tical experience. I had an opportunity of observing a 
case in -which this was exemplified. At a spot just in- 
ternal to the apex there were two distinct murmurs 
separated by pauses. The explanation of the pheno- 
menon appeared to be given to another case under my 
care, in which the only endocardial murmur was pre- 
systolic, but this was separated by a decided pause 
from the first sound. It was of such character that 
T called it a diastolic murmur. In this case the post- 
mortem examination revealed extreme narrowing of 
the mitral orifice, but in addition the ventricle was, 
in great measure, filled by vegetations depending from 
the lower surface of the valve. The latter condition 
seemed to me to explain the peculiarity of the murmur 
-the ventricle being already partially filled by the 207 
AUSCULTATION. 
vegetations, the murmur occurred only at the early 
part of the diastole, ceasing early because the small 
ventricular space left became quickly replete. 
In the great majority of cases the double mitral 
murmur can be readily resolved into two murmurs, 
having the distinctive characters which we have 
already discussed. The systolic element of the com- 
pound murmur is widely diffused, but the presystolic 
is heard only over its usual limited area. In the 
near neighbourhood of the apex the sound may be 
distinctly double: you hear the rolling presystolic 
murmur pass into the prolonged systolic. Or the 
presystolic may abruptly cease with a sharp first 
sound from which a soft systolic murmur tails off. In 
many cases, however, there is no spot where you can 
hear the two murmurs at one and the same time. 
This was well described bv the late Dr. Salter, who 
cited a case. Tn Dr. Salter's words-" At the apex 
a grinding bruit is heard, immediately preceding an 
apparently natural first sound, and terminated by it. 
On working back well into the axilla, and not until 
the axilla is quite reached, a systolic murmur begins 
to reveal itself, increasing in distinctness as you work 
round to the back, where it is loud and strong. It is 
audible over the whole of the left side of the back. 
On returning again to the front, to the region of the 
apex, it is quite lost, and the presystolic bruit is again 
heard."* I have no doubt that you will meet with 
examples verifying this description. 
The physical cause of mitral murmurs can be ex- 
plained according to the same principles as those 
which govern murmurs generated at the aortic orifice. 
* Lancet, July 24th, 1869, p. 114. 208 
AUSCULTATION. 
As regards the mitral systolic murmur we can thus 
explain its production :-So long as at the time of 
systole the curtains of the mitral valve are perfectly 
apposed there results only the sound of valve-tension 
-the normal first sound. Vibration is prevented by 
the coaptation of the valve-curtains. If from any 
cause, however, the segments do not meet, their 
borders are free to vibrate in the stream of blood, 
which of necessity regurgitates through the orifice 
left by their imperfect approximation. Where the gap 
is considerable, or the disorganization of the valve 
extensive, the normal sound of valve tension is alto- 
gether lost by the murmur entirely replacing it. When, 
however, a considerable portion of the valve curtains 
are capable of flapping back, the murmur is affixed to 
the sound of their closure. Such murmur is some- 
times termed post-systolic. It must not be forgotten, 
however, that the sound of valve tension may be that 
of the tricuspid ; if the murmur, when heard at the 
axilla and back, is accompanied by the flap of the 
valve, it may be fairly inferred that a considerable 
portion of the mitral valve is competent. The vibra- 
tions communicated to the boundaries of the imper- 
fectly closed orifice are not conveyed by the current, 
as in the case of the aortic regurgitant murmur, for 
in such case the " bruit" would be heard over the left 
auricle. They are, however, conducted by the solid 
structures, usually to the wall of the ventricle and the 
left apex, exceptionally, as lately explained, by good 
conductors, to theright apex and the adjacent sternum. 
The mechanism of the mitral systolic murmur is 
simple, and its occurrence pathognomonic of mitral 
regurgitation. The loudness of the murmur is by no 
means an index of the amount of regurgitation. In AUSCULTATION. 
209 
the earlier stages of valvular insufficiency it may be 
almost confidently stated that there can be no re- 
gurgitation without murmur. When, however, as in 
the last stages, the left ventricle becomes very feeble, 
the murmur may cease to be generated. So the en- 
feeblement or cessation of a mitral systolic murmur, 
when there are signs of increasing cardiac distress, is 
an evil omen pointing to failure of the left ventricle. On 
the other hand, when the disappearance of a mitral 
murmur is coexistent with amelioration in cardiac 
symptoms, and especially with enhanced power of the 
left ventricle, as evidenced by the cardiograph and 
sphygmograph, the prognosis is good; the regurgitation 
has been probably due to muscular enfeeblement, and 
not to structural disease of the valve. 
The presystolic mitral murmur I consider to be due 
to vibrations communicated to the abnormal mitral 
curtains, the solid structures in union with them, and 
the wall of the left ventricle, by the current of blood 
issuing under pressure through the narrowed mitral 
orifice during- the diastole of the ventricle. Such 
may be induced by the blood pressure in the 
auricle and pulmonary veins, independently of the 
auricular systole ; may be reinforced by contraction of 
the auricle during the period of diastole, especially at 
the conclusion of the period; or may be initiated only 
by the auricular systole just before the contraction of 
the ventricle. 
The mechanism of the presystolic murmur is more complex 
than that of the systolic, because the factors are more 
numerous and the conditions more variable. The sounds 
heard in connection with mitral stenosis can, I consider, be 
referred to the following types (see Fig. 9):- 
I. Reduplications, or seeming reduplications, of the normal 
sounds without murmur. I have already (p.. 119) called attem 210 
AUSCULTATION. 
tion to this as presumptive evidence of mitral narrowing. An 
apparent reduplication of the second sound is the most com- 
mon. Of thirty-seven cases in which I have made the diag- 
nosis of mitral obstruction, I have found such reduplication 
in eleven cases. This agrees with the experience of Guttmann 
(one in three cases) and Hayden (thirty in eighty-one). 1 
have already explained the mechanism of its production. 1 
Fig. 9. 
Diagram illustrating varieties of sounds observed in mitral 
stenosis. 
A, reduplication of second sound. B, reduplication of first 
sound. II. Prolonged murmur from second to first sound. 
III. The same, with reinforcement during its progress. IV. 
Presystolic murmur, with reinforcement at its close. V. Post- 
diastolic murmur. 
believe it to be due to the sudden floating-up of the valve- 
curtains of the mitral, owing to the increased pressure in the 
left auricle and pulmonary veins ; thus the valve is put on the 
stretch, and the sound of valve-tension results. Occurring at 
the earlier part of diastole, this appears like a doubling of the 
second sound. Occasionally such may be the only ausculta- AUSCULTATION. 
211 
tory sign of mitral stenosis, for the presystolic murmur may 
be absent. We have abundant experience that this murmur 
may appear and disappear ; at the periods of its absence the 
seeming reduplication may alone be heard. Much more com- 
monly, however, there is a short pause after the second 
element of the reduplication, and then a murmur of the pre- 
systolic character such as we shall presently discuss. In three 
eases I have noted reduplication of the first sound in connec- 
tion with mitral stenosis. I have discussed the mechanism 
of this, and have explained it by the view that in these cases 
the tension of the valve curtains takes place late in diastole- 
that is, synchronously with the auricular systole. Occurring 
just before the systole of the ventricle, this gives rise to a 
seeming reduplication of the first sound. 
The following types of sound, generated by the conditions of 
■mitral stenosis, are forms of the presystolic (before first sound) 
murmur. 
II. A murmur is heard occupying the whole of the interval 
between the second sound and the first sound (Fig. 9, II.} 
Usually this murmur receives a distinct emphasis near its 
termination; it often concludes with a rattle or roll, just as it 
is terminated by the sudden flap of the ventricular systole. 
You will observe that the murmur, so far as regards rhythm, 
may be identical with that of aortic regurgitation. Inamajority 
of cases the diagnosis between the two conditions will not be 
difficult. The area of audibility of the murmur of aortic 
reflux is usually notably different (as formerly pointed out) to 
that of mitral narrowing. Nevertheless, it is possible that 
difficulty may be experienced in the differentiation, for, as I 
have said, occasionally, though very rarely, the area of audi- 
bility of an aortic diastolic murmur is at the apex. In such 
-cases the diagnosis may be peculiarly difficult. My own 
belief is that the physical signs in the two conditions may be 
very similar-there may be in each, according to my own 
■observations, a thrill of presystolic rhythm, and in each a 
seeming reinforcement of the murmur just before the ventri- 
cular systole. Indeed, the physical conditions in the two 
-cases are very similar. In case of a presystolic mitral mur- 
mur such as this, a stream of blood is pouring during the 
whole period of diastole from the left auricle, and the veins in 
■communication with it, into the left ventricle; vibrations 212 
AUSCULTATION. 
capable of conveying sonorous impressions are communicated 
to the ventricle during the whole period, and are intensified at 
the close when the auricle adds the force of its contraction to 
the expulsive powers. In case of the aortic diastolic mur- 
mur vibrations are in ananalogous manner communicated to the 
left ventricle (in the instance we are now particularly considering 
to the apex of the left ventricle very probably, because the 
reflux current impinges directly on the upper segment of the 
mitral valve*) during the whole of diastole, owing to the 
gushing of the refluent stream through the chink occasioned 
by the imperfect closure of the aortic cusps, the backward 
impetus being due to the tension in the aorta and the whole 
arterial system, plus the gravity of the blood column. The 
physical conditions, therefore, in the two cases are closely 
analogous-a stream being urged under pressure during the 
whole period of diastole through narrowed orifice into the 
left ventricle, and the conduction of the vibrations being to 
the apex of the ventricle. The difficulty is by no means a 
merely imaginary one. Dr. Flint has recorded two cases 
in which murmurs presenting typically presystolic characters 
had been present, and yet post-mortem examination showed the 
absence of mitral stenosis and the existence of aortic insuffi- 
ciency. In regard to these cases, Dr. Flint says, in both " the 
mitral direct murmur was loud, and had the character of 
sound which I suppose to be due to vibration of the mitral 
curtains" (American Journal of Medical Science, vol. xliv.) 
Dr. Charlewood Turner also records a case in which there was 
a presystolic, alternating with a systolic, bruit at the apex of 
the heart, together with occasional thrill, and yet the autopsy 
disclosed no mitral stenosis, but aortic incompetency, the right 
and posterior cusps of the valve being chiefly affected. In 
another case mentioned by Dr. Turner a presystolic murmur 
and thrill were perceptible at the apex, as well as a diastolic at 
the base ; here the aortic valves were thickened, though there 
was no patency (it would seem most probable that there 
was, nevertheless, some regurgitation during life), and the 
curtains of the mitral valve were thickened and rough at their 
margins, though apparently competent. In a third case there 
were soft diastolic, presystolic, and systolic bruits at the apex. 
* Cf.. p. 153. AUSCULTATION. 
213 
with a slight diastolic thrill; here, as shown by post-mortem 
examination, there were aortic disease with incompetency 
and mitral disease with incompetency, but no stenosis. Dr. 
Turner does not consider that in any of these cases the 
murmur, which resembled that of mitral stenosis, was really 
one of aortic regurgitation, but adduces them to sustain his 
argument against the auricular causation of the presystolic 
murmur (St. Thomas's Hospital Deports, 1876). Dr. Hayden 
mentions a case in which the murmur of aortic reflux simu- 
lated that of mitral stenosis (" Diseases of Heart and Aorta," 
p. 907). It is a significant fact that in almost every case in 
which a presystolic murmur has been recorded, and the 
diagnosis of mitral stenosis has not been justified by the 
autopsy, there has been either a diastolic murmur heard 
during life in some part of the aortic area, or else the con- 
dition of aortic regurgitation has been demonstrated by the 
post-mortem appearances. 
To differentiate between the two conditions, therefore, aid 
must be called in from other sources than auscultation. The 
existence of hypertrophy of the left ventricle may be shown 
by the other signs, and thus the diagnosis will tend to that of 
aortic regurgitation; but the most important evidence is 
offered by the sphygtnograph and cardiograph (see Part II.). 
If under such circumstances the diagnosis between the two 
affections be difficult, the determination of the question of 
coexistence of the murmurs of aortic reflux and mitral 
obstruction may be still more difficult. We shall return to 
the question when we consider combined murmurs. 
In the case of the murmur occupying the w hole interval 
between second and first sounds, due to mitral stenosis, I can 
have no doubt that the early portions of such bruit may be 
due to the tension in the pulmonary veins and left ventricle, 
unaided by the systole of the latter. That such could be 
the case was held by Dr. Wilks. Dr. Galabin came to the 
like conclusion from cardiographic evidence. The crucial 
proof of the truth of the proposition is, I consider, furnished 
by cardiograms taken in cases in which I have found a 
presystolic murmur to occupy a considerable portion of the 
diastolic period, and yet the auricular systole is shown to 
occupy only its usual position just before the systole of the 
ventricle (see Part II.). 214 
AUSCULTATION. 
Ill. A murmur starting after the second sound and ceasing 
with the first sound is distinctly louder at a certain period 
in its course. This exaltation of the murmur is indicated by 
the swelling in the shaded portion of the diagram, which 
resembles one that was figured by Dr. Gairdner in his early 
exposition of the presystolic murmur. I have no doubt that 
this reinforcement is due to the systole of the auricle, which, 
owing to the obstruction at the mitral aperture, takes place 
out of the usual rhythm. I shall discuss the evidence which 
I believe to fully prove that such abnormal action of the 
auricle can, and does, take place in the section on the graphic 
signs of mitral stenosis (Part II.). 
IV. A murmur occupies a short interval just before the 
first sound, which abruptly terminates it. This is a common 
type of presystolic murmurs, and is due chiefly or wholly to 
the communicated impetus of the auricular systole (see 
Part II. p. 272). 
V. A murmur is affixed to the second sound, but ceases 
before the commencement of the first sound. Such murmur 
has been described by some observers as diastolic, by others 
as postdiastolic. The strictly diastolic form of murmur generated 
at the mitral orifice is very rare. Dr. Hayden states that he has 
not met with an example, but mentions a case under the care 
of Dr. Stokes in which it existed together with a systolic; 
murmur. I have recorded a similar case, with what I con- 
sider to be the explanation of the phenomenon in that instance. 
Dr. Fagge has mentioned cases in which a post diastolic 
murmur of mitral causation ceased before the commencement 
of the first sound, and it is quite conceivable that in such the 
tension in the left auricle was sufficient to produce a murmur 
as soon as the relaxation of the ventricle allowed the flow of 
blood to occur into it; but the muscular feebleness of the 
auricle was such that the murmur was not only not prolonged, 
but at the later period not even produced. In some rare cases 
the two last-mentioned murmurs have been combined : there is 
" a murmur of double rhythm, or broken into two fragments, 
one of which adheres as a prefix to the first sound, and 
represents the ordinary presystolic murmur, whilst the other 
succeeds the second sound, being appended to it as a suffix ; 
these two fragments being separated by a brief period of 
silence "(Dr. Hayden). AUSCULTATION. 
215 
We may now briefly consider combined murmurs. 
We have already discussed double murmurs-that is to 
say, murmurs generated at different periods of the 
heart's rhythm at one orifice : by "combined" mur- 
murs I mean those which take their origin from more 
than one of the orifices. The following may be taken 
as probably representing the relative frequency of the 
combinations :- 
(1.) Mitral regurgitation and aortic obstruction. 
(2.) Mitral regurgitation and aortic regurgita- 
tion, or mitral regurgitation and aortic obstruction 
and regurgitation. 
(3.) Mitral obstruction and aortic regurgitation, or 
mitral obstruction and regurgitation and aortic ob- 
struction and regurgitation. 
(4.) Mitral obstruction and regurgitation with tri- 
cuspid obstruction. 
(5.) Mitral obstruction and regurgitation with tri- 
cuspid obstruction and regurgitation. 
(6.) Aortic obstruction and pulmonic obstruction.* 
None of these combinations require particular com- 
ment from the point of view of diagnosis, except the 
third. You will distinguish them by the rules 
already laid down for the diagnosis of the individual 
affections. In all cases notice: 1. The positions of 
maximum intensity of any murmurs heard over the 
cardiac area. 2. Any differences of pitch and cha- 
racter. 3. The directions in which the sound is 
conveyed. 
There may be considerable difficulty in determining 
* The combination of mitral regurgitation and tricuspid 
regurgitation, or mitral obstruction and tricuspid regurgitation, 
is a very common one, but very frequently the tricuspid lesion 
is not betrayed by murmur. 216 
AUSCULTATION. 
the co-existence of aortic insufficiency and mitral nar- 
rowing1. A prolonged diastolic murmur may drown 
the presystolic. In carrying the stethoscope, how- 
ever, down the left border of the sternum you may 
probably arrive at a spot where the diastolic murmur 
ceases to be audible, and then as you approach the 
apex, a presystolic of different pitch and character 
may become manifest. The presence of a presystolic 
thrill at the apex may aid the diagnosis. 
Even though the ordinary means of diagnosis be used with 
all care, the question whether or no a mitral direct co-exists 
with an aortic regurgitant murmur may be difficult to deter- 
iniue. Witness the following cases under my care :-1. A 
man of fifty-one, in whom was diagnosed, from the physical 
signs, obstruction and regurgitation both at mitral and aortic 
orifice. There was no doubt concerning the signs of aortic 
obstruction and regurgitation; in addition, there was "a 
rolling presystolic murmur two inches below and an inch 
outside the nipple, this murmur terminating in a blowing sys- 
tolic bruit conducted to axilla." The sphygmographic signs 
were typically those of aortic reflux. 2. Alice B., aortic 
diastolic murmur with presystolic n^urmur presenting usual 
characters. Sphygmographic signs of free aortic reflux. 
Cardiograph shows no sign of mitral stenosis. 3. H. M., low- 
pitched murmur with first sound at aortic cartilage; second 
sound murmur left of sternum ; rolling typical presystolic 
murmur at apex. Cardiograph shows much hypertrophy of 
left ventricle, but no sign whatever of mitral stenosis. 
4. Walter F., aged twenty, murmur at first heard in 
mitral area, commencing very shortly after second sound, and 
after augmenting in intensity, ceasing abruptly with first 
sound ; in fact, closely resembling murmur of mitral stenosis. 
Coarse thrill also felt at apex. Afterwards, murmur heard to 
be diastolic down left border of sternum, but still typically 
presystolic at apex. Cardiographic and sphygmographic 
evidence indicated free aortic regurgitation, but no sign of 
mitral stenosis. 
I cannot think that in any of these cases, though there was 
a murmur which, in the absence of aortic regurgitation, 1 
should have considered pathognomonic of mitral stenosis. AUSCULTATION. 
217 
there was any other valvular lesion than aortic insufficiency. 
My belief is, as I have before indicated, that the murmur of 
aortic reflux may so closely simulate that of mitral obstruc- 
tion as to be absolutely indistinguishable from it. It follows 
that if you meet with a case in which, from the co-existence of 
the signs of the two conditions, you are inclined to make a 
diagnosis of the two lesions, it is right that you should 
hesitate and consider all the available evidence. Several of 
the cases which have been adduced as telling against the 
auricular causation of the presystolic murmur have been 
where the signs of aortic reflux have been undoubted. Now the 
combination of mitral stenosis and aortic regurgitation, as 
shown by post-mortem records, is a rare one; that of mitral 
regurgitation with aortic regurgitation being much more 
common. In my belief, the presystolic murmur heard in 
aortic regurgitation does not invalidate the auricular hypo- 
thesis, but, as I have said, the physical conditions are so 
analogous that the sonorous results may be identical. The 
quasi-presystolic murmur of aortic regurgitation is the con- 
cluding portion of a diastolic murmur heard at the apex; if 
the tension is great in the aorta, at the end of diastole, the 
murmur is generated with equivalent force to that exer- 
cised by the auricle in the mitral lesion ; moreover, the back- 
ward flow is capable of generating thrill, which, being most 
evident at the later periods of diastole, seems to be presystolic. 
I have never met with a case of co-existent mitral 
and tricuspid stenosis/ but Dr. Hayden, of Dublin, 
has recorded three such examples. The presence of 
tricuspid stenosis is to be suspected whenever a pre- 
systolic murmur is heard close to the left edge of the 
sternum. Dr. Hayden " would regard the existence 
of two centres of presystolic murmur, with or without 
fremitus-viz., at the apex and somewhat to the 
right of that situation, in conjunction with marked 
systemic venous engorgement-as evidence of the 
double lesion of mitral and tricuspid stenosis."* I 
* "The Diseases of the Heart and of the Aorta," by Thomas 
Hayden, &c. &c. (Dublin : Fannin & Co., 1875), p. 238. 218 
AUSCULTATION. 
had one case which seemed to present this com- 
bination, but the murmur simulating that of tricuspid 
stenosis was found to be due to a rough patch of 
pericardium over the right auricle. The probabilities 
of tricuspid stenosis were great, for there was very 
marked presystolic pulsation in the veins of the neck. 
There was tricuspid regurgitation. 
The diagnosis of complex pathological conditions 
of the heart sometimes presents very considerable 
difficulties, and requires great care and repeated ex- 
aminations. I would venture to give you one or two 
rules to observe when you meet with a difficult case. 
In the first place, do not be content to write in 
your notes, u rhythm of the heart irregular and 
tumultuous," but let there be order in your record of 
such irregularity, and system in your treatment of 
the seeming chaos. 
Record all the signs which you have observed 
previously to those derived from auscultation. 
Describe the sounds, normal and abnormal, heard 
over the situations of each of the orifices. 
Note, first, the characters of first sound and second 
sound at the aortic cartilage. Reduce these to dia- 
grammatic form (see p. 197 ct seq.), indicating' 
murmurs where present. 
Repeat the process at the pulmonary, tricuspid 
md mitral areas successively. 
Compare the observations and diagrams only after 
they have been completed, and then fill in the lines 
of conduction of normal and abnormal sounds (see 
p. 83). 
Do not unduly hasten to form your conclusions, but 
obtain all the evidence possible before you give your 
verdict. PART IL 
THE SPHYGMOGRAPH 
AND CARDIOGBAPH. PART II. 
THE USE OF THE SPHYGMOGRAPH AND CARDIO- 
GRAPH IN THE DIAGNOSIS OF DISEASES OF 
THE HEART. 
I. 
Invention of the Sphygmograph-Illustrations of its usefulness 
-Varieties of instruments-Mahomed's Sphygmograph- 
Pond's Sphygmograph-Galabin's Cardiograph. 
The sphygmograph is an instrument for enabling the 
movements of an artery which constitute the pulse to 
be automatically recorded; the term cardiograph is 
used for an appliance which writes the motions of the 
heart itself. The idea of making the pulse register its 
own movements dates from long-past ages: it is 
said to have occurred to Galileo. Anything like perfec- 
tion in the mechanism adopted has, however, only been 
obtained in recent years, when Marey devoted himself 
to the investigation of the phenomena of movement in 
the vital functions. His sphygmograph is the model 
on -which other instruments have been constructed. 
The mechanical difficulties of record being for the most 
part overcome, there remain difficulties of interpreta- 
tion-the pulse writes its own hieroglyphics, but these 
have to be expounded. The interpreter obtains the key 
by patient observation and by experiment. One advan- 
tage of the evidence obtained by such mechanical means 
is that, whilst the impressions we have gained by the 222 
THE SPHYGMOGRAPH. 
methods of physical investigation hitherto considered 
-whether those derived from our sight, touch, or 
hearing-may fade into the haze of half-forgotten 
memories, the story which the pulse writes of itself is 
permanent. " Literascriptamanet."* You may pon- 
der over the record, solve its intricacies at your leisure, 
and compare the evidence obtained at one time with 
that procured at another. But the question is asked, 
Are these practical instruments of diagnosis ? If by 
diagnosis we mean not merely the detection of definite 
diseases, but the estimation of the degree of deviation 
from standard health, undoubtedly they are. Is the 
value of the indications which they give commensurate 
with the trouble which must be taken to employ them ? 
Under present circumstances, certainly. Thanks to 
the ingenuity of physicians who are also mechanicians, 
the difficulties are so far overcome that the instru- 
ments may be used with very little expenditure of time; 
they are of daily employment, and every day gives 
evidence of their value and importance. They should 
be used, however, after the other means of diagnosis, 
not before. As Dr. Mahomed has said, they open up 
no "royal road to diagnosis," but they may check, 
confirm, or extend the diagnosis already attained, and 
often throw a new light upon a difficult position. I 
may illustrate the value of the sphygmograph by two 
examples. I was called hurriedly to a patient whom I 
found in the extremities of cardiac dyspnoea. She was 
unable to lie down; there was extensive oedema, and 
a loud systolic murmur was heard at the apex of the 
heart, conducted towards the axilla and audible at the 
♦"Segnius irritant animos demissa per aures 
Quam gate sunt ocnlis subjecta tidelibus."-Horace, Satire. THE SPHYGMOGRA PH. 
223 
'back. I had no doubt that the condition was that of 
mitral regurgitation. There was, however, in addition, 
■extreme anaemia, with haemic murmurs at the base of 
■the heart and over the vessels of the neck, and it was 
probable that this had been brought about by excessive 
h.emorrhage caused by uterine fibroid. The question 
which now presented itself was-Is this cardiac dys- 
pnoea with mitral regurgitation due to organic disease 
of the valve, or is it the result of weakness of the muscle 
of the ventricle ? Against the first view was the fact 
that there had been no rheumatism, acute nor subacute. 
On looking at the pulse-tracing, which I had at once 
•obtained, I was struck with the fact that it so nearly 
approached the normal; I concluded, therefore, that 
the imperfection of the mitral orifice was not the result 
of valvular disease. This diagnosis proved correct, for 
after treatment the whole of the cardiac signs and 
symptoms passed away, and no trace of the murmur at 
the apex remained. Another instance. I was called 
in consultation with a medical friend to the case of a 
■gentleman, past middle-age, who in appearance was 
hale and well-nourished, and who, it was well known, 
had led a careful, abstemious life. The signs were 
those of a limited pneumonia of the base of the right 
lung. The general conditions did not suggest a bad 
prognosis, the only reason in favour of which was the 
asserted debility of the patient on attempted movement, 
even while in bed; an expression which seemed not to 
be corroborated by the appearances. To the finger 
the pulse showed a fair regularity. The sphygmogra- 
phic trace, however, gave a different lesson ; though 
there was fair regularity in time, there were such 
variations in volume and in general characters that I 
feared the heart-fibres were degenerated. The prognosis 224 
mahomed's sphygmograph. 
founded on this observation was gloomy, and the pro- 
babilities which were then sketched out were exactly 
confirmed by the facts. The signs of pneumonia passed 
away, and it appeared that there might be a good 
recovery; then ensued a sudden syncope and a situation 
of grave peril. From this there was a rally and a 
renewed hope of recovery ; syncope, however, in spite 
of the most watchful care and abundant nourishment, 
recurred, and the patient died. These two instances 
are, I think, sufficient to show the value of the sphygmo- 
graph as an instrument of diagnosis : in the one case 
I consider that it determined the difficult question 
whether there was organic disease of the mitral valve or 
passive yielding of the ventricular walls; in the other 
it demonstrated an unsuspected condition of degene- 
ration of the muscular fibres of the heart. I propose 
now to examine more systematically its application and 
its uses in the diagnosis of cardiac diseases. 
Varieties of Instruments.-I have said that 
these are chiefly founded upon the model of Marey. The 
modification of Marey's sphygmograph usually em- 
ployed in this country is that designed by Dr. Mahomed. 
Mahomed's sphygmograph (Fig. 10) consists essen- 
tially of a framework containing an arrangement of 
levers adaptable to the pulsating vessel. Contact 
with the artery, the radial being usually chosen 
for convenience, s made by a steel mainspring, 
the movements of which, consentaneous with those 
of the artery' on which it is made to rest, are 
communicated to a lever of the third order, so that 
the slight motion may be much amplified (about 
ninety times). The writing lever consists of a fine 
slip of very light wood, and is so guarded as to 
allow vertical without lateral movement. The motions mahomed's sphygmograph. 
225 
of the pulse are thus converted into up-and-down 
strokes of the free extremity of the lever; these are 
made to impinge upon a slide, which, by means of 
clockwork, is caused to travel at a known rate-about 
Marey's Sphygmograph, improved by Mahomed. 
Fig. 10. 
four inches in ten seconds. Thus the movements of 
the free extremity of the lever, representing' the 
amplified movements of the pulse, are described upon 
the travelling slide in a series of figures. For a 226 
pond's sphygmograph. 
minute description of the instrument I must refer you 
to Dr. Mahomed's paper {Medical Times and Gazette, 
January 20, 1872, p. 63). 
An essential point is to he able to apply the main- 
spring- to the artery with definite degrees of pressure. 
This object Dr. Mahomed has attained with great 
success. By a very ingenious arrangement the pres- 
sure can be increased by turning a thumb-screw, and 
this pressure is registered in ounces (1 to 18 troy) 
upon a dial-plate. 
Pond's Sphygmograph (Fig. 11), which is also adapted 
for use as a cardiograph, has the great merit that it 
is very readily applied, and its application consumes 
so little time that it may be used in daily practice. 
I believe that every practitioner, however busy, would 
be able to employ it, and would find its indications of 
the greatest possible service. In this instrument the 
slide of paper or of mica on which the tracing is 
taken, instead of being vertical as in the other instru- 
ments, is horizontal, so that the operator looks down 
upon it. The throbbings of the pulse are communi- 
cated to an india-rubber diaphragm, or, by a late 
improvement of the instrument, to a vertical lever 
terminating below in a small metal button, and kept 
in constant contact with the artery by a spiral spring. 
A very ingenious, yet simple, arrangement of levers 
causes amplification of the movements which are 
recorded on the slide, which, as in the other instru- 
ments, travels by clockwork (about six inches in 
fifteen seconds). The upright stem of the instru- 
ment is provided with a pressure-gauge graduated 
from one to sixteen ounces, so that various degrees 
of compression can be exerted upon the artery 
The sphygmographs of Marey and Mahomed have pond's sphygmograph. 
227 
been used for taking tracings directly over the heart's 
impulse, but, in many cases with these instruments, 
the task is impossible-first, because with a strongly- 
acting heart the range of motion, amplified as it is 
by the sphygmograph, is too great to be recorded on 
Fig. 11. 
Pond's Sphygmograph. and Cardiograph. 
the travelling slide ; and secondly, because the mecha- 
nical arrangement adapted to the limited area of a 
pulsating artery is ill fitted for fixing over the chest- 
wall at the site of the heart's impulse. Marey first 
overcame the difficulties, and laid the foundation for 228 
galabin's cardiograph. 
the study of the movements of the heart by the 
graphic method, by constructing a cardiograph in 
which the cardiac motion of the chest-wall was 
transmitted to a drum or tympanum, communi- 
cating by a flexible india-rubber tube with a second 
tympanum, the two tympana, and the tube which 
connected them, forming- an air-tight cavity. Thus 
the motion imparted was transmitted by the oscilla- 
tions of the column of contained air; it was ampli- 
fied by a lever attached to the second tympanum, and 
recorded on a revolving cylinder termed a polygraph. 
Many observations of the highest importance were 
made by means of this instrument, but it is now super- 
seded by a modification of the sphygmograph adapted 
to the chest-wall. 
Galabin's Cardiograph is that generally 
adopted in this country. Its general construction is 
that of a magnified sphygmograph, with adjustments 
for its adaptation to the thorax. Instead of the rigid 
parallel bars of the sphygmograph, the base is consti- 
tuted by moveable wooden blocks, which can be 
separated to a width of nearly five inches; by means 
of these the instrument is made to rest upon the 
chest. Between them, by two transverse steel rods, 
the brass frame of the cardiograph is supported, and 
is attached, by joints which allow of both vertical 
and horizontal adjustment, to four vertical rods. It is 
possible, therefore, for the instrument to be applied 
to a chest of any size or shape. The brass frame 
differs from that of the sphygmograph in that the 
bar attached to the main-spring has an arrangement 
for its elongation and variation of position, so that 
the vertical height of the curve described by the 
recording style can be varied from 10 to about 100 galabin's cardiograph. 
22 
times the actual movement of the chest-wall. 
The mechanism for an exact determination of the 
pressure exerted by the main-spring- is unnecessary 
in the cardiograph, but there is an adjustment for 
reducing this pressure to nearly zero, so that very 
slight impulses-even the back-stroke in veins-may 
be recorded. (For Dr. Galabin's description vide 
" Med. Chir. Trans.," vol. Iviii. p. 353.) 230 
SPHYGMOGRAPHIC TRACINGS. 
II. 
Method of obtaining a sphygmographic tracing with Ma- 
homed's sphygmograph - Importance of recording the 
pressure employed-Tracings with Pond's sphygmograph- 
Cardiographic tracings with Galabin's cardiograph-With 
Pond's instrument-Varnishing tracings for preservation- 
To multiply copies of tracings. 
How to obtain a tracing-(1) with Mahomed's Sphygmo- 
graph.-The arm of a patient from whose radial artery 
a tracing- is to be taken must be placed upon a splint 
or rest, the palm being upwards. The stand of the 
instrument is then applied over the arm in the 
longitudinal direction, so that the ivory pad of the 
mainspring is just over the artery as the latter lieson. 
the inner side of the styloid process of the radius, and 
is crossing the anterior ligament of the wrist-joint. 
In this position the instrument is firmly maintained 
by strong bands passing over each extremity of the 
framework. The hand is to be bent slightly back- 
wards, and may be made to gently grasp a band 
stretched across the end of the splint or pad. If the 
wrist be strongly extended backwards, the parts are 
too tightly stretched and the artery rendered tense 
if the hand be firmly closed, the tendons of the 
muscles are tightened and made to interfere with the 
perfect application of the instrument, or, perhaps, ta 
produce vibrations in the tracing. The instrument 
being applied with these precautions, the artery will, 
now lie between the ivory rods, and the pressure of 
the spring upon it must now be varied (by the operator 231 
turning' the graduated thumb-screw) until the maxi- 
mum range of movement of the recording lever is 
attained. The slip" upon which the tracing is to be 
taken is now placed on the travelling- slide. This 
slip is generally of white paper, which should be well 
glazed on both sides, so that friction is reduced to a 
minimum. The style of the recording lever may be 
supplied with ink, so that it writes upon the white 
paper as the clockwork arrangement causes it to 
travel along ; this method, however, is often tire- 
some, the pen refusing to mark or the ink being jerked 
into unsuitable places. The best plan appears to be 
to allow the point of the style to make its mark 
upon the paper-slip, which has been previously smoked. 
In order to smoke the slip it is only necessary to hold 
for a brief period the paper over a small piece of 
burning camphor, a kindled pledget of cotton soaked in 
olive oil, or a smoking paraffin lamp : by either of these 
methods a uniform layer of black is obtained over the 
surface of the paper, and, of course, the end of the 
writing-lever makes, by displacing the smoke, a series 
of white markings as it moves over the surface. The 
blackened slip being introduced, and the clock move- 
ment wound up, a touch of the button is made to 
liberate the spring, and the slide commences to travel. 
It may be stopped at any time, and then the pressure 
varied. The most perfect tracing- is that in which, 
the spring following most perfectly the expansion of 
the artery, the summit is most sharply defined {i.e. 
free from rounding) and the various notches best 
marked. Dr. Mahomed says : " The use of incorrect 
pressure is perhaps the most common source of error 
in sphygmography, and the greatest care is necessary 
in deciding upon the amount of pressure to be 
SPHYGMOGRAPHIC TRACINGS. 232 
SPHYGMOGRAPHIC TRACINGS. 
employed. This, when ascertained, should be care- 
fully recorded, as it is one of the most important 
characters of the pulse. Notice should also be taken of 
the amount of pressure required to totally extinguish 
the pulse, so that the lever remains perfectly motion- 
less ; for by this means an estimate can be formed of 
the force with which the heart is contracting."* A 
number of tracings can of course be taken at one 
sitting : they may be at once examined with care lest 
manipulation rub off the coating of smoke. The 
name of the patient, &c., the pressure employed, with 
a brief note of physical signs, should then be inscribed, 
a needle or finely pointed steel pen being used for 
this purpose, and each slip be varnished for preser- 
vation. 
(2.) Tracings with Pond's Sphyymograpk are thus ob- 
tained. It is not necessary to use a pad or splint, but 
a metallic wrist-rest is supplied with the instrument; 
this is ingeniously constructed, so that it adapts itself 
to an arm of any size with no discomfort to the patient. 
Tracings may, however, be taken even without the 
wrist-rest. An upright bar is inserted into this sup- 
port, to which is clamped a transverse arm, which clips 
the body of the sphygmograph; this arm is provided 
with a screw adaptation to all necessary positions. 
The patient being in the sitting or recumbent posture, 
and quite at ease, the hand rests with palm upper- 
most ; then-the slip of smoked paper or mica having 
been introduced by momentarily setting free the watch 
movement, allowing the slip to travel for about a 
quarter of an inch, and then stopping again-the 
operator, holding the sphygmograph by the cylinder, 
* Medical Times and Gazette, Jan. 20, 1872, p. 64. SPHYGMOGRAPH1C TRACINGS, 
233 
applies the india-rubber base over the pulsating artery. 
Due contact between the upright bar immediately in 
relation with the india-rubber diaphragm, and the 
system of writing levers must now be made by suffi- 
ciently turning the small screw at the summit of the 
cylinder. The writing-needle will now be observed 
to move over the blackened slide. By slightly vary- 
ing the position of the india-rubber base over the 
artery, and by increasing or decreasing- the firmness 
of application of the instrument (this pressure be- 
ing determined by noting the pressure-gauge), the 
point of maximum movement of the needle will be 
observed. If the attachment to the wrist-rest be em- 
ployed, the instrument should be fixed in the position 
at which this maximum of movement is attained; 
but with a little practice the operator will be able to 
retain the sphygmograph with uniform pressure upon 
the artery, and to dispense with the clamp which fixes 
to the wrist-rest. Then the watch movement is libe- 
rated by a touch of the finger, and the slide travels. 
Several tracings should be taken at varying pressures. 
It is very easy to obtain tracings with this instrument 
from the carotids, the temporal arteries, the femorals, 
<tc., as well as the radials. 
I consider it best, when using Pond's instrument, to take the 
first slip with gradually increasing pressures every three or 
four pulses. Commence with the lowest possible pressure 
that will develop the tracing, then stop the travelling of the 
slide, and start it again, using slightly increased pressure ; 
observe whether increasing pressures increase the altitude and 
development. Note the pressure which gives the maximum, 
and the effect of higher pressures on the elements of the trace. 
Often one slip suffices, but it may be necessary to take two or 
three. Thus you are informed at what pressure you have the 
best tracing, and can proceed to take others at this, which 
gives you the most typical results. 234 
•CAaDioGnArnic tracings. 
(3.) Cardiographic tracings may be thus obtained 
with Galabin's Cardiograph. The patient being stripped 
to the waist, the position of the apex-beat should be 
determined and marked upon the chest-wall by means 
of a pencil. The pad of the lever is then to be ap- 
plied over the point of pulsation, and the instrument 
adapted by separating to greater or less degree the 
wooden blocks constituting the base, as well as by 
altering the position of the instrument in relation to 
the vertical rods until it rests suitably upon the chest. 
It may be fixed by two partially elastic straps passed 
round the body and fastened by buckles. In many 
instances it suffices to hold the instrument against 
the chest with the hand, the straps, &c., being dis- 
pensed with. The movements of the recording style 
being observed to be in suitable position upon the 
smoked paper, the clockwork is started and the tracing 
taken. Tn some cases the movements of respira- 
tion do not greatly disturb the position of the style, 
and the series of tracings is well comprised within the 
slide. Often, however, the movement of breathing 
causes too great excursion of the style, and the patient 
must be asked to hold the breath-the clockwork 
being started at the moment of arrest at the end of 
expiration. The position of the patient should be as 
much as possible one of ease : if the apex-beat be 
fairly defined, it should be that of as complete recum- 
bency as is consistent with comfort; if the apex-beat 
be ill-defined, a better tracing may be taken if the 
patient be in a sitting position, leaning- somewhat 
forwards. 
(4.) Cardiac tracings with Pond's instrument are 
often obtained with great ease. The preliminary 
arrangements having been made as when it is used CARDIOGRAPHIC TRACINGS. 
235 
as a sphygmograph, the instrument is simply held 
against the chest-wall at the point of pulsation, and 
the clockwork started. To obtain a satisfactory 
tracing it is usually necessary for the patient to bo 
recumbent; but it is possible to obtain one in the' 
sitting and even standing posture. The sphygmo- 
graph is held by the cylinder or by the barrel of the 
watch movement; the difficulty is, that the needle shall 
not by the force of gravity fly off the smoked surface £ 
sometimes this difficulty may be obviated by removing* 
the little weight which serves as a counterpoise to the 
needle, sometimes also by bending the needle itself. 
It is very important that there should be facility for 
taking tracings not only in the sitting* position, but 
even when the patient leans well forward. 
To preserve sphygmographic and cardiographio- 
tracings they must be varnished. Before this is done, 
upon each tracing should be inscribed the name and 
age of the patient, and a brief note of the physical signs- 
or the diagnosis arrived at by the hitherto employed 
means. This is easily done by writing on the smoked 
surface with the point of a pin or a needle fixed into a* 
convenient handle. The tracing should then be care- 
fully dipped in a rapidly drying varnish. The varnislr 
may be composed of gum benzoin and methylated 
spirit (one ounce of the former to six ounces of the 
latter). The following* is Pond's receipt:- Alcohol, 
one pint; gum sandrac, three ounces; castor-oil, half- 
ounce ; mix. 
To multiply copies of tracings the original should be 
taken on a slip of mica and well varnished. When 
quite dry it should be placed in a pressure-frame, such 
as used by photographers, with a slip of photo-sensitive- 
paper behind it, so that the latter becomes printed oft' 236 
as a positive impression from a negative photograph. 
A child's transparent slate provided with a clear glass 
forms a very efficient pressure-frame. The solution 
with which the paper is rendered sensitive is thus 
prepared:-(1.) Ammonio-citrate of iron, 1| ounce; 
water, 8 ounces. Make a solution. (2.) Red prussiate 
of potash, ounce; water, 8 ounces. Dissolve. Mix 
the two solutions and keep in the dark or in a yellow 
bottle. This solution being poured into a saucer, strips 
of white unglazed paper are to be wetted with it on 
one side only, and then allowed to dry in the dark 
until wanted. The sensitive side of the paper being 
pressed against the negative mica-slip, so that the 
tracing reads correctly, it is exposed to sunlight or 
daylight for a term varying from twenty minutes to 
two hours according to the intensity of the light. 
When removed from the pressure-frame, the paper 
must be washed in clear water for a minute or two, and 
the tracing will appear in blue lines upon a white 
ground. If properly managed, the copy is permanent. 
It is obvious that copies of many slides may be taken 
in one frame at the same time, and by consecutive 
operations almost any number may be procured from 
one mica. 
COPIES OF TRACINGS. THE PULSE-TRACE. 
237 
III. 
Interpretation of the normal pulse-trace-The first event, or 
percussion wave-The second event, or tidal wave-The 
third event, or dicrotic wave-The diastolic portion-Inter- 
pretation of the normal heart-trace-The systolic portion- 
The diastolic portion -Indications afforded by the sphygmo- 
graph-Frequency of pulse-Irregularity in time-Intermit- 
tency-Irregularity in volume, rhythmical and arhythmical- 
Relation of pulse to respiration-Respiratory line-Undu- 
lation of base-line in cerebral diseases. 
Interpretation of the normal pulse-trace.-The tracing 
of a single pulsation in a state of health' consists of 
(1) a line which is vertical or nearly so (Fig. 12, abf 
Fig. 12. 
The normal pulse-trace magnified ; a b, percussion up- 
stroke ; a b c, percussion wave; c d e, tidal wave; 
def, dicrotic wave; at e, aortic notch; f a, diastolic 
period. 
The contraction of the left ventricle forcing' the con- 
tained volume of blood into the aorta, suddenly dis- 238 
THE PULSE-TRACE. 
tends the systemic arteries; the lever, therefore, in 
•contact with the artery, receives a sudden impulse 
which jerks it upwards; the vertical line is the result 
of the movement of the vessel thus produced, amplified 
by the mechanism of levers and somewhat by acquired 
velocity. This, then, is the first event, an almost in- 
stantaneous up-stroke, often termed the percussion - 
•stroke. Having attained its maximum height, (2) the 
line now begins to descend at an acute angle to the 
up-stroke, the sudden force of elevation having been 
expended, but again rises at c d, so that it forms a 
-curve. This is due to the fact that the lever, which 
falls by its own weight after the expenditure of its 
'abruptly-communicated velocity, is again caught and 
lifted by the tide of the onward current of blood. 
This is the second event, and the wave thus produced 
is termed the tidal wave. The line inscribed by the 
lever now descends, and again rises, forming a second 
curve (ef). This is the third event,the dicrotic wave. The 
curve produced is an important one. It is due to a re- 
bound of the blood from the point d'appui constituted by 
the cardiac end of the aorta with its closed semilunar 
valves. Marking as it does the closing of the aortic 
valves, the notch thus produced is termed the aortic 
notch. So far, therefore, the trace has indicated only 
the systolic portion of the cycle; the brief remainder 
comprises the diastolic portion. This consists of the 
wave springing from the aortic notch and a gradually 
sloping line, ending at the base-line of the tracing. 
Its vertical height is about one-third of the percussion 
up-stroke. In delicate tracings a very slight elevation 
is sometimes seen just as the down-stroke ends and 
the up-stroke of the succeeding pulse commences ; 
this marks the systole of the auricle. THE HEART-TRACE. 
239 
Interpretation of the normal heart-trace (Figs. 13 and 
14).-As with the sphygmogram, the most promi- 
nent feature of the cardiogram is a sudden elevation 
denoting the contraction of the ventricle. Following 
Fig. 13. 
The normal cardiac trace (after Galabin). A, Typical 
apex tracing, a, auricular systole; a d, ascent due to 
sudden hardening of ventricles; def, continued sys- 
tole ; k, rebound after emptying of ventricles ; I, ascent 
from gradually increasing influx of blood into ventricles 
during diastole. Tracing from a healthy man ; tension 
low, and heart acting vigorously, g, notch indicating 
closure of semilunar valves. 
Fig. 14. 
Normal cardiac trace (after Pond). The references are 
the same as in Fig. 13. 
the chief elevation, on the broad summit of the 
trace, however, are one or two waves which have 
been said to denote oscillations of the auriculo- 240 
SPHYGMOGRAPHIC INDICATIONS. 
ventricular valves during systole. It seems to me 
more probable that they are due to the muscular 
movements of the ventricle. At the end of the 
elevated portion of the trace is a more rounded 
swelling, which marks the termination of the ven- 
tricular systole. The line then descends with a slight 
slope to the base-line. Now commences the diastolic 
portion of the tracing. In this is seen first an 
eminence, which indicates a shock lifting the apex 
after the relaxation of the ventricles; next, a slightly 
ascending line, broken by some slight undulations, 
marking the time during which the blood-pressure 
in the ventricle is increasing; and lastly, a small 
eminence immediately before the succeeding up-stroke, 
due. to the contraction of the auricle. 
It will be seen that the evidence obtained by the 
cardiograph is complementary of that afforded by the 
sphygmograph. By the latter we obtain a more 
complete record of the systole of the ventricle, and 
its effect on the peripheral arteries, whilst by the 
former we gauge more completely the conditions of 
blood-pressure in the ventricle during diastole. 
Indications afforded by the Sphygmograph. 
-The sphygmograph records the frequency of the 
pulse. Care should be taken as regards each instru- 
ment to estimate the time which the slide takes to 
travel. This maybe done by a stop-watch, and the mean 
of several observations should be taken. Occasion- 
ally the process should be repeated with individual 
instruments to ascertain whether in course of time the 
clockwork alters speed. The instrument is usually so 
constructed that six inches travel in fifteen seconds. 
To count the pulse, therefore, measure off six inches 
of the tracing, and multiply by four the number of SPHYGMOGRAPHIC INDICATIONS. 
241 
pulcations observed. This of course gives the rate of 
the pulse per minute. 
The sphygmograph also records irregularities in time. 
It registers intermittency in the pulse (see Figs. 15 and 
16). It is obvious that in these cases the heart rests 
Fig. 15. 
Irregularities in time. Tracings from right radials in 
cases in which irregularity disappeared after treatment. 
(In the upper tracing tension is moderate ; in lower ten- 
sion is low.) 
Fig. 16. 
Intermittency in pulses of high tension. 
during the period of a single pulsation, and that this 
intermittency is repeated at intervals. Such irregu- 
larities are not uncommon in old persons, or in the 
young- when convalescent from acute diseases. They 
•Jo •/ 
are usually of no serious prognostic import. Sometimes 242 
SPHYGMOGKAPHIC INDICATIONS. 
the condition is habitual, and uninfluenced by treat- 
ment ; in others it is remedied with ease. A change of 
dietary sometimes alone suffices; abstinence from tea, 
coffee, or other exciting- beverages, may soon restore 
the heart's regularity. In the case of one of my 
patients the irregularity entirely ceased after omitting 
potatoes as an article of food ; no doubt the error of 
•excess in this particular had been committed previously. 
The indication, however, may be very important; in 
one of my patients the advent of intermittency occurred 
in the early stages of the development of cancer of the 
liver, when the signs and symptoms were very obscure. 
A glance at the sphygmographic tracing shows also 
if there be irregularities in volume. These may be 
rhythmical or arhythmical. The most striking example 
of rhythmical irregularity of volume (Fig. 17) was in a 
case in which there was no cardiac disease, but hemi- 
Fig. 17. 
Rhythmical irregularity in volume in a case of cerebral 
disease attended with Cheyne-Stokes dyspnoea. Traces of 
right radial artery (5 oz. pressure). A, taken during 
period of excitement of respiration ; R, during arrest of 
respiration. 
plegia, aphasia and the phenomena of Cheyne-Stokes 
respiration (see p. 35). The autopsy showed that there 
was much cerebral disorganization, the remote effect of SPHYGMOGRAPHIC INDICATIONS. 
243 
embolism of some of the cerebral arteries. In my 
epinion, there was in this case a direct disturbance 
both of the respiratory and the cardiac centres. The 
pulse-tracing shows that each systole of greater is 
succeeded by another of lesser amplitude (Fig. 17).* 
Another example of double systole (the pulsus 
trigeminus') is seen in a tracing by Dr. Pond (Fig*. 18). 
Fig. 18. 
Pulsus bigeminus. 
Irregularities in volume in which there is no ob- 
servance of rhythm as indicated by the sphygmograph 
are of high importance both in diagnosis and prognosis. 
Here we observe the elevations in succeeding pulsa- 
tions to vary very considerably, and in an irregular 
manner; so in the trace the height of the percussion 
stroke in one instance may be four times greater than 
in others. Arhythmical irregularity in volume may be 
demonstrated by the sphygmograph when it is not 
detected by the finger. The tracing (Fig. 19) was 
taken from a case in which the finger failed to detect 
any notable irregularity. This wms no doubt due to 
the fact that the pulsations were fairly regular in 
point of time. The sphygmographic evidence alone 
led to the diagnosis of cardiac degeneration. 
* This has been termed by Traube the ''pulsus alternans." 244 
SPHYGMOGRAPHIC INDICATIONS. 
Irregularities in both time and volume are shown 
in the acute fevers when the muscle of the heart has 
Fig. 19. 
Arhythmical irregularity in volume. Tracing from 
right radial artery in a case of pneumonia, with probable 
cardiac degeneration. 
Fig. 20. 
Irregularity in time and volume (myocarditis in course 
of typhoid fever). 
been involved in disease (Fig-. 20), as well as in the 
later stages of valvular diseases. 
Inspection of the sphygmographic trace in series 
also indicates the relation of pulse to respiration. The 
base-line of a series-that is to say, aline drawn so as 
to join the lowest points of the percussion up-strokes- 
should be straight. A line so drawn is termed the 
respiratory line. If the arterial-tension vary, this 
line will be not straight but a series of curves. In 
health, if a deep inspiration be made during the time 
that the sphygmogram is taken the line curves down- 
wards, because, oXving to the suction-action of the 
thorax, general arterial tension is reduced ; on the RESPIRATORY LINE. 
245 
other hand, if a deep expiration be made, an elevation 
takes place in the respiratory line. In cases of dis- 
ease in which the rhythm of respiration is disturbed, 
this curving or undulation of the base-line is observed, 
and as each curve represents a respiration, the ratio 
of pulse to breathing is easily ascertained by counting 
Fig. 21. 
Marked undulation of base-line (from a case of 
tubercular meningitis). 
the number of traces in each curve.* In other cases 
there may be seen irregularities in the curves not 
corresponding to the obvious rhythm of respiration : 
thus one pulse-trace in every two, three, or live, may 
descend to the base-line; this is especially seen in 
cases where there are cerebral complications. (See 
Fig. 21.) 
* Such a trace is seen in Fig. 25. 246 
ABNORMAL PULSE-TRACE. 
IV. 
Interpretation of the abnormal pulse-trace-Causes of aug- 
mented and of lessened percussion wave-Oblique percussion 
-Causes of increase and of decrease of tidal wave-Of 
dicrotic wave-Estimation of arterial tension-Pulses of 
high and of low tension-Supernumerary vibrations. 
Interpretation of the Abnormal Pulse 
Trace. The elements which we have considered of the 
pulse-trace are all capable of modification under con- 
ditions of disease. The percussion-wave is increased 
by sudden and forcible contraction of the lift ventricle, and 
by a large amount of blood distributed by the systole. 
Fig. 22. 
Trace showing oblique ascent and descent (tidal wave 
only), taken from left radial artery in a case of aneurism 
of the left subclavian (Dr. B. Foster). 
It is lessened by feeble or gradual contraction of the 
ventricle, and by a small amount of blood distributed 
by the systole. When the up-stroke deviates from the 
vertical line, there is toiling on the part of the ventricle, 
or disease in the coats of the vessel through which the 
arterial current flows. In some cases in which the 
sphygmograph can be applied directly over the sac of PULSE-TRACE IN ANEURISM. 
247 
an aneurism the tracing shows only gradually sloping 
lines of ascent and descent; it is thus reduced to its 
simplest form, resembling that recorded by the mere 
pulsatile injection of fluid into an elastic tube. There 
is here only one wave-the tidal; it is exemplified in 
the tracing- (Fig. 22) taken from the left radial in a 
case of aneurism of the left subclavian artery by Dr. 
Balthazar Foster.* The aneurismal sac here acts the 
part of a mere elastic bag. In other instances the 
modifications are less notable, but a sloping line of 
ascent is characteristic (see Fig. 23). 
Fig. 23. 
Pulse-tracings in cases of aneurism showing obliquity 
of percussion-stroke (from left radial arteries in two cases 
of aneurism of the arch of the aorta). 
Whilst we look upon the percussion as the heart wave 
-an indication of the shock communicated by the 
grasp of the ventricle upon the contained blood-we 
may regard the tidal as essentially the blood wave, 
and a measure of the volume projected through the 
arteries. The tidal wave is increased by slow contraction 
of the ventricle, by a large volume of blood delivered through- 
* " Clinical Medicine'' (London, J. and A. Churchill, 1874), 
p. 297. 248 
ABNORMAL PULSE-TRACE. 
out the arteries by the ventricular systole, and by obstruction 
in the capillary circulation. On the other hand, it is 
diminished by sudden contraction of the ventricle, 
by a small quantity of blood delivered, and by increased 
outflow or free circulation in the capillaries. The 
tracing- in cases in which the tidal wave is exaggerated 
shows a broad, almost flat, summit; occasionally the 
tidal wave rises higher than the percussion up-stroke 
(see Figs. 24 (last tracing) and 47).* 
The dicrotic wave is the wave of recoil. The onward 
tide of blood having more or less distended the elastic 
arterial channels, the sudden closing of the aortic 
semilunar valves imposes a barrier against any flow 
towards the heart; the column, therefore, rolls back 
towards the periphery and distends a second time the 
arterial channels with this dicrotic wave. The dicrotic 
wave is increased by sudden contraction of the ventricle 
when the arteries are imperfectly filled, by increased outflow 
or free capillary circulation, and by a relaxed condition of 
the muscular coat of the arteries. It is decreased by a 
gradual systole of the ventricle, by a state of distension 
of the arteries, by contraction of the arterial wall 
upon its contents, and by obstruction in the capillary 
circulation. 
To estimate arterial tension.-By high tension in the 
arterial system is meant a condition in which the pres- 
sure of blood within the arteries is unduly great. The 
* The tidal wave should not extend beyond a straight line 
drawn from the summit of the percussion up-stroke to the 
bottom of the aortic notch. If any portion of the tidal wave 
encroach over such line, it is unduly developed. For many 
of these observations I am indebted to Dr. Mahomed's 
account of the Sphyginograph in Gant's " System of Surgery, " 
2nd ed., vol. i. ARTERIAL TENSION. 
249 
absolute amount of blood the arteries contain need not 
be greater, but may be much less, than normal, but 
the artery is tightly contracted on its contents. So 
the pulse may be either full, strong and incompressible, 
or small and wiry. One important sphygmographic 
evidence of increase of tension is the undue prominence 
of the tidal wave which we have considered, but it is 
a mistake to consider that this sign alone suffices. We 
Fig. 24. 
shall presently see that the tidal wave may be pro- 
nounced when the tension is low. The concurring' 
signs necessary for the demonstration of high tension 
are-(1) in taking the sphygmogram low degrees 
of pressure upon the artery fail to develop the trace, 
whilst firmer compression succeeds; (2) the dicrotic 
wave has a position higher than normal in the tracing' 
and is often but slightly pronounced (Figs. 1G and 24). 
Low tension, on the other hand, means imperfect 
repletion of the arteries, whose muscular coat is weak 
Pulses of high tension. 250 
DICROTIC PULSE. 
or relaxed. It is indicated by undue prominence of 
the dicrotic wave. We have seen that the dicrotic 
notch is decidedly marked in the normal pulse. In 
a sense, therefore, the pulse is dicrotic in health. 
The term " dicrotic," however, is usually applied to 
Fig. 25. 
Pulses of low tension, showing full dicrotism and 
hyper-dicrotism, (1) from a case of pneumonia which 
proved fatal, (2) from a case of typhoid fever which even- 
tually recovered. 
a pulse in which the aortic notch descends abnor- 
mally low. When this notch reaches to the level of 
the base-line, the pulse is said to be fully dicrotic, and 
ii it sink below this line it is called hyper-dicrotic 
(see Fig. 25). Such signs generally indicate serious 
conditions of debility. 
In some tracings the line of descent is broken by 
many vibrations. These may be due to oscillations 
Fig. 26. 
Extra or supernumerary vibrations (tracing of left 
radial in a boy the subject of haemophilia). ABNORMAL PULSE-TRACE. 
251 
extrinsic to the artery, but in many cases they arise 
in the arterial wall itself. When it is very pro- 
nounced in young persons, I consider that it may be 
taken to indicate an abnormal condition of the arterial 
coats (see Fig. 26). In advanced age the condition is 
much more common, and, taken with other signs, indi- 
cates arterial degeneration (see some of the tracings 
in Fig. 24). 252 
CARDIOGRAPHIC INDICATIONS. 
V. 
Indications afforded by the Cardiograph-Relation of cardiac 
revolutions to rhythm of respiration-Abortive systoles- 
Inversion of the trace-Interpretation of the systolic jiortion 
of the abnormal cardiac trace-The up-stroke ; its relation to 
the closure of the auriculo-ventricular valves-The summit 
and the prominence which terminates it-The down-stroke, 
and its relation to the closure of the semilunar valves. 
Indications afforded by the Cardiograph.- 
Inspection of the heart-tracing in series may show the 
relation of heart's action to respiration. When the 
breath is held the base-line is straight, but when 
respiration continues the curves are much more pro- 
nounced than is the case with the sphygmogram. 
Thus, on inspecting a heart-trace, you may find that 
each curve corresponds to from three to seven systoles, 
and these may vary much in definition and amplitude. 
Such variations and effacement of systoles are some- 
times due to the direct intervention of the lung, in 
inspiration, between the heart apex and the cardio- 
graph lever. Sometimes, this cause being excluded, 
the systoles are observed to be irregular or abortive. 
Thus, in Fig. 27 there is a systole of small ^volume 
interposed between two of larger, then follows one that 
is very small, and succeeding the seventh systole is an 
irregular rise not corresponding to a complete cycle. 
A difficulty which may beset the interpretation 
is inversion of the tracing. The spot at which the 
heart's apex impinges in such manner as to produce 
bulging outwards of the chest-wall, and consequently INVERSION OF CARDIAC TRACE. 
253 
an ascent of the cardiograph lever, may be very 
limited. At the moment of systole the muscles of 
the ventricles draw themselves inwards towards 
this centre of impulse. It follows that unless the 
lever be exactly over this spot it may be drawn inwards 
Fig. 27. 
Irregular and abortive systoles. Cardiogram from a 
case of mitral stenosis and regurgitation, with tricuspid 
regurgitation. 
with the motion of the ventricular wall, instead of 
being- forced outwards at the point of maximum 
elongation of the ventricle ; in such case the tracing- 
becomes inverted.* A tracing of this kind may be 
read as a positive if it be turned upside down and 
examined from right to left. Or, more simply, a 
small mirror, such as that of an ophthalmoscope, may 
be placed behind it, and the reflected image read as a 
normal tracing. Sometimes it happens that a tracing- 
is partially inverted, and then the difficulties are greater, 
and interpretation may be hopeless. In such case, 
tracings should be attempted at several situations over 
the impulse. From inversion of the tracing we are 
not justified in making any diagnosis of adherence of 
the pericardium as has been supposed. 
* Inversion often happens when the maximum of impulse is 
against a rib instead of being in an intercostal space, or where 
the heart is covered by emphysematous lung. 254 
ABNORMAL CARDIAC TRACE. 
Interpretation of the abnormal cardiac trace.-As 
with the sphygmograph trace, so with the cardiac, 
each element must be carefully examined. First, the 
vp-strohe. This is increased in vertical height by sud- 
denness of ventricular systole, but by no means ne- 
cessarily by hypertrophy of the ventricle. In my own 
cases the greatest height of up-stroke was attained in 
a, case of ulcerative endocarditis, in which the valves 
of the left chambers became rapidly diseased, and 
there were many embolisms. A reference to Fig. 28 
will show how sudden and vertical the up-stroke may 
Fig. 28. 
Cardiogram in a case of nervous palpitation; no organic 
disease. 
become in conditions of palpitation. One of the 
loftiest up-strokes in the cardiograms figured by Dr. 
Galabin was in a case of exophthalmic goitre-a con- 
dition which we know to be associated with the sudden 
systole of a feeble ventricle; with much palpitation, in 
fact. In this case there was also mitral regurgitation 
("Guy's Hospital lieports," 1875 ; Plate III. fig. 8). 
On the other hand, in cases of considerable hyper- 
trophy of the left ventricle, and in aortic regurgitation, 
where the ^wZse-trace shows very considerable ampli- 
tude, the cardiac up-stroke may have a vertical height 
much less than normal. ABNORMAL CARDIAC TRACE. 
255 
The closure of the auriculo-ventricular valves occurs 
during the up-stroke. The first sound is heard shortly 
after the lever commences to ascend, and its greatest 
intensity appears to be at about the completion of 
two-thirds of the elevation. This point marks the 
complete closure of the auriculo-ventricular valves, 
and in some tracings it is rendered visible by a slight 
Fig. 29. 
Cardiac tracings, showing the prominence b, due to 
closure of the auriculo-ventricular valves. A and B, taken 
by Galabin's cardiograph, from a case of aortic obstruc- 
tion and regurgitation with some mitral regurgitation. 
C, D, taken by Pond's instrument, C, from a case of 
mitral stenosis ; D, from a case of mitral stenosis with 
regurgitation and signs of hypertrophy of the left ven- 
tricle. 
interruption of the up-stroke. This is point 6 in the 
tracing's (see Fig. 29). It does not occur when the 
systole is sudden. In the cardiograms figured by 
Dr. Galabin (" Guy's Hospital Reports," loc. cit.) it is 
seen in the hypertrophy accompanying- chronic 
Bright's disease, in aortic disease (with regurgita- 256 
ABNORMAL CARDIAC TRACE. 
tion), and in mitral stenosis. Of fourteen cases in 
which I have found it well marked, ten presented 
the signs of mitral stenosis, the others being 
instances of aortic disease. 
In the next place, observe the summit of the trace. 
The extent of this summit is a measure of the duration 
of the systole. When the contraction of the ventricle 
is very sudden, there is an immediate tall. A refer- 
ence to Fig. 28 will show that this occurs at intervals in 
conditions of palpitation, the tracings of intervening 
pulsations having broader summits. When, however, 
the vertical up-stroke, followed by an immediate, or 
almost immediate, down-stroke, is the general cha- 
racter of all the individual tracings, feebleness or 
dilatation of the ventricle is indicated. I have said that 
the undulations which are visible in the horizontal 
portion of the summit of the cardiac trace are pro- 
bably due to the muscular movements of the ventricle. 
In cases of mitral regurgitation, sometimes the broad 
summit is formed by a vibratory line, which may be dis- 
tinctly traced to the sonorous vibrations of a murmur 
(examples are seen in Fig. 42 ; see also Dr. B. 
Foster's " Clinical Medicine," Fig. 18, p. 809). 
We have now to consider the termination of the 
horizontal portion of the summit in eminence f. 
In palpitation, and in cases of the sudden systole of 
a dilated ventricle, this eminence may be entirely 
lost. On the other hand, in hypertrophy of the left 
ventricle it is jurewiwcraf or rounded.* In some cases 
the prominence and amplitude of eminence f may be 
found to vary considerably in successive systoles. 
* I have noticed that the eminence has become markedly 
more rounded after the influence of digitalis. CLOSURE OF SEMILUNAR VALVES. 
257 
This I have found to occur chiefly in disease of the 
mitral valves, most frequently in stenosis, and in the 
double lesion of stenosis and regurgitation; but I 
have also observed it in combined aortic and mitral 
disease. I consider prominence of f to indicate 
forcible distension of the aorta at the end of ventri- 
cular systole. 
We have next to consider the downstroke, and 
observe whether there is any indication of the 
closure of the aortic semilunar valves. Practically, 
we may consider that the heart's second sound is 
synchronous with the downstroke ; but in some cases 
the shock communicated by the reflux of blood 
against the valves is rendered perceptible by a notch 
or wave (#) in the tracing. This is usually near the 
end of the downstroke, and is here observed espe- 
cially in cases in which arterial tension is low. It 
will be observed in the normal tracing (Fig. 13) taken 
when tension was low, but it is often very slightly 
marked. Dr. Galabin's cardiograms show it in mitral 
and in aortic disease. I have seen it in aortic disease, 
in which there is but slight regurgitation (especially 
where obstruction and regurgitation arc combined), 
and in mitral stenosis. You will observe it low in 
the downstroke in Fig. 27, 7th, 8th, 9th, and last 
systoles. 258 
RELATIONS OF SYSTOLE AND DIASTOLE. 
VI. 
Indications afforded by the Cardiograph continued-Relative 
duration of systole and diastole-Causes of variations- 
Interpretation of the diastolic portion of the abnormal 
cardiac trace-Difficulty of interpreting the eminence oc- 
curring immediately after the down-stroke-Its relation 
to suddenness of systole and suddenness of initial diastole 
-Line indicating rise of blood-pressure in the ventricle- 
Indication of auricular systole and its significance. 
I have said that breadth of the summit of the 
trace is a measure of the duration of the systole and an 
indication of hypertrophy of the ventricle. This indi- 
cation is of more importance when it is considered 
relatively to the period of diastole. It is usually held 
that § of the cardiac cycle are taken up by the ventri- 
cular systole, and £ by the diastole. According to the 
estimate of Landois, supposing the whole cycle to last 
1T30 second*, the systole occupies -451 second, and 
•the diastole '079 second.* A measurement of the 
tracing- of the healthy heart obtained by Galabin's 
cardiograph (Fig-. 13) shows that whilst the systolic 
portion of the cycle occupies || inch linear, the 
diastolic portion measures from to In the 
normal tracing obtained by Pond's instrument (Fig. 
14) the systole is measured by about and the 
diastole by about of an inch. It is important, 
as evidence of a morbid condition, to note any 
*Cf. Foster's "Tex* Book of Physiology," p. 102. 
London: Macmillan. 1877. RELATIONS OF SYSTOLE AND DIASTOLE. 
259 
variations from the normal relations of systole and 
diastole observed in the cardiographic trace. The 
diastolic portion of the tracing may be relatively dimi- 
nished in hypertrophy, but it is much more manifestly 
so in cases in which, in addition to hypertrophy, there is 
a condition inexistence in which the ventricle becomes 
too rapidly filled-such occurs in aortic regurgitation 
and in mitral regurgitation, and, a fortiori, in both 
combined. The diastolic portion is relatively increased in 
the following conditions:-(a) When the heart's action 
becomes slow ; "a frequent differs from an infrequent 
pulse chiefly by the length of the diastole."* This is 
exemplified by a tracing figured by Dr. Galabin,f 
which was taken from the exposed heart of a dog 
when circulation was beginning to fail-the diastolic 
interval is greatly prolonged (&) in dilatation of the 
ventricle (Galabin, loc. cit., Plate II. Pigs. 14 and 15). 
This may be inferred because the opposite conditions 
suggest, as we have seen, hypertrophy. The obser- 
vation is of the highest importance as indicating- in 
valvular lesions a want of compensation (loc. cit., 
Plate III., Fig 5) (c) in mitral stenosis. This is often 
very markedly shown by the cardiograph. The dias- 
tolic interval, besides having characters which I shall 
presently describe, is greatly prolonged. Thus the 
condition may be indicated when it has not been 
rendered evident by physical signs, and the proba- 
bility of combined stenosis may be shown when there 
are physical signs of only mitral regurgitation; so 
also may be determined the question of its co-existence 
with aortic disease (cf. p. 216). 
* Foster's "Text Book of Physiology," p. 109. 
+ " Guy's Hospital Rep." 1875, Plate I. Fig. 7. 260 
Again, when the diastolic interval is observed to 
vary greatly in duration, as in Fig. 27, there is con- 
siderable evidence of an impeded supply to the 
ventricle on account of mitral stenosis. 
Having considered the diastolic period as a w'hole, 
we will now look more closely into individual charac- 
teristics. First point It, the interpretation of which is 
undoubtedly difficult. The elevation k is a very 
marked feature in the trace, both in health and in 
disease. It is clearly established that it is not simul- 
taneous with the closure of the semilunar valves, but 
occurs subsequently to the second sound. In the trace 
it is observed after the downstroke. If we come to 
consider the various morbid conditions in which 
eminence It is either increased or diminished, we find 
many difficulties in the way of definite conclusions. 
A reference to Fig. 13 might give the impression that 
in health it is augmented in a condition of low tension, 
1 nt some of Dr. Galabin's cardiograms show that it 
may be also greatly augmented when arterial tension 
is high, as in hypertrophy of the left ventricle occur- 
ring with chronic Bright's disease. I have found it 
pronounced in conditions both of high and of lowr 
tension, and in disease of both mitral and aortic 
valves, but relatively of greater frequency in mitral 
lesions. On the other hand, I have found eminence 
k ill-pronounced or absent when the left ventricle 
has begun to fail, in the seemingly opposite con- 
dition of ventricular strength when there has oeen 
aortic disease, and again in the hypertrophy associated 
with Bright's disease. I think I may say that an 
ill-pronounced eminence k is considerably less com- 
mon in mitral regurgitation than is the opposite 
condition of exaggeration, excepting in cases wherein 
THE DIASTOLIC PERIOD. THE DIASTOLIC PERIOD. 
261 
there are signs of failure of cardiac power or the 
heart's action is notably slow. 
Dr. Galabin considers that eminence k, though not 
•synchronous with the closure of the aortic valves, is 
due to a reflux of blood against the valves-an 
explanation to me difficult to accept, when we con- 
sider that it is by no means constantly related with 
increased blood-pressure in the aorta, and often is 
associated with an opposite condition. 
Dr. Foster considers the eminence due to the first 
influx of blood into the ventricular cavity; and this 
would seem feasible, as it immediately follows the 
lowest point of the downstroke-i.e., the maximum 
relaxation of the ventricle. Dr. Galabin objects that 
if so the elevation would not be followed by so marked 
a fall, an objection which does not seem to me fatal, 
because the entry of blood, being sudden, might pro- 
duce the effect of a vibration. The frecpient want of 
relation, however, between the magnitude of k, and 
the conditions which would increase the volume and 
momentum of blood entering the ventricle, are serious 
objections to Dr. Foster's theory. The condition 
which I consider to be the most constantly related 
with the development of eminence k, is suddenness in 
the action of the ventricle. Thus a reference to the 
•cardiogram taken during* palpitation (Fig*. 28) will 
show that those systoles in which there is a high 
systolic rise and rapid fall, are immediately succeeded 
by a lofty eminence k, whilst the intervening cycles 
-show a more flat diastolic period. Again, in the 
normal tracing (Fig. 14) the more vertical downstroke 
is followed by the more pronounced eminence k. On 
the other hand, the sloping downstrokes indicating* a 
more gradual unfolding of the ventricle in Fig. 27 262 
THE DIASTOLIC PERIOD. 
are followed by only a slight or imperceptible 
eminence k. Suddenness of action of the ventricle, 
and especially of diastolic relaxation, appears, there- 
fore, to me to be the most probable cause of a 
high development of eminence It. Thus I think 
can be explained its magnitude in conditions of 
both low and high tension-in low tension when 
there is rapid systole and sudden relaxation of the 
ventricle followed by slight recoil; in high tension 
and ventricular hypertrophy when the diastole may 
be expedited by the sudden and forcible entry of blood 
through the coronary arteries into the heart-muscle. 
On the other hand, when from any cause there is 
slow or gradual relaxation of the ventricle, eminence 
It is ill-pronounced. 
Of less difficulty is the explanation of the condition 
when eminence k is lost or merged in the elevation 
intervening between the downstroke and the up- 
stroke of the following systole. This is well exempli- 
fied in Fig. 31. It indicates rapid impletion of either 
of the ventricles or both ; it is seen in mitral regurgi- 
tation, especially when co-existing with tricuspid or 
with aortic regurgitation. 
We turn next to line I, which is an indication of 
the filling of the cavity of the ventricle. Here, also, 
there is no room for doubt; the degree of ascent of 
the line is a measure of the degree of blood-pressure 
in the ventricle. If you compare Fig. 30, taken in a 
case of mitral regurgitation, with the healthy trace, 
Fig. 14, you will find that but little difference is 
obvious in the general characters; but the diastolic line, 
instead of being nearly horizontal, ascends progressively 
to the junction with the systolic. This, with a little 
broadening of the systolic portion, is the only point of THE DIASTOLIC PERIOD. 
263 
dissimilarity. These points suggest that the regurgi- 
tation causes a greater blood-pressure in the ventricle 
during the diastolic interval than in health, and there 
is compensatory hypertrophy. From this, in which the 
indication is but slight, turn to Fig. 31, in which you 
observe after eminence It a rapid and very marked 
Fig. 30. 
Cardiogram from a case presenting a soft systolic mur- 
mur at the apex, and a history of rheumatic fever three 
years ago, showing the line indicating the blood-pressure 
in the ventricle during diastole to ascend slightly. Com- 
pare with line I, in normal diastolic period, Fig. 14. 
Fig. 31. 
Cardiogram from a case of aortic regurgitation and ob- 
struction combined with mitral regurgitation, showing 
marked ascent of the hue indicating intra-ventricular 
pressure during diastole. 
ascent-here the ventricle is filled, not gradually as 
in health, but by a rapid influx both from the aorta 
and from the left auricle, owing to the insufficiency of 
both aortic and mitral valves. The progressive and 264 
PRESYSTOLIC VIBRATIONS. 
rapid rise of line I is chiefly seen in mitral regurgita- 
tion or aortic regurgitation, and especially when these 
lesions are combined ; but it may be seen also in 
mitral stenosis, and then is an indication of con- 
siderable hypertrophy (compensatory) of the left 
auricle. More commonly, in mitral stenosis, the line of 
ascent I varies considerably in different cycles. This 
is well seen in Fig. 32, in which there is regurgita- 
Fig. 32. 
Cardiogram in a case presenting variable systolic and 
presystolic murmurs, showing variations both in systoles 
and diastoles. 
Fig. 33. 
Cardiogram in a case of mitral stenosis, showing 
vibrations in diastolic period corresponding to presystolic 
murmur and thrill. 
tion as well as obstruction ; some of the diastolic 
intervals present only a sudden rise and fall, whilst 
others show a serrated line, which we shall consider 
as denoting- the sonorous vibrations of a presystolic 
murmur, or the vibrations, sensible to the touch, of a 
thrill. The latter is also seen in a very marked AURICULAR SYSTOLE. 
265 
manner in Fig-. 33. A great variation in the con- 
ditions of blood-pressure in the ventricle is also seen 
in Fig. 27, where tricuspid regurgitation existed as 
well as mitral regurgitation and stenosis. 
We have next to consider the eminence a, which in 
the normal trace we have no difficulty in ascribing 
to the auricular systole. When this eminence is 
exaggerated, we have evidence of auricular hyper- 
trophy. This is well illustrated in the two cardio- 
grams of Fig. 34. It might be considered d priori 
probable that, inasmuch as in mitral stenosis the left 
auricle is usually considerably hypertrophied, the 
Fig. 34. 
Cardiac tracings indicating hypertrophy of the left 
auricle. A, taken by Dr. Mahomed from point of apex- 
beat by ordinary sphygmograph in a case of great hyper- 
trophy of the left auricle with tricuspid regurgitation, but 
no valvular disease (yide Med. Times and Gaz., April 13, 
1872, Plate III. Fig. 16). b, taken by Dr. Galabin, by 
means of his cardiograph, in a case of mitral regurgitation, 
in which the left auricle was dilated and hypertrophied 
("Guy's Hospital Reports," 1875, Plate III. Fig. 6). 
evidence of a strong auricular systole would be a 
feature of the cardiographic tracings in this condition, 
and so would be a valuable aid to diagnosis. That 
in some cases of mitral stenosis exaggeration of emi- 
nence a, is a feature of the trace, is undoubted. This is 266 
AURICULAR SYSTOLE. 
seen in Fig. 37 a, a, b (see also Dr. Galabin's tracings, 
" Guy's Hospital Reports," loc. cit., Plate* III. Figs. 9 
and 15). A reference to the other tracings taken in 
cases of mitral stenosis will at once show, however, 
that a strong development of eminence a is by no 
means a constant feature; the reasons for-this we 
shall presently discuss. We may premise that when 
in a cardiogram, from a case of mitral stenosis, emi- 
nence a is exaggerated and in its normal position, the 
auricle is hypertrophied, and there is no extreme 
narrowing of the orifice, but the momentum of blood 
entering the ventricle is augmented by the abnormal 
force of the auricular contraction. PULSE-TRACE IN MITRAL STENOSIS. 
267 
VII. 
Evidence obtained by the graphic method in valvular 
diseases-Mitral Stenosis-Sphygmographic signs-Dif- 
ferent views as to irregularity of pulse-Interpolated pul- 
sations-Cardiographic evidence-Explanation of interpo- 
lated pulsations-Three forms of heart-trace in mitral 
stenosis-Tracings showing exaggeration of auricular systole 
-Tracings indicating that the auricle adopts an unusual 
rhythm-Tracings indicating a causation of the presystolic 
murmur independently of the auricle. 
We proceed now to consider the chief signs 
afforded by the sphygmograph and cardiograph in 
valvular diseases. 
I. Mitral Stenosis.-The sphygmographic evi- 
dence in cases of mitral stenosis is usually very 
characteristic. Various opinions have been expressed 
as to the general characters of the pulse in this con- 
dition. For the most part observers have attributed 
some irregularity to the pulse, but recently Dr. 
Hayden has combated this view, contending that in 
the earlier stages of the disease " the pulse of mitral 
obstruction is usually quite regular, and not above 
ninety in the minute, but small and that marked 
irregularity occurs only in the advanced stages of the 
disease when the left ventricle begins to fail, and 
congestion of the lungs, engorgement of the right 
chambers of the heart, general venous obstruction, 
and anasarca have taken place.* This experience by 
no means agrees with my own, for I have generally 
* " Diseases of Heart and Aorta," p. 895. 268 
PULSE-TRACE IN MITRAL STENOSIS.' 
found that a notable irregularity is the distinguish- 
ing mark of the sphygmographic tracing in mitral 
stenosis, and that this is rendered evident in very 
early stages of the disease, even when there may be 
no sign of cardiac discomfort whatever. The first 
two tracings of Fig. 35 were taken from a case in 
which a typical presystolic murmur had become 
developed whilst there were no signs pointing to 
Fig. 35. 
Thepulse-trace in three cases of mitral stenosis. The two 
first sphygmograms taken by Mahomed's instrument at 
different times in a single case ; the two lower taken by 
Pond's instrument. All show interpolated pulsations. 
cardiac mischief. It will be noted that in the top- 
most tracing the second pulsation is followed by a 
third before the base-line is reached, and in like 
manner the fourth is followed by the fifth. These 
interpolated pulsations are also seen with still more 
marked pronunciation in the second tracing-, and here 
it will be noted that after the fourth pulsation there 
is a prolonged diastole corresponding to an inter- PULSE-TRACE IN MITRAL STENOSIS. 
269 
mission or missed pulsation. After treatment by 
digitalis, the pulse was rendered slower, and the evi- 
dence of irregularity was only seen in the varying 
intervals between the systoles. Such peculiarity in 
the sphygmograms in mitral stenosis has been 
thoroughly recognized and described by Dr. 
Mahomed.* He mentions that the irregularity may 
be made more evident after the influence of digitalis. 
I have just asserted the converse, but I have no 
doubt that both propositions are true-the rhythm of 
the heart is altered by digitalis sometimes in the 
sense of developing-, sometimes in that of controlling 
the irregularity. Muscular exercise, or any form of 
respiratory trouble, will develop or increase the 
tendency, and in any doubtful case sphygmograms 
should be taken in the two conditions of tranquillity 
and excitement after exercise. 
We may conclude, therefore, that a pulse-tracing 
which shows irregularity in the diastolic periods 
sometimes missed pulsations, and, as described by 
Dr. B. Foster, the occasional appearance of a small 
abortive pulsation in the line of descentf is very 
strong evidence of the existence of mitral stenosis. 
We may now inquire as to the probable meaning 
of this form of tracing. It has been considered by 
Dr. Foster that the rise in the line of descent is due 
to a premature auricular contraction which propa- 
gates itself to the ventricle; but this proposition is 
untenable, because each abortive pulsation is seen to 
consist of all the elements of a ventricular systole. It 
always occurs after the dicrotic wave of the tracing 
* Cf. Medical Times and Gazette, May, 18, 1872, pp. 570 and 
427, Plate IV. 
+ "Clinical Medicine," p. 321. 270 
which precedes it. It is clear, therefore, that it is 
an abnormal repetition of a whole cardiac cycle. 
The conditions of its occurrence are, according to 
Dr. Mahomed, these :-a The left auricle, unable to 
thoroughly evacuate its contents, owing to the 
•obstruction at the mitral orifice, remains more or less 
full, and is generally distended at the termination of 
the ventricular systole, during which time it has 
been receiving more blood. It is thus stimulated to 
contract, and this it does slowly and with effort. But 
this is not always the case. The ventricle will not 
adapt itself to the altered rhythm of the auricle, but 
contracts immediately after the latter ; and when this 
occurs earlier than usual, following immediately the 
termination of the previous contraction of the ven- 
tricle, it gives rise to another peculiarity in rhythm 
-namely, the secondary contraction of the ventricle." 
By this altered correlation between rhythm of auricle 
and ventricle may be explained-(1) the occasion- 
ally skipped pulsation, the long wait in diastole, and 
the irregularity in time of the diastolic period; 
(2) the supernumerary systoles. We may have 
slightly to modify this explanation by ascribing to 
tension in the passive aftricle, as well as contraction 
•of its muscle, the initiation of irregular ventricular 
systole. 
Cardiographic Evidence in Mitral Stenosis.-Inspec- 
tion of the cardiac tracing in series shows the same 
irregularity that is rendered evident in the tracing of 
the pulse. If you turn to Fig. 27, which is a cardiogram 
taken in the later stages of mitral stenosis, where the 
right heart has consecutively suffered, and there is 
tricuspid regurgitation, you will observe that the 
characteristic is notable irregularity in time and 
PULSE-TRACE IN MITRAL STENOSIS. HEART-TRACE IN MITRAL STENOSIS. 
271 
volume. The diastolic periods greatly vary, and the 
systoles show differing degrees of magnitude. Turn 
now to the tracings in Fig. 36, where compensation is 
much more marked. In a and c there are varying 
characters of the diastolic portions, but d gives the 
explanation of the interpolated rise which is seen in 
the descending line of the sphygmogram. You will 
Fig. 36. 
Tracings by Pond's cardiograph in cases of mitral 
stenosis, a, loud, rolling, or bubbling presystolic murmur 
at apex, b, Typical presystolic murmur, c, Variable 
presystolic and systolic murmurs. D, Presystolic and 
systolic murmurs at apex. 
notice that in the second pulsation in d, the descend- 
ing- line of the cardiac trace fails to reach the base- 
line, but- is succeeded by a second pidsation, after 
which the line reachesits usual level; the same pecu- 
liarity is seen in the 5th and 6th pulsations. In 
some tracings two pidsations may be observed to 272 
HEART-TRACE IN MITRAL STENOSIS. 
occur with no horizontal diastolic period separating 
them; in others only a slight eminence divides them.* 
It is evident, therefore, that the rise in the down- 
stroke of the sphygmogram is due to a complete 
systole of the left ventricle, the condition of the 
normal rhythm being so altered, that two systoles 
may succeed each other with a very slight or an 
inappreciable interval. 
We will now examine the characters of the heart- 
tracings in mitral stenosis as individual revolutions. 
We may divide these into g-roups. 
(1.) Tracings in which the auricular systole is well 
marked. I have already said that the only legitimate 
deduction from an abnormal development of the emi- 
nence a is hypertrophy of the auricle, which may or may 
not co-exist with mitral stenosis (see Fig. 34). Fig. 
37b shows it considerably increased in a case mani- 
festing- well-marked presystolic murmur and thrill. 
In Fig. 36 a, the auricular rise seems not only to be 
very pronounced, but to contribute to the general 
elevation normally caused by the systole of the ven- 
tricle.! In Fig. 37a it is seen that the elevation, 
■which in all probability corresponds with the auricular 
contraction, has a double summit, and that this may 
be an indication of the vibration felt by the hand as 
a presystolic thrill. Similar tracings have been 
figured by Dr. Galabin. (Note especially Plate III. 
Fig. 10, in " Guy's Hospital Reports," 1875.) In one 
case, the period occupied by the heightened, broad- 
* Vide Figs. 33, 37c, where some of the systoles are divided 
only by a single eminence. 
t This is also seen, as produced by the high tension in the 
auricle, in Fig. 27. CARDIOGRAMS IN MITRAL STENOSIS. 
273 
ened, and reduplicated auricular portion of the tracing 
could be felt by the linger to be synchronous with 
" a slight beat, accompanied by a thrill, just preceding 
the main impulse." There can be no room for doubt, 
therefore, that an enlarged auricular eminence may be 
a feature of the tracing of mitral stenosis ; and further- 
Fig. 37. 
Tracings by Galabin's cardiograph in cases of mitral 
stenosis. A, A. well-marked harsh presystolic murmur 
at apex, with thrill. B, well-marked presystolic murmur 
and thrill. C, well-marked presystolic bruit, occupying 
greater portion of diastolic pause, at first of low pitch and 
" rolling " in character, becoming rasping and vibratory, 
and increasing in intensity up to a sudden stop with the 
first sound, d, presystolic murmur of low pitch (a sys- 
tolic murmur also at aortic cartilage). 
more, that it is an indication of the auricular-systolic 
causation of the murmur and thrill. A very slight 
consideration of the conditions would, however, sug- 
gest the probability that in many cases this auricular 
rise would not be manifest. The contraction of the 
auricle could not so influence the ventricle as to cause 274 
CARDIOGRAMS IN MITRAL STENOSIS. 
it to describe an elevation if the entry of blood were 
impeded owing to a very marked degree of stenosis. 
Supposing there were no stenosis, and yet marked 
hypertrophy of the auricle, we might presuppose a 
greater rise in the auricular period than would occur 
in the condition of obstruction. Both these proposi- 
tions are established by facts. We may conclude that 
if in any tracing we see a decided increase of ampli- 
tude of the auricular elevation, there is, from some 
cause, auricular hypertrophy; if there should be the 
physical signs of mitral stenosis, it is most probable 
that this hypertrophy is induced by the valvular 
lesion; if the auricular elevation is not only increased 
but broadened, and presenting undulations of its sum- 
mit, the probabilities of mitral stenosis, even where 
the other physical signs are doubtful, are very con- 
siderable. We turn now to another section of cases 
of mitral stenosis, in which there are- 
(2.) Tracings indicating that the auricle adopts an 
unusual rhythm. That the auricular systole may be 
-modified, is proved by the tracings we have just con- 
sidered ; the bifid or interrupted summit of the eleva- 
tion, which occupies the position of that known to be 
due to the auricle, leaves no room for doubt. I have 
observed this character in many tracings. Dr. Gala- 
bin has shown, however, that the rhythm of the 
auricle may be perturbed and altered in far greater 
degree. In the tracing (Fig. 38) it will be noticed 
that the two diastolic periods which are figured are 
abnormally lengthened. In the first of these periods 
are two elevations, a, a; these were found to corre- 
spond to two faint pulsations, which were not only 
audible but visible as slight waves in the fourth inter- 
costal space. They were not abortive systoles, for no 275 
sign of them was presented in the pulse-trace-there 
could be no doubt that they were produced by the 
contractions of the auricle. In the second diastolic 
period it is seen that the elevation indicating the 
auricular systole occurs, not in its normal position 
just before the systole of the ventricle, but nearly in 
the midst of the diastolic portion of the trace. It is 
evident, as Dr. Galabin has said, that " we have here 
a heart, the auricle of which sometimes contracted 
twice in the interval between two ventricular pulsa- 
tions, and sometimes singly in the midst of a long 
CARDIOGRAMS IN MITRAL STENOSIS. 
Fig. 38. 
Heart-tracing, showing unusual rhythm adopted hy the 
auricle. After Galabin ("Guy's Hospital Reports," 1875, 
p. 314, Plate II. Fig. 15). 
pause instead of just before the systole of the ven- 
tricle." In the case from which this cardiogram was 
taken, there was no proof from the other physical 
signs that mitral stenosis was present. Dr. Galabin 
has adduced it as showing that " it is d priori not im- 
probable that, in mitral stenosis, the auricle, perturbed 
in its action by the obstruction in front, may adopt an 
unusual rhythm." Further experience, in my own 
opinion, abundantly confirms this view. If you refer 
to Fig. 37 c, you will observe that the line indicating 
the rise of blood-pressure in the ventricle is broken 
into several eminences and depressions, so that it 276 
CARDIOGRAMS IN MITRAL STENOSIS. 
would be difficult to say which of these represented 
the auricular systole. In d a still stronger illustra- 
tion is afforded, the diastolic period being- represented 
by an undulatory line containing- four or five emi- 
nences or swellings. In Fig-. 40 you notice that the 
prolonged diastolic period is represented by a sinuous 
line more uniform and rounded. In some of the 
cardiograms of mitral stenosis figured by Dr. Galabin, 
the rise of blood-pressure in the ventricle is marked 
by a sudden elevation, followed by a vibratory line 
reaching- quite up to the next ventricular systole 
(loo. cit., Plate III. Figs. 11 and 13). The sudden 
rise can only be explained by the systole of the 
auricle, whilst the vibratory line indicates the expul- 
sion of the blood from the auricular into the ventricu- 
lar cavity. I have met with many tracings in mitral 
stenosis which can only be explained on the hypo- 
thesis that the auricular systole is exaggerated and 
occurs abnormally early. In some such tracings the 
line following the rise is broken only by fine vibra- 
tions ; in others there are two, three, or four more 
pronounced elevations, such as are seen in Fig. 37 d. 
In some tracings, however, in cases of mitral steno- 
sis, it is impossible to tell where the contraction of the 
auricle is recorded, because the whole diastolic period 
is marked by a serrated or vibratory line. Good 
examples of this are seen in Figs. 33 and 40. It is 
also to be observed in Fig. 36, 1) and d, and in c in 
some of the diastolic intervals. It is demonstrated by 
many cases that these vibrations may be the graphic 
records of thrill or murmur, or both thrill and mur- 
mur. They are highly characteristic of the lesion; 
and furthermore, in my opinion, they point the lesson 
that the presystolic murmur is not always auricular- CARDIOGRAMS IN MITRAL STENOSIS. 
277 
systolic. Such view was advanced by Dr. Wilks 
(" Guy's Hospital Reports," 1871), who, observing-that 
some presystolic murmurs extended throughout the 
whole period from the second sound to the succeeding 
first sound-that is, through the pause as well as 
through the auricular systole-considered that the 
first portion of such murmur was due to the blood- 
flow, unaided by the systole of the auricle, through 
the narrowed orifice. Experimental proof that such 
is possible has been afforded by Marey: if in an arti- 
ficial schema of the circulation a perforated plug be 
Eig. 39. 
Cardiogram (by Pond's instrument) in a case of mitral 
stenosis, showing coarse vibrations corresponding to a 
presystolic murmur of low pitch and presystolic thrill. 
interposed between auricle and ventricle so as to imi- 
tate the contracted mitral orifice, a diastolic murmur is 
produced when the pressure within the auricle exceeds 
a, certain point. In such case, therefore, the murmur 
■starts immediately from the second sound. And this 
seems to be only in exact accordance with probabilities 
-in the dilatable cavity formed by the auricle and 
pulmonary veins the blood, after being- impelled by the 
right ventricle, when exit is impeded by considerable 
contraction of the (mitral) orifice, must be subject to 
pressure. The walls of the cavity into which it is 
forcibly injected are elastic as well as contractile, and 278 
CARDIOGRAMS IN MITRAL STENOSIS. 
it is only reasonable to infer* that the pent-up tension 
in the cavity may be a cause of the early flow into the 
ventricle before such flow is aided by the proper systole 
of the auricle. Dr. Galabin, from cardiographic evi- 
dence, has formed the opinion that the presystolic 
murmur may in some cases be produced independently 
of the auricle, and I am entirely in accord with him. 
The positive proof of the proposition is, I consider, 
afforded by the next section-viz., 
(3) Tracings in which the auricular systole 2)rcscrves its 
normal position. The tracing (Fig. 40) was from a little 
F.ig. 4 J. 
Cardiogram from a case of mitral stenosis with presy- 
stolic thrill and murmur, showing the auricular systole 
in the normal position. 
girl, in whom there was a pre systolic th rill with localised 
presystolic murmur at the apex. The child suffered 
from right hemichorea. In the cardiogram the auri- 
cular systole is marked in all the individual cycles, and 
is in its normal position just before the ventricular 
upstroke ; it is obvious that the cause of the thrill 
and murmur must have been in this case independent 
of the auricular systole. 
The cardiographic evidence, then, in mitral stenosis- 
may be (a) an increase in magnitude of the elevation CARDIOGRAMS IN MITRAL STENOSIS. 
279 
denoting- the auricular systole; (Z») an increase in its 
breadth with a summit broken by undulations, a 
condition often felt by the finger as a thrill; (c) a 
perturbation of its rhythm so that it may contract at 
abnormal periods in the diastolic pause and may repeat 
its contractions; (d) a series of vibrations in the line 
denoting the rise of blood-pressure within the ventricle, 
often expressed also by presystolic murmur and thrill, 
and due sometimes to the prolonged auricular systole, 
sometimes to the accumulated pressure in the left 
auricle unaided by the contraction of the latter, and 
sometimes to both cases-viz., tension within the 
auricle at the commencement of the period of filling 
of the ventricle, aided subsequently by the muscular 
effort of the auricle. 280 
SPIIYGMOGRAMS IN MITRAL REGURGITATION. 
VIII. 
Graphic evidence in valvular diseases continued-Mitral 
Regurgitation-Sphygmograms often not characteristic- 
Two especial forms-(1) Pulse small, any elevation obtained 
with difficulty-Irregularity not observed until right 
chambers begin to fail-(2) Pulse ample, but of low tension 
-Cardiograms in mitral regurgitation-Ventricular hyper- 
trophy distinguished from dilatation by breadth of summit- 
Vibrations caused by murmur-Occasional bifurcation of 
summit-Shortened diastole-Indication of auricular sys- 
tole - Tricuspid Regurgitation - Arterial pulse-trace 
showing curves of respiration-Venous pulse-trace-Traces 
from pulsating liver-Characteristics of venous pulse-trace 
-The anadicrotic and katadicrotic waves-Cardiograms 
indicating irregularity-Right auricular systole not propa- 
gated so as to produce elevation in aj>ex-trace, bnt back- 
wards, producing anadicrotic wave in veins. 
IL Mitral Regurgitation.-The pulse-trace in cases 
of mitral regurgitation is often by no means character- 
istic. Where compensation is fairly maintained it 
may present no features differing from the normal. 
The notable forms of the pulse altered by the condition 
of mitral regurgitation can, according to my observa- 
tions, be divided into two classes. In one of these 
divisions the elevation is slight, the upstroke sloping. 
It is often difficult, on account of the small calibre of 
the artery, to obtain satisfactorily a graphic record; 
the systolic expansion is only represented by a slight 
rise, and the details of the gradually sloping down- 
stroke are undecipherable. In such instances there 
is, owing to the regurgitation, only a very small SPHYGMOGRAMS IN MITRAL REGURGITATION. 
281 
amount of blood thrown into the aorta; but the 
arteries are contracted upon their content. The 
sloping upstroke is an indication that the point d'appui 
afforded by the mitral valve in its normal state is 
impaired; the current which should produce the ele- 
vation flows not only towards the arteries, but back- 
wards into the auricle. It is generally supposed that 
a great characteristic of the mitral pulse is irregularity. 
So far as the mere valvular lesion is concerned, I do 
not agree with this view. The peculiar perturbation 
of rhythm which I have described in mitral stenosis, 
I do not think occurs in uncomplicated regurgitation. 
On the other hand, I am perfectly aware that very 
marked irregularities of time and volume are often- 
times features of the pulse-traces in mitral regurgita- 
tion. These characteristics closely resemble those of 
the tracing, Fig. 19, which I considered to represent 
no valvular lesion. What, then, is their significance ? 
I believe that they are complications of the trace 
induced by the secondary engorgement of the right 
chambers, by degeneration of the heart-muscle, or by 
both these causes combined. It is needless to say 
that, if this view be correct, it affords an important 
guide to prognosis and treatment. If in a case pre- 
senting the physical signs of mitral regurgitation you 
obtain a tracing- showing a sloping- upstroke with 
irregularity of time and volume, enjoin rest, and 
endeavour carefully to strengthen the ventricle by 
administering iron and digitalis; if, on the other 
hand, the tracing nearly approaches the normal, you 
may conclude that compensation is good, and anxieties 
at the present may be allayed. The action of 
digitalis, in conditions of irregularity arising from 
mitral regurgitation, is distinctly registered upon the 282 
SPHYGMOGRAMS IN MITRAL REGURGITATION. 
pulse-trace. It is remarkable how the disturbances 
of ill-compensation may be controlled, and an almost 
undecipherable tracing reduced from chaos to order. 
The second of the forms of tracing in mitral re- 
gurgitation to which I would call attention differs 
greatly from the former. In this case the tracing is 
easily obtained, the artery not being small and con- 
tracted, and the great feature is the pronounced dicrotic 
wave. This is well marked in the pulse tracing of 
Fig. 41. Here the pulse is fully dicrotic, the artery 
being relaxed and the capillary circulation engorged. 
In mitral regurgitation the appearance of a strong 
Fig. 41. 
Cardiogram and sphygmogram, from a case of free 
mitral regurgitation. 
dicrotic wave, associated sometimes with a full tidal 
wave, is a sign of considerable obstruction in the 
capillaries: such traces we meet with in cardiac 
dropsy. 
We turn now to the cardiac trace in conditions of 
mitral regurgitation. Inspection of the systolic 
portion of the trace indicates whether hypertrophy 
predominates over dilatation. If the condition be 
that of dilatation of the left ventricle, the upstroke 
is sudden and lofty, and the descent is also rapid. 
If, on the other hand, hypertrophy [predominates. CARDIOGRAMS IN MITRAL REGURGITATION. 
283 
the breadth of the systolic eminence is increased. 
The truncated summit is sometimes broken by serra- 
tions or undulations, indications of which are seen 
in Figs. 30 and 36 d. I have no doubt that these 
may be the result of the sonorous vibrations of the 
systolic murmur, just as we have seen that those 
occupying portions of the period of diastole may 
correspond to the presystolic murmur. There is this 
difference, however, in the record of sound in the 
two cases-the vibrations of the presystolic murmur 
are only written in the exact line of the cardiac 
trace, whilst it would appear that the vibrations of 
a systolic murmur may be communicated to a much 
wider area of the chest-wall, so that they may inter- 
Fig. 42. 
Cardiogram in a case of mitral regurgitation : a, taken 
at exact apex ; 6, taken in area of loud systolic murmur, 
showing sonorous vibrations. 
mingle, as it were, with the proper elements of the 
tracing-. This is illustrated by Fig. 42. At a the 
trace is unmodified ; but at 1), the position of the lever 
being slightly altered, a number of coarse vibrations, 
which I consider to be due to a loud systolic murmur 
which was manifested in the case, are interposed. 
Another character which I have observed in cardiac 
tracings, in cases of mitral regurgitation, is the 
doubling or forking of the summit, which is so 284 
marked in Fig-. 42 a. The like is seen in Figs. 32, 
36 c, and 41. The explanation I consider to be this: 
-After the first ascent of the lever, due to the 
hardening- and rounding of the ventricle, there is a 
fall, because the ventricle has lost the point d^appui 
afforded by the stretched curtains of the normal valve; 
the continuing contraction of the ventricle, however, 
renews the elevation at the end of the systole. 
The diastolic portion of the trace, when there is 
any considerable mitral regurgitation, is shortened ; 
the ventricle is filled more rapidly than under 
normal conditions. In some cases, as in Fig. 41, 
the rapid rise of blood-pressure causes a marked 
eminence, ending with a fall previously to the systole 
of the ventricle. In cases of mitral regurgitation, 
in which an increased volume of blood is impelled 
by a hypertrophied auricle, the eminence corre- 
sponding to the auricular systole is unduly developed 
(see Fig. 34). 
III. Tricuspid liegurgitation.- The chief charac- 
teristic of the trace of the arterial pulse in tricuspid 
regurgitation is undulation of the base-line, marking 
the variations of arterial tension during respiration. 
If in any case manifesting much dyspnoea, and accom- 
panied by engorgement of the right chambers of the 
heart, a line drawn through the bases of the upstrokes 
shows a series of marked curves, the probability of 
tricuspid regurgitation must be taken into account. 
So, also, in other valvular diseases, when a pro- 
nounced degree of respiratory curve is a superadded 
condition, it may be considered probable that the 
tricuspid has become insufficient. 
In tricuspid regurgitation, however, graphic evidence 
may be obtained from the venous, as well as from the 
CARDIOGRAMS IN MITRAL REGURGITATION. TRICUSPID REGURGITATION: SPH YGMOGRAMS. 
285 
arterial, system. A tracing may be taken of the venous 
pulse from the jugular or subclavian. Fig. 43 shows 
the graphic characters of such a tracing. The most 
conspicuous feature is the pronounced wave which pre- 
cedes the main upstroke; this is due to the systole 
of the right auricle, which causes a reflux into the 
venous channels. In the descending curve is seen a 
sharply-defined notch, analogous to the aortic 
(dicrotic) notch of the arterial trace. Tracings may 
Fig. 43. 
Tracing from subclavian vein in a case of tricuspid 
regurgitation with mitral contraction, after Galabin 
(Med. Chir. Trans., vol. Iviii. p. 365, Fig. 3); a, ana- 
dicrotic wave due to systole of auricle; b, hatadicrotic 
wave analogous to dicrotic wave of arterial pulse. 
•also be taken over the seat of pulsation of the liver when 
in tricuspid regurgitation this is observed (Fig-. 45), 
In such case the correspondence with the venous pulse 
will be noticed. There is the wave in the principal 
upstroke due to the auricular systole, and called the 
anadicrotic wave, and that in the downstroke the' 
liatadicrotic wave. The latter seems to be produced 
by like causes with those occasioning the dicrotic wave- 
in the arterial pulse, and maybe the more pronounced, 
as the veins are dilated and tensionless. 
The Cardiac Trace in tricuspid regurgitation pos- 
sesses no special characteristics, but in series it shows- 286 
TRICUSPID REGURGITATION : CARDIOGRAMS. 
that the systoles are irregular and unequal in volume 
(see Fig. 27). In the individual tracings the hyper- 
trophy of the right auricle is not marked; such 
hypertrophy is rather indicated by the venous reflux, 
as shown in the tracings from the pulsating veins 
which we have just considered. When, therefore, 
you observe a very marked auricular eminence in a 
Fig. 44. 
Tracing from pulsating liver in tricuspid regurgitation, 
showing a slight anadicrotic and a pronounced kata- 
dicrotic wave. 
cardiac tracing, taken in a case of tricuspid regurgi- 
tation, .you should suspect hypertrophy of the left 
auricle. This is strikingly exemplified in a case 
recorded by Dr. Mahomed, in which there was tri- 
cuspid regurgitation, with pulsation of the large veins, 
in the neck, and in which the apex-tracing showed 
the strong auricular elevation, Fig. 34 a. The ne- 
cropsy in this case showed a dilated right ventricle 
and wide tricuspid orifice, with greatly hypertrophied 
left auricle, but no valvular disease.* 
* Med. Times and Gaz., April 13, 1872, p. 429. AORTIC REGURGITATION : SPH YGMOGRAMS. 
287 
IX. 
Graphic evidence in valvular diseases, concluded-Aortic 
Regurgitation-Pulse-tracings referred to two types-A, 
associated with effects of rheumatic endocarditis-High 
percussion upstroke-Suddenness-Effacement of dicrotic 
wave, and its significance--Flatness of diastolic portion.- 
B, associated with atheroma-Trace of high tension-Heart- 
tracings-Evidence of slowness of systole-Signs of hyper- 
trophy of left ventricle-Shortening of diastole-Aug- 
mented blood pressure in the ventricle-Indications of 
diastolic thrill-Aortic Stenosis-Pulse-trace in extreme 
cases showing tidal wave only-Evidence •when tidal wave 
rises above percussion-Estimation of degree of stenosis 
when combined with regurgitation-Heart-trace occasionally 
registers sonorous vibrations - Vibrations recorded in 
Stenosis of the Pulmonary Artery. 
IV. Aortic Regurgitation. The pulse-trace 
which in cases of aortic regurgitation is usually highly 
characteristic, may be referred to one of two types, 
one of which (A) is usually associated with changes in 
the valves due to rheumatic endocarditis, and the other 
(B) with the incompetence due to degeneration of the 
aorta-aortitis deformans, or senile change. 
A. The pulse-trace presents characters correspond- 
ing to the splashing, wafer-hammer pulse of aortic 
regurgitation. The first point to be noted is, that the 
upstroke is loftier than normal. You find that the 
sphygmogram in such cases is easy to take. At low 
pressures the tracing shows great amplitude. The 
grasp of the strong left ventricle impels a sudden wave 
into arteries, lax at the moment of systole because of 288 
AORTIC REGURGITATION : SPHYGMOGRAMS. 
the leakage which has occurred during diastole 
through the imperfectly closed aortic aperture. 
This suddenness of impulsion gives rise to the lofty 
percussion wave recorded by the sphygmograph (vidc 
Figs. 45 and 46), as it does to the hammer-like quality 
of the pulse felt by the finger. Next in point of 
importance, as characteristic of the sphygmograms of 
aortic regurgitation, is impairment or effacement of the. 
dicrotic wave. This would appear to be d priori pro- 
bable. As the dicrotic wave is caused bv a rebound 
Fig. 45. 
Tracing from Brachial Artery in a case of free aortic regurgi- 
tation, showing effacement of dicrotic wave. 
from the closed extremity of the aorta, it is only rea- 
sonable to infer that, if the closure be imperfect, the 
dicrotic wave will also be ill-pronounced. That it 
may be so is proved by many tracings (vide Fig. 45). 
In the early days of the application of the sphygmo- 
graph it was considered that this impairment of the 
dicrotic wave was the chief sign of aortic regurgita- 
tion ; such view is not, however, borne out by facts. 
As a positive sign, effacement of dicrotism is of very 
high value, for it indicates very free aortic regurgita- AORTIC REGURGITATION- SPHYGMOGRAMS. 
289 
tion. It must not be concluded, however, that the 
presence of a marked dicrotic wave negatives regurgi- 
tation. In Fig. 4G a, you notice that the tracing of 
the radial, taken with Pond's instrument, has great 
altitude of percussion, the characteristic of aortic 
regurgitation : there is a sharply defined tidal wave, 
and near the base of the tracing- is a well-marked 
dicrotic wave. In this case there was undoubted 
aortic regurgitation, and it is well proved that in such 
cases a pronounced dicrotic wave may be recorded, the 
partially-closed aortic cusps forming a sufficient jwwi# 
Fig. 4G. 
Tracing from radial artery in aortic regurgitation : a, 
taken with light pressure showing dicrotic wave near the 
base-line; b, with slightly increased pressure showing 
obliteration of dicrotic wave. 
^appui for its production. It will be noticed, however, 
that in the tracings in which the percussion upstroke 
is high, the dicrotic wave, though it may be amply 
developed, is low or near the base-line. Another point 
of importance is its easy obliteration by pressure. In 
the type of aortic regurgitation, which we are now 
considering, I have said the elements of the trace 
are best brought out by low pressure, then the dicrotic 
wave may be full and rounded; but if the pressure 
upon the artery be only slightly increased, the wave 
may be altogether obliterated. This characteristic of 290 
AORTIC REGURGITATION-SPHYGMOGRAMS. 
the pulse of aortic regurgitation is demonstrated with 
great facility by Pond's sphygmograph. You com- 
mence to take the trace with low pressure, and all the 
elements of the trace become well marked, as seen in 
Fig. 46 a, which shows the dicrotic wave full and 
rounded. Then if, whilst the slide is travelling, you 
sliirhtly increase your pressure upon the artery, you 
find that the dicrotism is obliterated, as shown in 
Fig. 46 b, the diastolic portion of the tracing being* 
rendered fiat. We may conclude, then, as regards those 
sphygmograms of aortic regurgitation which present a 
high elevation that the dicrotic wave is either obvi- 
ously impaired or else, though apparently pronounced, 
is easily obliterated by increase of pressure. This leads 
us to the third characteristic of such pulse traces, which 
is fatness of the diastolic portion. The line succeeding 
the dicrotic notch is low in the tracing or is horizontal. 
Such flatness indicates the emptiness of the artery 
during ventricular diastole. 
The second type,.B, of pulse-trace in aortic regur- 
gitation differs considerably from the preceding: there 
is no notable exaggeration of the percussion upstroke 
with rapid fall, but a resemblance with the tracings 
indicating biyh tension in the arteries, as in Fig. 24. In 
such case the summit of the trace is broadened, the 
tidal wave being sustained; the dicrotic notch, though 
ill-pronounced, is high in the tracing; and the gradu- 
ally-sloping line corresponding to the diastolic period, 
tells of peripheral obstruction. As the former type 
of pulse was chiefly associated with the changes in 
the aortic valves induced by rheumatic endocarditis, 
so this is seen for the most part in conjunction with 
^leqen<raticc diseases of the aorta and arteries. 
JSo the sphygmograph becomes a valuable means of AORTIC REGURGITATION-CARDIOGRAMS. 
291 
diagnosis as regards the two pathological conditions. 
For example : a case presents itself with the physical 
signs of aortic regurgitation, the patient being past 
the prime of life, and giving a negative or obscure 
history of rheumatism. Your sphygmographic tracing' 
is not of the typical form Fig. 47 a, and you are only 
able to conclude from it that there is high tension in the 
arteries. Such conclusion is of the highest impor- 
tance. It either negatives the conclusion that the 
changes are due to rheumatic endocarditis, or indicates 
that any regurgitation so produced is slight and well 
compensated. But further, in a majority of cases it 
goes to prove that the condition giving rise to the 
aortic regurgitation is due to atheroma of the aorta- 
to endarteritis or aortitis deformans.* 
The Cakdiac Trace in aortic regurgitation does 
not present such important characters in regard to 
diagnosis as the pulse trace, but nevertheless affords 
evidence of much value. In the first place, it is 
noticeable that the quality of suddenness, so marked in 
the majority of the sphygmograms, is not a feature of 
the cardiograms. In a case in which the sphygmo- 
graph indicates a lofty, abrupt percussion wave, the 
cardiograph demonstrates a slow and prolonged ven- 
tricular systole. Dr. Galabin has proved by accurate 
measurement, that in a pulse-curve taken in a case of 
aortic regurgitation, in which the general shape dif- 
fered little from the. normal, the upstroke occupied 
about one-third less time than that of the healthy 
pulse.f On the other hand, " the interval occupied 
* Cf. Mahomed, Med. Times and Gaz., Sep. 21, 1872, p. 325, 
and " Guy's Hospital Reports," 1879, p. 419. 
+ Galabin, Med. Chir. Trans., vol. lix. p. 361. 292 
AORTIC REGURGITATION-CARDIOGRAMS. 
by the main upstroke of the trace, which indicates 
the time which the ventricles take in becoming fully 
hardened, may be increased in cases of aortic disease 
from its normal value of about one-twelfth of a second 
to as much as from one-eighth to one-sixth of a second; 
that is to say, that it may be nearly doubled."* The 
systolic portion of the tracing is usually broad, and 
the eminence^ well-marked and rounded-indications 
of hypertrophy of the left ventricle. In some cases, 
however, the opposite condition prevails, the summit 
is not truncated but narrow, and the diastolic fall 
rapid; this is an indication that dilatation of the left 
ventricle prevails. As regards the diastolic portion 
of the tracing, it is very important to note its relative 
duration. It is common to find in aortic regurgita- 
tion that this is much shortened. There may be 
scarcely any interval between one systolic upstroke 
and the next, or only a slight single eminence; this 
is an indication that the regurgitation is very free, for 
the ventricle becomes rapidly filled. Or the diastolic 
portion, instead of being horizontal, may present an 
ascending line (as in Fig. 31), indicating that the 
blood-pressure in the ventricle during diastole be- 
comes progressively increased; this is notably the 
case where mitral regurgitation, especially when com- 
bined with hypertrophy of the left auricle, co-exists. 
Occasionally, vibrations corresponding to diastolic 
thrill are marked upon the trace. Such is shown in 
certain of the cardiograms recorded by Dr. Galabin 
(" Guy's Hospital Reports," 1875, Plate II. Figs, 0 
and 10); and I have observed it in many others. 
In Aortic Obstruction, when the lesion is 
* Loc. cit., p. 363. AORTIC STENOSIS-SPHYGMOGRAMS. 
293 
extreme, the pulse trace may possess highly distinctive 
characters. The percussion wave is effaced, for the 
artery, owing to the narrowing of the aorta, is slowly 
and gTadually distended by the ventricular systole. 
The tracing in such cases shows sloping upstrokes 
and downstrokes resembling- that obtained sometimes 
in cases of aneurism (see Fig. 22). Such tracings 
are figured by Dr. Mahomed {Medical Times and 
Gazette, Aug. 10,1872, Plate V.) and by Dr. Hayden 
(" Diseases of Heart and Aorta," p. 869, Fig. LIL). 
This last was in the case of a boy aged seven 
and a half years. In these cases there is only one 
element of the trace, the tidal wave, all else being 
obliterated. In other cases the percussion upstroke 
Fig. 47. 
Sphygmogram in case of aortic obstruction (Dr. Gala- 
bin). A large tidal wave, c d, rises high above the percussion 
wave, a b, indicating prolonged ventricular contraction; 
there is a marked dicrotic wave, e f, indicating that there 
is little or no reflux through the aortic orifice; pulse very 
slow. 
is arrested, and from its point of arrest proceeds an 
ample tidal wave, which rises high above the per- 
cussion wave.* This is seen in Fig. 47. There is 
not such extreme narrowing of the aortic orifice that 
the element of suddenness is lost, but the percussion 
* Cf. Galabin, Med. Chir. Trans., vol. lix. p. 384. 294 
AORTIC STENOSIS CARDIOGRAMS. 
is short, and the pronounced tidal wave is an indica- 
tion of the prolonged systole of the ventricle. So 
important do I consider this form of tracing, that I 
would say, whenever you meet with a radial 
tracing in which the percussion wave is suddenly 
arrested and an ample tidal wave rises above it, 
suspect aortic stenosis.* I have before said that the 
signs of this lesion are often obscure, and that during 
life it often remains undiscovered. As an aid to the 
diagnosis of the condition, I think the sphygmograph 
is of great value. So also in combined aortic regurgi- 
tation and obstruction, a conjunction which is much 
more common than either affection singly, you may 
take the amplitude of the tidal wave as a measure of 
the degree of stenosis. A pulse trace, which at very 
light pressure has the typical verticality of aortic 
regurgitation with very slight pronunciation of the 
tidal wave, may, by increase of pressure, be made 
more and more to develop the tidal, and this I con- 
sider to be an indication of the accompanying stenosis. 
In certain cases of aortic stenosis there is a marked 
division between the percussion and tidal waves, so 
that the summit of the trace is forked (vide Fig. 47). 
Such tracings are figured by Dr. Mahomed (Medical 
Tithes and Gazette, Aug. 10, 1872; Plate V. Figs. 47, 
48, and 49); they may explain the thrill which is 
sometimes felt in the pulse of aortic stenosis. 
Cardiographic Tracings in aortic stenosis are 
not often characteristic. Traces taken by Pond's 
instrument with very light pressure, over the site of 
an aortic systolic murmur, may present vibrations 
caused by the conditions which produce the sound. 
* Vide Fig. 24, the last tracing. 295 
This is strongly insisted upon by Dr. Pond as a point 
of value, but considerable caution must be used in so 
accepting- it. These fine vibrations may have many 
causes-tremulous movements of the skin, vibratory 
contractions of the intercostal muscles, and rhonchi, for 
example. Nevertheless, I have had experience that 
such vibrations maybe recorded in the area of a systolic 
aortic murmur, just as I have already shown tliem to 
be made manifest in mitral regurgitation (see Fig. 42) 
and in mitral stenosis (Figs. 33, 3G, 37, and 39). 
In Stenosis of the Pulmonary Artery also 
STENOSIS OF PULMONARY ARTERY. 
Fig. 48. 
Cardiogram from a case of congenital Cyanosis with 
murmur over the site of the pulmonary artery: a, 
showing vibrations over the maximum of aloud super- 
ficial systolic murmur; b. tracing at the apex of the 
heart. 
such vibrations, due to a systolic murmur, may be 
registered upon the trace, as in the example Fig. 48. INDEX. 
Note.-The figures in darker type (eg-, 123) refer to Part IL 
PAGE 
Abnormal sounds 123 
Accent 98 
Albuminuria 19 
Anadicrotic wave 285 
Anaemia 29, 132, 156, 159, 169 
Aneurism, pulse-trace in 247 
Aortic area 97 ' 
„ obstruction 135,293 
„ regurgitation 43,50,73,144,212,287 
„ double murmur 147 
Aortitis deformans . 139, 291 
Apex-beat • 44, 56 
„ displacement of 57 
Aphonia .18 
Apoplexy 16 
Arcus senilis 32 
Arterial tension 248 
Atheroma 48, 139,182, 291 
Auricles, functions of 61 
„ pulsations of 64 
Auricle, right, hypertrophy of 64, 88, 286 
„ left „ 64, 186, 265,272 
Auricular systole 265 
Auriculo-systolic murmur 192 
Auscultation 90 
Basedow's disease 30 
Blueness 23 
Cardiac cycle 61,258 
Cardiograph 228 
Cardiographic indications 252 
Cerebral symptoms 15 
Charts, use of •. . 82 
Cheyne-Stokes dyspnoea 35 
Chorea 15, 170 
Chronometry of Murmurs 193 
„ Pulsations 66 INDEX. 
297 
PAGE 
Clubbing of finger-ends 28 
Coma 
Combined Murmurs 
Conduction of murmurs fo- 
■ Congenital lesions 1^1 
Convection of murmurs • 1^ 
Cyanosis H 24, lb2 
Diastolic murmur -I48 
„ period * 26U 
„ thrill 2q 
Dicrotic wave 248 
Dicrotism / 250 
Dilatation . . 45, 5.8, 60 
„ apex beat in 45 
„ dulness in 87 
„ of left ventricle 105, 184, 25 6 
Dropsy 
Dulness, praecordial "8 
Dyspnoea . . . 44, 33 
Effort, effect of • 
Embolism . . • 47, 204 
Endocarditis, rheumatic 1°8> 180, 186 
ulcerative 142, 182 
" villous 135, 141, 182 
Etiology 21 
Exophthalmos 
Fatty degeneration ■ 10^ 
Foramen ovale, patency ot -4, 162 
Friction-fremitus '4 
Friction-sound ...... ,24 
„ „ pleuro-pericardial 130 
Goitre, exophthalmic . 30 
Gouty kidney 
Graphic records 
Graphic Representation of Murmurs 107 
Graves' disease • 
Haemophilia onl 
Haemoptysis 204 
Haemorrhage . . . 1" 
„ intra-cranial 16 
Heart-trace, normal 239 
„ „ abnormal 254 
Hepatic pulsation 69, 285 
Hoarseness 1® 
Hyper-dicrotism . 259 
Hypertrophy 20, 45, 58, 86, 91, 99, 103 
„ pulse in • • 50 
• „ of right ventricle, pulse in .52 298 
JNDEX. 
n PAGK 
Hypertrophy of right ventricle 60, 87 
• „ of left ventricle .... GO, 87, 100, 104, 256 
„ of left auricle ...... 64, 186, 265, 2 72 
„ concentric . *187 
Inspection 23 
Intermission 12, 53, 241 
Intermittent pulse ......... 55 
Inter-ventricular septum, opening in 24 
Inversion of cardiac trace 253 
Irregularity 12, 53, 253 
„ arhythmic 243 
Irregular pulse 53, 241, 242, 268 
Jaundice 31 
Katadicrotic wave ... 285 
Kidney symptoms ... 19, 29 
Liver, pulsation of . . 69, 285 
Locomotive pulse ■ , 43,289 
Lung symptoms .14 
Mitral area .97 
„ „ murmurs in 191 
„ regurgitation . . . 51, 101, 183, 201, 203, 208, 280 
„ stenosis ... . 65, 108, 185, 200, 203, 209, 267, 270 
Murmurs, adynamic 175, 178 
„ anaemic 132, 156, 159, 169 
„ cause of 147 
„ combined 215 
„ conduction of 152 
„ convection of 153 
„ double aortic 147 
„ double mitral 203 
„ temporary 132, 170 
„ vascular 155 
Myocarditis .174 
Normal Heart Sounds 93 
Obstruction, mitral , . . 65, 108, 185, 200, 209, 267, 270 
„ aortic ......... 72, 135, 142, 293 
„ pulmonary 2Q, 160, 163, 295 
(Edema 14, 39 
Ophthalmoscopy . . . * 144 
Orthopnoea .33 
Pain 3 
Pallor 29 
Palpation 48 
Palpitation 11, 254 
Percussion 77 
Percussion wave, modifications of. 243 
Pericardial adhesions ............ 47, 68 
„ .effusion .......... ... 82 INDEX. 
299 
PAGB 
Pericarditis, decubitus in . .... 34 
„ pulse in . . ' ' ' rp 
„ apex-beat in . . ....... * os 
„ effusion in . 
fremitus in . . . • • 
friction sound in 1-' 
„ rheumatic .. .. . • 125 
,, prsecordial duhiess in 84 
Presystolic friction ^8 
thrill ... • 74 
" murmur 192,200,209 
Proptosis ' .„ 
Pulsation ™ 
venous . . ** 
„ visible arterial ' C7 
„ presystolic o7 
" hepS™69,285 
,, of retinal vessels • • 
- 
„ Corrigan's «. 
Pulse-trace, normal ' 
Reduplication • • „ 
Regurgitation, aortic 43, 50, 73, 144, 212, 287 
mitral . . 51,101,183,201,203,208,280 
tricuspid . ... . . . 42, 166, 284. 286 
Renal disease 10, 103, 1^6, 182 
Respiratory line . . . . • • • • 245 
Rheumatic endocarditis 138, 180, 186 
„ pericarditis . • . 12a 
Rheumatism 21, 125, 180 
Rhythm of murmurs 131 
„ of pulse 53 
Skoda's sign 
Sphygmograph 
,, invention of 221 
„ value of .... 222 
varieties of 224 
Mahomed's 224 
Pond's . . 225 
„ use of 230 
Sphvgmographic indications 240 
Stenosis, aortic 72, 135, 142, 293 
mitral .... 65, 108, 185, 200, 209, 267, 270 
pulmonary 26, 160, 163, 295 
„ tricuspid • 168, 218 
Stethoscopes . 91 
Stomach symptoms 17 300 
INDEX. 
PACK 
Symptomatology 1 
Systole ineffectual 52, 107 
Thrill 72 
„ pulmonary 165 
Throat symptoms 18 
Thyroid enlargement 30 
Tidal wave 248 
Topography of Heart 59 
Topography of Valves 96 
Tracings, cardiographic 234 
„ copying and multiplying 235 
,, sphygmographic 230, 237 
„ varnishing 235 
Tricuspid area 166 
„ obstruction 168, 218 
„ regurgitation 42, 166, 284, 286 
Tumultuous heart-beat 13 
Tympanitic resonance 78 
Typhoid fever, murmurs in 173 
Valves, closure of auriculo-ventricular 255 
„ „ aortic 257 
„ rupture of 182 
,, situations of 96 
Venous murmur 156 
„ pulsation 41, 285 
„ turgescence 41 
Ventricles, contraction of ,.63 
Visible impulse 44 
„ pulsation 43 
Vocal representation of murmurs 195 
..JUTTED BY BALLANTYNKAl'D HANSOM 
LONDON AND EDINBURGH