HISTORY OF MEDICINE
Year : 2012 | Volume
: 13 | Issue : 2 | Page : 77--83
Classics in Cardiology: On Cardiac Murmurs* (Part 3)
Professor of the Principles and Practice of Medicine in the Bellevue Medical College, N.Y., and in the Long Island College Hospital, USA
Professor of the Principles and Practice of Medicine in the Bellevue Medical College, N.Y., and in the Long Island College Hospital
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Flint A. Classics in Cardiology: On Cardiac Murmurs* (Part 3).Heart Views 2012;13:77-83
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Flint A. Classics in Cardiology: On Cardiac Murmurs* (Part 3). Heart Views [serial online] 2012 [cited 2022 Jun 29 ];13:77-83
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Mitral Systolic Murmur
I use the phrase mitral systolic instead of that more commonly used, viz., mitral regurgitant murmur, as applied to any murmur produced at the mitral orifice and accompanying the first sound of the heart. If the latter term be applied to any systolic murmur emanating from the mitral orifice, we fall into the solecism of calling a murmur regurgitant in cases in which there is no regurgitation. A mitral murmur may be produced by mere roughness of the valvular curtains when there is no insufficiency of the valve. In this case, the murmur cannot be correctly said to be regurgitant. A mitral systolic murmur, thus, may or may not be a regurgitant murmur, and to express this important distinction, we may say that a mitral systolic murmur exists with or without regurgitation. The question at once arises, how are we to determine whether a mitral systolic murmur be regurgitant or non-regurgitant? This point claims consideration.
A mitral systolic murmur, as is well known, generally has its maximum of intensity at, and the murmuring may be limited to, the situation of the apex beat, or to the point where the intensity of the first sound of the heart is the greatest. The murmur may be diffused, in the first place, within this point over the body of the heart, and in the second place, without the apex over the left lateral surface of the chest and on the back. I have been led to believe that when the murmur is diffused over the left lateral surface and more or less over the back, it always denotes regurgitation, and that when the murmur is not propagated much without the apex, although it may be more or less diffused over the body of the heart, it may be produced within the ventricle and not by a regurgitant current. In the latter case, I have distinguished the murmur as an intra-ventricular murmur, and not considered it as affording any evidence of insufficiency of the mitral valve. It is this intra-ventricular, or mitral systolic non-regurgitant murmur, which generally exists in rheumatic endocarditis.
The importance of the point involved is obvious, for a murmur emanating from the mitral orifice without valvular insufficiency or regurgitation denotes lesions of little immediate consequence, and they may be innocuous, not only for the present but also for the future.
The practical rule just stated, I believe, generally holds good; but there may be exceptions. The following is perhaps an exceptional instance. A case was recently under my observation in Bellevue Hospital, in which acute rheumatism was complicated with endocarditis, pericarditis, and pleurisy, with considerable effusion, affecting the left side. The patient presented, on admission, a loud pericardial friction sound diffused over the whole praecordia and a loud mitral systolic murmur. The latter had its maximum of intensity at the apex, but was diffused over the left lateral surface of the chest and heard on the back. After the lapse of about a week, the friction sound disappeared; but before the disappearance of the friction sound, the endocardial murmur had gradually diminished and disappeared. The pleuritic effusion also disappeared, and evidence was afforded in this case of pericardial adhesions by the immobility of the apex beat when the body of the patient was placed in different positions. The disappearance of an endocardial murmur developed by rheumatic endocarditis, so far as my observation goes, is rare, although I have met with other examples. I suppose that endocarditis does not involve actual regurgitation save as a remote consequence of lesions to which the endocarditis may give rise. I may be mistaken in this supposition, but assuming that I am not, here was an instance in which an intra-ventricular or non-regurgitant mitral systolic murmur was propagated entirely around the chest.
With reference to determining the existence of either regurgitation or obstruction, or both, resulting from mitral lesions, a comparison of the aortic and pulmonic second sound forms a beautiful and useful application of auscultation. Obstructive and regurgitant lesions, situated at the mitral orifice, involving an obstacle to the free passage of blood through the pulmonary circuit, give rise, as is well known, to hypertrophy of the right ventricle. In this way, they lead to intensification of the pulmonic second sound of the heart. This effect is due, in part, to the augmented power of the contractions of the right ventricle, and in part, to the resistance to the passage of blood through the lungs, both continuing to increase the dilatation of the pulmonary artery by the pulmonic direct current, and the consequent recoil of the arterial coats by which the pulmonic valvular segments are expanded and the pulmonic second sound is produced.
But the morbid disparity between the aortic and pulmonic second sound is not only due to the intensification of the latter in the manner just stated. The aortic second sound is weakened in proportion to the amount of blood which fails to pass into the aorta with the ventricular systole, in consequence of the mitral obstruction or regurgitation. It is obvious that the aortic direct current will be lessened by the amount of blood which, in consequence of valvular insufficiency, flows backward into the left auricle after the ventricle contracts, and by the amount of difficulty which exists in the free passage of blood from the auricle into the ventricle in consequence of a contracted orifice.
It is also obvious that other things being equal, the intensity of the aortic second sound will be greater or less according to the quantity of blood propelled into the aorta by the ventricular systole. Thus, it is clear how mitral obstruction and regurgitation lead to weakening of the aortic sound, as well as to intensification of the pulmonic sound, and both effects are abundantly attested by clinical observation. The degree of weakening of the aortic sound and of intensification of the pulmonic sound will be proportionate to the amount of mitral regurgitation or obstruction, or both. We have then, in this application of auscultation, a means of obtaining information respecting the extent or gravity of mitral lesions. And, in a negative point of view, this application is important, viz., as a means of determining that lesions which give rise to a murmur are not serious, in other words, of determining that they do not involve much, if any, obstruction or regurgitation.
As enabling us to exclude obstructive or regurgitant lesions in certain of the cases in which mitral murmurs exist, a comparison of the aortic and pulmonic sounds is of great practical value. But the circumstances which may stand in the way of this application of auscultation are to be borne in mind. The two sounds cannot he compared with reference to mitral, more than with reference to aortic lesions, if there be coexisting pulmonary disease, nor whenever the normal relation of the aorta and pulmonary artery to the thoracic walls is altered by either past UI' present disease of the lungs, by deformity of the chest, 01' any other cause . It is also to be recollected that mere enlargement of the heart may disturb the normal relation of these vessels to the walls of the chest. This application, moreover, cannot be made when mitral and aortic lesions coexist. Under the latter circumstances, it is, of course, difficult or impossible to determine how far an existing disparity between the aortic and pulmonic sounds is due to the aortic, and how far it is due to the mitral lesions.
Another important point pertaining to a mitral systolic murmur is its occurrence without any appreciable lesions. A truly mitral regurgitant murmur doubtlessly always involves lesions of some kind, for it is hardly probable that the papillary muscles, as has been supposed, may become spasmodically affected and thus give rise to insufficiency or regurgitation as a temporary functional disorder. But it is undoubtedly true that a systolic murmur either limited to, or having its maximum of intensity near the apex, has been repeatedly observed in cases in which mitral lesions were not apparent after death. Dr. Bristowe in a paper published in the Brit. and FOI'. Mad, Chiir . Review for July 1861 details six cases of this description. Dr. Barlow, in an article in Guy's Il ospiiai Reports, vol. v., 1859, states that a mitral murmur may occur (he does not state for what reason) in long-continued capillary bronchitis. I have met with some instances in which a systolic murmur, supposed to he mitral, existed, and no mitral lesions were found after death.
In the winter of 1859-1860, I saw a female patient in the Charity Hospital, New Orleans, in the service of my colleague, Prof. Brickell, affected with capillary bronchitis. After several days, there was improvement as regards the pulmonary symptoms, and then, for the first time, a systolic cardiac murmur was discovered. The murmur was loudest at the epigastrium, but heard over the site of the apex, and extended to, but not above the base of the heart. The patient subsequently died. On examination after death, the lungs were emphysematous; there were no valvular lesions, all the valves appearing to be sound. The foramen ovale was dosed. There were no clots. The right ventricle was distended with liquid blood. The walls of the heart were of normal thickness. The valves and orifices were not measured, nor was the water test of valvular sufficiency employed.
In recording this case, I have commented on the murmur as follows: "What could have caused the loud systolic murmur? I cannot say unless it was due to distension of the right ventricle and tricuspid regurgitation." In support of the supposition that the murmur was tricuspid, not mitral, it is to be noted that the greatest intensity was at the epigastrium. It was, however, considered to be a mitral systolic murmur during life.
During the winter of 1860-1861, a patient was under my observation in the Charity Hospital, New Orleans, for 4 months, affected with albuminuria and general dropsy. During all this time, there was a mitral systolic murmur at the apex and over the body of the heart, and not propagated throughout the apex. It was regarded as a mitral systolic, non-regurgitant or intra-ventricular murmur, and as such pointed out to several private classes in auscultation. The patient died by asthenia, and was found to have fatty kidneys and cirrhosis of the liver. On examination of the heart post mortem, nothing abnormal was found except some enlargement, the organ weighing 12 oz., and a little separation of the marginal extremity of two of the aortic segments. The mitral valve appeared to be perfectly normal. I expected to find some roughening of the mitral valve, but no insufficiency; there was, however, no atheromatous, calcareous, or other deposit, and the valve seemed to be sufficient. There was no aortic or pulmonic murmur in this case, a fact which excludes the supposition that the existing murmur was due to the condition of the blood.
During the winter of 1860-1861, a patient was under my observation in the Charity Hospital, New Orleans, for about 6 weeks, affected with chronic bronchitis and emphysema of lungs. He presented with habitual dyspnea, which was at times excessive, persisting lividity, and anasarca. The heart was evidently somewhat enlarged. There was a loud rough systolic murmur, having its maximum of intensity at the apex, propagated throughout the apex (the record does not state how far) and over the body of the heart. On examination after death, the volume of the heart was not much increased and its weight was 13 oz. The left ventricle was not dilated and the left auricle was small. The walls of the left ventricle did not exceed half an inch in thickness, and the appearance of the muscular tissue was healthy. The mitral valve was perfectly normal. The orifice was not enlarged, and the valve must have been sufficient. No lesion at the aortic orifice was found. The right cavities were much dilated. They were twice as large as the left cavities. The walls of the right ventricle were much thickened, the thickness falling but little short of that of the left ventricle. No lesion of the pulmonic orifice was found. The tricuspid valve was normal. The orifice was very large, admitting the extremities of all the fingers. I have appended to the record of this case the following comment: "'Whence the murmur supposed to be a mitral regurgitant? I suspect it was a tricuspid regurgitant."
Dr. Bristowe, in the article already referred to, discusses several conditions which have been supposed to give rise to the murmur in cases like those which have just been given, viz. clots in the ventricular cavity, spasm of the papillary muscles, and enlargement of the auricular orifice so as to render the valve insufficient. His own opinion is that the murmur is due to a "disproportion between the size of the ventricular cavity and the length of the chordea tendineae and musculi papillaries." He attributes this disproportion to dilatation of the cavity of the ventricle. He also accepts to some extent an explanation offered by Dr. Hare, viz. that the murmur may be due to a "lateral displacement of the origins of the musculi capillaries in consequence of the rounded form which dilatation imparts to the heart."
These several explanations may each be applicable to certain cases, but none of them is applicable apparently to the cases which I have given. Clots in the left ventricular cavity were not present in either of the cases; the murmur continued too long and too persistently due to spasm; the mitral orifice was not dilated, and the enlargement of the heart was not sufficient to occasion a notable disproportion between the length of the tendinous cords and papillary muscles, and the ventricular cavity. I am disposed to think that in each of the three cases, the murmur was erroneously considered to be mitral, that it was a tricuspid regurgitant murmur. As I have already said, I have, but little practical knowledge of tricuspid murmurs. I have met with two instances in which murmur was connected with well-marked tricuspid lesions as verified by examination after death. In both these cases, the murmur was heard over the body of the heart, within the superficial cardiac region. I suspect that a tricuspid regurgitant murmur is not so rare as is generally supposed, and that, not very infrequently, it is considered to be mitral. This opinion is expressed by Dr. Gairdner in an interesting article on cardiac murmurs in the Edinburgh Med. Monthly, Nov. 1861. According to this able clinical observer, a tricuspid systolic murmur is heard over the right ventricle where it is uncovered of lung, being but slightly audible above the third rib; and if the heart be much enlarged, it may be heard louder toward the xiphoid cartilage. A collection of clinical facts respecting the frequency of tricuspid murmurs, the physical conditions giving rise to them, and the means of discriminating them from mitral murmurs is an important consideration.
Mitral Direct Murmur
This murmur is not recognized by many auscultators, and its existence is denied by some. It is generally confounded with a mitral systolic murmur. For many years after I had begun to devote special attention to cardiac affections, I committed this mistake, and I was sometimes puzzled to account for a supposed mitral systolic murmur rough at its beginning and soft at its ending. In my records of some cases before, I had learned to separate the mitral direct from a mitral regurgitant. I have described the latter as presenting the variation just stated, the fact being that the two murmurs were present, the one rough and the other soft. It is only within the last few years that I have discriminated these two murmurs, but during this time, my field of clinical observation has been so extensive that I have had abundant opportunities to make the discrimination. With regard to the frequency of the mitral direct murmur, it is by no means so rare as is generally supposed and as I had thought some years ago. At one time during the past winter, in Bellevue Hospital, I knew of six examples of it, and several also at the Blackwell's Island Hospital. When the auscultator has learned to distinguish it, he will not be long in finding it if he be in the way of seeing a moderate number of cases of disease of the heart. From what has now been said, it is obvious that an important point pertaining to this murmur is its discrimination from other murmurs. This point will first claim consideration.
In order to comprehend this murmur, it is essential to understand clearly when the mitral direct current of blood takes place. The opportunity of observing the movements of the heart exposed to view in a living animal conduces greatly to a clear understanding of this point. The mitral direct current is produced by the contraction of the auricles; now, when do the auricles contract? When the movements of the heart are observed, it is seen that the contraction of the auricles immediately precedes the contraction of the ventricles. So close is the connection between the contraction of the auricles and the contraction of the ventricles that the former appears to merge into the latter; there is no appreciable interval between the two, but the successive movements, although distinct, appear to be continuous. Moreover, it is evident to the eye and to the touch that the contractions of the auricles are not so feeble as some seem to suppose. The mitral direct current of blood, therefore, occurs just before the ventricular systole; it continues up to the ventricular systole, and must, of course, instantly cease when the ventricles contract. The contraction of the ventricles causing the first sound of the heart, it follows that the mitral direct current caused by the auricular contractions must take place just before the first sound; that it must continue to the first sound; and that it cannot continue an instant after the first sound.
The mitral direct murmur is produced by the mitral direct current of blood forced by the auricular contractions through a contracted or roughened mitral orifice. Hence, the facts just stated with regard to the current apply to the murmur. The murmur occurs just before the ventricular systole or the first sound of the heart; it continues up to the occurrence of the first sound and instantly ceases when the first sound is heard. It is not strictly correct to call this a diastolic murmur; it does not accompany the second or diastolic sound of the heart. The aortic regurgitant is the only true diastolic murmur. The mitral direct is a pre-systolic murmur; this name expresses its proper relation to the heart sounds, and it is the only murmur which does occur in that particular relation. The time of its occurrence as just explained, and as expressed by the term pre-systolic, is sufficient for its easy recognition when once it is fully comprehended. Although when this murmur is fully comprehended, and has been repeatedly verified, it is more readily recognized than either of the other murmurs, there is often at first considerable difficulty in determining its existence. Let me endeavor to point out the way in which it may be ascertained. I have already said that by those who overlook this murmur, it is generally confounded with the mitral systolic or regurgitant murmur. This is in consequence of its close connection with the first sound and because it is heard at and near the apex of the heart. Now it is evident that a mitral systolic murmur cannot commence before the ventricular systole. It is equally evident that the ventricular systole and the first sound of the heart are synchronous.
It is, therefore, an absurdity to suppose that a mitral systolic or regurgitant murmur can be pre-systolic in the time of its occurrence. This murmur must necessarily accompany and follow the first sound of the heart, as clinical observation has established. We have, then, only to determine that a murmur is pre-systolic, and that it does not accompany the second sound of the heart (i.e. there is an appreciable interval of time between the second sound and the murmur), to recognize it as a mitral direct murmur. Generally it is sufficiently easy, after a little practice, to perceive that the murmur precedes the sound, but if there be difficulty or doubt, there is a ready mode of rendering it apparent; this is by placing the finger on the carotid pulse. The carotid pulse is synchronous with the first sound of the heart, or, at least, so nearly synchronous that there is no appreciable interval of time between them. Placing, then, the finger on the carotid and listening to the murmur at the apex, the murmur is found to occur before the arterial impulse and to cease instantly when the latter is felt.
The mitral direct murmur is to be discriminated from an aortic regurgitant murmur. These two murmurs may be confounded at first, but after a little practice, the discrimination is easy. The aortic regurgitant murmur accompanies and follows the second sound of the heart; the mitral direct commences after the second sound. Generally, there is a distinctly appreciable interval of time between the second sound and the commencement of the murmur. The aortic regurgitant murmur may be prolonged nearly or quite through the long pause up to the first sound; but the intensity of the murmur diminishes with the prolongation, the murmur being insensibly lost before or when the first sound occurs. The mitral direct murmur, on the contrary, always continues up to the first sound, and instead of losing any of its intensities, it becomes more intense and appears to be abruptly arrested, in its greatest intensity, when the first sound occurs. This is a striking characteristic. The difference in the situation in which two murmurs respectively are heard with their maximum of intensity is another point in the discrimination. The aortic regurgitant murmur is generally heard at the base of the heart and is heard loudest a little below the base near the left margin of the sternum on a level with the third intercostal space. The mitral direct murmur is heard loudest at or a little within the apex, is generally confined within a circumscribed space, not propagated much without the apex and rarely to the base of the heart.
The quality of the mitral direct murmur is, in many cases, characteristic. In my work on diseases of the heart, I have said that this murmur is generally soft. My experience since that work was written has shown me that this statement is incorrect. The murmur is oftener rough than soft. The roughness is often peculiar. It is a blubbering sound resembling that produced by throwing the lips or the tongue into vibration with the breath in expiration. I suppose that the murmur is caused, in these cases, by the vibration of the mitral curtains, and that the vibration of the lips or tongue by the breath represents the mechanism of the murmur as well as imitates the character of the sound. At one time, I supposed this blubbering murmur denoted a particular lesion, viz. adhesion of the mitral curtains at their sides, forming that species of mitral contraction known as the buttonhole slit; but I have found this variety of murmur to occur without that lesion, and in fact, as will he seen presently, when no mitral lesion whatever exists.
A mitral direct murmur may, or may not, be associated with a mitral systolic murmur. Without having analyzed the numerous examples which I have recorded during the last few years, I should say that while the mitral systolic murmur is much more frequent in its occurrence than the mitral direct, the former, indeed, being the most common of all the murmurs, the mitral direct is observed quite as often without as with the mitral systolic. But the two frequently coexist, and then the demonstration of the existence of the mitral direct murmur may be made more striking than when it exists alone, provided, as is usually the case, this murmur is rough and the mitral systolic murmur is soft. Listening at or near the apex in a case presenting a blubbering mitral direct and a soft mitral systolic murmur, the former, of course, precedes the latter, and between the two occurs the first sound of the heart, the apex beat, and the carotid pulse. The first sound, the apex beat, or the carotid pulse will be found to mark the abrupt ending of the mitral direct and the beginning of the mitral systolic murmur. The different relations of the two murmurs to the first sound are distinctly perceived in such a case if the observer be prepared to perceive them by a clear comprehension of the subject. And when once the discrimination between the two murmurs has been fairly made, it becomes sufficiently easy; indeed, the mitral direct murmur is then more readily recognized than either of the other murmurs.
The existence of a mitral direct murmur has been theoretically denied on the ground that the auricular contractions are too weak to propel the current of blood with sufficient force to give rise to a sound. It is undoubtedly true that other things being equal, the intensity of a murmur is proportionate to the force of the current, and clinical observation shows that sometimes a murmur is not appreciable when the heart is acting feebly, but becomes distinct when the power of the heart's action is from any cause increased. But murmurs do, by no means, always require for the production a powerful action of the heart; on the contrary, loud murmurs are often found when the heart is acting very feebly. For example, I have reported a case in which an aortic direct murmur and an aortic regurgitant murmur were well marked in a patient an hour before death and the patient was dying from paralysis of the heart due to distension of the left ventricle. Venous murmurs in the neck are often notably loud when, assuredly, the force of the current of blood in these veins is vastly less than the current from the auricles to the ventricles. The feebleness of the current in this instance is shown by the slight pressure requisite to interrupt it and arrest the murmur. It requires, but little force of the expiratory current of air to throw the lips into vibration so as to produce a loud sound. Moreover, one has only to see and feel the contractions of the auricle, when the heart is exposed in a living animal (the heart's action being much weakened under these circumstances), to be convinced that the power of these contractions is not so small as some seem to imagine; the blood is driven into the ventricles with considerable force. It is hardly necessary to say, however, that a priori reasoning with regard to the existence or non-existence of physical signs is not admissible. Their existence is a matter to be determined by direct observation. Clinical observation shows that murmur docs occur at the precise time when the mitral direct current takes place as shown by observation of the movements of the heart exposed to view in a living animal. And clinical observation shows that this murmur is not always feeble, but on the contrary, is not infrequently notably loud.
So much for the reality of the mitral direct murmur and the means of discriminating it from other murmurs. It remains to consider another important practical point, viz. the pathological import of this murmur. As already stated, it is developed in connection with a contracted mitral orifice, and so far as my experience goes, especially in connection with contraction caused by adherence of the mitral curtains, forming the buttonhole slit, the murmur, then, being due, not to the passage of blood over a roughened surface, but to the vibration of the curtains. And the sound, as thus produced, is peculiar, resembling the sound which may be produced, in an analogous manner, by causing the lips to vibrate with an expiratory puff. The murmur, however, may be produced by the flowing of the current of blood over a roughened surface, without contraction of the aperture. This is undoubtedly rare. As a rule, the force of the mitral direct current is not sufficient to develop a murmur unless there is mitral contraction. Is this murmur ever produced without any mitral lesions? One would a priori suppose the answer to this question to be in the negative. Clinical observation, however, shows that the question is to be answered in the affirmative. I have met with two cases in which a well-marked mitral direct murmur existed, and after death, in one of the cases, no mitral lesions were found; in the other case, the lesion was insignificant. I will proceed to give an account of these cases, and then endeavor to explain the occurrence of the murmur.
In May 1860, I examined a patient, aged 56, who had had repeated attacks of palpitation, sense of suffocation, with expectoration of bloody mucus and a feeling of impending dissolution, but without pain, the paroxysms resembling angina, excepting the absence of pain. In the intervals between these attacks, he was free from palpitation, did not suffer from want of breath on active exercise, and considered himself in good health. He had never had rheumatism. On examination of the chest, the heart was found to be enlarged, the enlargement being evidently by hypertrophy. At the apex was a pre-systolic blubbering murmur, which I then supposed to be characteristic of the buttonhole contraction of the mitral orifice. At the base of the heart was an aortic regurgitant murmur, which was diffused over nearly the whole praecordia. There was no systolic murmur at the base or apex. Three days after this examination, the patient was attacked with another paroxysm and died in a few moments after the attack, sitting in his chair. The heart was enlarged, weighing 16½ oz., with the walls of the left ventricle measuring four-fifths of an inch. The aorta was atheromatous and dilated so as to render the valvular segments evidently insufficient. The mitral valve presented nothing abnormal, save a few small vegetations at the base of the curtains, as seen from the auricular aspect of the orifice.
In this case, it is assumed that the mitral direct murmur, which was loud and of the blubbering character, was not due to the minute vegetations which were found after death. There was no mitral contraction. The mitral valve was unimpaired so that the murmur could not have been due to mitral regurgitation.
In February 1861, I was requested to determine the murmur in a case at the Charity Hospital, New Orleans. I found an aortic direct and an aortic regurgitant murmur, both murmurs being well marked. There was also a distinct pre-systolic murmur within the apex, having the blubbering character. On examination after death, the aorta was dilated and roughened with atheroma and calcareous deposit. The aortic segments were contracted and evidently insufficient. The mitral curtains presented no lesions; the mitral orifice was neither contracted nor dilated, and the valve was evidently sufficient. The heart was considerably enlarged, weighing 17½ oz., and the walls of the left ventricle were an inch in thickness.
In the second, as in the first of the foregoing cases, it is evident that a mitral systolic murmur was not mistaken for a mitral direct murmur, for in both cases, the conditions for a mitral systolic murmur were not present. In both cases, the mitral direct murmur was loud and had that character of sound which I suppose to be due to vibration of the mitral curtains. In both cases, it will be observed that an aortic regurgitant murmur existed and aortic insufficiency was found to exist post mortem. How is the occurrence of the mitral direct murmur in these cases to be explained? I shall give an explanation which is to my mind satisfactory.
The explanation involves a point connected with the physiological action of the auricular valves. Experiments show that when the ventricles are filled with a liquid, the valvular curtains are floated away from the ventricular sides, approximating to each other and tending to closure of the auricular orifice. In fact, as first shown by Drs Baumgarten and Hamernik, of Germany, a forcible injection of liquid into the left ventricle through the auricular opening will cause a complete closure of this opening by the coaptation of the mitral curtains, so that, these authors contend that, the natural closure of the auricular orifices is effected, not by contraction of the ventricles, but by the forcible current of blood propelled into the ventricles by the auricles. However this may be, that the mitral curtains are floated out and brought into apposition to each other by simply distending the ventricular cavity with liquid is a fact sufficiently established and easily verified. Now, in cases of considerable aortic insufficiency, the left ventricle is rapidly filled with blood flowing back from the aorta as well as from the auricle, before the auricular contraction takes place. The distension of the ventricle is such that the mitral curtains are brought into coaptation, and when the auricular contraction takes place, the mitral direct current passing between the curtains throws them into vibration and gives rise to the characteristic blubbering murmur. The physical condition is in effect analogous to contraction of the mitral orifice from an adhesion of the curtains at their sides, the latter condition, as clinical observation abundantly proves, giving rise to a mitral direct murmur of a similar character.
A mitral direct murmur, then, may exist without mitral contraction and without any mitral lesions, provided there be aortic lesions involving considerable aortic regurgitation. This murmur by no means accompanies aortic regurgitant lesions as a rule; we meet with an aortic regurgitant murmur frequently when not accompanied by the mitral direct murmur. The circumstances which may be required to develop, functionally, the latter murmur, in addition to the amount of aortic regurgitation, remain to be ascertained. Probably, enlargement of the left ventricle is one condition. The practical conclusion to be drawn from the two cases which have been given is that a mitral direct murmur in a case presenting an aortic regurgitant murmur and cardiac enlargement is not a positive proof of the existence of mitral contraction or of any mitral lesions. The coexistence of a murmur denoting mitral regurgitation, in such a case, should be considered as rendering it probable that the mitral direct murmur is due to contraction or other lesions, and not functional.
Dr. Gairdner, in a recent article already referred to, proposes a change of name for the mitral direct murmur. ·He proposes to call it an auricular systolic murmur. Inasmuch as the murmur is produced by the systole of the left auricle, this name is significant. And the usual name is open to this criticism, viz. it is not produced by the whole of the mitral direct current, but only that part of the current which is caused by the contraction or systole of the auricle. From the situation of the auricles as regards the ventricles, the former being placed above the latter, and the free communication by means of the auriculo-ventricular openings, the blood must begin to flow from the auricles into the ventricles the instant the ventricular contractions cease. During the first part of the long pause or interval of silence, i.e. the period after the second sound and before the subsequent first sound of the heart, the blood flows from the auricles into the ventricles simply in obedience to gravitation. It is not ascertained that this part of the current ever gives rise to a murmur. If it does, the murmur would follow immediately the second sound or when an aortic regurgitant murmur occurs. I have conjectured that such a mitral direct murmur may occur, and that it is confounded with an aortic regurgitant murmur. This conjecture is based on cases in which an apparent aortic regurgitant murmur existed and the aortic valves seemed to be nearly or quite sufficient on examination after death. However this may be, the mitral direct current giving rise to the murmur which has been considered in this article is not the current which immediately follows the second sound and is due to gravitation alone, but it is the current immediately preceding the ventricular systole and due to the systole of the auricle. Hence, as it seems to me, the name proposed by Dr. Gairdner, being more specific and accurate, is to be preferred to that in common use.