jpigniftrance of ihc |]r;u*sii‘ifolir JjJjWmnr. 
BY 
FKANK DONALDSON, M. D. Read before the Medical and Chirurgical Faculty of Maryland, 
Annual Session, April, 1874. 
of the Lurmur. 
By FRANK DONALDSON, M. D. 
Professor of Physiology and Hygiene, and Clinical Professor of Diseases Chest and Throat, 
University of Maryland. 
I propose detaining the Faculty a few minutes with some re- 
marks upon a point of analytical diagnosis in connection with 
disease of the heart. 
SIGNIFICANCE OF THE PRAESYSTOLIC MURMUR. 
Some years ago (in 1867), a case came under my observation, 
which made me question the explanation, which I had adopted on 
the authority of Barth and Roger, Walshe and Flint, of the 
sound which was described first by Fauvel in 1843, and then by 
Grisolle as the praesystolic murmur, afterwards by Dr. Gairdner 
of Edinburgh as the auricular systolic murmur, and by Dr. Austin 
Flint, Sr., as the mitral direct murmur. 
These authorities claimed that this sound was heard just preced- 
ing the ventricular contraction, and was caused by the systole of 
the auricle forcing the blood into the ventricle, through a diseased 
and contracted auriculo-ventricular orifice. 
The case was of a man 64 years of age, of grossly intemperate 
habits, who came to the Baltimore Infirmary with symptoms of 
advanced heart disease—great dyspnoea, a small contracted pulse, 
heart much hypertrophied, with a murmur of a rasping character, 
heard loudest between the second and third ribs at the base, not 
extending up the carotids, but down toward the base, and com- 
pletely obliterating the second sound of the heart. The murmur 
was audible after the apex-beat and the systole of the ventricle, 
and was followed by the pause of the heart. The first sound of 
the heart was normal. 
The diagnosis seemed clear and unmistakable, and was recorded 4 
SIGNIFICANCE OF THE FRAESYSTOLIC MURMUR. 
as insufficiency of the aortic orifice, by means of which the arterial 
blood was forced back into the left ventricle. 
The heart being-obliged to contract more frequently, so as to 
supply the organism with the proper quantity of blood, the mus- 
cular walls had become from this extra work enlarged, and thus, as 
the great dullness over the praccordial region indicated, there was 
compensating hypertrophy. 
For a time this increased size and force of the central organ 
accomplished the usual role of the heart, but the disease increas- 
ing, the individual suffered more and more, until shortly after 
admission into the hospital he died, suffering intensely from cardiac 
apnoea. 
The post-mortem showed atheromatous degeneration in the 
aorta above the semilunar valves extending to the sacks of 
Valsalva, and causing adhesion of one of the semilunar pouches of 
the aortic orifice to the wall, so binding it down that that portion 
of the orifice was unprotected. Thus, at the rebound of the artery 
the blood was partly sent back into the ventricle. The second 
sound could not be produced, and the insufficiency of the valve 
was evident. 
Th us far the diagnosis was correct, but on examining the 
mitral orifice we found, to our surprise, that it was reduced by 
thickening at its base to about the size of one-quarter of an inch in 
diameter. Yet during life, there was no abnormal sound preceding 
or during the ventricular systole. With such a contraction of the left 
auriculo-ventricular orifice, ought we not to have had a decided 
praesystolie murmur ? The whole heart, auricle and ventricle, was 
enlarged and increased in force, and yet there was no murmur 
produced from the passage of the blood through an orifice so re- 
duced in size ! I could not help questioning the received opinion as 
to the significance of the so-called mitral direct murmur. As it 
is a physical sound, heard at a particular period of the heart’s 
action, the physical cause which was said to produce it being 
present, it ought to have been heard, but it was not. 
Since this case I have been much interested in the articles that 
have appeared at different times, discussing the mode of produc- 
tion of this sound. I have had several cases in which I have 
heard this sound immediately preceding the impulse of the heart, SIGNIFICANCE OF THE PRAESYSTOLIC MURMUR. 
5 
or apex beat and the first sound of the heart. Although I have tried, 
I have never been able to get a post-mortem demonstration of the 
cause of sound. Yet I have insisted in my clinical teachings 
that I believed it was not caused by the passage of blood through 
the mitral orifice, but by intra-ventricular disease—not by stenosis 
of the orifice, but by abnormal friction within the ventricle. 
Before I give in detail the grounds, physiological and patholo- 
gical, upon which I base this opinion, I would refer first to cases 
which have been recently reported by others, where, notwithstand- 
ing there was found the post-mortem lesion of great contraction 
of the orifice, yet there was discoverable during life no praesys- 
tolic murmur. 
I will first give the facts bearing upon the point in discussion, 
and then deduce my conclusions as to the explanation of those 
facts. 
This abnormal sound is heard over a limited area, recognised 
as the mitral area. The position of its audition is limited ordi- 
narily above by the third rib, and below by the middle of the 
sixth intercostal space. Its rhythm or relation to the several phy- 
siological acts is easily recognised. During the period of the heart 
action, we have the ventricular systole synchronous with the apex 
beat and the first sound, the ventricular diastole synchronous with 
the second sound ; next, the period of cardiac rest, as it is called, 
but during which the blood is pouring into the cavities of the 
heart, on the right side through the venae cavae and coronary 
veins, on the left through the pulmonary veins; and lastly, the 
systole of the auricle, which is quick and sudden, and consumes 
two-tenths of the time of the heart’s action. This last period in 
the heart’s labor is apparently the moment when we hear this mur- 
mur. It is distinguishable immediately before the first sound, and 
has been regarded as produced by the column of blood passing 
through the constricted mitral orifice. 
We have mentioned our own case, and now briefly give those 
which have been observed by others. 
Hope, as far back as 1842, reports a case of a man named 
Christian Anderson, where the mitral orifice was so contracted 
that it would only admit the little finger, yet there was no murmur 
during life preceding the first sound. In his report he adds, “ I 6 
SIGNIFICANCE OF THE PRAESYSTOLIC MURMUR. 
have frequently known a contraction of the mitral orifice to the 
size of only two or three lines to occasion little or no murmur.” 
Mr. Prescott Ilewett has described a case in which the mitral 
orifice was reduced to the size of a quill, and during lifetime no 
signs of diseased heart were exhibited. 
Dr. James R. Learning reports the following case in the New 
York Medical Record: 
“ Mrs. B , 23 years of age, native of New York, widow, 
called Dr. S , in April, I860, for advice as to cardiac trouble 
and swelled feet. The Doctor found on examination a systolic 
murmur over the base of the heart, more distinct over the aortic 
valves, gradually disappearing to the right in the course of the 
aorta; there was also a diastolic murmur. 
“ Diagnosis.—Aortic obstruction and aortic regurgitation with 
hypertrophy of left ventricle. There were also casts in the urine, 
and albumen. She became dropsical, her condition gradually 
grew worse, and she died in September last. 
“I saw the case with Dr. S , in May, and found no different 
conditions than those already discovered. There was no mitral 
murmur of any kind. The specimens here presented show Bright’s 
small kidney of advanced disease. The heart is hypertrophied 
mostly in the left ventricle; the aortic valve is thickened at the 
base of the curtains ; shortened to incompetency—so far agreeing 
with the diagnosis. But the mitral valve presents the most notable 
feature. There was no sign of disease of this valve during life, 
and yet it is damaged in a very peculiar manner. It is thickened 
by lymph deposit; its color white, opaque ; the edges of the cur- 
tain are adherent, and the orifice is narrowed down till it will 
barely admit the tip of the index finger; and the whole valve 
extends down into the cavity of the ventricle like a funnel. The 
chorda? tendincao were shortened and thickened by lymph deposits, 
and the musculi papillares were thickened and lengthened. But 
everything was symmetrical, viz., the funnel-like condition of the 
valve, the hypertrophy of the cardiac walls, of the musculi papil- 
lares, and of the colnmme carneae. With perfect conditions for 
producing a mitral direct murmur, it was absent.” 
Dr. Stokes, in his work on diseases of heart and aorta, relates 
two cases of extreme contraction of the mitral orifice found after 7 
SIGNIFICANCE OF THE PRAESYSTOLIC MURMUR. 
death, bat where during life there had been no murmur audible, 
even to his practised ear. 
Dr. Waters, of Edinburgh, in the second edition of his work 
on diseases of the chest, just published, in the sixth chapter, writes 
of the praesystolic murmur. While he gives the received opinion, 
that it is caused by stenosis of the mitral orifice, he details cases in 
which lie shows there was no connection between the sound and 
the lesion. He speaks of them as exceptional cases. Ilis first 
case is where he heard a loud systolic as well as a praesystolic mur- 
mur. At the autopsy there was found insufficiency and slight 
contraction of the mitral orifice. In his second case there was no 
praesystolic murmur whatever, although the autopsy showed a 
constricted mitral orifice, only admitting the tip of the index 
finger. Next follow the details of four cases of extreme con- 
traction of the mitral orifice, where during life there was no prae- 
systolic murmur audible. He candidly adds: “ I have given 
you instances sufficient to prove that great constriction of the 
mitral orifice may exist without there being any murmur pro- 
duced by the passage of the blood from the auricle into the ven- 
tricle, and therefore that you must not look for a mitral diastolic 
or praesystolic as a constant sign of obstructive mitral disease. 
My belief is that this murmur is far more frequently absent than 
present, even when there is great obstruction at the mitral orifice.” 
Dr. Waters accounts for the presence or absence of this murmur 
as depending on the greater or less vigor with which the auricle 
contracts. 
We have now given ten cases beside our own where examina- 
tion after death showed the lesion which ought to have produced 
the sound during life, but did not do so. Dr. Waters says truly, 
<l Its absence is no proof that obstruction, even to an extreme degree, 
does not exist; ” and Balfour, an unwilling witness, confirms this 
view by saying, “.This murmur is not always audible when its 
cause is present.” Further, Dr. Flint records three cases in which 
the murmur was loud and clear, and yet the mitral valves were 
found at the post-mortem to be normal, but there was insufficiency 
of the aortic valves. Thus we have eleven cases of the lesion 
without the murmur, and three cases of murmur without the lesion ! 
These two sets of facts we consider valuable, as contributing to 8 
SIGNIFICANCE OF THE PRAESYSTOLTC MURMUR. 
prove that the praesystolic murmur is not due to stenosis of the 
mitral orifice. 
Before we get to what we believe to be the true explanation of 
this sound, let us look for a moment at the anatomical and physi- 
ological reasons against the usually received view. The sound is 
not a smooth, short one, but it is a rough, blubbering sound, often 
perceptible through thick clothing, and has been called “ the prae- 
systolic purring,” (Niemeyer). It is also prolonged, according to 
Flint and Balfour, up to the actual moment when we hear the 
apex-beat and the first sound, showing considerable force, whereas 
the muscular development of the auricle is very slight. Again, 
the time occupied by the murmur usually far exceeds two-tenths 
of a second, which, Marey tells us, is the time consumed by the 
auricular systole. The exceedingly wide orifice, between the au- 
ricle and the ventricle, measuring in circumference from four to 
four and a half inches, extending nearly through the whole sep- 
tum, shows us the facility with which nature intended the blood 
should pass into the ventricle through the auricles, and the absence 
of any necessity of any but feeble muscular power to assist it. 
The physiological objections to the old theory seem to be very 
well founded. We must bear in mind that the auricles are not 
first filled with blood and then contracted to force the blood into 
the ventricles, but during the diastole the blood flows onward, 
without obstruction and without force, except the feeble, gentle 
current of the venous system, and both cavities are nearly, 
if not quite full before the systole commences, the feeble mus- 
cular fibres of the auricles beginning to contract, and the contrac- 
tion going right on to the powerful fibres of the ventricles. I n 
fact, the ventricles are full before the auricles give their first 
impetus to the current that forces open the aortic valves and over 
them into the aorta. So true is this, that Chauveau has shown 
that the systole of the auricles is not immediately necessary to the 
preformance of the circulation, fie exhausted the contractility 
of the auricles, nevertheless the ventricles continued to act and 
keej) up the circulation without their aid. Even Harvey speaks 
of the harmony of the auricular and ventricular systole, the two 
concurring in such wise that but one motion is apparent. He 
compares it to a set of wheels acting upon each other when they SIGNIFICANCE OF THE PRAESYSTOLIC MURMUR. 
9 
appeal* to move simultaneously. We do not wonder at this aetion 
when we look closely into the histological structure of the walls of 
the heart, and find them composed of innumerable muscular fibres 
arranged like two balls of twine, each with a cavity in its centre, 
and both completely enveloped in a third ball. The free inoscula- 
tion of the fibres, a peculiarity of the muscular structure of the 
heart, and the absence, according to Robin, of the sarcolumna, 
favor the complete systole of the heart. 
When the auricles use their slight force the ventricles are nearly 
full, and the force is conveyed against the whole volume of blood, 
and is expended far beyond the mitral orifice. Before the auric- 
ular systole commences the blood has flown into the ventricles, 
and as demonstrated by Banmgarten of Germany, and by Doctor 
Halford, the flaps of the auriculo-ventricular valve rise on the 
surface of the liquid and come in contact. As the systole extends 
to the ventricle, they are brought forcibly together, and their 
tension gives us the valvular element, the real cause of the first 
sound of the heart. 
We hold that the contraction of the auricles is a secondary one, 
incapable of producing the prolonged rough sound recognised as 
the praesystolic murmur. 
Dr. Flint, Sr., thinks that the auricular force is sufficient to 
throw the curtains into vibration as the blood passes through the 
slit-like aperture, and thus produce the mitral direct murmur; but 
at that time there is no resistance to the force of the auricular 
systole, there is nothing to prevent their yielding. With due 
deference to so high an authority, we cannot consider this explana- 
tion as tenable. 
How then do we account for the sound which is heard and 
recognised as the praesystolic murmur? We believe it to be 
produced by endocardial causes within the ventricle, during the 
powerful ventricular systole, and not before the systole, although 
apparently so. The impulse of the heart and the forcible closure 
of the valves do not consume the whole of the time of the systole 
of the ventricle. They are produced at the culmination of the 
systole—the end. 
What occurs during the systole of the ventricles ? The blood 
is pushed both onward and backward with great force, equal, 10 
SIGNIFICANCE OF THE PRAESYSTOLIC MURMUR. 
according to Hales, to 51.5 pounds, which will raise blood in a 
tube connected with the aorta 7 feet 6 inches. We know if the 
onward current meets with asperities at the aortic orifice we hear 
a rasping murmur; so may it not be with the backward current, 
which passes between the cordae tendinae, and closes with a sharp 
sound the curtains of the mitral valve? In reading over carefully 
Dr. Balfour’s elaborate article in the Edinburgh Medical Journal, 
we were struck with the fact that in every case where he found 
the praesystolic murmur, there was also thickening from some 
cause of the free edge of the mitral curtains, or shortening and in- 
duration of the chordae tendinae. These lesions could have of 
themselves caused the murmur independently of the mitral con- 
traction. 
The abnormal friction, then, of the backward current of the 
blood against these rugosities up to the point of complete adjust- 
ment of the valves, and a twisting of the apex against the ribs, 
can give us precisely the sound we would expect. It appears to 
be praesystolic, because the sound strikes the ear before the com- 
pletion of the systole, as evidenced by the impulse and the first 
sound. 
Waters and the other authorities agree that the praesystolic is 
generally associated with a true systolic murmur. In chronic dis- 
ease of the heart we know that isolation is the exception and com- 
plication the rule. 
Several authors speak of a fact in relation to this murmur 
which is to us hardly consistent with the mitral stenosis theory. It 
is that this sound may exist at one time and not at another 
(Waters), may disappear temporarily, or even permanently (Bal- 
four. Dr. Gowers, in London Practitioner for Dec., 1873, gives 
four cases where it was heard in the recumbent position, but dis- 
appeared in the erect position. Stokes also speaks of its singular 
behavior in not being sometimes audible. 
Does this occur in aortic stricture and its characteristic sound ? 
No matter what the position of the body, the blood must be forced 
through the contracted orifice, and we ought to have the physical 
result of the extra friction. We can easily account for insuffi- 
ciency murmurs becoming inaudible as the space increases, Ixicause 
there is less friction. A smaller orifice with the same force will SIGNIFICANCE OF THE PRAESYSTOLIC MURMUR. 
11 
make a louder noise; but in obstructive lesions the orifice through 
which the blood is forced becomes smaller as the disease advances, 
and the murmur should be louder. Inside the ventricle the area 
is much larger, and we can see how it is much more probable that 
the blood-current may not so come in contact with the rugosities 
as to cause the fremissment cataire which Thauler considers charac- 
teristic of the praesystolic. 
If stenosis of the orifice is the physical cause of its production, 
then the intensity of the sound ought to be in proportion to the 
lessening of the size of the orifice. Again, how can the sound 
disappear? If we have given an orifice, a fluid of a fixed con- 
sistence and a force, the sound produced in one case must always 
be produced in a similar case. 
Flint tells us that praesystolic continues up to the occurrence 
of the succeeding first or systolic sound. Again, that it is more 
intense at its end than at its beginning. All these facts add 
probability to our conclusions as to the nature of this morbid 
sound, that stenosis of the mitral orifice is not the cause of its 
production. We claim with Dr. Learning, who we believe was 
the first, in a very suggestive paper in the New York Journal of 
Medicine (1868), to propose the ventricular origin of the so-called 
mitral direct murmur—“ That this murmur is only heard when 
the mitral valve is much diseased; and that the thickening and 
irregularity of the mitral valve, with the irregularly hypertro- 
phied ventricular walls and columnae carnae, are the physical 
causes of this sound, the blubbering character being produced by 
the irregular tension of the chords ; and the murmur is formed at 
the commencement of the ventricular systole, and not by the auricu- 
lar systole.”