COLUMBIA LIBRARIES OFFSITE HEALTH SCIENCES STANDARD HX641 32480 nCooi .C54 Lectures on diseases RECAP ^^ V Columbia Hmu^rBtlg tn % (Ettu 0f N^m fork QI0IU5F 0f pijgHtnanH unh ^ttrg? ona .^>rs.:.Cx'X^..Q.vm1h.e.r. LECTURES ON DISEASES OF THE HEART DELIVERED AT THE College of Physicians and Surgeons, New York BY ALONZO CLARK, M.D., LL.D. Emeritus Professor of the Principles a7td Practice of Medicine, Etc. BERMINGHAM & COMPANY 28 Union Square. East NEW YORK 1884 20 King William Street, Stranq LONDON Copyright. 1884, by Bermingham & Co. He lo 8 \ C -5r4- CONTENTS. LECTURE I. PAGE Heart Sounds • 9 LECTURE IL Pericarditis • 3^ LECTURE in. Endocarditis <> « 96 LECTURE IV. Myocarditis 116 LECTURE V. Hypertrophy of the Heart.' 122 LECTURE VL Dilatation of the Heart 132 LECTURE VIL Fatty Degeneration of the Heart 142 LECTURE VIII. Rupture of the Heart. 150 LECTURE IX. Fibrous Degeneration of the Heart 156 6 CONTENTS* LECTURE X. PACK Heart Clots.., *** *...* I59 LECTURE XL Valvular Disease • 163 LECTURE XIL Valvular Disease {continued) 179 LECTURE XIIL Prognosis and Treatment of Valvular Disease 204 LECTURE XIV. Angina Pectoris 216 LECTURE XV. Deformities of the Heart 222 LECTURE XVL Functional Diseases of the Heart 235 LECTURE XVn. The Effects of Certain Drugs on the Heart 242 PREFACE. This book contains the substance of my lectures lipoil " Diseases of the Heart," delivered at the College of Physicians and Surgeons for many years past, together with reports of cases collected from the literature of the subject, and from personal observation. The basis of the work being a course of didactic lectures, the style is colloquial, and though it may not possess that rhetorical rounding which is the offspring of elaborate revision, it is given to the profession as an exposition of the views which I have inculcated during the many years in which I have been a teacher. New York, March 21, 1884. DISEASES OF THE HEART. LECTURE I. HEART SOUNDS I WILL first make a few preliminary remarks upon what is essential to an understanding of endocarditis and val- vular diseases of the heart. Here you observe a heart, a very large one, laid open. You observe that the inner surface of this cavity is lined by a smooth, shining membrane. This is called the en- docardium, a serous membrane somewhat analogous to that which lies upon the outside of the heart. This mem- brane lines all these muscles, protecting the muscular structure entirely from contact with the blood. This same lining membrane is to be found in every cavity of the heart, and it is continuous in a certain way from one to the other. Now observe how a valve is made. Here is the semi- lunar valve of the aorta. If you will examine this you will see that the tissue is absolutely continuous from the wall of the ventricle on to this valve. Follow it on a lit- tle further ; it doubles down upon this valve, and then from there is reflected off on to the base of the aorta. Well, a valve of the heart is made, then, of a duplication of the lining membrane, of a duplication of the endocar- dium. The valve is closed when it lies against the aorta, to HEART SOUNDS* and you can then hardly see how it is constructed ; but open it and you see it is the same Hning membrane of the ventricle which doubles down to the bottom of this valve and then passes off, without being broken, into the great vessel. The mitral valve is made in the same way, but the lin- ing membrane of the ventricle goes down upon the pos- terior face of the mitral valve, doubles upon itself, and goes back into the auricle. To this valve are attached a considerable number of little cords that go down into the ventricle and are there attached to what are called the fleshy columns. The endocardium is no less continuous for that reason. Indeed, it doubles upon these cords, and covers them. Each valve, in each part of the heart, is made in this same way, but there is, however, a little more to each of these valves. There is a fibrous struct- ure in the middle of them — you may say a skeleton ; something like the frame of a house before there are any boards or plaster put upon it. The fibrous tissue of the valve lies between two folds of membrane. Now, it hap- pens that in endocarditis the aortic or the pulmonary valve, is most likely to show the results of inflammatory action. But the point I want to impress upon you is the way the blood circulates through the heart, and what the heart does in the course of the circulation of the blood through it. Suppose the blood is coming in from the lung. In the period of rest the left auricle is being distended by the blood coming in from the lung. The contraction of the heart begins in the auricle, and almost instantly spreads to the ventricle. The result of this little contraction of the auricle before the ventricle begins to contract is to send a little more blood into the ventricle, or perhaps to send a portion of it backward, because there is no valve HEART SOUNDS. 11 which Will prevent its going either way. Then the left ventricle contracts. What becomes of the blood ? It goes into the aorta, and if there is anything to obstruct it, it may make a noise, which is not normal, and which is known as a bruit or murmur. Then, when you have a murmur produced at the base of the heart when the ven- tricle contracts it is produced by an obstruction — it may be a narrowing of the vessel at the valves. Now, what else takes place when the ventricle contracts ? If there is any way for the blood to get out except the normal it will take that, as well as its natural way. Suppose the mitral valve is insufficient ; suppose it be diseased in such away that it cannot close perfectly ; what is there to prevent the blood, when the ventricle contracts, going back over the very track it came ? Nothing in the world. Well, then, when this mitral valve is insufficient, and you get a mur- mur from it, it will be when the ventricle contracts : this is regurgitation. When in systole, or contraction of the ventricle, there is a murmur at the aortic opening, it is due to obstruction. Now, suppose this aortic valve to be so far diseased, so far narrowed and shortened, that the three different por- tions of the valve cannot meet in the miiddle of the artery, and stop the blood going back ; there would be a murmur then. And when? Why, after the first sound of the heart has gone by, after the contraction of the ventricle — in the period of rest, or in the place of the second sound. A murmur, then, heard at the base of the heart in the place of the second sound, implies regurgitation ; a mur- mur heard during the contraction of the heart implies ob- struction. You may have both in the same person, at the same time. Again, if there is vegetation, if there is un- natural thickening of the mitral valve, when the blood passes from the auricle into the ventricle during the period of repose, there may be a murmur. It is almost always a 12 HEART SOUNDS. very faint murmur, and Dr. Williams described it, a good many years ago, as being like the sound produced by breathing the word awe — a very soft blowing murmur. That is in the period of rest ; it has been called presysto- lic. I have no objection to the name ; it is before the systole. Dr. Flint {Am. Jour. Med. Set., April, 1882,) recognizes two very distinct tones in the presytolic murmur : one soft blowing, compared by Williams, senior, to sound produced by the breathed word awe; the other rough, resembling the sound produced by blowing over a piece of paper, one end of which is attached to the lower lip. He recognizes with others the fact that the soft sound is but rarely heard, while the rough sound is not very uncommon. He thinks it is produced by vibrations of the curtain of the mitral valve caused by the passage of blood from the auricle into the ventricle. "A rough presystolic murmur," he says, " exceptionally is produced when there is no mitral lesion, aortic regurgitation existing whenever the murmur is thus produced." He says that Fauvel recognized the rough murmur in 1843, ^^^ called it bruit de rape, and established its connection with the mitral obstructive lesion. Then you may have two murmurs at each one of these valvular openings ; in which case it is obstruction in the one instance and regurgitation in the other. Now, to satisfy yourself whether it is obstructive or regurgitative, you have only to remember the course of the blood. From the auricle it passes into the ventricle during the period of rest ; then the ventricle contracts and it passes over these valves into the aorta, or if the valves are diseased the blood is regurgitated. Then, too, it sometimes happens, as I shall explain to you further on, that these valves are subjected to a cer- tain amount of inflammatory action when endocarditis occurs, and their action is disordered. The mitral valve, HEART SOUNDS. 1 3 we know, is composed of fleshy columns, which are com- posed of fibres that are continuous with those in the walls of the heart. Now, if these be diseased, one or more of them, or a part of one may become contracted and leave an opening in the mitral valve. This fact shows that regurgitation may take place without disease of the valves, that is, without deforming disease of the valves. As the blood comes from the ventricles it is forced over the semilunar valves, which lie smoothly up against the aorta, presenting no obstruction to the outgo of the blood. If they are rough, thickened, contracted, then they will present an obstacle to the course of the blood, and there will be produced a murmur during the contraction of the heart, that is, during systole — the time when you feel the impulse of the heart against the ear when it is applied to the chest. Now, that is easily remembered, I think ; the murmur in systole, the murmur in the contraction of the ventricle, heard over that part of the chest which corre- sponds to the aorta, an aortic obstruction. When the blood reaches the aorta, the aorta dilates, and on account of the many little elastic fibres which it contains it has a disposition at once to contract ; and in contracting it of course starts the current backward toward the heart, which instantly closes these valves and thus prevents its return. But if these valves have become so thickened, so hard and inelastic that they will not close, a portion of the blood is sent back into the ventricle, which has to do its work over. This produces a murmur which occurs during the period of repose or in the place of the second sound. This constitutes aortic regurgitation. We often have obstruction and regurgitation in the same person, so that we will have a " whewing" sound during contraction, which is repeated during diastole of the ventricle. It has come to be the fashion of late to use the terms " direct" and " indirect." I do not think the terms nearly as good 14 HEART SOUNDS. as obstruction and regurgitation, for these are descriptive, while only " direct" can be regarded as descriptive in the other choice of terms. Then the blood passes on in the general circulation, and comes back in the veins to the other side of the heart, to the right auricle. The right auricle in turn contracts after it is full, and sends its blood into the right ventricle, which, being connected with the left ventricle by the septum, is really a part of the same organ, and liable to contract at the same time ; and the right and left ventri- cles then do contract at the same instant, and a sound produced by the passage of blood into the pulmonary artery occurs in systole. You observe that the pul- monary artery has valves corresponding with those of the aorta, and they work in the same way. They fall up against the artery, and allow the blood to flow over them easily and freely. But these, too, are sometimes found to be diseased. The valves of the right side of the heart, I say, are sometimes found to be diseased, and here is as good a place to state the fact as any, that in persons who have disease of the right side, if it is not due to laceration or breaking of the tendinous cords, you may pretty rea- sonably infer that the disease belonged to the period before birth. The right side of the heart is more subject than the left to disease in utero. The left side of the heart becomes diseased after birth. If you can find a murmur, then, that belongs to the pulmonary valves, you will be pretty sure to find it in a child, and it will be pretty safe to infer that there was endocarditis in that child before it was born. It is not a common occurrence, and yet it has happened a few times in my experience. Then the same law applies to the current of blood and to the sound that will be produced by disease of the valves of the right side as on the left. There are two valves here, the tricuspid, which guard the opening be- HEART SOUNDS. 1 5 tween the auricle and ventricle, and act in the same way as the mitral valve on the left side, and the pulmonary- valve. Now, I will repeat the formula by which you can recog- nize disease at different points of the heart. Remember that these fleshy columns are connected with the heart at a distance of from one inch to an inch and a half above its apex ; these tendinous cords run into the heart, and may be regarded as conducting media, and the fleshy columns also may be regarded as conducting media. The point where, physiologically, in audition, you can get nearest to the heart, is not at the apex exactly, but about an inch above. There you will be more likely to hear sounds produced in the mitral valve than at any other part of the chest ; and when I say " heard at the apex," I mean at the apex, or an inch above. When, then, you have a murmur during the time the ventricle is being filled, you ascertain, by listening at different points, where it is most distinct. If it is most distinct at or near the apex in systole, it is a murmur of regurgitation at the mitral valve ; if, on the contrary, it is heard in the period of repose, the blood is flowing from the auricle into the ventricle, and that will be an obstructive sound in the mitral. The mitral is roughened, and throws the blood or itself into sonorous vibrations, as the blood flows over it ; that, however, is almost always a very feeble sound. As I said before. Dr. Williams described it by breathing the word " awe,'' opening the throat well and breathing a little loud. A murmur heard most distinctly on the third rib, at the sternum, and heard in systole, must be obstruction at the aortic valve. Then, if it is repeated immediately afterward, in the interval, you can hardly appreciate it, and yet you do appreciate that there are two sounds — the latter is regurgitation ; the valve acts insufificiently. l6 HEART SOUNDS. it cannot perform its office, and thus the murmurs are produced. Every little while you get two murmurs. I have heard four in the same person, two produced at the aortic valve, two at the mitral. Now, the same law applies to the right side of the heart. You listen to the right side of the heart, at the lower part of the precordial region on the right side. I do not say the lower part of the sternum extends below the heart region ; but on the sternum at the fifth rib, and outside the sternum a little, on the same level, you will get a sound from the right heart more distinctly than anywhere else. If, then, you get a murmur in that region, heard most distinctly in contraction of the heart, in systole, that would be regurgitation, at the tricuspid valve. If, on the contrary, you get a myrmur which you are not quite sat- isfied is aortic, and it is a little to the left of the sternum, you may, perhaps, conjecture tjjat it belongs to the pulmonary artery. The pulmonary artery is given off a little further to the left than the aorta, and you listen for the aortic murmurs on the middle of the sternum and a little to the right ; for the pulmonary murmurs on the left edge of the sternum and a little to the left of the sternum. If you get a murmur there in systole it is due to obstruc- tion at the pulmonary valve. If it is repeated, it is then regurgitation at the same valve, and is heard most distinctly at the base of the heart. But if it is a tricuspid murmur you will hear it most distinctly over the right side of the heart, at the right edge of the sternum ; I never have heard a direct or obstructive murmur at this point. Indeed, a good many .years ago Dr. King thought he demonstrated, and probably he did, that this particular part of the heart, the opening of the tricuspid valve, has considerable power of dilatation without injury, and when the veins are overcrowded with blood, surcharging the left ventricle, he claims that the right ventricle has the HEART SOUNDS. I7 power of sending it back into the veins again through the tricuspid opening and without a murmur. I can easily comprehend that it may be so. It is what he called the safety-valve arrangement. The right ventricle being over- distended the right auriculo-ventricular opening would be dilated also, and a part of the blood can be thrown back into the veins of the general system without being compelled to go forward into the arteries that lead to the lungs. With reference to the tones of these murmurs. You hear them in different stages of cardiac disease ; mildly when the valves begin to be deteriorated ; more strongly when the deformity has become considerable. And then again, perhaps not at all after the disease has continued for a length of time, and the heart has become weakened by it. Almost every person who has cardiac disease which finally terminates fatally reaches a period, before death, when the murmur cannot be heard, and the simple reason is that the heart cannot contract upon its contents with sufficient force to make the blood run swiftly enough to cause a murmur. It is probable that these murmurs are made in the solid tissue and not in the blood itself. The vibrations that produce the murmur are probably in these deformed valves. You have a great many terms by which to designate these murmurs, according to their tone. The French have used terms which represent a filing sound, a rasping sound, a sawing sound, which, of course, are harsh, and given to distinguish the harsh sounds from those which are soft and blowing. But it is not necessary for you to learn these terms. The coarse sounds are almost always produced by deformity or defect of the valves. The blowing sounds are often produced by the same thing, but they are also produced under circumstances in which the valves are not diseased ; when, for example, the blood becomes watery and thin, by a law which I cannot j8 HEART SOUNDS. I ^ explain to you, the blood makes a noise in going over the aortic valves. It is the anaemic sound ; and, therefore, if you hear a, blowing sound at the aortic opening, as if it were obstructive, your next business is to look in the patient's face and see if she is anaemic — for anaemia occurs more frequently in women than in men. If the face is pale and has a chlorotic look, you will be very likely to get a soft murmur— a blowing murmur at the aortic open- ing, and it will not authorize you to infer that there is any disease of the aortic valves under such circumstances. Dr. G. W. Balfour* has lately published an article enti- tled "Arguments in Favor of the Theory of Dilatation of the Heart as the Cause of Cardiac Haemic Murmurs and of the Appendix Auriculi Sinistri being the Primary Seat of this Murmur." So far as I can judge from the analysis of the abstract which I have seen (for I have not read the whole paper as published in the Brit. Med. Jour., Aug. 26, 1882), it is arguments, not demonstration. He does not even adduce convincing proofs from auscultation. The idea has met with criticism already. We are not, then, converted wholly from the old doctrine that the haemic or chlorotic murmur is produced at the valves of the heart. That in the same state of the system, the pressure of the stethescope on a vein, the jugular, for example, will pror duce a continuous murmur {bruit de diable) would seem to show that, in chlorosis, the blood changes have given to that fluid the capacity of producing sound, from causes that do not operate in that way in health. These sounds are often called anaemic, but immediately after a large loss of blood they do not occur, but they are found, if at all, after the vessels are replenished by absorption of fluid, and its constitution thereby greatly changed. This has * Medical Record, Nov. i8, 1882, p. 572, whiqh sep, apd N- ¥• Med, yi(7«n, Dec, 1882, p. 657. HEART SOUNDS. I9 been denominated hydraemia, and the name is not an improper one. But the term chlorosis is appHed almost exclusively to a condition that is not preceded by loss of blood, but by bad assimilation, and ends in great reduction of the nourishing power of the blood ; in paleness and a puffy condition o.f the skin, with moderate oedema and loss of force. This is the disease in which we most frequently hear the haemic anaemic sound. There is another thing connected with thin blood which may perhaps help you to distinguish the sounds that are produced by deformity of the valves and those that occur when the valves are sound. Jan. 21, 1883, a boy from M , 8 years of age, was brought to me by his parents. He had been very much reduced by disease, so that he was very pale and thin and had aortic systolic murmurs, and his physician found serious heart disease. From his anaemic state he had rapidly improved, so that now he looked healthy and was strong, appetite good, almost voracious, and digestion good. Examining him to-day there is no murmur, the heart is of proper size for a boy of his age. The inference is conclusive that the late systolic aortic murmur was a blood (haematic) murmur, which his im- proved health has removed. In most of these persons in whom anaemic murmurs occur there will be heard, through the stethoscope applied over the jugular vein in the neck, a continuous humming noise. They call it bruit de la toupie, which a friend of mine has interpreted with a little liberty, ''devil of a noise." This briiit de la toiipie is not the work of the devil. The French have a little toy which children whirl around, and as it goes around, a spring works on a wheel of cogs and makes a repetition of clicks. That is the devil that this is compared with — bruit de la toupie. This sound is not connected with disease of the heart, but as it so frequently occurs in anaemic persons it is worth while to allude to it in this connection. The 20 V HEART SOUNDS. harsh, rasping sound is almost always produced by sorae defect of the valves ; the soft, blowing murmur may be so produced, but it is occasionally found in persons whose hearts are sound enough, but whose blood is diseased or in a watery condition. I do not think there is any practical use in making any other distinctions between the soft and the harsh, or the blowing and the rough murmur. Dr. E. Hyler Graves* concludes: i. The presence of murmurs does not necessarily indicate the existence of incurable lesions, or their absence that such lesions are not present ; but other symptoms must be looked to for a correct diagnosis. 2. The persystolic murmur of mitral stenosis may disappear and the lesion remain. Mitral regurgitant, when due to simple relaxation of the heart's muscles and dilatation of its cavities and orifices, as in chlorosis and fever, in most cases completely disappears. 3. Tricuspid regurgitation is occasionally temporary, due to bronchitis, etc. 4. Aortic systolic murmurs, due to permanent lesion, may undergo changes in intensity but never completely disappear. 5. Aortic diastolic murmurs in rare cases have been known to disappear. The sys- tolic aortic murmur in these cases is always present and is persistent. 6. The pulmonary systolic is permanent when due to organic lesion, but is non-organic ; may dis- appear temporarily or permanently. There is another thing that I must call your attention to before discussing endocarditis itself. At the 83rd meeting of the Medical and Chirurgical Faculty of Maryland, April, i88i,t Dr. John S. Lynch communicated a new plan in the differential diagnosis of cardiac and pericardial murmurs. He said, ^' Whenever the friction murmur is produced at or near the apex of the * Med. Rec, Sep. 29, 1883. \ Am. Jour, of Med, Sci.j Oct., 1882, tiEART SOUNDS. it heart, if we cause the patient gradually and slowly, but en- tirely to inflate the lungs, we will perceive that the friction murmur becomes gradually progressively more intense until the act of insufflation is complete. Now make the patient * hold his breath ' while the lungs are in this state, and the murmur will be steadily maintained at its maxi- mum intensity; cause him then to expire in a like slow and gradual manner," and the reverse will be observed. He thinks the sound at the apex is the only one that presents any difficulty in diagnosis. The heart itself has two sounds. They are denominated first and second, and it will interest you to know what is the cause of these two sounds ; and, perhaps, as great di- versity of opinion has been expressed in regard to this, it may be of some little interest to you to know which opin- ion I have chosen. As a consequence of the arrangement of the muscular fibres of the heart, as the heart contracts, all these bun- dles of fibres contract at the same time, and one rubs against another. It is not exactly a fiddle-string opera- tion, and yet it is not without analogy to it. These fibres cannot rub upon one another actively, as they do when the heart contracts, without producing some sound, and this first sound continues during the contraction of the heart. It begins with the beginning and ends with the end of that contraction — that is, of the ventricles. The auricles are placed a little out of hearing, so that you can- not know what is going on in them by audition. You can imitate the sound very closely by placing the stetho- scope upon the ball of the thumb and opening the thumb. You will hear a sound exactly like that which is produced by the first sound of the heart. Another very good illus- tration of this sound may be had by placing the arm against something that is firm and extending and con- tracting it, and listening to the action of the muscles. ±2 HEART SOUNDS. It has been said that the first sound is produced by the tension of the mitral valves, in consequence of the sudden jerk made upon them by their muscular columns. I do not know that that does not enter into the first sound and make a part of it ; I do not know that it does. It has been said, again, that the first sound is produced by the rush of blood from the auricle into the ventricle (?). I do not know but that this aids in the pro'duction of the first sound, and I do not know that it does. The current is easy, the flow is at a pretty good rate, to be sure, and I should not be surprised if concussion against the empty walls of the ventricles would produce some effect of that kind ; and yet I do not know it. I think when you have tried these little experiments I have spoken to you of, and then listen to the heart sounds you will be pretty well satisfied that the chief element in it is the contraction of the muscles, and the rubbing of these cross-fibres one against another. They are sepa- rated, to be sure, by a little layer of connective tissue, but even that is put upon the stretch by the action of these muscles that are working at right-angular contrac- tion. The first sound, therefore, is confined entirely to the systole, to the contraction. The second sound there are no debates about ; experiments have been performed that explain that perfectly. A number of physicians in London tortured some honest old asses and worn-out horses, by opening the chest and having little hooks that were sharp enough to penetrate the tissue, laying the hook- handle along the course of the aorta and penetrating it, then carrying the hook forward and getting it over one of the folds of the semilunar valve, and drawing it back up to the wall of the artery. It is an experiment that can be pretty easily done. The result of the experiment was a cessation of the second sound. Then by depressing the handle and raising the point of this hook the valve would Heart sounds. . ^5 be let loose, and be at liberty to play again, and then the second sound was reproduced. They repeated the ex- periment a great many times, and in a great variety of ways. A Philadelphia committee of doctors repeated it with the same result, so that we have the fact pretty well established, that the second sound, which you will recog- nize as instantaneous as a click, results from the falling together of these three segments of the valve in the cen- tre of the aorta. When the second sound of the heart is unusually loud, it has been the habit of late to say that it is accentuated. This word may not be the best that could have been chosen, but it appears to have the sanction of usage, and that entitles it to the place it occupies. This intensified second sound may be noticed on either side of the heart, that is, it may be seated either in the pulmonary or in the aortic valve. In either, two conditions of the organ are neces- sary. It must retain a good deal of its natural strength, and the valves referred to must be sound, or if not entirely free from disease, not diseased in a way to impair their efficiency. Another condition is equally necessary — that the flow of blood from the half of the heart in which it is produced be resisted. The familiar second sound in the pulmonary artery, when there is stenosis of the mitral is an example. Any obstruction in the pulmonary circulation, the heart retaining its strength, the valve its integrity, and the quantity of blood in the system undiminished, will pro- duce it in the same way. Pneumonia produces it unless the heart is feeble. Phthisis does not, because the vol- ume of blood in the body is diminished, as is also the strength of the heart. Dr. Begbie has found that sacculated aneurism and dilatation, or true aneurism of the aorta, produce, with a good deal of constancy, exaggerated second sound at the aortic opening. The probable explanation of this is that 24 HEART SOUNDS. as neither of these changes occurs spontaneously without atheromatous deposit in the vessel, that while the strength of its walls is diminished, their distensibility is also decreased. You would naturally expect, if these aortic valves were inefficient, and did not guard the opening, that there would be no second sound produced. But call to mind the fact that I just now stated to you that the two hearts beat at the same time, and it is almost never found to be the case that the pulmonary valves and the aortic valves are diseased in the same person. You have, then, the pulmonary valves to give you the second sound. The aortic valves may not participate in it, may not fall to- gether at all ; they may be too short and too inflexible. The cause, then, of the two sounds of the heart you can easily carry in mind. The reflux of the blood from the aorta in its attempt to get back into the ventricles, closes, as I told you, these valves; they close with a click, and that is all there is of the second sound. The sphygmograph is now pretty well known, and its indications pretty well understood. It will indicate aor- tic obstruction by the sloping rise of its tracing ; aortic regurgitation by the rapid fall ; irregular action of the heart by its writing down the small and varying action with more correctness than the finger on the artery can possibly attain ; and yet its diagnostic value is not great, for almost all that it teaches that is important can be learned by other and shorter methods. But now there is a compound sphygmograph, by which the beating of the pulse of any artery, and the beating of the heart are recorded on the same paper, one tracing over the other with a time index at the bottom. It shows how much the pulse wave in any artery chosen for the experiment is delayed, after the heart has contracted, or on the other hand, if the pulse wave reaches the artery HEART SOUNDS. 25 under examination in less time than the normal, how much it is accelerated. As each contraction of the heart and the pulse produced by it is traced one above the other, it is easy to compare them, and to learn the time difference between them. But that this difference may be useful, the natural or normal difference between the heart beat and the pulse beat in the several arteries must be known. This basis fact is apparently ascertained. Dr. A. T. Keyt announces that the time consumed by the pulse wave in passing to the carotid artery is -^ of a second ; to the temporal in front of the auditory meatus, ■^ o{ 2i second ; to the radial, ^ ; to the femoral, -I-; to the artery on the upper surface of the foot, ^. These are averages. If they are confirmed they make an interesting demonstration of the rate at which the blood travels in the vessels. It is» claimed that dilatable aneurism, stiff aortic valves and mitral regurgitation delay the wave, and make the time longer; while aortic regurgitation and rigid arteries make it shorter. Dr. A. B. Isham of Cin- cinnati has pubhshed a paper on the application of this instrument to diagnosis {Am. Journ, of Med. Science^ July, 1882,) in which he gives a considerable number of cardiac and arterial tracings, one over the other. The greatest difference that he has recorded is ||- of a second between the heart and the right subclavian, while in health the time should be -f^. This is certainly a marked re- tardation — one that could be recognized but not measured without the aid of the instrument. It occurred in a per- son who had aneurism of the aorta and mitral regurgita- tion. In a case of mitral regurgitation the pulse in the carotid (right?) was delayed \ to \y instead of ^ of a second. But these are large delays. In a case in which the aortic opening was greatly obstructed, the delay in the carotid (right?) was J of a second, while the natural delay is-^oidi second. This case is narrated by Dr. A. T« ^6 ittEARt SOUNDS. Keyt, in the Cincinnati Clinic, April 19, 1879, ^^^ ^^ the Medical Record, June 4, 1881. I have been sufficiently interested in the use of this instrument to try to obtain one, but it must be imported, and my confidence in its prac- tical value has not yet overcome this trifling obstacle ; for so far its teachings are more confirmatory of what can be learned by other means, than an instrument communicat- ing new information. But as the shrub may grow into a tree, the moderate beginning of the cardiac sphygmo- graph may have a large and expanded growth. Heart Scanning. — Dr. Samuel W. Francis says that the normal beat of the healthy heart is iambic ^^ — ; that when it is trochaic — ^^, pyrrhic -^ -~- or spondaic , these measures indicate disease. He also reports a case in which the pulse was only 29 in the minute, and the beat dactylic — ^ ^-^, a long and two short being well marked. The patient was a lady sixty years of age, who recovered under diffusive stimulants, and counter-irrita- tion. {The Medical Record, Feb. 24, 1883.) Dr. Henry Cook has quoted three cases published by Dr. Hyde Salter, and added three of his own, in which the rhythm of the heart was lost in a double beat, one following the other so quickly, that there was hardly time enough between them to perceive that there were two — the end of one instantly followed by the beginning of the other. The second systole was followed by a second sound, but the first was not. Thus, instead of In these cases the first of the double beat sent a pulse to the wrist, the other did not; but in one of Dr. Salter's cases this was changed. At the first examination it was the first of the two beats that produced the radial pulse ; HEART SOUNDS. 2^ at another, he says " the second beat of each couple was the strongest, not the first as formerly, and the only one reaching the wrist, though the first and feebler was plainly visible in the carotids." In four of these six cases it was noticed that the time occupied by this double beat and the pause following, was just double that required for a single beat and pause. For example, if, while the heart had a single beat and pause, the pulses were io6, when the double beats occurred it would be 53. Both observers had the opportunity of listening to the heart at the moment the change from double to single beat occurred, and Dr. Cook witnessed the change from single to double. The change in each direction was not attended with the slightest disturbance ; indeed of one patient it is said he did not know that any change had occurred. In a man who had aortic obstruction, and both tricuspid and mitral regurgitation, Dr. Cook says, " each impulse was accompanied with the systolic bruit." He does say that there was disease of the pulmonary valve, and no post-mortem examination is reported. These double beats were strong, each a good deal stronger than the single beat, though not always of equal strength. Neither of these gentlemen entertained any doubt that it was a double action of the left ventricle, and Dr. Cook devotes considerable space to conjectural explanations of the mode in which it was effected, none of which seem to himself wholly satisfactory. Was it not that the beat of the right heart followed that of the left when the radial pulse was produced by the first contrac- tion, and opposite when the pulse attended the second? But can the action of the two hearts be partly separated in that way? Some recent experiments referred to else- where seem to prove that it can be, in animals, and to a 28 HEART SOUNDS. much greater extent than is necessary to explain Drg. Salter and Cook's cases. But I have myself, not fre- quently, to be sure, but two or three times recognized a double second sound, one following the other quickly, but each perfectly distinct, and have called the attention of persons who were with me to the fact as showing a lack of strict coincidence in the action of the two hearts. Dr. Cook has given sphygmographic tracings of his cases, which appear to be conclusive on this point. If the two beats were both left ventricle contractions, when the trac- ings reached the highest points, they must be held there during all the time of the second beat of the couple, with perhaps a downward notch between the two. But there is nothing of the sort. The descending line pays no at- tention to the second beat, but descends at the acutest of angles, greatly more acute than when the tracing is of the normal and regular beats. The only facts that seem inconsistent with this expla- nation are, first, the statement that Dr. Salter noticed a pulse in the carotids when it did not reach the radial artery. But may not a full wave in the heart give a pulse to the aorta and pulmonary artery that would extend to the carotids ? The two ventricles so commonly contract at the same instant that observations are yet to be made which will enable us to answer this question positively. But the affirmative answer seems to me probable. Second,. Dr. Cook says that in the case in which all the valves were diseased except the pulmonary *' There were now two impulse beats, then a second sound, and then a long pause, and each impulse was accompanied with a systolic bruit." If this statement is strictly correct, there must have been disease of the pulmonary valve also. At least it is easier to suppose this than to admit that a ventricle just emptied of blood could empty itself again on the in- stant, without time to get a new supply, and further, HEART SOUNDS. 29 with no power to make a pulse. — New York Medical Ab- stract, Feb., 1882. Cardiac Irregularities. — Dr. Lukjanow, not long ago, tried the effect of closing one, and then the other of the coronary arteries of the heart ; and asphyxia on rabbits and dogs. The function^-l connection of the different parts of the heart was interrupted by the closure of one coron- ary artery. A difference in the number of contractions of the auricles and ventricles was easily produced, and almost as easily a difference between the two auricles. '' Asyn- chronism is produced in the auricles much more readily than in the ventricles." The closure of one coronary is found to influence, first, the ventricle on the same side ; then the other ventricle, and lastly the auricles." The car- diac muscle may contract, he says, in paristalsis, or in anti-peristalsis. Sudden asphyxia especially effects some- times one, sometimes the other side of the heart. He attributes these phenomena to '' the effect of sudden ischaemia, and to the retention in the tissues of the products of such action as may occur." — Am. Jour, of Med. Sci., Apr., 1882. If these experiments can be relied on, asynchronism can be produced by local anaemia and by asphyxia, and if by these causes in all probability by others not yet under- stood. There is no chance closure of either coronary artery in either of these patients, but the circulation may have been modified by atheromatous or calcareous de- posits in one of them, or, as is most probable the asyn- chronism came from some unexplained condition of the nerves of the heart. As to these heart nerves Dr. E. P. Hurd {The Medical Record, Oct. 28, 1883,) writing of the Physiology of the Jleart, says the cardiac innervation comprehends certain intra-cardiac ganglia, extra-cardiac ganglia and nerves derived from the sympathetic and cerebro-spinal system. 30 HEART SOUNDS. Intra-cardiac Ganglia. — These are in the walls of the heart, and regulate the rhythmical working of the cardiac muscle. This is a property of the myocardium itself also. The ganglia of Remak are placed at the point where the sympathetic and pneumogastric nerves enter the heart, whose terminal filaments are lost in these ganglia. They occupy thesinus of the vena cava. Other gangHa, those of Bidder and Ludwig, are situated in the auriculo-ventricular furrow. In these ganglia originate fibres, some of which, centrifugal, are distributed to the muscular fasciculi, others, centripetal, terminate in the endo-cardium. These ganglia and these nerves constitute the excito-motor arc, and are to a certain extent inde- pendent nerve centres. Extra-cardiac Gajiglia. — Almost every nerve centre has some connection with the heart, but the cardiac centre emphatically is in the rachidian bulb between the tuber- cula quadragemina and the thalamus. When this is stimulated by a strong electrical current the heart's action is arrested or slowed by a less powerful current. If previously the pneumogastric nerves are cut excitation here produces cardiac acceleration. The medulla ob- longata is especially the centre of impressions which reflexly affect the frequency and rhythm of the cardiac movements. Other extra-cardiac ganglia exist in the cervical portion of the spinal cord. These maybe regarded as the centres of the accelerator nerves. Von Bezold has shown that excitation of the spinal cord, especially in its upper por- tion, augments the energy of the heart and the arterial pressure. These auxiliary cardiac ganglia are in the closest relation with the vaso motor centre, and any ex- citation which raises the arterial tension may be attended by accelerated cardiac action. Ludwig and Thery have clearly proved this intimate relation. .^ HEART SOUNDS. 3! The depressor nerve of Cyon is a sensory nerve found among the filaments of the pneumogastric, coming with it from the medulla oblongata. An excitation of its terminal branches, endo-cardial, is reflected on the splanchnic nerves opens the splanchnic vessels, so that the heart work is lessened and the blood pressure lower. The vaso-motor nerves, when they contract the vessels, make more work for the heart and increase its beatings. This effect is witnessed when the splanchnic nerve is ex- cited by electricity, the blood pressure is increased and the heart beats are quickened, and contrarywise. There are a few points in reference to the anatomy of the heart which are necessary to the clear understanding of the diseases of the organ, and these we shall proceed to touch upon. Other investigators report observations on the blood pressure in the coronary artery and the carotid. Simul- taneous tracings taken in a branch of the left coronary artery, and in a carotid agree in every respect. If the aortic valve closes the coronaries during systole, the period of greatest pressure in the arteries of the heart should follow the same period in the carotid. When one inspects the aortic valves (N. V. Med. Jour., March 3, 1883,) lays them up against the aorta, and sees how completely they cover the openings of the coronary arteries, and must cover them when the valve is open, it is much easier to believe that these gentlemen have made some mistake in their experiment, or in their ex- planation of it, than to abandon the apparently inevitable inference from this piece of anatomy. But if the experi- ment is correctly reported, does it prove any more than that the blood pressure is greatest in the coronary ar- teries, when the muscular pressure is greatest 07t them (in systole), for at the moment of greatest pressure tbdr 32 V PERICARDITIS. mouths are closed and held closed by a force equivalent to that very pressure. Mr. Geo. C. Karop says {N. Y. Med. Jour., July 7, 1883) that while the best authorities are divided, some asserting, some denying that the coronary arteries an- astomose, when junior Demonstrator of Anatomy at Middlesex Hospital, he made some injections, and found that in some cases they anastomosed, and in others they did not, the latter being as two to one. The question requires further attention, " but the con- clusion will probably remain as before, that in some cases the anastomosis is very free, in some slight, and in others does not occur at all.'* LECTURE II. PERICARDITIS. The pericardium is the sac or bag about the hearty containing it. It is double in two senses. The real sac is made up of two structures or. tissues. The outside one is formed of fibrous tissue, not unHke that which forms the ligaments of the joints, but less condensed, and is continuous with cordiform tendon of the diaphragm below, and the outer covering of the large vessels above. The inner layer is a serous membrane, no more and no less incorporated by interchange of fibres with the outer layer, so that it cannot be separated by the scalpel without considerable labor. These two constitute the heart sac. From this, at or near the origin of the great vessels, the inner or serous layer is continued on to the heart and wholly invests it, forming a closely adhesive layer. Serous membranes everywhere are constructed on the same plan, PERICARDITIS. 33 lining the parietes and covering the viscus without break of continuity. The term pericarditis is used to designate the inflam- mation of this serous lining of the fibrous pericardium and this serous covering of the heart. Here, when we have to use percussion as a means of diagnosis, is as good a place as any to give an explana- tion of a method by which the auscultation of percussion is in certain respects improved — into which a new principle is introduced. The percussion of Laennec gives information regarding the condition of the different organs of the body by the greater or less volume of sound, and by modification in the tone of sound pro- duced by it. This results from vibrations produced in the cov'ering structures, and will be freer and of deeper note if air or gas or a rarefied structure be underneath, but of higher pitch and scanty volume if a solid body or fluid be in contact with the percussed surface. Every carpenter in the land understands the practice growing out of this principle and applies it when he is to drive a nail into the plastered wall of a room. He taps with a light hammer on the wall from side to side till he strikes a spot where he finds the sound is not *' hollow" and is of less volume, and he knows that he has found a timber that "will hold his nail." Persons keeping fluids in wooden casks apply the same principle to ascertain how much fluid is left in them. The farmer strikes the cider barrel with his knuckle, from above downward. At first the sound produced is clear and free, and soon it is suddenly changed in volume and tone. He knows that is the cider level. The sound in all these cases is pro- duced in the containing wall. In the year 1840, probably in January, the late Dr. Cammann called on me with a new idea. It was no more than a thought. He had not attempted to prove or 34 PERICARDITIS. apply it. May not vibrations be produced in solid or thick walled organs which can be brought to the ear as sound? He had no sooner stated his point than I saw, or thought I saw, a new field of useful investigation. We agreed at once to give our leisure time to the inquiry. We met day after day at the dead house of Bellevue Hospital, where I was already an accepted volunteer, and with stethoscopes of solid cedar wood, one inch in diameter, and six inches long, or wedge-shape, or almost pointed at the objective extremity, each furnished with an ivory ear-rest through which the cedar projected slightly, we began and prosecuted the study. Dr. C. S. Mitchell, then of New York, now of Brooklyn, often met with us and gave us his assistance. The m.ode of pro- ceeding was this : The objective end of the stethoscope was in central position over the heart, for example, or over the spot where the lung does not overlap it, and the ear was applied to the aural end, leaving the two hands free. The forefinger of left hand was the pleximeter, and the first two of the right the hammer. By standing on the right side of the body, and then on the left, we could easily percuss in the whole circumference of the heart. We percussed first off the heart and made the percussion approach it in a right line on every side in succession. While the percussion had not reached the organ, the sound was distant and of small volume; but when it reached the outer border of it, on either hand, the sound grew instantly louder and acquired a half metallic ring. This point was accurately marked. In this way the whole circumference was mapped out, and then sharpened knitting needles were driven into the chest, at these marked spots, perpendicular to the plane of the body. We were surprised at the accuracy of our measurements. The needles were always in contact with the pericardium, often entering it without wounding the heart. Tkese , PERICARDITIS. 35 experiments were repeated day after day by ourselves and by friends, and always with the same results. Upon the dead body, then, the demonstration was complete. We tried the same method for fixing the boundaries of the liver, the spleen, and the kidneys, and found it equally accurate on them, with this exception, that the liver was the least conductive of them all, but that the limits of this could be easily defined when the stethoscope was not more than two inches and a half from the border. These facts and others of the same kind were arranged for publication by myself, and appeared in the July num- ber, 1840, of a journal edited by Drs. Watson and Swift. Soon after this paper appeared, a meeting of the New York Medical and Surgical Society was held in the Library of the New York Hospital, and a patient was brought in on whose chest the boundaries of the heart had been marked by an ink line, and the members, one after another, tried the new method, and, as I now re- member, each member indicated the same line, some at once, some after a second trial and some hesitation. I state this to show that the art of this plan is not difficult of acquisition. My lamented friend Dr. Powers, of Baltimore, soon after reading the paper, was called to see a patient who carried a large abdominal tumor, the nature and relations of which were not determined. He could not himself per- cuss anteriorly and listen behind; another percussed for him, and he carried the stethoscope from near the point of percussion backward to the usual place of the kidney of that side, and finding no break of continuity, only a uniformly diminishing volume, he pronounced the kidney and the tumor continuous structures. The size of the tumor rendered this opinion improbable, but inspection after death proved it to be correct. Not long ago a gentleman was brought to me from the 36 PERICARDITIS, West by his physician, who was not satisfied with the term malignant which had been applied by a surgeon to an apparent tumor in the right side of the abdomen, and much less with the surgeon's proposition to remove it. I found it movable, and especially that it could be pressed upward and backward toward the place the kidney should occupy, but particularly on placing the patient in a horizontal position, his elbows on a chair. I found, by auscultatory percussion, that there was no organ where the kidney should be to give any sudden change, at its borders, to the percussion sound. On these two facts was based the opinion that the *' tumor" was a floating kidney. I am not informed, and may never be, whether this opinion was correct. Last winter a large consultation of the Me'-J 'r ,, — ■ — r- — f JliQ Medicql Record, IVlay §, ;88^. 122 HYPERTROPHY OF THE HEART. LECTURE V. HYPERTROPHY OF THE HEART. When I was a student of medicine hypertrophy was described under three divisions : First, simple hypertro- phy ; second, eccentric hypertrophy ; and third, concen- tric hypertrophy. We do not use those terms now. It is hypertrophy, and hypertrophy with dilatation. Hy- pertrophy with contraction, concentric hypertrophy, is probably, in every instance, no hypertrophy at all. The last act of the heart was to contract, and to force out the blood that was, just the instant before, within its cavity. It is very much contracted, its cavity is nearly obliterated and it may be taken for a diseased condition. But it is a natural office of the heart to contract, and if death strikes at the instant that the contraction is completed you will, of course, find no blood in the ventricles of the heart : you will find it smaller than natural, and that would not be consistent with the term hypertrophy. The walls are thicker because they are contracted. I think it would be found that every instance that was, of old, called concen- tric hypertrophy could be resolved into the condition that I have described. So that now we have hypertrophy, and hypertrophy with dilatation. The first question that presents itself is, what is hyper- trophy of the heart ? Well, the obvious answer is, enlarge- ment of its walls ; increase in the bulk of matter that constitutes the walls of the heart. Well, what constitutes the walls of the heart? Mainly, muscular fibres, and some connective tissue. Then it is the muscular fibres of the heart that are increased ; and how increased ? I HYPERTROPHY OF THE HEART. 1 23 asked myself that question a great many years ago, and I resorted to some old specimens I found at the hospital for the answer. A point to be investigated was, the size of the muscular fibre in hypertrophy of the heart ; is it larger than the muscular fibre in the heart of natural size? I procured about twenty or twenty-five, and drew fibres from different parts of the heart, from one ventricle, and then from the other, and, compared those from the nat- ural heart with those from the hypertrophied heart, and though occasionally I would find enlarged fibre the average was pretty nearly the same in the healthy and in the hy- pertrophied heart. Well, then, the conclusion is inevita- ble that if the same proportion exists between the size of the muscular fibre of the natural and of the hypertro- phied heart, there must be a multiplication of the fibres of the muscles in the latter, and that is a fact. There is a new production of muscular fibres. From what origin they spring I cannot tell you, but nature has so ar- ranged it that if the heart needs additional strength it can get additional fibres. The size to which the heart may grow is, perhaps, limited to sixty ounces. When we meet next I intend to show you one that weighed fifty-seven ounces — within three ounces of the largest heart the weight of which has been recorded. The natural weight of a heart in a full grown person, not remarkably broad upon the shoulders, is eleven ounces ; if, then, it is increased to sixteen or eighteen ounces, you see there is some hypertrophy ; if it is increased to twenty-five or thirty, there is very consid- erable hypertrophy ; and if it is increased to anywhere in the neighborhood of sixty ounces it is cors bovinmn, an ox- heart, and here I may say that that enormous size is never attained except in persons in whom disease of the heart began in infancy. This, the largest heart I possess, perhaps the largest heart in the country, was taken from 124 HYPERTROPHY OF THE HEART. a man who, at six years of age, was taken over by his physician from Randolph, Vermont, to Dr. Nathan Smith, and was shown by him as an instance of heart dis- ease arising from inflammatory fever, rheumatism. The boy had had articular rheumatism, and his heart became involved, and Dr. Nathan Smith had interest in it as an instance showing there might be some connection be- tween articular rheumatism and disease of the heart. It was fourteen years after that — more than that — -twenty odd years, before the connection between articular rheu- matism, pericariditis, and endocarditis was made out ; so that, really, had it been published, that discovery of Dr. Smith would have been put first, as showing the relation between rheumatism and inflammatory affections of the heart. The boy grew up, attained the age of twenty- eight years, and to show you his was not a useless heart, he was foreman of a manufactory in the immediate neigh- hood of Springfield, Mass. He was only incapacitated for work about a month. He kept his men all in line, all at work, until his breath became so short, probably through involvement of the kidneys, that it was so painful to him he was forced to give it up. He remained at home after that, and died about a month after ceasing to work, and yet carried this enormous Heart. I have never seen a very large heart in a person in whom it did not begin to grow in early life. The heart may be hypertrophied in the wall of one of its cavities. The hypertrophy usually found about the heart is that of the walls of the left ventricle. The left ventricle is hypertrophied oftener than any other portion of the heart. You will find, also, hearts that are hyper- trophied in all of the cavities ; perhaps some such among those that I shall show you at our next meeting ; and others, perhaps, that are hypertrophied in the two ventri- cles ; and one or two, I think I have, that are hypertro- HYPERTROPHY OF THE HEART. 12$ phied in the right ventricle, the right auricle, and the left ventricle. So that hypertrophy may be single, or it may occupy each one of the walls of the heart cavities. The causes of hypertrophy are various. The most common cause is the need of more strength in the walls of the cavity that is immediately affected. Obstruction,, then, at the aortic opening, as has already been stated ta you, is attended by hypeftrophy; but the heart does not seem to know exactly when to stop growing, though it does know when to begin to grow, and it may go on to become diseased. A moderate hypertrophy, then, with obstruction at the aortic opening, may not be regarded as a grave disease. Then, regurgitations will lead to hypertrophy. That the obstruction not requiring in- creased strength in the walls of a cavity will not produce hypertrophy, you will see in the fact that stenosis of the mitral valve is attended by no change in the left ventricle. If there is regurgitation, then the left ventricle may become hypertrophied. It needs more strength for the work it has to do. But if it is simply an obstruction of the blood coming from the left auricle into the left ventricle, and the left ventricle becomes in the end fairly filled, and does not throw the blood back again into the auricle, then there is never any hypertrophy of the left ventricle. It is only in regurgitation with this lesion that hypertrophy comes. Here, then, is one cause. Another cause is increased strain upon the heart ; an increased demand continued for a long time, attended by a nutritive, non-deteriorated condition of the blood. You see why I make that limitation ; because a man with typhoid fever may have his heart beating rapidly and pretty strongly for four weeks continuously, and no hypertrophy follow. But then his blood is deteriorated ; all his tissues are, throughout. If by mental or physical excitement his heart should beat this way, at the same 126 HYPERTROPHY OF tPIE HEART. rate and for the same length of time, and his blood were in a nourished condition, his heart would become hyper- trophied to a certain extent. Disease that produces increased action of the heart and full action of the heart, does not, then, cause hypertrophy, unless the blood is in good, full, nutritive condition. Occupations that are at- tended by great mental excitement and by heart beating are dangerous in this respect, producing hypertrophy without valvular disease. The little tyrants that command on vessels at sea sometimes are very passionate men. I have seen them beat their men about and swear at them as if they belonged to orur army of Flanders ; and those men are very apt to get hypertrophy of the heart. They do not observe the rule of Scripture, let not the sun go down upon thy wrath. They are wrathful at night. A French physiologist has interested himself in the cardiac condi- tion of the domestic fowl, and he found that where one rooster had to be the husband of ten or twelve hens, he was apt to get hypertrophy of the heart. This may be a warning in regard to sexual indulgence. Then, again, hypertrophy comes from causes that are not known. We say in general that it is an error of nu- trition, but why, we do not know. Persons of quiet tem- per and of easy life, not subject to particular excitements, and having no valvular disease of the heart, do once in a while get hypertrophy of the heart ; but it is uncommon ; decidedly uncommon. The time seems to be passed when it was necessary to ascertain the effect of the contracted kidney on the heart by experiment on animals. There appears to be very general assent to the proposition that it causes hyper- trophy of the left ventricle. But in the reports of those who have studied the matter experimentally there is a remarkable disagreement, and it is worthy of notice that HYPERTROPHY OF THE HEART. 12/ while the clinical studies have been settling the question the experimental should be so inharmonious. Dr. Straus, of Paris, tied one ureter in twenty guinea pigs to cause atrophy of the kidney to which it belonged. These animals were killed four to six months after this was done, and the left ventricle was found enlarged in every one of them. The hypertrophy was not great — only -J- to J the original weight, but the time was short. The muscular fibres were healthy. Grawitz and Israel asserted that while hypertrophy of the heart might follow a kidney lesion in old animals in which the other kidney did not grow to compensation this result was not to be obtained in young animals. But nearly all of Dr. Straus' animals were young. Rollet * records the following case of hypertrophy con- fined to the left ventricle, the walls of which were pale and presented here and there small spots of sclerosed tissue. The aortic orifice was normal. A fibrous band was found extending from the under surface of the aortic lip of the mitral valve to the intraventricular septum and aortic portion of the ventricle at a little distance from the sig- moid valves. The new growth narrowed the aortic cone to such an extent that one finger could with difficulty be in- troduced. The author thinks this band was produced by endocarditis before birth. A similar case affecting the right ventricle is recorded by Dettrich, 1849. The patient was a woman forty-seven years of age, ad- mitted with palpitations, thoracic pain, dyspnoea and cephalalgia ; cardiac rhythm irregular. There was an in- creased area of dulness, apex beat strong and to the left of its normal place. There was a distinct thrill, percepti- ble only under the lower part of the sternum, to the left of that bone and at the apex. There was a rather pro- * The Medical Record, Oct. 7, 1882. l^B HYPERTROPHY OF THE HEART. longed systolic murmur of greatest intensity in the fourth interspace at the left border of the sternum. The second sound was audible at the base and in the carotid, showing the integrity of the sigmoid valves. Now the question comes, how to recognize hypertrophy of the heart. A heart like that one that is passing around, which I told you is hypertrophied, occupied a greater space in the chest than it did when it was of normal size, and what will that do ? It will crowd the lung away. The space over which a heart of natural size will practically come in contact with the walls of the chest, or, in other words, not be covered by lung, is about equal to two su- perficial inches ; but when a heart grows, as that has, it must crowd the lung out of position. In a healthy per- son you can hear the respiratory murmur over the whole praecordial region ; but when you listen to a person who has considerable hypertrophy of the heart you will very likely fail to find the respiratory murmur over the anterior portion of the heart, because the lung has been crowded away. That comes to be, then, one sign for the recogni- tion of it. The same thing, however, occurs when the pericardium is dilated with fluid. The lung then is neces- sarily crowded away in the same manner. Another point is that the region of dulness is in- creased more or less markedly. The point to which the apex of the heart can be pushed to the left by its hyper- trophy is perhaps six inches and a half from the median line. Then you get to about the outer curve, the outer limit of the curve of the chest. It may be pressed back- ward beyond that, but I do not remember to have meas- ured a heart which extended to the left more than six inches and a half. I have found it six inches a great many times, and five inches and a half a great many times. You can measure it in either one of two ways. Find the apex, and be sure that there is no heart beat HYPERTROPHY OF THE HEART. I 29 beyond that, and you can pretty safely measure up to that point from the median line. But it is always better to make percussion, so that you will be sure of the point to which you should measure. Dulness over the lung upon an enlarged lieart is very decided. The line of division between them is pretty clearly cut. Yet, even suppose you get dulness over six inches from the median line, your diagnosis is not yet made. The same thing may happen with pericarditis and an enlarged pericardium. Then seek for the apex of the heart. If there is marked enlargement of the right side of the heart the apex will be tilted up toward the axilla. It will be, perhaps, as high as the fifth rib, following the curve of the rib up- ward, or it may not be as high as that. Its direction is upward and outward, and to the left. If it is the left side of the heart exclusively that is hypertrophied, the apex may be situated in the seventh intercostal space, outward, downward, and to the left. Of course it will be in the sixth before it is in the seventh. It is in the intercostal space, of course, that you can most easily feel the impulse of the heart. And then, again, you must make percussion to verify the indications of the apex- beat. There is nothing that is likely to trouble you in the attempt at diagnosis but pericarditis. It is true, the heart is sometimes the seat of tumors ; and the pericar- dium becomes enlarged sometimes by air, but that will not give dulness. In general practice, with the exception of the extraordinary cases, that you do not expect to see, these two things will give you the only trouble there will be. Hypertrophy is otherwise easily recognized. There is a point, however, to be borne in mind. I examined a gentleman yesterday who had been educated to the profession, but had gone into business. He had pleurisy filling the left side of the chest, and his heart was pushed over so that the apex beat was about in the position on I30 HYPERTROPHY OF THE HEART. the right side that it would naturally occupy on the left, crowded over by this accumulation of fluid in the left side of the chest. Now, a person who has hypertrophy of the heart may have pleurisy as well as anybody else, and the heart may be displaced in the same way. It may be displaced to the left also. An effusion upon the right side will encroach upon the right side, will encroach upon the mediastinum sufficiently to crowd the heart over an inch further to the left than it naturally would be. Such a case as that you may mistake for hypertrophy when it is only a displacement. It will be important to know, then, whether there is any effusion upon the right side of the chest. Then, again, the history of hypertrophy and of peri- carditis will be found different. Hypertrophy is a chronic affection, and a man who has it, and is sent to you for it, will have had for a good while some shortness of breath in going up stairs. Then, again, the dulness extends, in pericarditis, as I have already told you, in a direction dif- ferent from the dulness in hypertrophy. You get a cer- tain degree of dulness in pericarditis, with copious effu- sion, on the right side of the sternum, and you get it above the third rib. It is only effusion in the pericardium that does that. The physical signs of hypertrophy, there- fore, are pretty clearly made, pretty clearly cut, and you need hardly make any mistake about it. The rational signs are more obscure. You cannot be sure, by any study of the general symptoms, that you have hypertrophy and nothing else. You can pretty easily determine, from the rational symptoms, that there is heart disease, but exactly what it is, is almost impossi- ble to determine. The usual symptoms of heart disease are to be observed in these patients — that is, a certain de- gree of shortness of the breath on exertion, frequently a disposition to rest the head on two or three pillows, in- HYPERTROPHY OF THE HEART. I3I stead of one, in sleep ; a disinclination to sleep upon the right side of the body, not because it gives them pain, but because it disturbs them, it makes them nervous; they feel the heart beat, and that makes them nervous. Palpitation cannot be relied on as a means to distinguish hypertrophy. It is wonderful how much of thumping the heart will have, and the patient be entirely unaware of it in some instance ; afid it is really surprising how lit- tle of real palpitation will give other persons much un- easiness. There is a real palpitation and there is a sub- jective palpitation. Persons of particular habits will be- come nervous and feel palpitation when there is only natural action of the heart. It arises alone from their in- creased sensitiveness or the heightened state of nervous perception. And then, as I said before, a man who has real hypertrophy of the heart, who has been accustomed to hard knocks in life, may pay no attention to it, while it may lift your head half an inch at each beat when you apply your head to the chest. It knocks like a hammer against the face and ear ; and yet, ask him if his heart palpitates. " O no, O no, my heart is good !" But pal- pitation is not a certain guide to diagnosis. The man we saw at the clinic yesterday had no palpitation ; that is, nothing that you could feel with the hand. You could feel that the heart was beating, but not with extraordinary force. He had had his disease for a considerable time, and it is to be presumed that the heart had lost some of its energy. But even in persons in whom the disease may be gradually growing there may be decided palpi- tation, and there may not be, so that you will have to consider what is the cause of the palpitation, if you find it. * Shortness of breath is common to almost all the forms of cardiac disease, so that there is nothing particularly distinctive in that. Then comes the question, what can 132 DILATATION OF THE HEART. be done for the relief of these patients ? and then, again, as all the diseases, or nearly all the diseases, of the heart, have about the same physical history, their treatment will be substantially the same, so that I will say what is to be said about that further on. B LECTURE VI. DILATATION OF THE HEART. There is another condition of the heart that deserves particular attention. I say particular, as it is not nearly so common as hypertrophy with dilatation. It is dilata- tion alone, and this brings me to the question, what pro- duces dilatation of the heart, whether it occurs with hy- pertrophy or singly ? The answer to this question, I think, has been given by Niemeyer: dilatation of the heart is caused by a reflux of blood into it, which blood has just been thrown out of a cavity. For example, the blood is thrown into the aorta, there is a reflowing, a re- flux of it into the ventricle ; perhaps one half of it that was thrown out comes back again, and this is in the pe- riod of non-resistance of the heart ; its muscle is all re- laxed, flabby. If it were to come during contraction there would be resistance to enlargement, but the muscle is, so to speak, dead at the moment ; it is in the period of re- pose that this reflux takes place. It stretches it, together with the blood flowing in from the auricle. It is com- pelled to contain more than it was made to contain, and the result is a moderate dilatation, and this continued seventy-two times a minute, for days, and weeks, and months, will produce an effect. One occurrence, proba- bly, would not be felt, but a repetition is what produces DILATATION OF THE HEART. 1 33 the dilatation. Well, this dilatation, then, is caused by an unnatural flow of blood into the ventricle, and the heart, feeling its contents, naturally acts with more than ordinary force, so that hypertrophy and dilatation often go together, step by step. Dr. Peabody * showed to the N. Y. Pathological So- ciety a heart of which the following is a description : The endocardium was generally thickened, as were the aortic cusps. The chief lesion was in the muscle of the heart. It had been replaced by connective tissue largely in two places ; the most marked was a circular spot of nearly two inches in diameter between the papillary muscle and the attachment of the aortic valve, and there was distinct aneurismal bulging of the septum ventriculorum and also of the left border of the left ventricle. The depth of the sac was three quarters of an inch. A second sac was near the apex of the ventricle in the septum. The mus- cular tissue was in the state of brown atrophy. The coronary arteries open at their origin ; their branches were obstructed or occluded by a growth from their lining membrane. Patient was a man fifty-five years old. I told you, in speaking of hypertrophy, that I would show you a heart that is, probably, the largest that has been noticed in this country. This is the specimen. There are several interesting things about this : first, that it is, probably, \h.e largest heart that has been in this land ; second, its history is well preserved. I gave you the history in a previous lecture. The patient could carry this large heart only because he grew up with it. These large hearts, as far as I have noticed, always begin to be diseased in early childhood, possibly in infancy, and the person becomes accustomed to the extraordinary develop- * Medical Hecord, July 29, 1882. 134 DILATATION OF THE HEART. ment, and so it gives little inconvenience. It grows with his growth, and may attain this monstrous size. I told you, when speaking of pericarditis, that I would exhibit to you a heart to which the pericardium was at- tached. You observe here is the pericardium, and it is attached to the heart. The patient had had endocarditis and pericarditis, and this is an instance in which we can pretty safely say we have twenty-two years from devel- opment of the pericarditis till death. You will see the manner in which the pericardium is trying to separate it- self from the heart. By just raising up the flap of this pericardium on either side you will see threads running from one side to the other. They have been considera- bly torn up by handling, but still I think you will notice them better on the upper side. This pericardium, had the man lived long enough, would have been separate. The attachment, as you see, is loose. Then, as a speci- men of aortic disease, it is extraordinary. Opening the aorta by '' its ears," and getting down to the valves, you see they are thick and leathery. They are more than a Hne in thickness, nearly an eighth of an inch in thickness, and they are much distorted, and are, you see, quite inca- pable of performing their office. They feel hard, like sole leather. Then the right auricle, together with the right ventricle, you observe, is somewhat dilated, but very much encroached upon by the septum ventriculorum. The mitral valve is not so very much diseased. That is to say, its offices are not very much hindered. It is thick, scarcely leathery, its posterior valve is contracted. It is contracted considerably, and I am not sure that it would perform its office perfectly. But the amount of disease there is trifling compared with that which effects the aortic valves. Here, too, has been pericarditis. You observe how rough the heart is. There is something of that thready DILATATION OF THE HEART. 1 35 appearance, not so much, however, as in the other speci- men, in this pericardium. I do not know the history of this case as I do that, but you observe here is very marked shortening of the valve. That valve is not one half its proper height, and it would be impossible for its parts to meet in the middle of the artery and prevent re- gurgitation. In this instance the right heart is more hy- pertrophied than the left — that is, in proportion to its natural thickness the walls are thicker, and in regard to capacity it seems to be just about as great as the left. The thickening here is quite remarkable. The tricuspid valve does not seem to be diseased. The aortic valve is firm, and shortened to a certain extent, and here again the posterior more than the anterior curtain of the valve. But the great defects, or rather the principal diseases of the heart, are the hypertrophy, particularly of the right side, and the valvular disease at the aortic opening. The pulmonary valves are about natural. Here is another specimen of marked hypertrophy, and here again you observe a septum of the aortic valve thickened and drawn down. The valves, you observe, are very imperfect, and allowed regurgitation, while the mitral valve is in tolerably good condition. The right ventricle is small, comparatively. It will not hold one half, it will hardly hold a quarter of what the left will, and that of itself is a kind of disease. The blood can be thrown out from the left heart a great deal more rapidly than it can be received by the right ; and the result is exactly the same as when the valves are defective. I was speaking to you, w^hen we were last together, of dilatation, I had begun to describe to you the peculiari- ties of that disorder of the heart. We will go on with that, and I will show you at our next meeting a speci- men that is rather striking ; a dilated heart, in which, if I remember right, all the cavities are dilated, and they are 136 DILATATION OF THE HEART. stuffed with hair, so that the heart has about the size that it had in life, and yet in the cuts made into the walls you will see to what a very marked thinness it has been reduced. Dilatation, I told you, considering it in the sense in which we are using the word now, is a thinning of the walls of the heart. We have hypertrophy with dilatation, in which there may be considerable thickening of the walls of the heart, but this is spoken of by a distinctive name. We now refer to simple dilatation of the heart, in which the walls of the heart of the left side come to be little more than a line in thickness. The walls of the right heart are from three to five lines in thickness in the nor- mal state, that is, three at about half an inch from the base, and growing a little thicker toward the apex, and at the apex five lines in thickness. But this heart that I shall exhibit to you at our next meeting will give less than a line in thickness of any portion of the left ventricu- lar wall. The first question that presents itself to us is, how can this thinning occur? A good many speculations have been offered in explanation of this occurrence, but I am inclined to think that the German explanation is the best : that it may occur in two different ways : First, by a reflux of blood when the blood is in a non-nutritive state, dilating the natural walls of the heart till they are thinned down to a condition I shall exhibit to you ; the other, that hypertrophy with dilatation may have oc- curred, and that by fatty degeneration, which I shall ex- plain to you a little further on, the material constituting the muscle of the heart may be absorbed, taken up, car- ried away, leaving very little but the two serous mem- branes, the endocardium, and the pericardium. That implies, of course, very marked feebleness in the heart's action. Simple dilatation of the heart to the extent of DILATATION OF THE HEART, 1 37 becoming a disease is a rare occurrence. I have met with two or three cases, and that is all. The indications of it, the means of recognizing it during life, are both physical and rational. Among the physical signs will be one that belongs to hypertrophy, extended region of dulness. The lungs will be pushed away, in the same way, from their natural position, and in auscul- tation for the respiration you will find it silent over the dilated heart. That is, the lung is pushed so far away that the sounds of respiration will not be brought to the ear placed in the middle portion of the pericardial region. There is no palpitation proper. It frequently happens, however, that the patient complains of palpitation. His sensitiveness is increased at the same time that the action of the heart is rendered feebler ; though he complain of palpitation you put your hand over the heart, and you can scarcely feel it beat. In one case that I saw it was remarkable that the contraction of the heart was in a wave. It was not a sudden contraction of all the muscles of the^ heart at the same moment, but the contractile effort seemed to pass up under the hand. Beginning below I could feel the wave pass the length of my hand. That is, so far as it was applied to the intercostal spaces. I could not feel it, of course, through the ribs, but the intercostal spaces being thin, as I exerted some pressure they would indicate to my hand the kind of action that was taking place in the heart. A feeble beat of the heart, then, with an increased region of dulness, and a consideration of the kind of sound, will be the chief physical signs. The sounds of the heart are changed in relation to each other ; the time is changed, or the rhythm, as it is called. As the heart beats naturally, the second sound follows instantly upon the cessation of the first, and then there is a period of rest, about as long as the period occupied by the first and 138 DILATATION OF THE HEART. second sounds together. In this condition you are very apt to have the motion of the heart, or rather the sounds of the heart, resembling the ticking of a watch, the first and second sounds at even distances apart. The first sound is short, scarcely exceeding in duration the second. Tick, tack ; tick, tack ; in about that relation. Then the appearance of the patient gives a marked indication of dilatation. The force with which the heart contracts upon the blood is so far diminished that a small quantity is sent into the arteries at any one beat, at any one time. This does not dilate the arteries, does not keep them of their natural size. They are apt to grow small therefore. I referred the other day to the filling of the ventricle during the period of rest of the heart. I perhaps should have said the ventricle has no power of dilating itself, but it is dilated by the force that it has impressed upon the blood when it went out from the ventricle into the arteries. The residual force of the cir- culation when the blood returns to the heart is really the dilating power. In that sense it dilates itself. The ve- nous power is considerable, as when we tie the arm to bleed a man the force of the current is such as to throw the blood quite a considerable distance from the arm. This force is not all exhausted when it comes to the right heart, and it is that residual force impressed upon the circulation by the contraction of the left side that opens the right. In this case the force impressed upon the blood going out of the right side of the heart opens the left ventricle, or causes the left auricle to fill, and this is really the cause of the filling of the left ventricle. Now, in this dilated heart, you have a very feeble force impressed upon the blood when it comes out of either ventricle. It will, of course, flow into the opposite ventricle in an equally feeble stream. It will dilate the veins, because there is not force enough behind to empty them, and you get DILATATION OF THE HEART. 1 39 oedema of the face, of the feet, and of the surface of the body, and you get at the same time enlarged veins ; the blood seems to rest in the veins. Of course it does not absolutely rest, but the current is slow. The oppression of the breathing is very marked in these cases. It belongs to almost every form of disease of the heart, but is developed earlier, and is, perhaps, more severe in this than in any other, and that depends upon the failing force with which the blood can be circulated through the lungs. There are at least three distinct causes of dyspnoea besides the nervous causes that would produce the same thing. One is an over-charged or con- gested lung or lungs ; another, very slow circulation of the blood through the lungs ; and the other, some physical obstacle to the dilatation of the lungs by the air entering them. These three conditions all produce dyspnoea more or less severe, and why? You would suppose that, mechanically, they would not act in the same way. Mechanically, they do not, but physiologically they do. They each one interfere with the aeration of the blood. When the lungs are congested the blood is circulating slowly through them, and though the blood that is in the lungs may become aerated it is not given to the system with sufficient rapidity to answer the demands, and conse- quently a sense of dyspnoea. And, then, too, when the quantity circulating through the lungs is very small and the current slow, there is not enough aeration of the bulk of the circulating blood, and there is dyspnoea. Then, when both pleuritic cavities are filled with serous fluid, or any other fluid, and the lung room is not great enough, there is not space for very much aeration of blood, and there is dyspnoea. And these three conditions of the lungs explain most of the dyspnoeas that occur with the diseases of the heart, and in none of them is that dyspnoea more perceived, more apt to cause sufl^ering, than in this 140 DILATATION OF THE HEART. dilatation of the heart. These are the leading facts by which you are able to recognize simple dilatation of the heart, if you should happen to meet it. With reference to its treatment I will say a word. There is something to be said in regard to this that does not belong to all forms of diseases of the heart. I see recom- mended in some of the text-books, and in special papers on this affection, as a means of relief, bleeding — bleeding from the arm. Well, I will tell you my experience. When I was house physician in the New York Hospital a man came in in whom we recognized dilatation of the heart, and it was in that particular man that I got that wavy motion of the contractile fibres of the heart. My principal, seeing how much he suffered, said, bleed him. I looked at him with surprise, and said, " Doctor, I would not dare to bleed him. He cannot lose five ounces of blood without dying." *' Pooh, pooh !" says he. ** If you don't like to bleed him, give me the lancet." He tied up the arm and took the lancet. I was accessory in holding the bowl, and the vein was opened. The man bled a little spurt, it may have been four or five, possibly six ounces, and rolled over on the bed — I had him sit on the bed on purpose — rolled over on the bed, and breathed no more. Of course that did not make me very much in love with bleeding for dilatation of the heart. And yet, even in Niemeyer, if I remember right, it is recommended, but, I suppose, theoretically, inasmuch as bleeding does in some conditions of dyspnoea give relief. But I do not think it applicable to the dyspnoea which arises from dilatation of the heart. Well, then, there is very little you can do. The man cannot take any exercise. He would drop down of dyspnoea if he were to make any great exertion. He may walk about the ward a little, if he is in a hospital, or in his room, if at home ; but that is about all he can do. He cannot go up stairs and can DILATATION OF THE HEART. I4I scarcely go down. About all you can do is to induce him to take as much food as he can digest, with the hope of enriching the blood a little, and delaying the progress of the disease ; to give him chalybeates, which will help in this change of the condition of the blood, almost any form of iron that is a favorite with you ; it matters very little, for they all go to about the same thing ; and create an active condition of the .kidneys to carry off the oedema. This latter is applicable to almost all the forms of cardiac disease where dropsy has occurred. I shall recur to the matter of diuretics by and by. With these remarks on dilatation of the heart, we will leave that subject and turn to another conditionof disease of this organ. Prof. Maragliano* gives the results of the administra- tion of strychnine in dilatation of the heart as follows : I. In two or three days the size of the heart was reduced, and in five or six days very considerable dilatations were caused to disappear. 2. If immediately on the reduction in the size of the heart the strychnine were withdrawn, the dilatation was frequently reproduced. 3. The daily dose of sulphate of strychnine required was from -^^ to -^ of a grain. *The Medical Record, Jan. 27, 1883. 142 FATTY DEGENERATION OF THE HEART. LECTURE VII. FATTY DEGENERATION OF THE HEART. You hear a great deal about fatty degeneration of the heart. You will hear a great deal more than you will see. I scarcely ever see a fat man advanced somewhat in years who has trouble with the heart, that the attend- ing physician does not say, "Why, doctor, don't you think he has fatty degeneration of the heart?" My reply is uniform, " I cannot diagnosticate fatty degenera- tion of the heart, and I have no right to assume it in any case without proof." You will see where the difificulty lies pretty soon. Fatty degeneration, to the extent of producing real disease, is quite a rare occurrence ; occur- ring, to be sure, now and then, but in comparing it with dilatation and hypertrophy together, it hardly bears the relation of one to fifty. There are two kinds of fatty degeneration of this organ. One I have«sometimes designated as adipose degeneration, or adipose deposit upon the heart. The other is an integral degeneration of the muscle of the heart into fat. The latter is called, commonly, Quain's degeneration, as he was the first to describe it. The two are very easily distinguished by the appearance after death. But neither of them can be confidently recognized during life. The latter, Quain's disease, you will be more likely to dis- tinguish than the other. The fatty degeneration of the adipose variety is merely a deposit of fat upon the surface of the heart. I have some better specimens than this which I can show you, perhaps, at our next meeting, though this is well enough marked to give you an idea of FATTY DEGENERATION OF THE HEART. 1 43 what is meant by it. Always there is some fat upon the exterior of the heart in the pericardium, but you will observe in examining this specimen that here it has encroached somewhat upon the muscular element of the organ. The whole heartis covered with a more or less abundant layer of fatty tissue, but chiefly upon the right side. Well, that is the part of the heart that is most commonly overloaded with this fat. You take a portion of this fat and examine it under the microscope, and it will present exactly the same appearance as adipose tissue taken from any portion of the body — a multitude of cells filled with oil. It is a healthy fat enough, but it is out of place here, for the reason that as it becomes abundant the muscular heart becomes weakened. But many per- sons, no doubt, carry this condition for a considerable time without knowing it. The heart performs its office with fair regularity and with fair force. But in a few instances it will happen that the fatty encroachment is unequal, and it weakens one part of the heart more than another; as, for example, the septum ventriculorum may be just as strong as it ever was, while the wall opposite is weakened. The result is that the heart sometimes gives way first at that point ; at the point where the greatest weakness of its muscular tissue is it bursts itself. I will refer to that again a little further along. This is the heart, then, and you may examine it and see what it means. The fat is very abundant upon the base, but that does not do so much harm as that deposited along the course of the ventricular wall. This heart is also hypertrophied. I told you the heart beats with perfect regularity, and that it is not enlarged in any such degree as that you can recognize it by physical signs. Well, then, how can you recognize it at all? Well, just make up your minds, now» and forever, that you cannot recognize it, except after 144 FATTY DEGENERATION OF THE HEART. death. And we will not spend a great deal of time in talking about fatty degeneration of the heart, when you cannot tell what is the matter with the patient when he has it. Now, the other kind is altogether different in its effects upon the heart, and altogether different in its pathological aspect. The heart muscle is a striped muscle. It has cross markings, lines in the direction of its length, and lines across dividing those muscles, as the muscles of the arm and leg, and all the voluntary muscles of the body are divided into little checks. Well, these checks, when Quain's degeneration occurs, come to hold first a little oil globule. A muscular element seems to be removed from it. The place of the muscular element is taken by oil drops, minute, microscopic drops. I can show you a plate the next time that will, perhaps, give you a better idea than any of my drawings, but you may get some idea of it from this drawing. Well, then, this sort of heart has become useless. No, not quite, because this sort of degeneration is unequal in the walls of the cavities. It will be here marked, and at another place scarcely noticeable. The result of this production of oil within a muscle, covering the sarcolemma, is to change the color of the heart, and to change its consistency. Here, for example, are three specimens of this kind of degeneration. This one is not so very much softened. It seems to be small. The walls of the heart are thin, but the cavities are not dilated. The peculiar color that the oil gives to it is noticeably yellow. Here is another which is soft and yellow, and the walls of the heart are a little thinned, but not reduced so much as that you would be able to recognize it during life. And here are several other speci- mens which you will examine with regard to color, etc. In regard to the recognition of this form of disease, it is more nearly possible than to recognize an adipose FATTY DEGENERATION OF THE HEART. I45 deposit Upon the exterior of the heart. For example, I was called to see a lady, not quite middle aged, in whom there was marked irregularity in the action of the heart. I measured its size; that was natural. She was of an age that would hardly admit of the supposition that she had bony degeneration of the heart structure. That belongs to advanced age. She was not more than thirty, or per- haps thirty-five. She could lie down flat in bed — that is to say, she could lie down on her back without any pillow or bolster, and felt better in that position than with her head raised. She was dizzy, and disposed to faint when she walked about, and particularly when she made any exertion. The peculiar irregularity — I say peculiar; I do not know that that is the proper name — the marked irregularity, the irregular irregularity in her heart fixed on my mind that there was some disease of it. In using that expression, irregular irregularity, I ought, perhaps, to define it. When a heart beats on for five, six, or seven minutes, and then drops a beat, that is an irregularity; but there is a certain degree of regularity in its recurrence. You may count a certain pulse, and find that the sixth is dropped through a whole minute. But when there comes a kind of irregularity that you cannot describe, when the heart beats perhaps rapidly in this way and then holds up, beats slowly, and then directly begins with a sort of fluttering that is hardly describable in words, that is what I mean by irregular irregularity as contrasted with the regular recurrence of certain phenomena in the action of the heart. Well, this lady had that. The heart beat with an irregularity that is hard to describe. Now, it will be well for you to remember that that belongs to some particular disease of the heart; that that particular irregularity that you cannot well describe does not come of mere functional disturbance, but is always, as far as my memory goes, associated with a change of some kind 146 FATTY DEGENERATION OF THE HEART. in the structure of the heart or its valves. I said to the doctor who called me in, " I am confident there is some disease of the heart here, but I cannot tell what it is." Had I known the fact that in this kind of degeneration it is not uncommon that patients can lie down with the head low in bed, and feel better than when the head is raised, I might perhaps have made a reasonable conjecture. But at that time I did not know it — thirty or forty years ago. This lady died, and we had a post-mortem examina- tion, and the heart I think is one of these. I examined various portions of it under the microscope, and found the kind of degeneration that I have been trying to describe to you, more or less in all parts of its walls. But it was very marked, more marked than anywhere else, in the fleshy columns, and this, perhaps, was one reason of the marked irregularity. They performed their office very imperfectly, and by sympathy disordered the heart. This kind of degeneration is, again, of rather rare oc- currence. It may occur at any age. It may occur upon hypertrophied and dilated hearts, and it may occur upon hearts that are perfectly normal in size, and up to the time of its occurrence perform their function properly. I do not know what causes Quain's degeneration. It. is something connected with the nutrition, the nerves of the organ. Persons who have it do not become oedema- tous, they do not become always very pale. This lady that I refer to was pale and icteric, but I did not refer the icteric element to the heart, unless, perhaps, the liver was deranged by imperfect circulation of blood through it. As to the treatment of this particular form, if you make it out, there is but little. A rather extraordinary recommendation has been given, however, by one physi- cian of some authority, and that is to advise the patient to run up-stairs. I think it would kill more than it would FATTY DEGENERATION OF THE HEART. I47 cure. The idea is to make the heart active, and to cause it to be nourished by healthy muscular tissue in this way. But my own opinion is that this cannot be done. The treatment that I should adopt, and have recommended in cases where this disease was suspected, is of an en- tirely different character. It is aimed at causing the ab- sorption of the fatty matter, and reduction of the supply of fat in the body ; for example, the patients, as in two or three other forms of disease that depend upon fatty disorders that I shall describe to you further on, are di- rected to take moderate exercise, to walk upon the level ground, or upon the floor of the house, and take, accord- ing to their strength, the exercise they can endure. The second element of the treatment is to exclude from the diet all fatty food, including butter, milk, cream, fat of meats, and in a manner all fatty food. I sometimes al- low them enough of milk to flavor their tea or coffee, but nothing beyond that. Only lean meat^, and the vegeta- ble foods that contain the least oily matter. Well, the grains ; perhaps you ask whether they contain oily mat- ter; yes, they contain oily matter. Wheat contains about three per cent. Indian meal contains about ten per cent — that is the reason it fattens the hogs. Then I should prescribe food made from wheaten flour rather than from Indian meal. And next, and perhaps the most important element in treatment, is to administer the bicarbonate of soda, and to administer it in as large amount as will be borne, and that fact to be judged of by a daily examination of the urine. In giving alkalies you are to bear in mind that some of them have the power of producing calculi in the kidneys or bladder, but there is no danger of their producing anything of this sort as long as the urine is in the slightest degree acid. Furnish your patient, then, with slips of litmus paper, to be kept in a convenient place, as in a box about two and a half inches 148 FATTY DEGENERATION OF THE HEART. long and an inch and a half wide, and let the patient take every morning, or every evening (better in the evening), one of the papers by one of its ends and dip the other in the water, and when it comes out, notice whether it is red or purple. If it is purple the patient is taking too much soda ; if it is in a very slight degree red, that is all right ; if it is very red, he is not taking enough ; give more. And in this way, from day to day, by applying the test, you may give what will be safely borne, and what will produce most effect upon fatty degeneration of any kind in the body of the patient. I do not know from experience that it will do any good in this kind of fatty degeneration; but it does so much good in other kinds of fatty degeneration that I deem it important that it be tried. Of course, the most nourishing food that the patient can take is to be preferred ; beef and mutton, all lean, and not excluding chicken and fowls of various sorts. Any good whole- some meat food, is better than vegetable food in this case; at the same time some vegetable food may be taken. Before I go on with the matter of rupture of the heart it is probably best that I give you a few statistics from different authors referring to the frequency of disease in the several valves of the heart. Here, for example, in 300 cases of endocarditis in the adult, 297 were on the left side, 32 on the right side ; 268 were confined to the left side, 3 confined to the right side ; 29 in both. (Taken from statistics.) In the foetus and newborn child, the evidence of endocarditis was in 192 cases in the right side, and in 15 in the left. Observe the very marked disproportion between the adult record and the infant record ; 192 in the right side in the infant or newborn, 15 only in the left ; in the adult 297 out of 300 cases on the left side ; but 29 of these were on both sides at the same time. In regard to the particular valve that is most liable FATTY DEGENERATION OF THE HEART. 1 49 to disease, in the 300 cases 255 were in the mitral ; a por- tion of these were in the aortic also, as you will see further on ; 129 aortic ; in the tricuspid valve, 29 ; in the pulmonary valve, 3 ; or one in a hundred. Of these 300, 159 were of the mitral only ; 40 were of the aortic valve only ; 3 of the tricuspid valve only ; and none of the pulmonary valve only. Here I have a record obtained from Bouillaud ; and observe it is in hospital practice, for children in Paris are sent to a hospital separate from the general hospital. He found endocarditis occur in 55 per cent of cases of articu- lar rheumatism. Budd, an English physician, finds it in 48. Fuller, in 23, Wunderlich and Lebert, in 23 per cent in a hospital for adults. In regard to embolism, of which I have said something to you, in endocarditis or after it, different parts of the body are the seat of embolism, or parts that obstruct the flowing mass. In 84 cases that were observed in the Berlin anatomical museum, 57 were of the kidneys, but not of the kidneys alone ; the kidneys were the seat of embolism in 57 out of the 84 cases. But these emboli are not always single ; the spleen was the seat of the same accident in 39 of the cases; the brain in 15 cases; the liver and alimentary canal in five cases only out of 84 ; and the vessels of the skin in 14. Of course, in several of these the emboli were multiple ; that is, different organs were affected at the same time. I50 RUPTURE OF THE HEART. LECTURE VIII. RUPTURE OF THE HEART. , Now, with reference to rupture of the heart. I do not beHeve the heart is ever ruptured when it is in a sound condition. You have just seen some illustrations of rup- ture of the heart, but bear in mind that some previous disease may have existed ; it may be there was what they call myocarditis, a form of disease that I have not yet described to you. That produces, as you will see when I shall describe it, a weakening of the muscles here, and makes a place of least resistance, and a place that is liable to give way under the power of other portions of the heart. The specimens that you are examining show fatty degeneration, or rather adipose degeneration, a weaken- ing of the muscular tissue, for fatty tissue has little con- sistency, gives but little resistance to the power that is acting on it. Now, if you had the means of determining in what particular cases this adipose degeneration of the heart has occurred, you might anticipate such an occur- rence, or rather you might conjecture that it might occur. And that is about as far as you can go in the diagnosis. I told you when we were last together that we have no means of diagnosticating fatty degeneration of the heart. You observe in these plates that the organ is not enlarged. There is no valvular sound to indicate the presence of any new structure ; therefore, auscultation amounts to noth- ing. The heart beats naturally and easily until the rupture comes. It may come during some period of considerable exertion, and the first you know of it is sudden death — and then you do not know what is the cause of death RUPTURE OF THE HEART. 151 until you have made a post-mortem examination. So that speculation in this direction is really a loss of time. You can, in the language of Goldsmith, be sure, after she is dead, that her last disorder was mortal, and that is about all you can say. The accident may surprise you, then, at almost any time. Still, it is not a very frequent occurrence. When it occurs from a weakening of the walls of the heart, of th^ muscular tissue of the heart, from previous disease, other than fatty degeneration, it will be likely to take you by surprise equally, because there is no murmur, there is no friction sound, there is nothing that is unnatural in the action of the heart, unless perhaps, occasionally a little feebleness which you can account for in a dozen other ways. When it follows myocarditis you have no means of anticipating it. It is, then, practically a post-mortem disease and you can prescribe no treatment. Dr. Ferguson * reported to the N. Y. Pathological Society a rupture of the heart in a man fifty years of age. His health was good till a few hours before his death, when he suffered from dyspnoea. He died in the water closet, a linear rupture in the anterior wall of the left ven- tricle began half an inch above the apex and extended up- ward three quarters of an inch. There was an increase of the fibrous tissue and pus in the muscular wall of the ventricle. Also another instance of rupture during a convulsion in tetanus. This was in a man forty-four years of age. He had a laceration of the left hand, and three weeks after tetanus began on the anterior of the heart an inch to the right of the apex there was a circular opening of one eighth of an inch in the right ventricle, the wall of which at this point was a line in thickness. * The Medical Record, Nov. 24, 1883. 152 RUPTURE OF THE HEART. Dr. Da Costa ^ in his Toner Lectures relates a most ex- traordinary breakage. A man of forty years had parox- ysms of severe cardiac pain happening at irregular intervals. They were attended by venous pulsation. This pulsa- tion was noticed while he was suffering pain, but was marked only while this lasted, or just before or after. At this autopsy the heart was found to be enormously hy- pertrophied ; one of the papillary muscles of the tricuspid valve was torn from its attachments both to the walls of the heart and to the tendinous cord, and a piece was found floating in the pulmonary artery. The right auri- cle and ventricle formed a continuous pouch that was filled with coagulum. Dr. Coupiand f reported a case of spontaneous rupture in a man aged sixty, from sudden fright. He says that perhaps the fullest information on this subject is given by Dr. Quain in his Lumleian Lectures, Lancet, 1872 ; I. p. 460, where he states that in yy out of 100 cases there was fatty degene- ration of the heart walls and that 63 were over sixty years of age. He also points out what all writers have noticed, that the exciting cause of the rupture was some sudden mental excitement or physical exertion. This patient, till the accident occurred, had had no symptoms pointing to heart disease, yet the coronary arteries were advanced in calcareous degeneration, and there was considerable adi- posity of the heart wall as well as true fatty degeneration. This case resembled the majority in the fact that the lesion was on the left side. In most cases the lesion is in the anterior wall, either in the region of the apex or close to the septum. In this case it is on the posterior wall, at some distance from the septum and about midway be- tween the apex and the base. According to Dr. Quain 71 deaths in 100 were sudden, occurring in one or two * Lecture m. f Medical News ^ Dec. 30, 1882. RUPTURE OF THE HEART. I 53 minutes, one patient, however, lived eight days ; i five days ; i nine days, etc. This patient Hved forty-eight, and the inspection disclosed two clots in the pericardium of different ages, and between the two effusions he rallied considerably. Dr. Van Santvoord* reported to the N. Y. Pathological Society a case in which death seemed to have been hastened by entrance of air into the pleural cavity in the operation of tapping. The heart was markedly hyper- trophied and dilated. The pericardium was thickened and seemed to be undergoing atheromatous change. The valves were healthy. The microscopic examination of the fibres of muscle showed no degeneration on the left side. One exhibited a marked tendency to longitudinal spHtting of the muscular fibres. On the right side the muscular fibres were in a state of moderate fatty degene- ration. Why there was heart failure was not shown by the examination. Dr. Displatz f relates a case in which a sharp fragment of bone lodged in the oesophagus about half way down. An abundant hemorrhage occurred on the eighth day which ceased spontaneously. Thirty-six hours later it was re- newed and was followed by death. There was ulceration of the oesophagus and perforation of the aorta about an inch below the junction of the transverse and descending portions. Dr. Wm. Axford if reports two cases, one in a boy aged 16, the other in a boy of 15 years. The first *' while car- rying a heavy weight made a sudden and great muscular effort. Soon he complained of considerable pain in the centre of the sternum, also of uncomfortable feeling in the left arm ; expectorated some blood ; short dry cough." A * Medical Record, March, 17, 1883. flbid., June 2, 1883. J Ibid., March" 24, 1883. 154 RUPTURE OF THE HEART. time after his pulse was lOO, temperature g7i°, respiration 26, irregular. There was an aortic regurgitant mur- mur. Since this accident the boy has not been able to do any hard work, but earns his living by bookkeeping. In this second case, a boy in good health made a sud- den and violent effort to control horses he was driving, and immediately felt pain in the region of the heart and said he could not get his breath for several days. Syn- cope and a sense of impending suffocation followed mental excitement or muscular effort often, and up to the time of the report he could not make any physical exertion. All who saw him found mitral regurgitation. Dr. Axford adds that Corvisart was the first to point out the fact that this injury was possible and that it could by caused by muscular exertion. Dr. Peacock, he says, in 1865, had collected seventeen cases, four of which came under his own observation. The valves injured were : the aortic ten ; the mitral four ; the tricuspid three. Dr. Brenner"^ reports the following : A woman fifty- five years old, had repeated hemorrhages from the stom- ach and died in consequence. She had had pleurisy of the left side six weeks previously. The left lung was retracted and closely adherent to the diaphragm. The two surfaces of the pericardium along the left border of the heart were closely adherent and the dilated stomach along the lesser curvature to the diaphragm. About two inches from the cardiac orifice on the lesser curvature was a round ulcer almost as large as the palm of the hand, at the edges of which were seen gaping coronary vessels. At the bottom of the ulcer was a sinus communicating directly with the cavity of the left ventricle through an opening in the endocardium the size of a pea. There were no serious cardiac disturbances during life. " The * The Medical Record, Oct. 7, 1883, ^ RUPTURE OF THE HEART. 1 55 hemorrhage was from the coronary arteries of the stomach and not from the heart." In two cases of perforation of the left ventricle of the heart by gastric ulcer Oser,* at autopsy, discovered a round ulcer of the stomach which had penetrated the left ventricle of the heart. The communication between the organs was through a long narrow canal. No air was found in the heart or vessels. The woman was seventy-one years old. The perforation was indicated three days before death by the vomiting of bright arterial blood and by tarry stools. Brenner had just published a similar case occurring in a woman 55 years old. She had had for years attacks of cardiac pain, occasionally attended by vomiting. A few days before death she vomited blood, had black tarry stools and great cardiac distress. A circular ulcer was found in the lesser curvature of the stomach, which com- municated with an opening in the wall of the left ventricle. Dr. Blockf of Dantzig has been trying to show that the heart when wounded can be sutured and life saved by experiments on dogs and rabbits. Four experiments with rabbits showed that both thoracic and pericardial cavities can be opened for a short time with impunity. An open- ing of the right and left ventricle as well as an entire com- pression of the heart, for the application of suture, can also be supported by animals for a few minutes, and he pre- sented a dog in good health in which there had been a wound of the cardiac muscle with opening and suture of the three thoracic cavities. In order to prevent the escape of blood in the applica- tion of the sutures the heart is to be seized at the apex and drawn forward until pulsation and respiration cease * Am. your, of Med. Sci., April, 1882. t Ibid., Jan., 1883. 156 FIBROUS DEGENERATION OF THE HEART. (the animal not being necessarily killed by the procedure) or the traction on the heart can be made only sufficiently strong to arrest the escape of blood from the wound. The wound can then be ligatured or sutured. LECTURE IX. FIBROUS DEGENERATION OF THE HEART. Now, then, I have something to say to you about the heart clot. No, not yet ; fibrous degeneration of the heart comes before that, because it is of the heart struc- ture itself. Dr. Quain, who gave us our first ideas of fatty degeneration of the muscular fibres of the heart, a few years ago, described what he regarded as hypertrophy of the heart arising from increase of its connective tissue. He called it fibrous hypertrophy. I have been, from the time he made this statement, a little skeptical in regard to the correctness of his opinion. But during the present winter I have examined by the microscope some speci- mens that are unquestionably of the character that he described, and a little further on, when you have fewer specimicns to handle, I will show you some specimens under the microscope that will illustrate this form of dis- ease. In specimens in my possession newly formed fibrous tissue or connective tissue is seen by the micro- scope in great abundance. In parts it is laid in between the muscular fibres of the organ. This new material, thus deposited, may have the width of one muscular fibre, or that of ten or twelve and more. In other parts it cuts across these fibres, causing their absorption so far as the new deposit extends. Then again it is laid in in- termittently, leaving a short fragment of a muscular fibre FIBROUS DEGENERATION OF THE HEART. 1 57 isolated, and then another and another, all lying in the same line, contiguous fibres all broken up in the same way over a space which may fill two fields of the micro- scope. Thus, in the field, which seems to be four or five inches in diameter, fragments of muscle, appearing half an inch long, broken by a layer of connective tissue and disappearing, reappear at variable distances, presenting another semi-fragment,' and so the field is checkered, the connective tissue showing its peculiar cells, and the muscular fragments their double striation. Thus in cer- tain parts of the heart the muscular fibres are broken up and their continuous action wholly lost. It seems that the connective tissue can take on hypertrophy by itself alone. The quantity of it that may be found upon the spleen, sometimes called a cicatrix, is enormous, and it is perfectly well formed connective tissue, with the fibres and with the nuclei, and it may be half an inch in thickness. The con- nective tissue in the liver is multiplied very much in certain forms of disease, as is also the connective tissue in other parts of the body occasionally. But in the heart it seems to have had but a recent discovery. All the hypertro- phies that have been noticed have been deemed to be hypertrophy of the muscular tissue only. As to the mode in which this particular form of disease presents itself under the microscope, when you make a section of an enlarged heart, you follow the muscular tissue a certain distance, and then it breaks up, and in the place of it you find connective tissue, and the connective tissue may be wide enough to reach the whole breadth of the field of the microscope, and no muscular tissue in it. But you see muscular fibres ending, one here and another there, then gone, and then by and by they will be observed again — that is, at a little distance from where they disappeared. It seems then to destroy the muscular tissue, when the hypertrophy of the connective tissue is marked. But fre^ T5§ FIBROUS DEGENERATION OF THE HEART. quently it seems to occur without being really a disorder. There is always between the layers of muscular fibre of the heart some connective tissue. The bundles are separated by something more than a myolemma, sarcolemma, or what- ever name you may give it ; some real connective tissue thrown in between the sarcolemma of the different bundles of fibres. You see that in passing a micro- scope over a thin section of the heart in almost any instance. Well, this increases in quantity, of course increases in thickness, and by just so much as it in- creases beyond a certain point it seems to diminish the muscular fibres by compression ; that is, causes their ab- sorption and removal. When, then, this form of disease presents itself in any decided manner, you can easily comprehend that you will have an enlarged heart with diminished power ; this deposit is for the most part in lieu of, or a substitution for, the muscular fibres, and as it has no contractile force, upon itself, it will only diminish the strength of the heart. I do not know that we are advanced far enough in our knowledge of disease to dis- tinguish between fibrous hypertrophy and muscular hypertrophy ; it requires some further observation ; but it is important that you know that there is such a thing as fibrous degeneration of the heart with increase in size. It is a matter that is open to study yet. The study has not been pursued far enough to enable us to lay down rules and principles in regard to it. HEART CLOTS. 1 59 LECTURE X. HEART CLOTS. Now, then, we come to heart clot. I give a little time to the matter in the lectures, as I used to receive from the graduates of the college long letters in regard to it. I remember one, four sheets of foolscap, written on each side of the page, describing a something that was terri- ble. A clot had formed in the heart, and extended out in the vessels about as far as the examiners could pursue them, and it was wonderful that a man could live with such a thing in his heart ; well, he did not. All that formed after he died. A distinguished physician of Philadelphia wrote a book on the frequent occurrence of ante-mortem heart clot. He thought they were of very frequent occurrence. I do not believe that. That clots can form in the heart pre- vious to death, and may cause death, I fully believe, but the occurrence is rare. I will make you understand that, I think, before we get through. Now, to distinguish between the clot that is formed before death and one that is formed after, there are two or three rules that will be diagnostic. You come to a heart, the left ventricle of which is filled with coagulated blood, and the blood runs on out through the aorta, and you can follow it to some of the ramifications of the large vessels ; or it forms in the right side, and extends through the pulmonary artery into even minute branches of the pulmonary vessels, and it does really look like a very formidable thing, and a per- son who does not understand it would assume that it was as bad as violent death. Now, then, if a clot form in l6o HEART CLOTS. the heart before the heart ceases to beat, it can never be attached to all the periphery of the heart. If the heart has ever beaten upon the clot that has formed in it, the contraction that must follow, if life continues, will separate the clot from all the external walls, from every- thing except the septum ventriculorum ; and when clots are found in the heart that have been formed during life, they are always attached to the septum, usually to the lower part of the septum, where are the greatest number of pectinean muscles. The very act of contraction must separate it. If you will think of it for a moment, you will see it cannot be otherwise. These clots are of two colors, buff and black. The buff is uppermost with reference to the position of the body after death ; the dark colored is the dependent portion. Now what is that buffy coat ? Exactly what takes place in the blood when withdrawn into a bowl and allowed to stand. The upper layer has been formed by the sinking of the blood corpuscles into the deeper layer, and that takes time. There is not time between two heart beats for anything of that kind to take place, and the occur- rence of a clot with a buffy portion and a dark portion is conclusive evidence that the coagulation took place after death. The heart was full ; it died expanded, and the coagulation took place in a manner that would require several minutes to form it, perhaps an hour or two. The blood does not coagulate quickly within the body. It has been estimated that it requires about six hours for the blood to become firmly coagulated after death. Sometimes it takes a much longer time than that, but a quick coagulation does not take place. As the blood- corpuscles are a little heavier under most circumstances than the fluid portion of the blood, their specific gravity being a Httle greater, they have time to sink to the deeper portions of the pool of blood, and allow the surface to HEART CLOTS. l6l coagulate with a buffy coat, a yellowish, semi-transparent substance. That, then, is conclusive evidence against the chances of ante-mortem heart clot. It has been assumed frequently enough that the in- dentation of the clot at the point where the valves are placed is evidence of an impression made upon it by the action of the heart during life. But this is altogether another thing. When death takes place and the heart ceases to send a current of blood through the aorta, the upper portion of the valve of the aorta falls downward of its own weight into the blood ; the lateral ones fall a little but not so much. The anterior is the point where quite an indentation in the coagulum has been noticed ; it falls into the fluid blood, and when the coagulation takes place, it will take place about that valve that hangs in it, and of course it will leave an indentation in it. So far from being an evidence of ante-mortem clot, that particular thing is evidence that it formed after death. Almost all the clots that are found after death are formed after death in the heart and great vessels. If the clot has formed before death, and the heart has beaten upon it, it has become compressed and will be found attached to the lower part of the septum ventricu- lorum and not to the walls of the heart, unless it be the very apex. Clots are formed in the heart. Here is a figure of one, and you observe it is rather crab-like in form ; it has several legs. Cardiac Thrombosis in Acute Disease. — Dr. Goodridge * bases his opinion on three cases in which death occurred with greater or less degree of suddenness and with attend- ant symptoms of dyspnoea, thoracic oppression, rapidly diminishing heart power, and a sense of impending disso- lution. In these cases there were found firm decolorized * N, Y. Med. Journal, Oct. 20, 1883. l62 HEART CLOTS. coagula, occupying in one case the left ventricle and the beginning of the aorta; in another, extending from the right ventricle into the pulmonary artery, and in the last blocking up the right auricle and the superior vena cava. In the last case the fibrous coagulum was distinctly lam- inated, and the symptoms pointed to a progressively in- creasing interference with the function of the right heart. At a meeting of the section in Practice of the Academy of Medicine, Dr. J. Lewis Smith* defended the opinion always taught from this chair since I have occupied it, that the white clots and those that have an upper layer of white and a deeper one of very dark color are always and necessarily of post-mortem origin. He brought into his argument a very important case. He had in the hos- pital a man whose symptoms led him to suppose that the right heart was overloaded with blood. Feehng that benefit might follow the withdrawal of some of this blood he introduced a hypodermic syringe and removed a cer- tain quantity. This blood was of dark color and perfectly fluid. The heart had ceased beating before the syringe was introduced,* and cardiac action did not follow. Dr. Janeway then injected a solution of carbonate of am-' monia into the same cavity, but it also failed to excite the heart to action. At the autopsy there was found a firm white clot entangled in the chordae tendiniae and columnae carneae and not any dark fluid. Immediately after the heart ceased to beat, the right cavity contained fluid dark blood. At the autopsy there was no fluid dark blood in the same cavity, but a firm white clot entangled, as de- scribed. *The Medical Record, Jan. 13, 1883. VALVULAR DISEASE. 163 LECTURE XI. VALVULAR DISEASE. It is necessary to refer to other causes of valvular dis- eases. The most common is the deposit of that substance that looks like mucine, that'I have described to you. Its organization and contraction, producing what I have already denominated the shortening, thickening, and stiff- ening of the valve. These same results may be obtained when other agents are at work. One of the things that operates most actively after inflammation is atheroma. Atheroma originally meant an abscess, but it has come to mean, in these later years, a particular deposit that is confined almost entirely to the heart and arteries, much more common in the arteries than in the heart itself, but in the valves not infrequently met with. This atheroma you can form an idea of by the specimens which I can exhibit to you. When you first find atheroma in the dead body it is almost always of a yellow color, or a faint yellow color. Here it is white. It has been bleached by alcohol, in which the specimen I show you has been kept. If you handle the specimen you will find that at different parts it is of uneven thickness. There are little warty, flattened eminences upon the whole circumference of it, and at the edge you can get an idea of its thickness. Here is another artery that is, to a certain extent, warty, exhibiting the same thing, lacking the yellow color which belongs to it when it is first seen. You observe it runs up the artery a considerable distance, that is the aorta. You observe, too, that it has narrowed the openings of the three arteries that are given off from the aorta. Here 164 VALVULAR DISEASE. is an interesting specimen of an atheromatous deposit in a valve and not in the artery, or if any, very little. The valve has undergone one of the changes that I will describe to you directly, and it has ulcerated a hole through the valve. Not only that, but it seems to have been deposited upon the substance of the heart, probably not in the sub- stance, and an opening has been made at the same time from one ventricle to the other. A broom straw has been passed through the whole, from one ventricle to the other, and you will observe what an ulcerated and damaged condition this valve is in. Here are a number of other specimens which you will examine. Now, then, the first question that comes is, what is this — this atheromatous matter? Well, it is an effusion on the outside of the inner lining of the artery ; the intima, as it is the fashion to call it now. It lies outside of the lin- ing membrane of the artery. It is to a certain extent infiltrated into the fibrous tissue of the artery, but it is much more commonly found just between the lining membrane of the artery and the fibrinous layer, called media in these later days. Between the intima and the media, then, is to be found this deposit. And it is con- stituted sometimes of a material very much resembling that which I have described to you as thickening the valves in endocarditis, a sort of mucous matter, and that is thick set with cells that do not grow, do not develop themselves according to the rules of cell growth in other parts of the body, but become attached to each other on almost any point where they may touch, and thus form a kind of tissue. Then that is pretty fully infiltrated with little globules of oil, and occasionally a few fibres are formed by the coalescence of these cells, but they possess very little power of permanent life. And the result of this is a pretty early change in their constitution. The cells disintegrate, and oily globules seem to take their place. VALVULAR DISEASE. 165 The fibres gradually disappear, being broken down into granules, and soon the means of organization have passed. This takes place very soon, that is in a few months, or a year or two at most. The result of the breaking down of the structure is a softening, and you can sometimes find these little deposits of soft material, looking exactly like pus, except a little yellow. Put them under your micro- scope and you will find' that there are no pus globules in them. The result of this is, sometimes, to leave an ulcer on the artery, or, as in the specimen you are examining, in the valves, and more frequently at the base of the valves than at any other part of them. A weakening of the structure is therefore produced, without softening. This atheromatous matter has no strength and it has no elas- ticity. It cannot replace in function, as it replaces in position, the fibrous tissue of the artery. The wall grows weak by the deposit of this matter in it, therefore, and you may start, with regard to aneurism, with this asser- tion, that aneurisms in the human body do not occur except by violence or by the weakening of the coats of the artery or through an atheromatous deposit. An aneurism in any of the large trunks of the circulatory system will not occur without atheroma ; the artery must be weakened before it will yield, and weakening is always effcted by atheroma of the artery. You may search for twen- ty years among aneurisms, and you will not find a single one that has occurred in a sound artery. Even those minute ones that have been lately described in the brain circula- tion have for their base atheromatous weakening of the arteries of the brain. Well, this is a pretty grave matter, then, for it is the parent of aneurism ; it also produces the weakening that precedes what is called dissecting aneu- rism. The artery may break partly in two, the inner lay- ers may be broken, and the blood may find its way be- tween the layers of the artery for a very considerable dis- 1 66 VALVULAR DISEASE. tance. This, however, I believe only occurs in the large arteries, the thoracic and the abdominal. I do not know but it occurs in the iliac sometimes. That, also, I say, has its origin in the weakening of the arterial coats by this atheromatous deposit. This is one of the courses that an atheroma pursues when it is once deposited in the ves- sels. Another is interesting perhaps, not to say impor- tant, in its bearing. The atheromatous matter is broken down very much in the same way as I have described to you, but more gradually, and the fat which seems to be taken up by the circulatory vessels, and deposited in the place of the atheromatous matter is bony structure, bony scales. Such a specimen as that I will try to show you the next time we come together, in which the whole ar- tery has been converted into scales, a multiplication of scales, some of w^hich have a real bony structure — have the lacunae and the canaliculi ; and some of which are mere calcareous accretions, without anything which dis- tinguishes bone. These render the artery inelastic, and so interfere with the circulation. As I have already told you, the heart sends the blood into the artery and dilates it, and the artery, by its natural contractile power, propa- gates or continues the action produced by the heart, car- rying the blood forward in the circulation. But in an ar- tery that has been deformed in this way the elasticity is gone. Hence, in such cases it is not uncommon that hy- pertrophy occurs. There is another evil that may come of these bony scales ; they are sharp at the edge ; they are thin. I say sharp ; they have almost a cutting edge ; and the gradual action of the artery, or so much as is left of it, may cut through the inner lining and let one of the sharp edges stand out like the edge of a nail, or the end of a nail rather, and on this may form the accretions of fibrine, the coagulations of fibrine, or vegetations, and these, in their turn, may wash off and make emboli. In VALVULAR DISEASE. 167 a few instances, when the process is softening, and it has occurred between the valves, the soft matter may remain between the valves some time. I had a specimen — I do not know but I may have it now, but I have not seen it for two or three years — in which the mitral valve was the seat of atheromatous deposit, which made a material looking like pus. It was found after death. It at first merely separated the two folds of the mitral valve, and formed a kind of abscess. The quantity of softened ma- terial it contained was perhaps half a teaspoonful ; it had not, as in the specimen you are examining, destroyed the lining membrane, or at least the folds of the valve. There is one other point to be referred to in this con- nection. You hear a good deal, or something, at any rate, of bony deposits in the heart, and particularly in the valves. They almost always result from a changed athe- roma. The atheromatous matter is deposited in the valves, and there is, perhaps, some thickening, too, from inflammation, produced by the irritation of this substance, and at length absorption of the material takes place and calcareous matter is deposited instead. I shall be able to show you, probably, two or three hearts, perhaps, some in which you can feel the bony roughness in the valves. Occasionally this bony deposit occurs in the heart itself. I was consulted in regard to a physician who was pretty well advanced in life. It was supposed that he had heart disease. His heart was beating irregularly, sometimes palpitating, sometimes beating very feebly, and he was subject to fainting spells. On examining his heart I found no enlargement. I found nothing to indicate val- vular disease, and I said, from the manner in which it be- haved, there must be some disease of it, but I cannot tell what. In a month or two this gentleman died, and a post-mortem examination was made, and a mass of cal- careous matter was found in the body of the heart, begin- l68 VALVULAR DISEASE. ning at the base, and extending downward an inch or more, and, to a certain extent, thickening the particular part of the base of the heart in which it was deposited. It had crippled the heart in its muscular contractions, and the heart resented it as well as it could, but it could not tell the story to the outsider. It was plain that the heart was not working properly, but why, nobody could guess, because there are other forms of disease that behave in the same way, particularly fatty degeneration, Quain's degeneration of the heart. You can frequently see that there is something wTong in the heart, but you cannot tell what it is. This atheromatous matter is not usually deposited in the muscular fibres of the heart; and whether it was the result of a previous deposit of this material in the heart, or whether it was a bony deposit or a calcareous deposit in connection with atheroma, I cannot tell. The importance of atheroma, then, will impress itself upon your minds mainly with reference to the deposit in the valves of the heart and the formation of calcareous or bony concretions in the valves, or, perhaps, in the sub- stance of the organ. There is no way of distinguishing, before death these several forms of diseased valves. You cannot tell, as you hear a certain murmur, whether it is produced by inflammation of the pericardium or by an atheromatous deposit, or atheromatous deposits that have passed into calcareous or osseous formation. To determine this you will have to wait until after death, and as almost all, and probably all, the vegetations of the valves are incurable, to distinguish the varieties is of no practical importance. A remark or two more in regard to endocarditis before we pass to diseases of the valves to consider them in de- tail. Endocarditis, Hke pericarditis, is very apt to show itself to a certain degree upon the heart itself. An cede- matous effusion may take place in the fibres of the heart VALVULAR DISEASE. 169 exactly as you see an oedematous effusion occurring in the leg when the knee is the seat of inflammation, or in the arm when the muscles of the shoulder are involved in inflammatory disease, as rheumatism. For example, in February of last year I woke one morning with a pain and stiffness in the left shoulder. I found that I could not get my coat on without assistance. So I got assist- ance to put on my coat and went about my business. The arm, however, grew worse and worse, and I recog- nized after a few hours that I had rheumatism in the del- toid muscle, and directly my arm and hand began to swell and my hand looked very fat. As soon as I saw it swell- ing I took off my rings for fear they would be fastened upon the finger and could not be gotten off. The swell- ing continued until, after a pretty free use of the bicar- bonate of soda, the inflammation was subdued. Then the swelling all went away. So in the heart, the parts neighboring to those that are the seat of inflammation may become the seat of oedematous effusion, and thus weaken the heart — the same thing that I stated to you when speaking of pericarditis. Pericarditis and endocar- ditis commonly occur together, and of course there will be on this account all the more of this oedema of the heart. Dr. Livingstone does not believe the little nodules on the edges of the mitral and tricuspid valves are of in- flammatory origin, for out of 136 autopsies of children either stillborn or a few hours old up to three and a half years of age, he had never failed to find them when he had looked for theiUy and he says they are the more pronounced the younger the child. He does not admit that they re- sult from the rupture of the intravalvular blood-vessels, causing haematomata from which the blood has been ab- sorbed and only a semi-transparent substance remaining. But he is inclined to the idea of Richard Pott, that they I/O VALVULAR DISEASE. are the remains of the foetal valve, whatever that may be. He says : " They are composed of a collection of the normal elements of the valve and do not appear microscopically like the deposits of an endocarditis." Dr. Livingstone raises the question whether the nodules on the mitral valve or the movement of the blood through the ductus arteriosus produced the systolic murmur heard at the apex, or whether it was produced at foramen ovale, citing de Gassicourt as authority for the idea that the current through the ductus arteriosus can cause a mur- mur. Endocarditis is perhaps the most prolific cause of de- rangement of the valves, and it may occur as the result of acute disease commonly associated with rheumatism, occasionally found in connection with Bright's disease, sometimes occurring in the course of measles, and rather frequently in the dropsical sequelae of scarlet fever, some- times occurring in septicaemia. And still again, I told you it may occur independently of any of these causes as a spontaneous, I might say almost idiopathic disease. That it does occur frequently in this manner is rendered evident by the large number of persons that suffer from disease of the valves who have not had any sickness pre- ceding the development of heart disease ; who. have not had rheumatism ; who do not remember that they have had scarlet fever ; who have not had Bright's disease, etc. I have told you of atheroma, a particular deposit, more frequently found on the inner, or rather under the inner, lining of the arteries encroaching upon the elastic tissues of the walls. I told you that it undergoes, whether in the valves or in the artery, one of two changes as a rule. It may soften and form a yellow collection looking like an abscess, and this may rupture the intima and escape into the blood, and do mischief or not according to the fineness of its division. Or it may harden and undergo VALVULAR DISEASE. I7I calcareous degeneration. It does not seem possible that the elements of atheroma can be converted into bony matter. It would seem altogether likely, therefore, that it is substituted for these after they are softened and have been absorbed. I told you that this deposit in the valves causes a thickening, an inflammation, a bony deposit especially causing constant irritation. I told you that the valves are sometimes ruptured, and I pointed out to you a specimen in which the inferior or lower portion had given way, so as to render that part of the valve useless in retaining the blood in the artery. I told you of a case in which a man, while lifting a heavy beam, felt a sudden something give way, he could hardly tell what, but he said there was something gave way, and he fainted, and sat for a considerable time in the mill before he attempted to go home, and then reached home only with assistance. In a few days he revived again and went to his work. He lived twelve years after that with the heart largely hypertrophied. At the post-mortem the longest portion of the tricuspid valve was found to have been flapping backward and forward in the current of blood. As the blood ran down, the strand was in the ventricle, and when the heart contracted it would double back on the rest of the valve. A tendinous cord had given way when he had felt the sensation described. He had a murmur heard in systole ; not in diastole. The valve may give way in a considerable variety of cases. I recall one of a gardener who had loaded his cart too heavily. His horse could not draw it, and he put his shoulder to the rear of it to help the horse, and exerting about all his strength, he also felt something give way and was very much crippled after that. He came to Bellevue Hospital. There I had an opportunity of examining him before and after death. A portion of one. of the folds of the aortic valve had given way in his 172 VALVULAR DISEASE. case and I thought almost without previous disease. Atheroma is a very common precedent of the breaking of the valves. This man lived about two years after the accident occurred to him. I once was with a gentleman who was making great haste to reach the top of a hill. He was within about fifty feet of it, when he started on a run up the steep ac- clivity. The result was he was brought into the same condition as the gardener, and from that time on, as long as I knew him, there was a regurgitant murmur at the aortic opening. He broke something at that time. Pre- cisely what, whether the bottom of the valve gave way, or whether it split down, I cannot tell. One thing, how- ever with regard to the splitting of a valve is worthy of notice. You remember there is on top of the valve a kind of cord, and immediately below that cord the valve is not as strong as at the edge. The common way for a valve to break is to give way at the cord, and it vibrates in the current of blood, and frequently makes a musical sound, a sort of ^olian harp sound ; making a noise that is not altogether unlike that of a cord stretched across a little opening in a window. It is quite a musical note, and I don't know that there are any other circumstances in which that musical sound is produced. Then I should add, in this enumeration, that the tendinous cords are occasionally found welded together, two or three or more of them, and, of course, a great deal crippled in their action. In certain instances the two folds of the mitral valve and the three portions of the aortic valve grow together, in the latter case leaving a slit by which the blood can go out and by which it will return in re- gurgitation. How in the world that can occur I do not know, but it does occur. They are almost always thick- ened, so that they do not play freely before this adhesion or coalescence takes place. But moved, as they are, con- VALVULAR DISEASE. 173 tinuously, by the current and reflux of blood, it is very difficult to understand how these three portions of the aortic valve can grow together, leaving only a little slit for the blood to pass through. It is easier to understand how adhesion may take place between the two curtains of the mitral valve, for by contraction they can be grown together, and contraction is affected by the material that is deposited between the two folds of the valve. I will put in your hands, now, for example, a few speci- mens of valvular disease. Here is one, in which, as you open it you see that the wall is the seat of spots of atheroma, and some of these have passed into a calca- reous condition. Even the valve itself is shortened and thickened, but not remarkably. In this one the aortic valve is very much diseased. If you put your finger on it you will find that it has hard scales on it. It is not very much contracted, except one fold of it. One fold is thickened and hardened, and on the inside of it is a little calcareous matter. This has been a pericarditis, and the outside of the heart is roughened by the adhesions that formerly existed on the pericardium. The mitral valve is in a state of very marked stenosis, that is, contracted, and you see here almost nothing of the tendinous cords, they are shortened so much. The fleshy columns are a little elongated, to make compensation for the shorten- ing of the tendinous cords. This is a striking speci- men of stenosis of the mitral valve, and in this con- nection it may be that we shall find an illustration of the rule that applies to such cases generally — that is, stenosis of the mitral valve induces hypertrophy of the right ven- tricle ; stenosis of the left auriculo-ventricular valve in- duces hypertrophy of the right ventricle, and frequently of the right auricle, and also sometimes of the left auricle. This you see illustrated here. The right ventricle is thicker than natural, but not very much hypertrophied. 174 VALVULAR DISEASE. This stenosis, marked as it is, did not disturb the circula- tion as it sometimes does. Then in this specimen you have two lesions, the aortic valves thickened and a little calcareous deposit in them ; and at the mitral valves, stenosis. In this specimen the mitral valve is thickened and hard, but not disorganized, and it is large enough to allow the circulation to go on with ordinary freedom. The aortic valves are thickened, shortened, and hardened. In this specimen the aortic valves are a little but not much dis- eased. The chief lesion is probably in the mitral. You observe the mitral valve is thickened, not exactly disor- ganized. There is some hypertrophy of the heart. This is not a very striking specimen. Here is a very good one, and opened in such a way that you can see the change that has taken place; it is in the aortic valves. You observe they are contracted in their length, contracted in height, and thickened, but not nearly as much as in some specimens I shall show you hereafter. Now comes the question, what sort of disturbance will these lesions of the valves produce? Of course it will be first felt in the circulation. Let us take a mitral stenosis, such as you have in two or three of the specimens now going round, and its effects are perhaps as simple as the effects of any of these lesions. Indeed, they all follow in the same track after they have taken the first step. Re- member, now, that the blood in the left auricle has just come from the lungs, and it is seeking its way into the left ventricle. It is obstructed at the valves ; well, what will that do ? The circulation by the right heart we are to assume is natural. The blood goes into the general system, and empties into the right side of the heart, and from that is thrown into the lungs, and it begins to come from the lungs into the left heart and is obstructed VALVULAR DISEASE. 175 What then ? The first thing will be a certain amount of engorgement of the lungs. They receive blood faster than they can discharge it ; the consequence is, therefore, an engorgement of the lungs, greater or less, depending upon the extent of the stenosis. Next after that comes a strain upon the right heart, which is attempting to send blood all the time into the lungs, and associated with this may be what is called an emphasized condition of the second sound in the pulmonary artery. That is pretty full of blood, the right heart pumps more into it, the reaction is stronger, and makes the valves strike with more force than natural. Hence, there may be an increase in the second sound from the pulmonary artery, in an instance where the disease is at all considerable. Well, what more ? Stop the blood from coming into the right heart and what will be flooded ? Why, every impor- tant organ of the body. The blood cannot return from the veins with anything like its natural freedom. The liver will be engorged, the spleen will be engorged, the brain will contain more blood than it should, the face perhaps will be a little puffy, from a little effusion into the tissues from the veins. The veins cannot empty themselves freely. Little clusters of enlarged veins are found upon the surface of the body, chiefly upon the chest. The external thoracic veins frequently become enlarged. There is general hindrance of the blood in the general circulation, because there is obstruction of the blood in the lungs, and consequently obstruction in the right heart, to which the blood in the general system should naturally go. One consequence of this accident, then, is enlargement of the liver ; not in all cases, not in the majority of cases, but now and then. And some- times quite considerable hypertrophy of the heart, and enlargement of the spleen, from the same cause, namely, obstructed return of blood. The effect upon the stomach 176 VALVULAR DISEASE. is often noticeable. There being more blood in the stomach mucous membrane, the digestive membrane, than can be used, the digestion becomes impaired. It is imperfect, and the appetite feels the effect of this. Then, too, the effect of the obstruction is sometimes so consid- erable as to hinder the contribution of the thoracic duct to the general nutrition of the body. The thoracic duct, you remember, receives the material that is digested in the intestine, and carries it to a vein through a duct, and that vein delivers it to the general circulation. Well, that is obstructed also ; it cannot freely give its nutritious fluid to the blood, and it not infrequently happens that the patient becomes pale, in consequence of imperfect nourishment, though he may eat a considerable quantity of food ; and you will observe, frequently — I am referring now to an advanced case — that the patient speaks of his feet "being swelled, particularly at night, if he is on his feet during the day, and you observe yourself some pufifi- ness about the face. You will particularly be able to notice what has been called the tear line ; that is, a some- thing looking like a silver thread or a thread of transpar- ent glass lying upon the upper edge of the lower eyelid. It is a little oedema of the conjunctival covering, and as the eyelid presses considerably upon the eye it is forced up along the ridge, above the tear line. There may not only be oedema of different parts of the body, but the whole body may be swollen. The kidneys have suffered congestion, and have taken on a condition analogous to that of Bright's disease, generally the large white kindey, and they are unable to perform their function properly. The urea remains in the blood, or a part of it, at any rate, and produces its systemic effects. The urine is com- monly scanty, sometimes even bloody, and there is not unfrequently effusion found in the chest, a double pleuritic effusion. I recently examined a gentleman from the VALVULAR DISEASE. 1 77 country, or rather from a distant city, who had been ill for some months, and in the course of the examination found fluid effusion coming nearly up to the lower angle of the scapula on both sides. My thought was, he has Bright's disease. He had heart disease, for his heart was enlarged, but there was no valvular murmur at the time I examined him. On examining the water I found it con- tained a large quantity of albumen. It was one of the cases that interested the late Dr. Stephens so much when this matter was first investigated. There was a large amount of amorphous urates in his urine. On heating it up to about the point of boiling, it became cloudy with albumen, and heating it till it boiled it became almost thick. I have a scale for estimating the amount of albu- men in the urine, ranging from one to ten. Ten repre- sents a coagulation of albumen in the tube, so that noth- ing will run out ; invert the tube and nothing is dis- charged ; the whole of the urine is imprisoned in the co- agulated albumen. When there is but a trace of albu- men it is represented by one. In the specimen of the patient spoken of the amount of albumen was represented as six ; or more than half of the urine was composed of al- bumen. I did not know that this gentlemen had Bright's disease when I found a double pleuritic effusion (although I felt pretty sure of it), for double pleuritic effusion does once in a while occur with Bright's disease. This, then, is substantially the series of consequences that will result from obstruction, from stenosis of the mitral valve. And you can see that when the blood is returned through this valve, that is, when it has entered the ventricle, and a part of it is returned into the auricle, that it is going to do exactly the same thing when the condition becomes marked. It it all the same, save that in the one case it is stenosis, in the other it is insuffi- ciency. The valve is incapable of serving as a gate, a 178 VALVULAR DISEASE. watch, and a part of the blood that enters the ventricle goes back into the left auricle, and obstructs the blood that comes in from the lung, so that the result in the end is exactly the same — congestion of these various parts, sometimes cyanosis. This latter belongs also to mitral stenosis. Then there is another point which I may as well refer to here. You sometimes see a pulsation in the veins of the neck, the jugular. There are two modes in which what appears a little like a pulsation is to be accounted for. When this obstructed circulation occurs the vein is seen to fill in expiration. In expiration the blood does not flow so freely in the lungs or into the chest, as in in- spiration, and in expiration you may watch the vein and see it fill, but it fills from above. It is not a wave coming up from below. About the only conditions in which the wave will come up from below are when there is insuf- ficiency of the tricuspid valve, that is, the valve of the right side of the heart, or when there is hypertrophy, a tumor like an aneurism resting upon the vena cava de- scendens. In either of these cases a regular wave may come up the vein, but I know of no other condition in which it does occur ; but in the cases referred to you observe the filling of the vein is a different thing from an aneurismal tumor. It is not necessary to dwell longer upon regurgitation at the mitral valve, as the effects of it in the end are the same as those of stenosis. VALVUI-AK iJiSEASE. 179 LECTURE XII. VALVULAR DISEASE — [Continued), Now turn to the aortic valve, to the two conditions that have been named — obstructive disease and regurgita- tive, or direct and indirect, jf you choose to so call it. When there is obstruction at the aortic valve the sound produced by it will be heard in the contraction of the heart in systole, and it will be loudest at the base of the heart, near the sternum. This may exist in a moderate degree for a long time, and no very grave aonsequences result. But if it is a growing disease, if it is a form of valvular disease that is irritating in itself, like a spicula of calcareous matter in the valve, action of the valve will excite an inflammation, and cause a deposit of material that can contract and still further deform the valve. But there are a great many persons who can carry both mitral regurgitation and aortic obstruction a very long term of years. Indeed, my colleague, the late Dr. Gil- man, came to me with mitral disease at a certain time, and he said, '' Am I going to die of it?" '' Well, maybe," said I, " but I think you will live twenty years." The years rolled on, and I heard nothing more of it, until at length Dr. Oilman came to my house, and exclaimed : " Doctor, my lease is out ! I want to renew it !" He lived about four years after this. I remember a patient who carried a valvular lesion fifty years before a fatal sickness occurred ; a young man, at first, all activity, but, of course, he could not go up-hill or up-stairs as well as other people, but his mind was active, and as an evidence of his industry, in the old time, when l8o VALVULAR DISEASE. speculation did not fill a man's pocket in a day, he had made by speculating in oil a million of dollars, and built up the fortunes of two brothers in this period of fifty years. I am in the habit, in this connection, of referring to a certain case because it is rather impressive. Many years ago I had occasion to listen over a certain gentleman's heart, and I found a mitral murmur. He appeared per- fectly well, and I went on, making no sign of surprise, and afterwards thought the 'thing over. He is of phleg- matic temperament, and I do not think he will be very much excited ; he will take the world pretty easy ; I think he will take the world quite as easy without as with a knowledge of the disease of his heart. Now that gen- tleman is in active practice to-day ; you see his name not infrequently in the medical journals, as having performed this or that operation, and he is a great deal happier than he would be if he knew that he had mitral regurgitation. There is no knowing, then, when the unfavorable issue will take place ; but I can tell you this about it : when a patient comes to you complaining of a great deal of short- ness of breath, when he has oedema of the feet, and pos- sibly some swelling of the face, look to the kidneys. They probably have become involved by that time, and in a few weeks, in a Aveek or two, he may be pretty gravely sick, having carried disease of the heart for twenty, thirty, forty, or possibly, fifty years, as in the case I have just referred to. And here it is perhaps proper to say that the last generation of doctors, and the present generation of people who are not doctors, look upon the statement that they have heart disease as equivalent to signing their death warrant. The profession have out- grown the idea that heart disease must be fatal in a few months ; but the older physicians, physicians of past gen- erations, not having auscultation to guide them, were not VALVULAR DISEASE. l8l able to detect diseases of the heart until the kidneys, and perhaps liver, and possibly the spleen were involved. In other words, not until oedema came. Their post-mortem examinations told them what oedema meant. They were able to recognize then, by the general signs, what was the trouble, but the patients generally died pretty soon, in a few months after the oedema occurred. But they may have passed forty, fifty, or even sixty years before that, with the same disease of the heart, only it had not until the oedema appeared, come to be obstructive to the venous circulation. But to go on with the obstruction at the aortic opening. If it is moderate there is compensation. The heart has the faculty of growing in size and in strength to meet an emergency, and we speak of compensating hypertrophy of the heart. If the blood does not flow easily through the aortic opening, the heart will gain additional strength by gaining additional fibres, and will overcome the obsta- cle, so that a man may carry a disease of that kind a great while without knowing that he has it. But when regur- gitation occurs, and that is only in the advanced stages of obstructive disease, when the valves become shortened and thickened, so that they cannot fall together, a certain quantity of blood that has been sent into the aorta goes back again into the ventricle every time the heart dilates, and here is work to be done over and over again. The heart has to do its work twice over, substantially ; at any rate, once and a half. The ventricle has just been filled from blood forced in from the auricle, and half filled from that which comes from the aorta. The effect of this is ex- actly that which I have been describing to you, and you will see how it must be so. When blood from the aorta falls back into the left ventricle it prevents blood from coming in from the left auricle. Only about half the con- tents of the ventricles can come in from the left auricle, 1 82 VALVULAR DISEASE. and consequently the blood will set back upon the right heart, and engorge the lungs, and it will also produce very much the same general symptoms as those I have de- scribed to you. Well, then, these all come to about the same thing. Their consequences are substantially the same. So also in contraction of the mitral valve. A contraction of the aortic valve, you observe, is compen- sated for very generally, and that is not so grave a trouble. A stronger current of blood is sent over it, and of course into the general circulation more blood is sent in a given time, and consequently the general circulation does not feel it so much. These are the general effects relating to the advanced stage of cardiac disease. The question has been often raised and discussed, which comes first, the kidney disease or the cardiac disease? My own answer is very positive : that while the cardiac disease may come after the kidney affection has begun, in the great majority of instances in which they are con- nected, the connection is as I have been describing to you. The kidneys become congested because the circu- lation is obstructed at the heart, and after they have suffered a certain length of time they will begin to give albuminous urine ; they do not secrete the urea in full measure, and cede*ma then begins in different parts of the body. It is my strong conviction that in nine cases out of ten where the two are associated the cardiac disease came first, and the other case will be an instance in which kidney disease from some other cause has occurred, and the cardiac disease has followed ,it, possibly by the influ- ence of congestion in a certain degree. But the order is almost always cardiac disease first, and renal disease afterward. I have noticed so often what I have already explained to you that I cannot have a doubt about it. I examine a man and find he has valvular lesion of one sort or another ; I watch him for a year ; he gets along very VALVULAR DISEASE. 1 83 well ; and perhaps ten, fifteen, or twenty years after I have examined him for the first time he begins to suffer ; he begins to get oedema of the lungs, which is one of the effects I have not mentioned. We may have an oedema- tous condition of the lungs, as well as of the legs, body, and face. With reference to the right side of the heart, we have had but little experience with disease of the valves on this side. For forty-nine cases of valvular disease of the left heart there will hardly be one of valvular disease of the right heart. I have told you that after birth the left side of the heart is the seat of disease, and before birth the right. In the right heart there are lesions of the valves, though they are rarely met with. In a little boy about e-ight years old, when the college was in Crosby Street, I found a very peculiar sound in listening over the base of the heart. It was not a murmur, but it was a snap, and it was heard in both actions of the heart. It was a double snap, very much such as you get by pulling a piece of ribbon suddenly. He died, and at the post-mortem examination that sealing together of the pulmonary valves was found which I have already described to you. The edges of the three portions of the valve were sealed together, with the exception of an openings which must have been less than half an inch in the middle, and one of the lips of that opening was a little longer than the other, and it was this which snapped when the blood came against it from the heart, and snapped again when the pressure from the artery was felt. That was the only lesion about it. I did not distinguish that from the aortic disease, for it is a difficult thing to do it, but some per- sons claim to be able to do so by getting the sounds of he pulmonary valves a little to the left of the sounds that^come from the aorta. I dare not trust my ear for the diagnosis ; and besides, there is another mode that is 1 84 VALVULAR DISEASE. worth something, but not worth a great deal either, and that is, if the sound is at the base of the heart, to follow it to the artery, and particularly to the left and right clavicle. Listen to the sound from the heart there ; if it comes up there pretty fully, it is in all probability in the aorta. I say, in all probability. I make that modifica- tion because the two vessels, the pulmonary artery and the aorta, are sealed together by loose connective tissue, and for a certain distance after they leave the heart they run together. I have some curiosities here, some that are so rare that you may never see anything like them, and some that you will see plenty of. Here, for example, is a heart, the peri- cardium of which is attached to the heart, but between the pericardium and the heart is a layer of bone that makes a perfect hoop, or did make a perfect hoop about the heart. This bony material, you observe, is covered over by the pericardium on the outside, and attached to the heart on the inside. It flattens out to make quite a broad covering, then it grows narrow, and is broken, and you can feel the rough bone on each side — it then goes on up to the point of starting. How a heart hooped in this way could pump out blood is a matter of wonder. It was probably by a change in its usual motion. The contraction was probably from the point towards the base. There is also in this heart a considerable amount of thickening and hardening of the aortic valves, but not so much as in some specimens I shall show you. The amount of effusion that took place during the pericarditis, between the pericardium and the heart, was too large to undergo organization, and for some reason bony matter has taken its place. It was very likely broken down and absorbed in part, and calcareous matter deposited in its place. VALVULAR DISEASE. 1 85 Here is a heart that I shall have occasion to refer to, perhaps, at our next meeting. Observe, particularly, its flabbiness, and its color, which is yellow. This color is not so very deeply marked, however. It is a fatty heart. It is an example of Quain's degeneration. It is a feeble heart also ; the walls are hardly of the usual thickness. But I will touch on this again further on. I have but little more to say regarding valvular diseases. I told you that the valves are occasionally torn out ; the aortic valves are torn out at the bottom, at the attachment to the aorta. The cup is made no cup by having its bottom fall out, so to speak. That is almost always the conse- quence of atheromatous degeneration, weakening the valve at that point. There is another atheromatous change that is met with occasionally, and that is athero- matous deposit at the point where two of these valves are together attached to the aorta. You will observe as you examine these specimens that each pair of the valves, each of the two valves that are near to each other, have their attachment to the aorta at the same position ; that is, one is in immediate apposition to the other. Now, it sometimes happens that the aorta at that point becomes atheromatous, and that the attachment is torn down. It is torn down so that it comes to be about a quarter of an inch below the attachment of the other valve, and this produces insufificiency. The valves will not, even suppos- ing they are not diseased, meet in the middle of the aorta ; one will fall in below the others, and consequently the valve is incomplete. These, I think, with those enumerated before, will con- stitute the changes which you will be most likely to meet. Possibly not all the changes, but they are all that occur to me as occurring with any degree of frequency. There is a point which I omitted to refer to, but was reminded of by one of the students, and that is with re- 1 86 VALVULAR DISEASE. gard to the pulse in regurgitation at the aortic opening. There is a peculiar pulse. It has not, as our Methodist friends say, the gift of continuance. It is a blow, short, sharp, I cannot say decisive, and then it seems as if the pulse is instantly cut off as soon as you feel it. There is a little duration to the swelling of the artery in the healthy condition, and still more in hypertrophy of the heart. Supposing there is no obstacle, but if there is regurgita- tion at the same time, the pulse has that short, quick, sud- den beat aud sudden subsidence; the force that created the pulse seems to be withdrawn instantly after you feel the pulse, and then there is not infrequently, on account of the smaller wave of blood that is sent out, a little retarda- tion ; that is, the pulse does not come to the finger as soon after the heart-beat as in health. But this you can only appreciate by putting one hand on the praecordial region and the other on the pulse. The arteries in the neck, in instances of hypertrophy and regurgitation at the aortic opening, are apt to be enlarged and to have a wide beat. You observe I do not say stronger beat, but a wider beat than usual, and the pulse in them is apt to be feeble ; and further, the arteries in time not infrequently grow tortuous — they wind about instead of going direct to the point of distribution. From a number of examinations of hypertrophied hearts, with valvular lesions, Dr. Putjatin* concludes that in chronic affection the nerve ganglia are affected by an inflammatory process. In early and slight disease the changes are limited to hyperaemia and granular de- generation. In chronic and extended disease of the heart the connective tissue is produced and there is fatty and pigment degeneration of ganglion cells. In one case there was entire destruction of the ganglion cells and calcifica- * The Medical Record, July 7, 1883. VALVULAR DISEASE. 18/ tion of the tissues between them. Changes in the ganglia may also be produced by chronic constitutional disease. In this fact may be found the explanation of the function disturbances and even paralysis of the heart. Another observer found that in hypertrophy with chro- nic interstitial nephritis with the growth of the muscular tissue the medullary sheath of the nerves is lost, and a process of nuclear proliferation commences. Should an acute disease supervene, then the change in the affected nerves assumes the character of an acute parenchymatous inflammation. In the nerve cells lying in the course of the fibres as well as those in the ganglia of the septum arteriosus the changes were confined to thickening of the capsule and increase of the nuclei. The protoplasm itself was not affected. As bearing upon valvular disease of the heart both in reference to etiology, pathology, diagnosis, and treatment, I have collected several cases, some from those which have come under my own observation and others which have been reported in current medical literature, and shall also enumerate various experiments which have been made, and conditions which have been observed in valvu- lar diseases of the heart. Dr. C. S- M., seventy years of age, applied to me forty years ago for advice regarding a disorderly heart. I found that he had moderate enlargement and a murmur, I think mitral chiefly, because he has now that murmur feebly, and no murmur at the aortic opening. He was advised to eat moderately, not to walk up hill when he could ride, and when obliged to do this to take plenty of time, and go very slowly ; as his profession would compel him to ascend stairs many times a day, to apply the rule of mod- eration with great rigor to this part of his duty. He has lived in obedience of these rules. He has taken no intox- icating liquors except when needed as medicine. He 1 88 VALVULAR DISEASE. has had nearly all his professional life a large practice, but as soon as he had won the confidence of his patients sufficiently to do so he refused to go out after bedtime, and has long had a partner on whom that work has de- volved. He has, until lately, appeared like a healthy man, and it is only in the last four months that he has not been able to follow his practice. A month and a half ago he came to my house suffering from shortness of breath, and having some cedema of the legs, and fluid in each pleural cavity, filling one half its capacity. He took diuretics. The kidney secretion soon amounted to seventy ounces a day, and he improved rapidly, so that he felt that he was all but restored to health, and ceased to take any medicine. He went from home, as he says, " on a summer vacation." While away the urine dimin- ished in quantity to three or four ounces, was of very high color, and highly albuminous. With this came con- vulsions, and he had of these in a day and a half they say thirty, none very violent, but all with a short period of unconsciousness. With a digitalis poultice over the loins and other medicines the urinary secretion was restored to a healthy quantity and more, and he has had no more convulsions. After recovering some strength he returned to his home, where I saw him to-day (Aug. 23, 1883). He has now no oedema at all. The fluid is wholly re- moved from the chest, but he has lost flesh since I saw him a month and a half ago, yet for most of the time he has taken about his usual rations, avoiding meat since the convulsions, but taking milk and eggs. The urine amounts to thirty ounces and over daily, and he says he feels well but is not strong. He walks the floor, but is not willing to go down stairs, fearing he cannot get back Albumen had not been found when I saw him first, and no casts; but I felt certain of Bright's disease because it so often follows heart disease even forty years after the VALVULAR DISEASE. 1 89 discovery of the heart affection ; and because there was double pleural serous effusion, without pain, or other evidences of pleurisy, and because with these there was oedema of the legs. I did not examine the urine, but others have ; and since his first call on me albumen has been found, uniformly, more or less varying, and casts not uniformly, but often, mostly hyaline. Now comes the peculiarity, to record which I have written up the case. When I saw the doctor in July I made out a double mitral murmur, which was not very distinct to-day, but his pulse at the wrist was twenty-eight beats in the minute^ and no faint indication even of any more. But when the impulses of the heart were counted by putting the ear over it, there were twenty-eight pul- sations that were distinct and strong, and twenty-eight more alternate ones which could just be heard and no more, and which sent no pulse to the wrist. Occasionally the feeble heart pulse would be strong and forcible, but for almost the whole of a minute it was the faint and the strong alternately. Dr. Herman Tittenger* describes a peculiar murmur characterized by the distance at w'hich it is audible (it can be distinctly heard through the bed covering) by its stability (it is but slightly influenced by the intensity of the heart's action) and by its character. Together with the murmur is perceived a widely propagated tremor. This phenomenon occurs only with rupture of the valves or tendinous cords. The primary murmur is caused by insufficiency of the valves, the secondary sound by the flapping of the loose valves and tendinous cords in the returning blood stream. A diastolic murmur indicates the rupture of the semi-lurrar valves, while a systolic * Medical Record, Aug. 18, 1883, p. 184, from Centralb.Jiir Klin. Med., June 9, 1883. 190 VALVULAR DISEASE. sound points to the (much less frequent) lesion of the mitral valve. Aneurismal Dilatation of the Heart and Mitral Steno- sis — Fibroid Induration!^ — The heart is large ; the ante- rior wall of the left ventricle is bound to the pericardium by a firm band of connective tissue. The left ventricle is enormously dilated, and the left ventricular wall in places is less than one eighth of an inch in thickness, and at the apex there is a portion of the wall where the pericardium and endocardium are separated only by the interposition of a thin layer of fat. Posteriorly the ventricular wall is much thicker, being uniformly nearly one inch. The papillary muscles are much hypertrophied. The right ventricle is moderately dilated, and the valves of that side are normal. The segments of the aortic valve are slightly thickened and retracted. The stenosis of the mitral valve only admits a cylinder of half an inch diameter. The endocardium is markedly thickened, and in all the ven- tricular wall there is increase of the fibrous tissue be- tween the muscular cells (fibroid induration of the heart) especially marked where the ventricular wall is thinnest, except at the apex, where there is no muscular tissue. There is atrophy of the fibre cells, and much pigment arranged around the poles of their nuclei. The cells in places contain a small amount of fat, but generally the transverse striae are well preserved. Dr. Ferguson, who reported this case to the N. Y. Pathological Society, May 23, 1883, has examined the most of it. He finds parts hypertrophied, parts dilated, in parts fibroid substitution for muscular fibres, and here and there a little fatty degeneration of the muscular fibres. The patient was twenty-seven years of age ; had had rheumatism. His chief suffering was from dyspnoea * Med. Rec, Sept. 8, 1883. VALVULAR DISEASE. I9I and palpitation, cough and expectoration, the latter scanty and sometimes streaked with blood. There was a double mitral murmur. Pulse 80 to 140, temp. 99° to 102°. He died unexpectedly. A complete diagnosis was impossible. Dr. Ferguson exhibited at the meeting, June 27, 1883, a heart resembling this with aneurismal clots adherent near the apex in the left ventricle, wall there thin and wholly fibrous, muscular tissue gone. Tricuspid Insufficiency. — M. Frangois Franck,* by a specially contrived valvulotome, has produced tricuspid insufficiency and has noted the effects, i. Systolic pul- sation in the jugular veins and in the thoracic veins, dila- tation and hepatic pulsation. 2. Systolic murmur in the heart, whose pitch is in inverse proportion to the extent of the sound ; increased frequency of cardiac action ; diminution in the arterial pressure. 3. Increased fre- quency of respiration ; and 4. After a time the phenomena of general venous stasis ? — ascites, anasarca, albuminuria, etc. M. P. Dureoziez concludes that a tricuspid regurgitant murmur can be heard over the entire anterior surface of the heart, the points of maximum intensity being some- times at the xiphoid cartilage, sometimes at the cardiac apex, and it may be heard at the latter spot only. It is not, however, transmitted to the axilla ; and is not heard in the back. It is not, necessarily, associated with venous pulsation. Mitral Obstruction and its Consequences. — Dr. E. R. Bruch,f at a meeting of the Pathological Society of Phil- adelphia, exhibited a heart the mitral opening of which was nearly occluded by an epigglotic-shaped enlargement * N. Y. Med. your., March 3, 1883. \ Ibid. ig2 VALVULAR DISEASE. of one of its leaflets, permitting during life reflux. The result was dilatation and hypertrophy of the left auricle to twice its proper size. The right ventricle is very much dilated, the walls of less than half their proper thickness, and the capacity of its cavity doubled. The tricuspid valve was insufficient on accourtt of this dilatation. There was during life a broad area of dulness, extending to the right of the median line. The murmur heard was both systolic and presystolic. The second sound was much accentuated. The first sound was distinct over the ven- tricle, but obscured by the murmur at the apex. The immediate cause of death was pulmonary repletion with blood which induced right heart failure, as in cases of aortic obstruction it is induced by left ventricle failure. Pleurisy with Heart Disease. — Dr. Bucquoy* has ob- served a number of cases of pleurisy occurring in the course of heart disease. He says that though the patient may be weak from this disease of the heart often associ- ated with albuminuria, the inflammation has all the char- acteristics of subacute idiopathic pleurisy, and is entirely distinct from hydrothorax. It usually pursues a favora- ble course, ending at length in absorption. He would hasten a cure, and if absorption is tardy recommends tap- ping, especially if there is dyspnoea or other urgent car- diac symptom's. Mitral Stenosis — Prognosis. — Dr. Dureoziez f finds that mitral stenosis, simple or combined with other valvular diseases, permits, in exceptional cases, the life to pass the sixtieth year. The complication of mitral regurgitation does not aggravate the prognosis. The co-existence of aortic insufficiency renders it more grave. The complica- tion of tricuspid lesion is of very serious import. * The Med. Rec, March lo, 1883. f Ibid, Oct. 27, 1883. VALVULAR DISEASE. I93 Aortic Regurgitation Make$ the Pulmonary Second Sound Inaudible. — Every auscultator has noticed that the sound of aortic regurgitation may be pretty loud at the base of the heart, and at the same time be nearly or quite inaudible at the apex. This is not true of the louder class of murmurs, but is true of those which are loud enough to obscure or wholly cover the pulmonary second sound. It is possible, in such case, to find the pulmon- ary second sound audible, more or less clearly, at the apex, while the regurgitant sound will be conducted down the sternal bone much more loudly than down the heart tissues. Dr. Begbie has called attention to these facts. Stenosis of the Right Auriculo-Ventricular Opening. — Dr. Kucher reports the cure of a child twenty-four hours old in whom the right auricle was larger than the left, the borders of the thin curtains of the tricuspid valve were sealed together, and made a funnel with two openings in the bottom of the funnel that would admit a Simpson*s sound. The material of the valve was thickened and hard. This he ascribes to fcetal endocarditis confined to this valve. He also found in the left auriculo-ventricular opening a transverse chorda tendinea, and says that such a chord was recognized during life by Schroetter by a peculiar musical note. There was nothing striking in the ante-mortem history except that the chest arched as in rachitis, and that the child was bluish. At the end of twenty-four hours the child became cold, and the doctor was sent for. On his arrival it was dead. Dr. Kucher says that while foetal endocarditis is not uncommon, tricuspid stenosis is very rare. Rauchfuss found only two similar cases on record ; one reported by Peacock and one by Romberg. In Romberg's case, a boy 194 VALVULAR DISEASE. of four years, the opening was very narrow, and the tri- cuspid valve had disappeared. In Peacock's case, a girl of seveo months, the stenosis was not considerable, and was apparently due to the thickened valves with inflam- matory deposits on their outer walls. There were two defects in the intraventricular septum. Tricuspid and Mitral Stenosis. — At a meeting of the London Pathological Society Dr. Bedford Fenwick* showed a specimen of tricuspid stenosis from a woman aged thirty, who had rheumatic fever at fifteen and after- wards suffered from winter- cough and dyspnoea. There was marked distention of the jugular veins, but no cya- nosis, cardiac dulness extending far to the right, a well- marked presystolic apex thrill, and systolic and presys- tolic apex murmur, to the right another systolic and pre- systolic murmur. At the post-mortem examination both auricles, but particularly the right, were very much dilated, the ventricles small. The tricuspid and mitral valves were greatly thickened, shortened and agglu- tinated. Cases of this kind are now known not to be very rare. Since his table of forty-six cases he had been able to collect twenty-three more, twenty of whom were in females, average age 31.7 years. In every case the mitral valve was more changed than the tricuspid, and in all the general health had been good. The great dilata- tion of the right auricle caused increase of dulness to the right, and afforded a means of diagnosis. Dr. Vohsen f finds that in nearly one half of the chil- dren suffering from acute articular rheumatism endocar- ditis occurs and results in marked valvular insufficiency. The mitral valve was most frequently attacked. Endo- carditis appears usually in the first or second week. * The Medical Record, Jan. 20, 1883. t Ibid. VALVULAR DISEASE. I95 Pericarditis is also a frequent complication. Salicylate of soda, while it exerts a favorable influence on the joint disease, seems not to prevent the cardiac complications. The mild forms of articular rheumatism are especially liable to be followed by cardiac disease. Dr. O'Hara reported to the Pathological Society of Philadelphia,* the casQof a patient, a laborer thirty years of age. At first the usual symptoms of cardiac disease. On admission, with the forearms flexed to a right angle, the brachial arteries became prominent with each impulse of the heart ; the pulsations of the carotids were wavy and prolonged ; the temporals were tortuous and pulsated vis- ibly ; no retinal arterial pulsation was seen. Retinal ven- ous pulse was marked, but venous pulse was found else- where. In the second left intercostal space a systolic impulse was observed. The pulse struck the finger with considerable force, but at once lost most of its volume. This was exaggerated by raising the hands above the head. No hepatic pulsation was felt over the second right costosternal articulation, the closure of the aortic valves was distinctly heard and a slight diastolic murmur. A systolic murmur was also heard over the same spot. The systolic murmur was nearly lost in the carotid and sub-clavian arteries. The aortic valves were insufficient and thickened ; the posterior leaflet was normal in shape, but the others were curled on themselves on the aortic side. The stenosis was slight. The mitral orifice was buttonhole shape, and the valves failed to close on account of calcareous deposit in their tissue, extending into the auricle. Attached to the valve a bony substance hung into the ventricle one eighth of an inch in diameter. The left auricular appendix was much hypertrophied. The valves of the * N. V. Med, Jour., Jan. 20, 1883. 196 VALVULAR DISEASE. tricuspid and pulmonary orifices were normal. The pul- monary artery was considerably dilated. Dr. Eskridge thought that the demonstration of the left auricular pul- sation was important, as Dr. Broadbent had so recently advanced an opposite view : ( Was there a functional murmur in the pulmonary opening due to enlargement of the artery?) Dr. Bruch said that he would like to go on record among those who had observed auricular pulsation in cases of mitral obstruction, in which the stenosis was ex- treme. Trtwipet Bruit. — Dr. Eskridge said that Hayden * re- ferred to bony deposits in the aorta and its valve as fol- lows : Sir Dominic Corrigan exhibited before the Patho- logical Society of Dublin (Proceedings, vol. ii., new series, Feb., 1864) the heart of a young woman, in which the root of the aorta had undergone osteoid transformation ; it was likewise greatly dilated, and the aortic valves had been rendered thereby inadequate. During the patient's last illness a systolic murmur of metallic quality, appropriately designated a ' trumpet bruit,* was audible at the base and in the ascending aorta and carotid arteries. There was likewise a soft diastolic murmur. He regards a " trumpet bruit*' as absolutely diagnostic of bony de- posit in the aorta, either in the form of a '' rim of bone," of a projection, or "tongue of bone." In the same para- graph Corrigan refers to Dr. Banks' specimen of a tongue of bone projecting into the aortic orifice. Lying-in Murmurs of the Heart. — Dr. Angel Money f publishes a paper on this subject, the chief conclusions of which are the following. One kind is endocardial-like, and may be heard over any part of the precordia. The * Diseases of the Heart and Aorta. Vol. ii., p. 839. \ Medico-Chirurgical Transactions, Vol. 65, 1882. ' VALVULAR DISEASE. 1 97 second is friction-like and not conducted just above and to the left of the xiphoid cartilage. The third is very loud, of curious quality, not conducted, and very capri- cious. Some of these murmurs occur in seventy-five per cent of the lying-in, and a large part of them are heard over the right heart. These murmurs are for the most part functional murmurs and need not excite any alarm. Relative Stenosis of the Cardiac Orifices. — A theoretical explanation of the transient heart murmurs has been advanced.* In the normal heart, the size of the orifice multiplied by the velocity of the blood-current must equal the cubic contents of the heart cavity. If the latter be greater, we have stenosis. Hitherto but one factor has been taken into account, viz., the diameter of the orifice, but it is clear that if with a normal exit the capacity of the heart be increased, the former becomes relatively too small, and we have a relative stenosis. The auriculo-ventricular opening partakes in the dilatation of the cavities, to the extent indeed that the unchanged valves become too small, and insufficiency results. But the arterial orifices do not dilate as the ventricles enlarge and hence become too small. As regards the third factor — the velocity of the blood-current — a certain relation exists between the capacity of the heart and the size of its ori- fices, which permits. changes in the velocity of the current within certain limits. But when through congenital de- fect or in consequence of pathological changes the ven- tricle can barely empty itself, a slight increase in the velocity'will produce a murmur. On the other hand, a pre-existing murmur may disappear on the retardation of the blood current. Witness the disappearance of a sys- tolic murmur after a severe hemorrhage. We should make a distinction between organic and functional or clinical stenosis. Organic valvular changes are sometimes * The Med. Record, Sept. 23, 1882. 198 VALVULAR DISEASE. found after death that gave rise to no murmurs during life. In acute endocarditis or during a high fever, there may be a weakening of the muscular walls of the heart and consequent dilatation. Here the relation between the ventricle and its orifice is altered, and the latter be- comes stenosed. The sound produced is a blowing mur- mur, heard oftenest and loudest over the left heart, and of course systolic. After copious hemorrhage loud blow- ing systolic murmurs arise, often not till the vessels are refilled by the absorption of the water of the tissues. From insufficient nutrition, the muscular tone of the heart is lowered and there is consequent dilatation. When this condition exists, the orifice being relatively too small for the ventricle, only a part of the contents of the latter can pass out ; the balance recoiling against the advancing blood-stream causes a murmur. Before proceeding with the consideration of the treat- ment of valvular disease, I append a letter, in which my opinion is asked regarding the relation between heart and kidney lesions, and the reply, in which are set forth the views I have entertained upon this subject for many years. Springfield, Vt., Aug. 20, 1883. Prof, Alonzo Clark, M.D. Dear Sir : The following case reported at a local medical society excited some interest among the mem- bers, and it would be gratifying to them to know your opinion of it. Is it possible, do you think, to decide which is the initial lesion when the heart and kidneys are involved (as in this case) by the clinical history, and by the stage of development of each lesion, as shown by the autopsy? If it would not encroach too much upon your time, would you have the kindness to give us your opinion T With high esteem, I am, very respectfully, yours, Daniel W. Hazelton. VALVULAR DISEASE. 1 99 Case. — Nov. 1880. J. B., male; age 72; married; farmer by occupation, and a man of good habits. When first seen he gave a history of repeated attacks of acute ar- ticular rheumatism during the preceding 20 years. For a long time he had had dyspnoea, which was made worse by exertion. The dyspnoea persisted and was more marked than ever before. For days he was unable to maintain any but the sitting posture. Pulse was inter- mittent. There was a cough and expectoration occasion- ally streaked by blood. There was fulness of the super- ficial veins of the neck, and distinct pulsation of the jug- ulars. Lower extremities were oedematoeus, auscultatation gave a systolic murmur heard best at the apex of heart and indistinctly at angle of scapula. Percussion showed the area of cardiac dulness to be increased, extending from J to I inch farther to right of sternum than normal. Urine on first examination and for some time subsequently was about natural in quantity and color ; specific gravity about 1015, and contained a truce of albumen. At dif- ferent times during the succeeding year the patient had small hemorrhages from the lungs, and at various times the lungs gave dulness on percussion, when dyspnoea was increased. He also had hemorrhages from the bowels, one of which was profuse. Patient died with symptoms of uraemia and pericarditis December, 1882. Autopsy: Pericardium congested and bound by recent adhesions to heart. Heart was moderately dilated. Right side more dilated than left. Left side about normal — weighed 22 oz. Mitral valve had an abundant deposit on it of calcareous matter, also the margins of the auriculo-ventricular orifice. The kidneys were slightly atrophied. Their capsules were easily removed. One cyst about the size of a pea was found between the capsule and cortex of one kidney. They were of about the natural reddish color, but were studded with very fine and rather indistinct millet seed granulations. 200 VALVULAR DISEASE. On section, the cortex and pyramids, presented their natural color and structure so far as the unaided eye could determine. The cortices were not diminished in breadth. Other viscera were normal. *' Dear Doctor : "It has been the subject of much discussion, when car- diac and renal disease are found in the same patient, which preceded. This question, in my mind, divides itself into two, and would be answered as follows : When it is the large kidney, with albumen and casts in the urine and much oedema during life, then in nine-tenths of the cases the heart disease is primary and the kidney affection is secondary and consequent. When, on the other hand, the kidney is contracted, and during life the albumen is scanty and often absent, the casts are uncertain, there is but little oedema, and there is no distressing valvular dis- ease, then the chances are at least even that the renal disease is primary. ** In your case the articular rheumatism had been re- curring for twenty years, and " for a long time the pa- tient had had dyspnoea." How long ? This question is important. If he was pretty well and could attend to his business for six months or for some years after the rheumatic attack or attacks, and then the difficulty of breathing came slowly, with perhaps at times an urgent attack, and if especially this difficulty increased rapidly after the oedema appeared, then you have the history of rheumatic mitral disease as the primary affection and the renal is secondary. " In your case there was calcareous deposit on the mitral valve and in the margin of the orifice. That means years. " Then, again, *' the left side of the heart was about nor- mal," the right was dilated, and the heart weighed 22 oz. It is evident, then, that there was hypertrophy some- VALVULAR DISEASE. 20I where- It was not in the left side. There must have been hypertrophy with the dilatation of the right side. This should be looked for because of the long standing stenosis of the mitral valve. You do not state that there was a diastolic mitral murmur. Yet, from the hypertro- phy of the right ventricle and the condition of the mi- tral valve and orifice, I, infer that it did exist at one time and had been lost as the strength of the heart diminished toward the end of life. '^ Then as to the kidneys. They do not appear to have been in a state of advanced disease. They were " slight- ly atrophied." They were finely granulated, but their capsules were not unnaturally adherent, while the internal structures were not perceptibly changed. There was one serous cyst, but only one, and that was small. This ap- pears to be the early stage of the contracted kidney, a disease which sometimes reduces the weight of the organ to one and a half ounces. " When the small kidney produces disease of the heart it is the left side that is affected and hypertrophy is asso- ciated with it, or it is hypertrophy alone. In my judg- ment, then, the chronic disease of heart antedates the disease of the kidney, but probably was not the cause of it. The contracted kidney is not that which usually follows cardiac disease, but the large one. How a kidney of the kind you have described should have occurred in such a case is a problem I cannot solve. If it was really produced by the heart it is a noteworthy exception to the rule I have referred to. If it was the result of the unknown agencies which usually produce the contracted kidney^ even then the concurrence is worth remembering. One other supposition is possible. The influences that pro- duce the contracted kidney may have been operative be- fore the dyspnoea was experienced and when that came, the congestive state of the kidneys, which comes with it, 202 VALVULAR DISEASE. may have counteracted the contraction and suspended it. Whether this is possible I do not know, ' If it is, then whether it explains this case can be better judged of when we know for how many of the twenty years the dyspnoea existed. The duration of the cirrhotic kidney may never be known, but after it is recognizable the patient often lives three or four years. Still it is difficult to suppose that it can have a total duration of twenty years. " There is one other point in the case. Your patient had pericarditis at the end. You state that the urine con- tained a little albumen, and your idea that he was also uraemic is altogether probable. This state of the blood is quite capable of producing pericarditis and probably did in your case. " The other points in your case are easily explained. The cough, the expectoration, and the blood stains were produced by the distention of the vessels consequent on the mitral regurgitation and stenosis. The intestinal hemorrhage from the overloaded state of the right heart and its unwillingness to receive the blood of the hepatic and portal vessels and the consequent rupture of some intestinal veins. The fulness of the veins in the neck and the pulsation in the jugulars were due to regurgitation through the tricuspid opening, for while the right ventri- cle was dilated its auriculo-ventricular opening would be enlarged also, and so render the valve insufficient to guard it. *^ You say ' at various times the lungs gave dulness on percussion,' but you do not state in what part of the chest this dulness was found, or whether it was on both sides. If it was on both sides and in the lower part of it, it was dependent on double pleural serous effusion — an event not uncommon in cardio-renal disease. It is a part of the dropsy not caused by inflammation, and it is therefore painless, but it greatly embarrasses the respiration. It is VALVULAR DISEASE. 203 possible for congestion of the vessels of the lungs to so far exclude the air from the air cells as to make dulness. This, is however, somewhat peripatetic, moving from place to place in the lung or from one lung to the other and is apt to be attended by haemoptysis. " Finally, you appear to have found no fluid in the peri- cardium only lymphy adhesions, yet you found percus- sive dulness on the right of the right edge of the sternum one half to an inch in extent. This was probably due to a serous effusion in the pericardium that was absorbed before death." 204 TREATMENT OF VALVULAR DISEASE. LECTURE XIII. PROGNOSIS AND TREATMENT OF VALVULAR DISEASE. In regard to the treatment of valvular disease, it is so entirely bound up in the subject of treatment of cardiac diseases in general that it does not require atten- tion at this time. The question will naturally occur to you, how much havoc can be made by these diseased valves ? How dangerous is it ? The reply would be this : Obstruction at the aortic opening is the least dangerous of all, because of the compensation that can be furnished by hypertrophy of the heart. Obstruction at the mitral opening will be grave or not, depending upon its extent. As I told you, one day it may become a very grave matter, producing cyanosis that may be visible in the face, a con- gestion of all the important organs of the body, and lead- ing to rather a slow death, that is, an illness that may be protracted through several months, or half a year, or even a year, and finally terminating in death. But diseases of the mitral valve usually have a slow ending through affections of the kidneys and dropsy, particularly oedema. Regur- gitation at the mitral valve goes in the same class ; it stands with obstruction of the mitral valve in regard to its mode of termination ; that form of disease that is most likely to have a sudden termination, that condition in which the patients are sometimes told they may drop down dead in a moment ; and this is a very unwise thing to tell a patient ; it makes him anxious all his life, fearing at every moment he may drop down dead. The condition that is most likely to be attended by this sudden result is regurgitation TREATMENT OF VALVULAR DISEASE. 20$ at the aortic opening, by a return of blood into the ven- tricle after it has once entered the aorta. You can easily see that in this case, depending upon how much regurgi- tation there is, there will be a diminished quantity of blood circulating in the arteries of the body. The brain will not receive its due amount, and syncope may take place, you cannot say \yhen. It does not require a very grave lesion of this kind to lead, in certain instances, to sudden death, and it almost always occurs by a sort of syncope, the brain receiving too little blood to stimulate it to proper action, and to react upon the heart. The heart ceases to beat and the patient is dead. And yet do not give these patients unnecessary alarm. They may carry this lesion that leads to regurgitation from the aorta into the ventricle for a great many years. The number of instances in which persons die with this lesion suddenly, compared with those who die a lingering death, is very small. It is an old error to suppose that persons who have cardiac disease must die suddenly. They may, and others may. A good many years ago, when I was just entering upon the profession, I took up the study of the cause of sudden deaths ; and one of the first that occurred which I studied was of a young woman in Bellevue Hos- pital. She had had typhus fever. It was in 1847. I was not so young in the profession as I was thinking. Well, typhus fever was prevailing there to a remarkable extent. She had got through with her typhus fever, and was in a condition of convalescence. She was able to go about the wards and take care of other patients to a cer- tain extent, but she felt a little weary at times. After eating dinner she had lain down upon her bed and taken a nap. Another patient, her next neighbor, had done the same thing. She woke from her nap, raised herself in bed, and said to her neighbor, '* I have not felt so well as I do at this moment since I was first taken sick," and 2o6 TREATMENT OF VALVULAR DISEASE. had scarcely finished the sentence when she fell back senseless, dead. At post-mortem examination we found there was an effusion of blood at the base of the throat, in- volving all the nerves of respiration, compressing them to a certain extent, so that the respiration stopped suddenly. In following up the inquiry, I found within six months six cases of the same kind. Since then I have not seen one. Sudden death, then, has a variety of causes. In a person who is known to have cardiac disease it is usually ascribed to that affection, but it is not a matter of course that it will be so. And then you are to bear in mind that in certain forms of disease of the heart there is greater dan- ger at the brain than there is at the heart itself. That is, hypertrophy of the heart without obstruction is a rather frequent cause of apoplexy. An hypertrophy of the heart without obstruction between the arteries of the brain and the heart itself is apt to lead to apoplexy. /;/ Regard to Remedies. — In cases of dizziness from heart disease, See* asserts that iron *is absolutely indicated, though in many cases the iodide of potass gives excellent results. Anginous attacks should of course be combatted by hypodermics of morphine, the administration of chloral, or the inhalation of nitrite of amyl during the access, and by the bromide of potassium and digitalis or con- vallaria during the intervals. Excellent results are claimed in the treatment of car- diac dropsy by caffein. Begin with a dose of 7 grains, gradually increasing to 15, 30, and even 45 grains per diem. Such large doses, however, often cause severe pain in the stomach. Adonis vernalis\ has long been used as a dropsy ^ Med. Rec. Sept. 22, 1883. \ The Medical Record, Oct. 6, 1883. TREATMENT OF VALVULAR DISEASE. 20; remedy in Southern Russia, and Prof. Bolkin has em- ployed it extensively, and Dr. Budnoff reports the result. It was found to be of value only in the dropsies that were preceded by cardiac disease. The heart-beats were much strengthened. The size of the organ was diminished, and its tones were much louder. The systolic murmur of aortic stenosis especi^illy was intensified. The heart's rhythm became more regular, and the pulse slower and fuller. The daily excretion of urine was increased greatly, sometimes rising from ten or twelve to eighty or ninety, ounces a day. The subsidence of oedema was propor- tioned to the flow of urine. The medicine was given in infusion of the strength 3 i. to | vi., to which two drops of the oil of peppermint was added. The dose of this was a tablespoonful every two hours. Dr. Bubnow"^ of St. Petersburg, says that it is a popu- lar remedy in Russia for dropsy. Under its influence the cardiac contractions are increased in force and diminished in frequency, and the urine was augmented, and no longer contained casts or albumen. Experiments on both cold and warm-blooded animals with different preparations (infusion, aqueous and alcoholic extracts), showed that its action is to stimulate both the motor ganglia, and the imbibitory apparatus of the heart, and to raise arterial tension. Dr. Bubnow prefers adonis to digitalis, and says that, like convallaria, it has no cumulative action. A glu- coside adonidin containing the active principle has been isolated. The effects of adonidin are very similar to those of digitalin. It is not improbable that the same similarity may be found to exist between adonis and digitalis as exists between hyoscyamus and belladonna. The therapeutic uses of convallaria are thus stated by Prof. Seef : *N. Y. Med. Jour., June i6, 1883. \Ain. Jour, of Med. Sci., Oct., 1882. 208 TREATMENT OF VALVULAR DISEASE. 1. In palpitation due to an exhaustion of the vagus nerve or paralytic palpitation. 2. In simple want of rhythm with or without hypertro- phy, with or without lesions of orifices or valves. 3. In mitral stenosis the contractile power is increased as shown by the sphygmograph. 4. In insufficiency of the mitral valve, particularly when there is passive congestion of the lungs and consequent dyspnoea. 5. In aortic regurgitation (Corrigan's disease) the good effects are shown in the pulse and easier respiration. It gives strength and energy to the heart. 6. In dilatation, w4th or without hypertrophy ; with or without fatty degeneration ; with or without sclerosis of the muscular tissue. 7. In all cardiac affections giving rise to dropsy and anasarca surpassing all other drugs. The combination of convallaria with the iodide of po- tassium is most valuable in cardiac asthma. In the Medical Record for Feb. 24, 1883, may be found the report of twenty-one cases treated with this drug, all heart disease in some form ; the ages of the patients from eleven to seventy years. The preparation was an infusion 3 ^ to | i. to a pint, in tablespoonful doses every two hours. In seventeen cases there were absolutely no results, and in the others the im- provement was trifling. The writer therefore does not admit that convallaria is an efficient substitute for digita- lis. He does admit, however, that the specimens of convallaria used by him may have been of a quality infe- rior to that used by other observers, who have reported such brilliant results. Dr. B. Robinson* exhibited to the N. Y. Pathological * The Medical Record, Jan. 13, 1883, TREATxMENT OF VALVULAR DISEASE. 209 Society the hearts and kidneys of two persons who were similarly affected, and in whom both digitalis and con- vallaria were equally ineffectual in producing diuresis, in both of whom the contracted kidney was found, regard- ing which Dr. Robinson expresses the following opinion: *' We should be prepared to assume that with a small quantity of urine, with, nothing specially abnormal about the specific gravity, and failure on the part of the kidneys to respond to cardiac stimulants, as in the case recited, we might reasonably expect to find that form of kidney degeneration." Dr. A. A. Smith's* experience with convallaria had led him to think it a good diuretic. It had seemed to him that in cardiac hypertrophy the remedy was not indicated. In chronic renal disease, with chronic hypertrophy, ac- cording to his observations, it aggravated the symptoms. In cases of enlargement of the heart in which dilatation predominates it serves a very good purpose. He was not however, prepared to give up digitalis, and substitute convallaria. Nor was he quite sure the experiments of Ott had not demonstrated that it does not act through the pneumogastric. Dr. Vanderpoelf found in a case in which there was mitral stenosis and insufficiency with irregular action of the heart and cedema, that eight minim doses of the fluid extract of convallaria twice a day brought marked im- provement, removed the oedema in ten days, and brought a more regular heart action. Dr. Delafield said it made the heart action more regular and slower in certain cases, and in general condition the patient improved very much. He had found, like Drs. Vanderpoel and Barker, that there was a great difference ■ * Medical Record Q^. Y. Acad, of Med.), April 14, 1883. t N. Y. AUd. Jour., Apr. 14, 1883. (N. Y. Med. and Surg. Soc.) 2IO TREATMENT OF VALVULAR DISEASE. in patients as to dose. For some five drops of fluid ex- tract every three hours was enough, while other patients required drachm doses. He thinks he saved the life of a woman, over seventy years of age, overwhelmed by pneumonia, with twenty-drop doses of the fluid extract every three hours. Dr. Hurd" has translated Prof. Germain See's opinions of this new medicine, which are mostly embraced in the following extracts : In the form of aqueous extract of the entire plant, given in doses of half a gramme to a gramme and a half daily, it produces on the heart blood-vessels and respiratory organs, effects constant and constantly favorable, viz.: a slowing of the beatings of the heart, with often a restoration of the normal rhythm, augmenta- tion of the energy, also of arterial pressure, the respira- tory force is increased. ... In all cardiac affections in- differently, from the moment the watery infiltrations ap- pear, it has an action prompt and certain. Dr. Hurd has tried the fluid extract in doses of five drops every four hours in two cases with very satisfactory results. Dr. Troitsky t says it may be used to make the heart's contractions stronger, slower, and more regular, especially in cases of organic disease, or those in which increased fre- quency depends on changes in the nerve centres ; to lower the temperature so far as its influence on the heart may permit ; to increase arterial tension ; to in- crease the secretion of urine in dropsy ; to lower reflex action. He says that it acts better in mitral regurgitation than in the diseases of the aortic valve and mitral ste- nosis. In this respect it is like digitalis — ten or twelve grains of the flowers to six ounces of water, three or four tablespoonfuls a day. Convallaria in large doses does not *The Medical Record, Sept. 9, 1882. \ N. Y. Med. Abstract, April, 18S3. TREATMENT OF VALVULAR DISEASE. 211 stimulate the cardiac terminations of the vagi — does not stimulate the cardiac nerves. It stimulates the central inhibitory apparatus. It paralyzes the motor centres situated within the heart itself. It at first accelerates then retards the respiration, and finally stops it just after the heart has stopped, and he thinks, because the respiratory centres are paralyzed by the venosity of the blood. Temperature at first rises half to one degree C, then falls considerably because it paralyzes the vaso- motor centres. It first stimulates then paralyzes the vaso-motor centres, hence increased and then diminished vascular tension. On the brain it produces anaemia and sleep ; applied directly to striated muscle the extract pro- duces complete loss of contractility. The trial of this drug in the Roosevelt Hospital, under the direction of Dr. Delafield, reported by Dr. Taylor,"^ is summed up as follows : " Of the five cases of cardiac disease four improved — one veiy markedly — after digitalis had failed ; one improved at first, then grew very much worse and recovered on digitalis. One was hopeless. Case XL, already referred to, was as brilliant an example of the benefit to be derived from a drug in certain in- stances as I saw during my hospital experience." Fifteen other cases are reported in which the medicine was used in other diseases. One, a case of pneumonia, hardly a less brilliant illustration of the power of the medicine than the Case XI. of. heart disease. The fluid extract was given X minims three times a day to XX minims every four hours. Dr. Polkf reported to the Practitioners' Society a case of palpitation in which the heart would beat 240 times in the minute, in one instance for three days. Drs. Polk, *The Medical Record, Feb. 13, 1883, and a previous number, flbid, Feb. 3, 1883. 212 TREATMENT OF VALVULAR DISEASE. Peabody, Flint, and Metcalfe had all failed to find any organic change in the heart. The patient was a young man of twenty years. In one of these attacks Dr. Polk gave him ten minims of the fluid extract of convallaria hypodermically, and one half hour later repeated it. Five to ten minutes after this the pulse fell to 120, and fell not gradually, but suddenly. Fifteen-drop doses every three hours. The next morning the pulse was 90 in the min- ute. The intervals were lengthened to four hours, and the next day the medicine was suspended. There was no return of palpitation. Dr. Beverly Robinson* reported to the Practitioners* Society an eleven years old asthma in a man sixty- three years old, inherited, which was greatly relieved by the fluid extract of the root of convallaria. The first dose of fifteen minims gave sensible relief. Then it was four minims in eight of syrup of tolu and water sufficient to make a drachm, every three hours, then five drops of the extract every three hours. It was con- tinued through December, having been begun Oct. 4, 1883. Dr. Ott finds that the slowing of the heart by digitalis is due to a cardiac inhibitory excitation ; with convallaria some other part of the heart is acted on (he thinks the muscle). Digitalis, as a rule, does not primarily accel- erate the heart ; convallaria does. After section of the spinal cord digitalis is powerless to increase arterial tension, while convallaria is not. If we compare the action of the drug with other cardiac agents, as aconite, or astragalus molissimus, it is found that it does not belong to this group. As these resemble each other in their action, yet many important differences exist. So does convallaria differ from digitalis in several important * The Medical Record, Feb. 3, 1^83. TREATMENT OF VALVULAR DISEASE. 213 particulars. The great rise of arterial tension would indicate its value in dropsies. It is a drug which must not be pushed to any great extent for fear of producing spasm. Salicyl Compounds in Rheumatism. — Dr. Maclagen * again brought forward his views. He urges that small doses are ineffectual, .but that we employ large doses and at frequent intervals — say twenty to forty grains every hour for six hours, or until there is relief from pain. Dr. Maclagen thinks that we may, by the early and free use of salicin, prevent valvular inflammation. Dr. Sansom, while indorsing much that Dr. Maclagen has said, was not so sanguine as to the preventive action of salicin. Cactus GrandifloriLs in Heart Affections. — Dr. M. O'Haraf at a meeting of the Philadelphia County Medi- cal Society said that his attention was first called to this cactus some time ago, and failing with the usual remedies in a case of mitral disease with oedema, dyspnoea, etc., he gave five minims of the fluid extract of the cactus grandiflorus. Every symptom improved, and in two weeks the patient was quite another man. He had two other similar cases which give similar evidences of the virtues of the cactus. He says that if he can trust a limited experience the cactus is a pure heart tonic. He refers to various other remedies recommended by different persons who think that their action is similar to that of digitalis, but he has not tried them. Dr. Finny :j: thinks that too much dependence may be placed on the physical signs of mitral regurgitation as evidence of organic disease; that such signs may be due to purely functional derangements and weakness of the *The Medical Record, April 7, 1883. f N. Y. Medical Journal, Nov.. 17, 1883. X The Medical Record, March 17, 1883. 214 TREATMENT OF VALVULAR DISEASE. heart, or to an altered condition of the blood ; that the blood murmurs in the heart and large vessels may be louder than those produced by valvular lesions; that the danger of valvular disease is enormously increased by weakness of the cardiac walls; that the lowering treat- ment of the heart's force is rarely if ever required in heart disease; that indications for treatment in diseases of the heart should be sought from the evidences of the condi- tion of the heart muscle, and not from those of the condition of the valves. Dr. Leech* said his general plan in the treatment of cardiac dropsy was to place his patient in bed, secure rest for some time, and then administer diuretics. When diuretics failed, purgatives rarely succeeded. He had not seen benefit from the use of the hot air bath. He had entirely failed to see any benefit from the use of pilo- carpin. Unlike tapping in cirrhosis, he had seen but little loss of strength in tapping for cardiac dropsy. He had but once had peritonitis follow tapping. Southey's capillary tubes for draining the legs in general anasarca were of great value, although he had seen phlegmonous erysipelas follow their use in one case. He had found that diuretics would act often after rest and good diet, though they had previously failed. Dr. Allbutt had found diaphoretics very uncertain. He regarded hydragogues as very useful. The air bath was unsuccessful. He hesitated to tap the patient's leg in fear of erysipelas, but otherwise the operation was almost brilHantly successful. He used Southey's tubes with satisfaction. He delayed tapping on account of the exhaustion it produced. Dr. Thomas had found diaphoretics inactive, but some- * British Med. Association, Aug., 1882; Med. Record^ Aug. 26, 1882. TREATMENT OF VALVULAR DISEASE. 21 5 times they were satisfactory after purgatives, but generally no real benefit from attempts to act on the skin. Dr. Carter had used the hot air baths and hot drinks with marked benefit, especially in dropsy after scarlet fever, and had frequently seen diuresis follow. For cardiac and other dropsies digitalis had in his hands proved to be exceedingly useful. He had resorted to early tapping, but he had used a very small trocar, whi<:h would allow only a slow removal of the fluid, believing that thereby the liability to exhaustion was considerably diminished. He referred to three cases. The first was ascites from cirrhosis, and tapping was followed by gradual exhaustion. The second was ascites with Bright's disease. In this tapping, doubled the quantity of urine and was followed by relief. The third was ascites with cardiac disease, and each tapping was followed by diminution of the urine one half, although relief was afforded. The patient was tapped seventeen times. The patient with cirrhosis died, the other two left the hospital in a com- paratively comfortable condition. He had used Southey's tubes for the legs with good results. He believed the use of hydragogues should not be constant, but occa- sional. He preferred rhubarb, jalap, etc., with elaterium. Dr. Roden recommended iodide of potassium combined with full doses of nitric acid. Some preparations of iron with saline cathartics possessed special advantages. Dr. Phillip's had used Southey's tubes successfully, but regarded hypodermic injections of pilocarpin as one of the most valuable agents that could be used. 2l6 ANGINA PECTORIS. LECTURE XIV. ANGINA PECTORIS Is pretty plainly a neuralgia. Whether the change that produces it is in the muscle of heart, caused by scanty supply of blood to the organ, or is in the terminal branches of the cardiac nerves, or as the Medical Record'^ expresses it, referring to Dr. Allen Sturge's opinions, due to " a commotion spontaneously developed in the gray sub- stance of the sympathetic ganglia of the cardiac plexus, this being transmitted to the spinal cord and brain; a commotion spontaneously developed in the cervical sym- pathetic ganglia, which give off branches to the cardiac plexus, or in the ganglia of the vagus; a spontaneous commotion in the part of the gray substance of the cere- brum which may receive impulses coming from above and below ; or to a spontaneous commotion in the parts of the gray substance of the cord in communication with these ganglia, by means of bands of nervous substance passing from the cord to the great sympathetic." Angina arising from tobacco is a rare thing. Tobacco causes intermittence, arythmia, etc. When it causes angina it is due to the slow action of the nicotine on the coronary arteries. Angina arising from alcohol signifies endarteritis of the coronary arteries as well as degenerations or sclerosis of the myocardium. The mischief is done, the suppression will not avail. Gouty angina of the Germans is a cardio-vascular *Med. Rcc, Sept. 22, 1883. ANGINA PECTORIS. 217 lesion and resists treatment ; it is like alcoholic angina caused by endarteritis ; the alkalies can do little for gout of the heart. Angina of organic origin, alterations of the coronary- arteries, degeneration of the cardiac muscle, dilatation of the cavities, and lesions of the aorta, oftener cause attacks than mitral lesions. Hysterical angina is very rare. These neurotic anginas are nearly as dangerous as those of organic origin. There is, in fact, no paralysis of the sympathetic in angina pectoris. The disease is in reality attended by excitation of the cardiac sympathetic nerves and coronary vessels ; the latter being in a state of erethism, there is no paralysis in the case ; but there is not even excitation of the sympathetic nerves, accompanied by the contraction of the blood-vessels in general, the disease, so far as nerves are concerned, being partial and limited. If it were possible to galvanize the cardiac sympathetic nerves, would you not augment rather than diminish the vaso- motor contractility? Obstruction and Regurgitant Mitral Murmur with Healthy Valve ; also Angina Pectoris. — A case is reported in the Lancet, Jan. 27, 1883, in which the patient died in a paroxysm of angina pectoris, left hypertrophy and dila- tation and the mouths of the coronary arteries obstructed. The writer believes that angina pectoris is caused by ischaemia of the heart. The patient had a presystolic and a systolic murmur, yet the mitral valve was normal by the water test and was perfectly healthy in appearance. The presystolic murmur had in this case its usual distinctive feature — a rough vibrating quality resembling in this respect the sound produced by the lips when thrown into vibrations by the expired breath. The writer calls it a blubbering sound. The author explains the murmurs as follows : " I do 2l8 _ ANGINA PECTORIS. not propose to discuss the various explanations of the production of a mitral systolic murmur without mitral lesion. Suffice it to say that in this case, taking into view the considerable dilatation of the left ventricle, it seems to me probable that, although the ventricle held water when filled from an opening made through the apex, the ventricular contraction during life occasioned some regurgitation. A regurgitant stream, be it ever so small, may give rise to a murmur. I submit this explanation without undertaking at this time to account for the ap- parent incongruity that the mitral may admit of some regurgitation during life and yet be found competent after death." Hysterical Angina Pectoris. — Marie* reports two cases in hysterical patients. In one the pain commenced in the left little finger, ran up the arm to the breast of that side. During the attack, which often lasted some hours, the pulse of the left radial artery became imperceptible, the lower parts and the whole left side became cold. In the second case the attack was often preceded by general malaise ; then a sudden violent pain in the prsecordial region ; accompanied by extreme anguish, invincible ter- ror. The pain then extended towards the neck and left arm and little finger, and sometimes toward the leg. The attack lasted ten to twenty minutes, and the face, which was at first pale and cold, became red and warmer. He compares them to a form of angina called vaso-motor by the Germans, but does not say whether there was heart disease. Prof. Sees Treatment of the Paroxysm, — See has aban- doned the use of chloral. It induces sleep, but has no effect on the circulation. Hypodermic injection of morphine, a centigramme ^- *T\izM€d. Rec, June 2, 1883. ■- ANGINA PECTORIS. 219 of the hydrochlorate, one sixth of a grain, may be re- peated, may be given daily to prevent return. Nitrite of amyl is one of the most active and useful means, three or four drops inhaled from the open palm. In the first period of the action the vascular tension is lowered, the vessels are dilated, the action of the heart is very much quickened, the respiration is more free and easy. At a more advanced period, the pressure remain- ing lowered, the heart and respiration become slowed. There is sanguineous irrigation of the coronary arteries, as in other vessels, the cardiac ischsemia ceases. From more than the dose indicated there is risk of cardiac syn- cope. The patient soon becomes accustomed to the rem- edy, so that its good effects become less and less. Nitro-Glycerine. — The effects of this are very much like those of the nitrite of amyl, only slower. The dose is one or two drops of a one per cent solution. Sees Treatment in the Intervals. — Bromide of Potass- ium. Under its action the patient becomes less impres- sionable to physical and psychical influences which might provoke a paroxysm, but it produces debility, which is more or less permanent. Digitalis. When the attacks result from cardiac atony or degeneration it is better than the bromide ; it sustains the action of the heart and is every way preferable. Of electricity he speaks very doubtfully; it may even kill, as in Duchenne's case. Angina Pectoris and Counter Irritation. — Dr. W. A. Sturge * explains the pectoral pain as well as the associ- ated dyspnoea, gastric disturbance, brachial soreness, etc., by the conversion of an efferent impulse conveyed along certain nerve trunks (the cardiac nerves) into a general commotion of a group of spinal nerve centers with which * N. Y. Med. Journal, May 26, 1883. 220 . ANGINA PECTORIS. these trunks are connected, and by the consequent in- volvement of other trunks springing from the same cen. tres. So in visceral inflammations he believes we relieve pain by counter irritation^ the latter exhausting the sen- sitiveness of the centre which supplies nervous force both to the viscus and the overlying integuments, so that by making a powerful impression on the latter we inhibit the irritation of the centre upon the former. Nitrous Compounds in Angina Peetoris. — Dr. Hay,* after experimental observations, concludes that nitrous acid in any combination, whether as an ether or metallic salt, is useful in the treatment of angina pectoris, and that in the case of the nitrite of amyl the action of the acid is aided by that of the base. But all the compounds of nitric acid are useless unless they are so composed that the acid is converted into nitrous acid in the system. So far it appears that nitrogen containing remedies for angina pectoris may be divided into two classes, the one consist- ing of combinations of nitrous acid with metallic oxides or alcoholic radicles, the other comprising a peculiar class of nitric ethers obtained from higher alcohols. In both classes the action of the compound is ultimately on the nitrous acid present. Examples of the first class are the nitrite of sodium, and the nitrite of ethyl, and of the sec- ond class nitro-glycerine. Then there are the compounds of amyl whose action is similar to that of nitrites. But they are limited at present, the dose required is large, the action is not rapidly produced ; and disagreeable after effects are apt to be produced. They are not to be chosen in the treatment of angina pectoris. Nitro-Glycerine is a vaso-motor paralyzer and dilator of the peripheral vessels, and is of service in diseases of the heart, especially those of the aorta. It opposes the symp- — _______ — . — — _ « — , * The Medical Record, July 7, 1883. ANGINA PECTORIS. 22 1 toms of cerebral anaemia, as Dujardin Beaumetz* has shown to be the case with the nitrite of amyl. In cardiac affections characterized by feeble state of the myocardium amyl nitrite has been regarded as a cardiac stimulus, and nitro-glycerine has doubtless the same action. Nitro- glycerine has been especially productive of good results in angina pectoris in doses of three drops a day of a solu- tion of one to a hundred. It has also been successfully used in tendency to syncope and in palpitations, but only in those cases in which there is a nervous or anaemic state. Free diuresis has been produced. Formula : Dis- tilled water, fl | x, solution of nitro-glycerine — i-ioo, gr. XXX ; three teaspoonfuls a day, one after each meal. Angina Pectoris and Nitro-Glycerine. — Dr. Jacob Frankf of Buffalo treated a woman aged thirty-one years with morphine, electricity, etc., with little benefit. He then tried nitro-glycerine m. j. of one per cent solution, grad- ually increased m. vj. three times a day and then decreased. The patient had no more of the disease. After she had been taking the medicine for six weeks, aphthae appeared on the tongue, mouth, and fauces. The medicine was stopped, and these ulcers were treated with borax, etc., after which the treatment was resumed. * Dr. Henri Huchard Am. Jour. Med. Science, July, 1883. \ The Medical Record, May 5, 1883. 222 DEFORMITIES OF THE HEART, LECTURE XV. DEFORMITIES OF THE HEART. Certain congenital malformations of the heart take place, the result of imperfect foetal evolution ; to enter into a lengthy discussion of these conditions would in- volve an extended inquiry into the science of embryology, which is not intended. The principal deformities to which the organ is subject may be briefly summarized, as arrests of development during some period of intra- uterine existence, in which the heart may either consist of two or three cavities : those in which, although four cavities exist, there is a deficiency in the septa between the right and left sides, and those cases in which the heart is not confined to its proper cavity. These condi- tions may be best elucidated by the following cases. Disease of Puhnonary Valve and Open Septum. — Dr. Bruen,* in the Pathological Society of Philadelphia, de- scribes a heart thus : Two of the semilunar leaflets of the pulmonary artery are nearly destroyed by atheromatous changes ; the third segment is much thickened and pro- jects as a leaflike fold, roughening the mouth of the pul- monary artery. This vessel is dilated to twice its natural size, forming nearly an aneurism. The vessel's walls are covered with vegetations of inflammatory origin, or due to atheromatous changes. The right auricle is very small and imperfectly developed, the bulk of the cavity being formed by the auricular appendix. The tricuspid valves are much thickened, but probably competent. Between * Medical Ne^vs, Dec. 23, 1882. DEFORMITIES OF THE HEART. 223 the ventricles is an orifice that will admit the forefinger. It is directly beneath one of the tricuspid leaflets and is lined with endocardium. The walls of the right ventricle are thinned and its cavity somewhat dilated. Dr. Bruen ascribed the perforation to the pressure of blood in the right ventricle. The dilated artery made a pulsating tu- mor to the left of t^e sternum, between the second and fourth ribs. Over the tumor a ** post diastolic and presys- tolic bruit-like murmur could be heard," while close to the junction of the second and fourth ribs to the ster- num a hoarse systolic murmur could be heard. There was no cyanosis. Dr. Wilson thought that in this case the left heart by its greater strength had sent its blood into the right and overloaded it, and that the condition of the pulmonary artery was due to this. Open Ductus Arteriosus. — Dr. Beverly Livingston* re- ported to the N. Y. Pathological Society a case of this kind. In a newborn male child there was no indication of disease till the morning of the third day. Then there was a sudden arrest of respiration ; an irregular action of the heart, cyanosis, first of the face, then of the whole surface of the body. In a minute and a half the pulse resumed its regularity, and the skin its natural color. At intervals of about an hour the same symptoms recurred, and as they recurred they lasted a little longer, about two minutes, and artificial respiration was neces- sary for the restoration. In the sixth attack the best efforts were unavailing. The heart ceased beating for- ever. The lungs showed numerous small regions of collapse (atalectasis), and the right heart was distended with blood. *Path. Soc, June 27, 1883. 224 DEFORMITIES OP THE HEART. Open Foramen Ovale. — Dr. Ferguson exhibited at a meeting of the N. Y. Pathological Society two hearts il- lustrating persistent foramen ovale. One opening admit- ted a tube half an inch in diameter. Dr. Allchin of Lon- don asked Dr. Ferguson why he supposed the blood in one of his specimens passed from one auricle to the other. He had seen the lesion very frequently, and supposed that it was generally accepted that the pressure of the blood in both cavities was so nearly equal that it kept the opening sufficiently closed to prevent any evidence that the blood passed from one auricle to the other. Dr. Ferguson replied that the arrangement of the tis- sues was such in one of the cases that he thought pres- sure on one side would close the foramen, and that pres- sure on the other would open it. Ductus Arteriosus Open in a Dog. — Dr. W. H. Howell and Professor Donaldson* found in a dog the pulse rate greater and the cardiac impulse stronger than normal. The apex was further to the left than it should be, show- ing marked hypertrophy. Over all the cardiac region Prof. Donaldson heard a loud rasping cardiac murmur with maximum intensity over the base, also a slight murmur with the second sound. Experiments showed a normal arterial pressure and no abnormality in the sphyg- mographic tracings except an unusually marked dicro- tism. The ductus arteriosus was found open, its calibre being at least equal to that of either of the pulmonary arteries. With such free communication between the aortic and pulmonary circulation it is noticeable that so good an average arterial pressure was maintained (as meas- ured in the femoral artery). Only one such case is found on record. I have not the ** circular" in which this account was * N. Y. Med. Jour., March 3, 1883. DEFORMITIES OF THE HEART. * 22 5 first published, but this abstract, as I suppose it is, leaves the impression that " the loud rasping mur- mur" was produced by blood flowing through the open ductus arteriosus. But there is no reason to suppose that the ductus arteriosus produces any more noise when the blood passes through it than does the aorta, or the carotid where it divides into internal and external. It is easy enough to hear the sounds of the heart in utero, yet '* a loud rasping murmur'' is almost never heard. The report does not mention the aortic valves. Then the blood pressure was apparently taken in the femoral artery, where it would represent the strength of the left ventricle, and a good part of that of the right, and until the heart became enfeebled, the pressure ought to be considerable, at least compared with that in the carotid artery. Congenital Communication between the Right Side of the Heart and the Aorta.—Dr. B. Livingston* exhibited to the N. Y. Pathological Society the heart of a child, a male three months and twenty seven days old, that had been strong and healthy, and had never given any symptom of heart disease. He died of entero-colitis. Thymus gland large ; heart enlarged ; at root of the aorta on the right side was a communication with the right heart. ''Above and below the tricuspid valve it was closed by a part of this valve, and most Hkely no blood passed through it." The valves of the aorta were only two in number, but were sufificient to close the opening. The mitral and tricuspid valves were normal. On the mitral were plenty of those semi-transparent nodules referred to in other cases. Congenital Pulmonary Stenosis. — Dr. B. Livingstonf * Med. Record, Sept. i, 1883. flbid. 226 DEFORMITIES OF THE HEART, reported to the N. Y. Pathological Society an instance cfi this obstruction that occurred in a female child one year and eight months old. The parents believed that the dis- ease existed at birth. When Dr. Livingston first saw her she was pale, not cyanotic, short of breath, disposed to rest. A systolic very loud murmur was heard most dis- tinctly at the union of the fourth left rib with the sternum, and nearly as distinctly at apex ; was also heard in sixth intercostal space to left of apex beat and between the scapulae. There was a distinct fremitus over the prse- cordia4 region felt by the hand. She died of septicaemia following mild ulcerative stomatitis. "The three semilunar valves of the pulmonary artery had grown together, so as to leave a round hole two millimetres in diameter, and on one side there was a small vegetation, which must have been an obstacle to the cur- rent of blood. The foramen of Botal was enlarged and open, and the interauricular septum was very much thinned, and there were some small holes through it, so that it had a cribriform appearance." The heart was hypertrophied and the left side dilated. Stenosis and Atresia of the Piilmonary Artery and Opening in the Ventricular Septuin."^ — A boy of thirteen years. He was under observation about four and a half months. In the boy's opinion and memory he had been cyanotic from four years of age (probably from both). He had attacks of deep cyanosis lasting some days, during which he would become wholly or partly uncon- scious, the respiration slow and sighing, the pulse rapid and feeble, 120 to 150, the pupils widely dilated and insen- sible to light ; the temperature at first somewhat elevated, 100° to 102°, but later it would fall slightly below the standard, while the extremities would be cold and covered * Dr. B. A. Watson, N. V. Path. Soc. Med. Record, March 10, 1883. DEFORMITIES OF THE HEART. 22; by a slight perspiration. These attacks were generally produced by slight fatigue, or exposure to the sun (it was in summer) and were always preceded by several hours with severe headache and a general feeling of illness. He died in such an attack in which for the first time he complained of a severe pain in the praecordial region. Two murmurs were heard at the base and two at the apex. During the attacks only, subscrepitant rales were heard over the whole chest. The heart was found to be large ; the left auricle was only half the capacity of the right ; the tricuspid and mitral valves were healthy. Two segments of the aortic valve were sealed together by a material of cartilagin- ous firmness ; the valve was atheromatous and covered with vegetations. There was marked stenosis of the pulmonary valve. There was an opening through the ventricular septum which permitted the little finger to pass through it easily. The left carotid artery arose from the innominata and the left subclavian nearer the median line than usual. It is not probable that there were two murmurs at the apex distinct from those at the base, but it is probable that the base murmurs were con- ducted so strongly as to deceive the observer. It seems that no murmur was recognized that could be referred to the opening in the septum. Dr. Eskridge exhibited, at the meeting of the Patholo- gical Society of Philadelphia, March 3, 1883, an unusual deformity of the aorta and the aortic valve. The speci- men was taken from a man about seventy years of age, who had suffered a number of years from severe heart disease. The walls of the large arteries were thickened, rigid and contained numerous deposits of inorganic mat- ter. The left ventricle was enormously enlarged. The first half inch of the aorta was hard and unyielding from fibrous thickening' and calcification. Each section of the 228 DEFORMITIES OF THE HEART. valve was almost wholly transformed into a bone-like matter, and at points the valves were a quarter of an inch in thickness. They were immovable and almost entirely closed the opening. ''One of the leaflets, about three fourths of an inch in all directions, with its vegetations stretched across the aorta, lay against, and was apparently adherent to the other segments of the valve, the latter being curled upon themselves. The central portion of the aorta was entirely occluded, and only two small open- ings remained" between the segments of this valve near the artery : — one three m. m. by one, the other about two thirds this size. Then other similar openings had existed, but were obliterated before death by a thin fibrous trans- parent membrane. The valves on the aortic side were very rough, but on cardiac side were rather smooth. A vegetation ten m. m. long was attached to one of the segments. One segment was adherent to aorta for about half an inch, while the free portion was folded on itself and pointed toward the orifice. Dr. H. Horace Grant* reports the case of a mulatto girl aged i6, who was poorly developed, had never menstru- ated, had often coughed up blood, had remarkable clubbed fingers and toes, had a great deal of dyspnoea, had a loud tricuspid regurgitant murmur, and increased praecordial dulness. Her ill-health was traced back to her birth. Her complexion forbade the recognition of cyanosis. The right auricle was greatly dilated, the right ventricle moderately, the tricuspid valve was insufficient. There was no pulmonary artery. The aorta was given off just above the septum, one half from the left ventricle and one half from the right. The three sections of the aortic valve arose, one on the right, one on the left of the aorta, Am. Jour, of Med, Sci., July, 1883. DEFORMITIES OF THE HEART. 229 and the third, posterior, from the top of the septum. The two coronary arteries arose from the right sinus of Valsalva. The puhnonary arteries were given off from the front of the aorta at the pericardial attachment each about half an inch in diameter. Sundrifold Pulmonary Valve, — A young man 20 years of age died from fracture of the skull caused by a fall down a flight of stairs when intoxicated. The valves of the pulmonary artery were tested by water and were found slightly incompetent. There were four valves (or cusps) ; three of about the ordinary size, the fourth much smaller than the others, and imperfectly separated from one of them. The other valves of the heart were healthy, and the heart was of natural size. He had been examined by Dr. Begbie repeatedly dur- ing the three years preceding his death. A very decided thrill and a loud blowing murmur attended the systole at the left border of the sternum at the third rib. The thrill was very limited. The murmur was diffused over the upper part of the chest, but was scarcely appreciable in the carotids. There was a much fainter diastolic mur- mur almost limited to the same spot. (Begbie's Works, Sydenham.) Double Ventricle and Insufficient Septum. — Mr. Stone, in St. Thomas's Hospital Reports,* gives the following : Heart not excessively large, the vessels given off nor- mally. Ductus arteriosus closed; water injected by the aorta comes out freely by the pulmonary artery. The finger passed into the pulmonary artery meets obstruc- tion an inch and a half below the valve. The auricles communicated by a slit-like fissure such as is not uncom- mon without producing any pathological effect. The walls of the right ventricle were hypertrophied to exactly * Am. Jour, of Med. Sci., Oct., 1883. 230 DEFORMITIES OF THE HEART. an equal in thickness to those of the left. The cavity of the ventricle was divided into two chambers, one much smaller than the other, and almost completely shut off from it by a firm fleshy partition. These were in com- munication with each other by a small circular aperture with cartilaginous margin, studded with vegetations of the size of a millet seed, about a quarter of an inch in diame- ter. The small oval chamber was an inch and a half long, situated between the general cavity and the pulmonary valve. This was quite healthy. The septum between the ventricles was perforated by a large semilunar orifice in its upper space. During life there was a distinct systolic thrill over the cardiac region, most marked at a part half way between the left mamma and the sternum, and conveyed upward in a diagonal line from the midsternal toward the outer extremity of the left clavicle. This was accompanied by a loud, rough sound, also systolic, most accentuated at the point covering the origin of the pulmonary artery. It was not loud at the apex of the heart, was also lost to the right of .the sternum, but was audible over the up- per part of the»scapula posteriorly, and less distinct lower down. The heart was somewhat enlarged toward the left side. '* The pulmonary valve was healthy," and as nothing is said of the other valves it is wrong to infer that they were healthy also. The thrill and rough sound must have been produced at " the small circular aper- ture." No Aortic Orifice. — Dr. Alfred Meyer* reports the fol- lowing case : A male infant twenty-four days old, cyanotic all over the body, suffering great dyspnoea, no radial pulse on either side, distinct pulse in the dorsalis pedis, 135. Nothing abnormal was found in the lungs, but there was * The Med. Record, April 21, 1883. DEFORMITIES OF THE HEART. 23 1 a loud, distinct blowing systolic murmur in the neighbor- hood of the second and third ribs to the right of the sternum. The mother said he had been short of breath from his birth, but that the skin was not discolored till the third week. The gradual increase of the dyspnoea while nursing and the deepening cyanosis alarmed her. The child was found' dead in bed forty-eight hours later. The pericardium contained three fourths of a drachm of clear serum ; heart substance of dark blue color. The right auricle and ventricle greatly dilated; foramen ovale pervious ; pulmonary artery fully twice its normal size ; ductus asteriosus pervious ; left auricle one third the size of the right ; walls of the left ventricle half an inch thick; its cavity just large enough to hold a small pea; pectinean muscles fused into a solid mass ; mere traces of the chordae tendineae. Aortic orifice completely closed ; dictus arteriosus leads into the arch of the aorta, which is about one eighth of an inch in diameter and ends in a blind sac at the base of the heart. The septum ventric- ulorum complete. This patient lived twenty-seven days. Two other re- corded cases give a life of two and four days respectively. Atresia and stenosis of the aorta at or above the open- ing of the ductus arteriosus is comparatively common. Eppinger collected 42 cases and adds 2 of his own. The patient may live 50 or 60 years ; one lived to 92. Both Septa of Heart Deficient. — Dr. H. A. Gallatin* re- cords the case of a male infant thirty months old, in whom the heart was as large as that of an adult female, the increase almost wholly in the right cavities, the auricle and ventricle having each a capacity of two ounces, and the walls of the latter were half an inch thick ; a probe passed through the valves of the pulmonary artery appeared *The Medical Record, Oct. 20, 1883. 232 DEFORMITIES OF THE HEART in the aorta. There was an opening in the ventricular septum at the top three quarters of an inch in diameter, so that the aorta and pulmonary artery both communi- cated freely with either ventricle, or with both, most freely with the right. The semilunar valves of the aorta and pulmonary artery were, however, perfect. The fora- men ovale was open three quarters of an inch. The Eustachean valve had disappeared. The patient was tall and delicate, upper parts of the body usually cedematous, subject to turns of cyanosis, and even fainting; surface cold and patient chilly; there was dyspnoea by turns. Varying murmurs not constant; the most constant was a presystolic rippling sound. A Diverticulum, or Glove-Finger Extension of the Left Ventricle. — Dr. Gilbert* records the case of an infant who lived to the age of ten months in whom was a ventral hernia and defective abdominal wall in the middle line from the umbilicus upward. The diaphragm was found to be defective also, so that the pericardium opened into the abdominal cavity ; and projecting into the abdomen was a pouch-like diverticulum attached to the apex of the left ventricle, with muscular walls and having internally fleshy columns like the ventricular cavity itself. This ap- pendix was thirty-eight millimetres in length, and shaped like the finger of a glove. Dr. Peacock in his " Malforma- tions of the Heart," though he refers to several cases of defect of the pericardium, does not mention any such abnormality. Dextro-cardiUy the other Viscera in their Proper Places. — Dr. D. Frank Sydstonf reports the case of a man twenty- four years of age, a barber. He says : " The heart occupies precisely the same relation on the right side that it * Med. Record^ Aug. ii, 1883. \ Ibid., July 21, 1883. DEFORMITIES OF THE HEART. ^ 233 ordinarily does on the left, the apex being in the right fifth intercostal space." Otherwise the heart appears to be perfectly healthy. " The abdominal viscera are in their normal positions, a point to which especial attention is directed, inasmuch as such cases are usually accompanied by a transposition of the liver and spleen." He refers to the pathological displacements of the heart of which this is not one, as he has none, and has had none of the diseases which cause such displacement. He calls it, therefore, "An instance of a quite rare anomaly, congenital dextro- cardia. Open Foramen Ovale; Perforated Septum Ventriculorum. — Reported by Dr. Toupet.* A child, seven years old, had had measles and whooping cough ; cyanosis from birth, blue, temperature, 96.5°; eyes prominent; nails enormous- ly hypertrophied ; heart very large ; respiration rapid and labored ; at the level of the third costal cartilage, near the left border of the sternum a loud blowing systolic sound. On inspection the heart lay nearly in the median line owing to the greater size of right ventricle, right auricle normal, but left rudimentary ; aorta greatly dilated up to the origin of the left subclavian artery, beyond that, normal. The pulmonary artery only one fourth the size of the aorta ; the walls of the right ventricle very thick, tricuspid valve healthy ; the infundibulum separated by a partition from the right cavity, which was pierced by an opening of the size of a small goose quill ; the mitral valve was normal; in the upper part of the ventricular septum was a hole that admitted a finger; the aorta arose exactly at the septum, communicating with both ventricles ; valve of the foramen ovale was not adherent and was pierced by two openings of the size of a crow-quill ; the lungs were congested. * Med. Record, Aug. 4, 1883. 234 DEFORMITIES OF THE HEART. Malformation {?) Aortic. — Dr. Thomas B. Peacock* gives the following description of the condition of a heart and thinks the lesion was congenital. "The right and posterior segments of the aortic valve were blended together so that the aortic opening had but two valves ; both of them were very much thickened, and the under curtain fell below the level of the other curtain, so that there was obstruction and regurgitation. • The action of the heart was tumultuous and visible over a large space ; there was decided prominence in the praecordial region. Dulness on percussion began in the second interspace and became entire in the third. Laterally it begins to the right of the sternum and extends beyond the line of the left nipple. At the base there was a systolic murmur heard most distinctly at the right side and upper part of the sternum ; it was short and rough and followed by a soft diastolic murmur which was propagated down the course of the sternum. Toward the apex there was a creaky murmur which was independ- ent and perhaps presystolic, not heard posteriorly. Per- haps a slight passing tremor felt at the apex. Ectopia Cordis. — M. Tarnierf exhibited at a meeting of the Academic de Medicin a woman whose sternum was bifurcated at the lower part, so that the beating of the heart could be seen to take place immediately under the skin of the epigastric region. The ventricular part could be seized between the fingers ; by palpation over the upper part of the notch the contractions of the auricles could be detected. Apparently the diaphragm did not exist under the heart. M. Beau believed that the beat of the heart was due to dilatation under the influence of the afflux of blood at the time of the \ Am. Jour, of Med. Sci., Oct., 1883. * The Medical Record, Oct. 6, 1883. FUNCTIONAL DISEASES OF THE HEART. 235 ventricular systole. According to him the apex of the heart contracts during the diastole. In this case it was easy to perceive that the ventricle was soft during diastole, and hard during the systole. In systole the apex of the heart struck the thoracic wall. LECTURE XVL FUNCTIONAL DISEASES OF THE HEART. Forced Heart. — There is a diseased condition of the heart observed for the most part in those who have made great and prolonged physical exertion, whether in violent games, heavy labor, climbing ladders, running matches or forced marches, heavy drills, and the like, which has been called "the overwrought heart," "the forced heart," the irritable heart. This condition most physicians have seen, and perhaps have not distinguished it from irritable heart arising from other causes. It has been described in France and Germany, and in England by Maclean and Myers. Cases have been seen in fifties abroad, but as our war brought into conflict a greater number of men than were ever mustered into the field before, the medical muster should be correspondingly large. Dr. Da Costa alone, in a military hospital under his charge, saw more than three hundred cases. He had the means, therefore, of giving, and probably has given, the best description of the disease which we possess. It may be found in the Am. Jour, of Med. Set., Jan., 1871. I also had large numbers of army patients in the years of the war. But as Bellevue Hospital stands on the river, and the helpless 236 FUNCTIONAL DISEASES OF THE HEART. cases had to be carried on stretchers only about two hundred feet, they were all landed there, while the walk- ing cases were sent to hospitals more distant from the river. These cases of irritable heart are almost all walk- ing cases, and therefore passed by us to the upper hospitals. I am not ignorant of this disorder, but am about as familiar with rupture of the valves or heart wall from strain as with the "overworked heart." It is wise then to take the portraiture of the disease from Dr. Da Costa, whose opportunity of studying it has so far excelled that of anybody else. Dr. Da Costa says in substance that a soldier in active duty is debilitated by a diarrhoea or fever, but soon cured, returns to duty, but finds that as he exerts himself he gets out of breath, and falls behind his comrades in the march ; has dizziness and palpitations of the heart, and pain in, the chest. He is oppressed by his gun and knapsack. At the hospital his rapid pulse proves his infirmity, although he looks like a man in sound health. Any associated disorders may soon pass away, but the irri- tability of the heart, the excited organ only slowly return- ing to its healthy action, or the excitement may continue till the patient is discharged from the army or is sent to the invalid corps. There are, he says, many others in whom the irregularity of the heart's action and pain in the region of the heart occur more suddenly without previous disease. Dr. Da Costa describes the symptoms, and says that in those not having organic disease of the heart they were as follows : Palpitatiojis. — In some the attacks lasted many hours. They occurred at all hours of the day or night, and were repeated in some six or more, in others occurring but once in twenty-four hours, while some were free from FUNCTIONAL DISEASES OF THE HEART. 237 them for days. Sometimes the attacks were so violent as to produce unconsciousness, while physical exertion was a uniform cause of palpitation ; they occurred also when the patient was in bed and even asleep. Some were worse at night and early morning. The attacks were accompanied by cardiac uneasiness and pain, and pain under the left shoulder and in some by headache, dimness of vision, and giddiness. With some exceptions the patients would not lie on the left side in bed, fearing that that position would provoke an attack. But there were some who preferred the left decubitus, and somd who could lie on either side or on the back. Pain. — This was almost a constant symptom, varying in character from a dull ache to sharp and lancinating. In a few it was a burning sensation, or tearing. Some- times it preceded the palpitations, and sometimes oc- curred without them. In rare instances it was relieved hy muscular exertion, but was generally caused by it. Deep breathing in some increased the severity of the pain. The chief seat of the pain was over the heart near its apex ; it was also felt above the inferior angle of the left scapula, in the left axilla, and down the left arm, attended there with numbness. Sometimes it radiated from the heart in every direction. With the pain there was hyper- aesthesia in the cardiac region. The pain, the author thinks, was not an intercostal neuralgia, but that affection sometimes occurred as a complication. Pulse was generally very rapid — 100 to 140 — small and compressible. It might or might not have the jerky character of the heart beat, and was subject to great vari- ations. It was noticed the change in frequency was greatly affected by change of position. In one case, the patient standing, it was 105 to 108, after lying down less than 80, and fuller, in another it changed from 124 to 94. These 238 FUNCTIONAL DISEASES OF THE HEART. pulse records were made during the absence of palpita- tions ; during these the frequency was increased. The author also observed a frequent tendency to cyano- sis. Respiration. — Respiratory oppression on exertion and in the palpitations was constant ; a little of it was felt at all times, and there were occasions when the patient could not lie down. The normal ratio of the breathing and heart beats was quite broken up. A man with a pulse at 124 breathed 25 times a minute, one with a pulse at 146 breathed 26 times, and one whose pulse beat 192 times breathed 26 times. Nervous Disorders. — The headache was constant as a symptom, or in duration. It is most likely to follow se- vere palpitations. Dizziness was not uncommon. It was increased by exercise and -stooping ; often preceded the palpitations, and in one case at least caused a fall from a horse. Disturbed sleep, jerkings in sleep, and frightful dreams were not uncommon. Itchings of the skin and excessive perspirations, or of the hand only, were complained of by several. Digestive Disorders^ with "irritable heart," indigestion, abdominal distention, and diarrhoea are very common, but Dr. Da Costa regards them as more connected with the cause of the disease than a consequence of it. The Urine contained oxalate of lime and other products of impaired digestion sometimes, but never anything that was peculiar to this affection. Physical Examination. — The beat of the heart was quick, and not remarkably strong, often irregularity of rhythm. The first sound of the heart is feeble and short, resembling the second in duration. The second sound is sometimes increased, always distinct. Sometimes, he says, " the sounds of the heart are split," " there were double beats and intermissions." FUNCTIONAL DISEASES OF THE HEART. 239 The disease, for the most part, either slowly subsided or was followed by degrees, by enlargement. Dr. Da Costa, referring to causes, has constructed the following table, showing its relation to fevers and diarrhoea. The symptoms did not generally appear till the patients were sent back to duty. 200 CASES. p. c. Fevers \ , 17. Diarrhoea 30.5 Hard Field Service 38, 5 Wounds, Injuries, Rheumatism, Scurvy, Soldier Life, and Doubtful 18. 100. He has another table in which the '^ results" are shown in 200 cases, and in which death finds no place. Treatment. — In Dr. Da Costa's remedies rest has the first place — rest in bed, not only at night, but for many hours of the day. His most esteemed drug is digitalis. He gives the next place to veratrum viride. Aconite found but little favor with him ; gelsemium none at all. Belladonna corrected the irregularities of the heart, but did not reduce the frequent beat. Opium he used only for the diarrhoea and severe pain, but he decHned to use it against the irritability, fearing that in a long use of it he would establish the opium " habit." Hyoscyamus while not valueless, was not much praised. Conium, can- nabis indica, valerian, ergot, and the bromides did not win his confidence to any great degree. Tonics were often valuable, and zinc had some control over the disease. Iron was valuable in the anaemic cases. Dr. Da Costa's paper is one of the most valuable of the age. It is a structure built by square and plurnmet. Heart Sympathies. — The heart bounds with joy, it sinks in great disappointments, at sights of horror. Some persons faint at the sight of blood. Fear does not often paralyze the heart, as it often does the muscular strength, 240 FUNCTIONAL DISEASES OF THE HEART. but it causes rapid and small pulse, while it contracts the capillaries of the surface and brings paleness and nervous tremors or large shakings. A gentleman was brought to me by the physician of a life insurance company for my opinion as to the freedom of his lungs from phthisis. On the first examination, for some reason, now forgotten, I was not willing to answer the question : should the risk be taken ? On a second examination, I answered affirma- tively. This fixed the gentleman's attention strongly on this liability to consumption. Two or three months afterward a messenger summoned me to visit him at once. I replied, " Call his physician" (the late Dr. Van Buren). The messenger soon returned stating that Dr. Van Buren was not at home and urged that I must go at once. It was raining a deluge, but I waded to the gentleman's house. He was on a sofa, was as pale, or rather white, as the pillow on which his head rested ; his movements were as tremulous as if he had the '' shaking palsy." His pulse was small and rapid. His voice was low and on a monotone. I asked what had happened. He said 'he had been raising blood. I asked him, How much ? An attendant raised and unfolded a handkerchief which had on it numerous stains of blood. The blood had spread into and was diffused in the threads of the cloth, not in coagulated masses with slight diffusion, as blood from the lungs would be. It was blood that was mingled with the saliva, which had delayed its coagulation. I asked him if he had hurt his tongue while at dinner. He did not know that he had. I asked for a candle. His wife brought it in a hand trembling hardly less than her husband's. I found a laceration, a penetrating wound in the left side and back part of the tongue, as if a wood- splinter or the fragment of a nail from a flour barrel had been forced by a molar tooth into the tongue. I informed him of my discovery, and then he remembered FUNCTIONAL DISEASES OF THE HEART. 24I that he did have a pain in the tongue while at dinner. But when he was informed that the blood came from the tongue and not from the lungs, he exclaimed : *' Why, wife, I feel better. Why, I can sit up, I can stand up, I can walk," which he did then and there across the floor. I returned through the rain to my dinner and heard no more from. my patient. The load of fear lifted from his heart, it resumed its natural mode of working, and the vaso-motor nerves relaxed their grasp on the capillaries. Cardiac Neurasthenia!^ — In some cases of exhaustion from continuous over-work, the symptoms centre chiefly about the heart. The symptoms are feeble cardiac action, giddiness, weakness, intermittent beat. There may be palpitations, dyspnoea, and even syncope. A physician who suffered in this way writes that he was relieved entirely by the following prescription : 3 Quin sulphate gr. xxiv. Mist camph ad. § vj. Acid hydrobromic dil 3 iij> Tinct digital § ss. Liq. aurant § j. Tinct. Nuc vom 3 ij. M. Half an ounce three times a day. Cardiac Typhoid, — Mr. Bernheimf designates by this term cases in which, without notable organic alteration of, without pulmonary complication, or others capable of explaining the occurrence, the pulse becomes small, fre- quent and depressed. The patient succumbs to this para- lytic acceleration of the heart, which may occur at the beginning of the fever, with or without concomitant nervous adynamia or at a more or less advanced stage of it. The temperature may be moderately febrile, normal or * The Medical Record, Jan. 20, 1883. f Ibid., Jan. 20, 1883. 242 EFFECTS OF CERTAIN DRUGS ON THE HEART. subnormal. He considers this nervous asystole in typhoid fever to be due to the direct action of the poison on the cardiac innervation. The author bases his conclusions on six cases with autopsies. They ended in sudden death and no alteration of the heart correspondent. Cardiac Vertigo^ I cannot say I am very familiar with, aside from that faintness which may attend grave aortic obstructions and regurgitations. The^ Medical Rec- ord, however, quotes Germain See as saying that when it occurs in the course of heart disease, we need to look no further for its cause, as a rule ; that in cases of troublesome vertigo the heart should always be examined for its cause, especially if extreme pallor, a prominent symptom of aortic insufficiency, be present, and will not yield to med- ication. . . In these cases there are also the characteristic pains of angina pectoris, coming on every few months — another prominent, though not constant, symptom of aortic incompetency. LECTURE XVII. THE EFFECTS OF CERTAIN DRUGS ON THE HEART. Accidents Caused by Tobacco. — Vallinf has lately re- ported to the Societe de Medicine Publique some cases of poisoning by tobacco in smokers that are very emphatic. In M. Vallin's cases symptoms akin to those of angina pectoris were produced. Indeed, he calls the affection angina pectoris. Take a case. It is a "young lieutenant of vigorous constitution who for a year had been subject to attacks of angina pectoris. The * Med. i?