Volume 3 — DISEASES OF THE BLOOD, AND OF THE HÆMATOPOIETIC SYSTEM. (continued 2)

Another special danger is rupture of the blood-vessels, particularly of the brain. In the condition of general arterial degeneration associated with contracted kidneys and hypertrophied left heart apoplexy is common; indeed, we may say that in the majority of cases of cerebral hemorrhage there is sclerosis of the cerebral vessels, often with the development of miliary aneurisms, and the rupture is directly induced by the forcible action of the heart.

Hypertrophy of the right ventricle in the adult is rarely induced by valvular disease on the right side, but is a result of increased resistance in the pulmonary circulation, as in cirrhosis of the lung and emphysema, or in stenosis of the mitral orifice. When the compensation is perfect, and the hypertrophy fully maintains the equilibrium of the circulation, there are no symptoms. Extra exertion, as in ascending stairs or running, may induce shortness of breath, but in many respects hypertrophy of the right ventricle is the most enduring and salutary form in the whole range of cardiac affections. For long periods of years the effects of mitral stenosis may be counterbalanced completely, and only sudden death by accident or an acute disease reveals the existence of extensive unsuspected heart disease. In the hypertrophy secondary to pulmonary disease, particularly emphysema and cirrhosis, there may be sensations of uneasiness in the cardiac region, with cough and shortness of breath; but so long as the dilatation is moderate the symptoms are not marked. With great dilatation and tricuspid regurgitation come the venous engorgement, oedema, and pulmonary troubles. The increased pressure in the lesser circulation not uncommonly leads to atheroma of the pulmonary artery, and the full state of the capillaries leads ultimately to a deposition of pigment and increase in the fibrous elements in the lung—the brown induration. Pulmonary congestion and apoplexy from thrombosis or embolism are more often associated with dilatation. Hæmoptysis may result from rupture of vessels during sudden exertion.

The physical signs of hypertrophy of the right ventricle are not so marked as those of the left. Bulging of the lower part of the sternum and left cartilages is occasionally met with. The apex-beat is forced to the left, but is not so often displaced downward. The most marked impulse may be in the epigastrium, in the angle between the ensiform cartilage and the seventh rib or beneath the cartilages of the sixth and seventh ribs. The pulsation is rarely the strong heave of left-sided hypertrophy, and is apt to be diffuse, not punctuate, particularly if there is much dilatation. In thin-walled chests there may be pulsation in the third and fourth right interspaces. The area of dulness is increased in the transverse direction, particularly toward the right, where it may extend an inch or more beyond the border of the sternum. On auscultation the first sound at the lower part of the sternum is louder and fuller than normal, but the differences are not very marked unless there is much dilatation, when it is clearer and sharper. The second sound is accentuated in the pulmonary artery on account of the increased tension, and there may be reduplication. The pulse at the wrist is usually small. The jugular pulsation occurs when there is tricuspid incompetence, which arises when the eccentric hypertrophy reaches a certain grade.

Hypertrophy of the auricles is always associated with dilatation. It is most common in the left chamber, which hypertrophies in mitral stenosis and incompetency, and assists materially in restoring the balance of the circulation and protects the lungs. There are no special physical signs, and we usually can only infer its presence by the existence of mitral stenosis and a presystolic murmur. Increased dulness may be determined at the left of the sternum, and there may be a presystolic wave in the second left interspace.

Hypertrophy and dilatation of the right auricle occur not infrequently, and are almost invariably associated with a similar condition in the right ventricle, and incompetency of the tricuspid. In emphysema, cirrhosis of the lung, chronic bronchitis, and in mitral disease, it is very common, much more so than the statement of some authors would lead us to expect. In comparison with the left auricle the greater development and hypertrophy of the appendix and its musculi pectinati is very striking. The latter may be distributed over the anterior wall of the sinus to a much greater extent than in health. There may be increased dulness in the third and fourth interspaces, with pulsation presystolic in rhythm. Usually there are signs of venous engorgement, jugular pulsation, and other evidences of dilatation of the right heart.

The DIAGNOSIS of cardiac hypertrophy does not usually present any serious difficulties. Increase in size, more forcible contraction, with displacement of the apex-beat, and the character of the pulse, are the most important signs. There are certain conditions which require to be carefully distinguished. Neurotic palpitation, from whatever cause, may be accompanied with forcible contraction, but it has not the heaving impulse of genuine hypertrophy. Actual enlargement of the organ may, however, result from prolonged over-action, as in Basedow's disease, in the smoker's heart, and the irritable heart of neurasthenics, but it is usually slight. Increased dulness in the cardiac area may be due to a variety of causes, some of which may simulate hypertrophy, as pericardial effusion, aneurism, mediastinal growths, or displacement of the heart from pressure or the existence of malformation of the chest; but with the exercise of ordinary care the diagnosis can usually be made. There are two opposite conditions which not infrequently give trouble. When the left lung is retracted from pleurisy, phthisis, or cirrhosis, there is a large surface of the heart exposed, and the pulsation may be extensive and forcible, and at first sight resemble hypertrophy. There is usually in this condition some dislocation upward and to the left. The history of pulmonary or pleuritic disease, and the evident fixture of the lung on deep inspiration, will usually suffice to prevent mistake. A similar exposure of the heart occurs without any disease in very narrow-chested persons with ill-developed lungs; and here, though the area of dulness may be much increased, yet the normal position of the apex and the absence of forcible heaving impulse, pulse signs, and of any obvious cause of hypertrophy will afford satisfactory criteria for a diagnosis. Just the reverse occurs in some cases in which a moderate cardiac hypertrophy is masked by emphysema of the lungs or of their anterior borders. The area of dulness may be normal, or even diminished, and the pulsation diffuse and chiefly epigastric. The general condition, state of the pulse, and character of the sounds would help in the diagnosis, but it is sometimes a matter of no little difficulty.

The symptoms and physical signs above narrated sufficiently indicate the points of difference between hypertrophy of the two sides of the heart.

In all cases the greatest possible care should be exercised in ascertaining the presence or absence of conditions likely to cause hypertrophy.

The COURSE of a case of ordinary hypertrophy may be divided into three stages: 1st. The period of development, which varies much with the nature of the primary disease. Thus in rupture of an aortic cusp or in sudden overstrain from exertion it may require months, or even years, before the hypertrophy becomes fully developed. In these cases it may never do so, and then death results. On the other hand, in sclerotic affections of the valves with stenosis or incompetence the hypertrophy develops pari passu with the lesion, and may continue to counterbalance a progressive impairment of the valves. 2d. The period of full compensation, the latent stage, during which the heart's vigor meets all the requirements of the circulation. There may be no signs whatever of heart weakness, but the hypertrophied muscle completely equalizes the valvular or other defects. It may last an indefinite period of years. In some cases this fortunate period is never fully attained, and indications of incomplete compensation remind the individual that he has a heart affection. 3d. The period of disturbed compensation, which sooner or later awaits all victims of hypertrophy. It may come suddenly during an extra exertion, and death follow from acute dilatation; or more commonly it takes place slowly, and results from degeneration and weakening of the heart-muscle, with consequent dilatation and all its evils. There may be repeated failures before the end is reached, represented clinically by attacks of cardiac dyspnoea and dropsy.

The breaking, as it is called, of a compensatory hypertrophy may be induced by many causes. Among the most important is failure of general or local (cardiac) nutrition. In many a chronic heart case readmitted to hospital, perhaps for the third or fourth time, with dyspnoea and dropsy, exposure, poor food, and whiskey are responsible for the failure. Gradual sclerosis of the coronary arteries leading to fatty or fibroid changes is a fruitful source of disturbed compensation. It is well known that during or after an acute illness, pneumonia, fever, or a bronchial attack the first symptoms of heart disease may be manifested. Mental emotions, severe grief, or fright have been known to bring on symptoms of heart failure in hypertrophy. One of the most frequent causes is sudden or prolonged muscular exertion, which may disturb a compensation perfect for years, and induce death in a few days.⁵⁹ The intimate pathology of broken compensation is not always clear. It certainly does not always depend on degeneration of the muscle-fibres, so far as microscopical examination can tell, and in many cases we are forced to conclude that the ganglia are at fault and the breakdown is nervous, not muscular.

⁵⁹ Traube, Gesammelte Beiträge, Bd. iii.

The PROGNOSIS depends entirely upon the nature of the cause which has induced the hypertrophy. When remediable or removable, the heart may return to its normal size, as after pregnancy, acute Bright's disease, and some cases of hypertrophy from deranged innervation and muscular exertion. When the cause is irremediable, as in chronic valve disease, sclerosis of the arteries, or obliteration of pulmonary capillaries, the case is quite different. Here the prognosis depends largely on the capability of maintaining in its integrity a sufficient hypertrophy to compensate for the obstruction: so long as this keeps up all is well; the evils come with failure of the hypertrophy and increase of the dilatation. Conditions of general and local nutrition are all-important factors, and when these can be supported to the highest possible degree the prognosis is favorable. Ill-health may be indicated at once by the onset of cardiac symptoms, pointing to disturbed compensation. Much depends on the seat of the original disease. Mitral stenosis carries with it as good prognosis, quo ad longevity, as aortic stenosis,⁶⁰ and the latter much better than aortic insufficiency. The nutrition of the muscle of the heart demands a full and constant supply of blood, but in aortic incompetency the rapid regurgitation does not permit of the complete distension of the coronary vessels,⁶¹ and the strain is such that atheroma of these arteries is very apt to follow and still further diminish the blood-supply. Hence the prognosis in aortic insufficiency for enduring hypertrophy is bad. The hypertrophy which accompanies general arterial degeneration, though compensating for peripheral obstruction, carries with it certain dangers, as already indicated, in the liability to cause rupture. With care such patients may survive for years, though exposed to risks other than cardiac.

⁶⁰ Brückes held that the coronary vessels were filled in diastole alone, but there can be no question that blood also enters during the systole. The sigmoid valves certainly do not in the majority of cases cover the orifices of these arteries during this act. Undoubtedly, however, the heart-vessels are more distended in diastole. The pallor of the muscle in systole is a proof that the coronary vessels are not well filled at this period.

⁶¹ This is not the usual statement, but my experience—limited, it is true—seems to point to the conclusion that mitral stenosis may also exist for many years without exciting symptoms of heart disease. It may, I think, be safely affirmed that a larger number of persons with mitral valve disease live in blissful ignorance of the existence of serious heart lesion than any other group of cardiac cases. Particularly is this the case in women. Two points have attracted my attention in this connection: the frequency with which we find evidence of stenosis—as shown by the presystolic thrill and rough murmur—in women complaining, perhaps, of shortness of breath on exertion and slight cardiac distress—symptoms which are readily relieved—and the discovery post-mortem of stenosis of the mitral orifice in cases of sudden death by embolism or from some intercurrent disease occurring in persons in whom heart disease had never been suspected. The narrowing may be extreme—an orifice only 13 millimeters in width in one case in which a woman was stricken with hemiplegia while attending to her household duties. Such cases, and they are not very uncommon, teach us how perfect compensation may be in this lesion.

The TREATMENT of hypertrophy consists largely of measures directed toward its maintenance in a degree proportionate to the extra work which the heart has to do. In organic disease the well-being of the patient depends on this: we cannot remove the cause, but we can by careful hygienic and dietetic regulations maintain the balance between the defect and the compensation. The original lesion is usually beyond control, and the special indications are to moderate certain dangers associated with hypertrophy, and to promptly meet the earliest symptoms of heart failure. The utmost moderation in food, drink, and exercise must be enjoined. Quiet, regular habits are all important; excesses of all kind quickly lead to impairment of the heart's action. In the hypertrophy associated with arterial and renal disease a special danger exists in the tendency to rupture of vessels. In these cases vigorous heart-beat, with very high tension in the peripheral arteries, indicates mischief which may be met by taking prompt measures for the reduction of the high pressure. A brisk cathartic may avert an apoplectic attack, and there are cases in which the old practice of bleeding—formerly so much in vogue for hypertrophy—is justifiable. Palpitation and shortness of breath are among the earliest signs of failing compensation, and call for the treatment to be considered under Dilatation. The condition of hypertrophy from organic disease is not directly amenable to treatment; we cannot diminish the size of the organ, but we can regulate its action by measures which control the contractions when from any cause they become too forcible or irregular. More particularly is this the case in hypertrophy due to disturbed innervation. When vigorous, rest and the administration of cardiac sedatives, such as aconite or veratrum viride, will generally suffice to reduce the force of the contractions. The palpitation and irregular action in cases of irritable heart from over-exertion, the abuse of tobacco, or sexual excesses may subside with the removal of the cause. The steadying action of small doses of digitalis is often well seen in these cases.

Dilatation of the Heart.

DEFINITION.—An increase in the size of one or more of the chambers, with or without thickening of the walls.

VARIETIES.—Two varieties may be recognized: (1) dilatation with thickening, and (2) dilatation with thinning. Dilatation with thickening is the most common, and corresponds with the dilated or eccentric hypertrophy and the active dilatation of some writers. Those cases of dilatation with walls of apparently normal thickness—simple dilatation of authors—also belong to this category, for if the chamber is distended, and yet the walls maintain their normal diameter, they must of course be hypertrophied. The dilatation with thinning—passive dilatation—is specially met with in the auricles, and is characterized by increase in the size of the chamber and attenuation of the walls.

The diastole of the heart is partly an active, partly a passive act. The cavities behave as would rubber balls, and their distension after contraction is partly due to their elasticity. The heart is a suction- as well as a force-pump. In the ventricles, for example, after systole the active dilatation draws blood from the auricle—must do so, in fact, in the very process of dilating—and then the auricular systole completes the process, fully accomplishing the diastole. Dilatation occurs during this period, and results from distension beyond the limits of the contractile power of the wall. More blood is contained in the cavity than the muscle of the wall can control—i.e. expel—but if the organ is healthy, hypertrophy ensues and the chamber accommodates itself to the altered condition. It is the heightened pressure during diastole which is dangerous; during systole the pressure may be extreme, and yet no dilatation may ensue, as in aortic stenosis, in which condition the size of the chamber may remain normal, and yet the walls hypertrophy to meet the greatly-increased resistance to the outflow of the blood during the systole. In the auricles, however, the increased tension during contraction may be accompanied with considerable dilatation, as in mitral stenosis.

ETIOLOGY.—There are two important causes in the production of dilatation: increased pressure within the cavities, and impaired resistance due to disease of the muscular substance of the heart. They may act singly, but are often combined. Weakened walls may yield under normal distending force, or normal walls may yield under a heightened blood-pressure, or both factors may prevail.

1. Increased endocardiac pressure—which results, as before stated, either from an augmented quantity of blood to be moved or an obstacle to be overcome—is the most frequent cause of dilatation. It does not necessarily cause it. Simple hypertrophy may be the result, as in the early period of aortic stenosis and in the hypertrophy of the left ventricle in Bright's disease.

Most of the important causes of increased endocardiac pressure have already been considered under Hypertrophy, but we may refer to one or two more particularly.

The size of the cardiac chambers is variable in conditions of health. With slow action of the heart the dilatation during diastole must be much more full and complete than with rapid action. Physiologically, the limits of dilatation have been reached when the chamber cannot be emptied during the systole. We find this as an acute, transient condition in severe exertion—during, for example, the ascent of a steep mountain. There may be great distension of the right heart, as shown by the increased epigastric pulsation, and even increase in the cardiac dulness. The safety-valve action of the tricuspid valves may here come into play, and by permitting regurgitation into the auricle relieve the lungs. Rest causes it to pass off, but if it has been extreme, the heart may suffer a strain from which it may recover slowly, or, indeed, the person may never again be able to undertake severe exertion. In the process of training the getting wind, as it is called, is largely a gradual increase in the capability of the heart, particularly the right chambers. A degree of exertion can be safely maintained in full training which would be quite impossible under other circumstances, because by a gradual process of what we may call physical education the heart has strengthened its reserve force—widened enormously its limits of physiological work. Endurance in prolonged contests is measured by the capabilities of the heart, and its essence consists in being able to meet the continuous tendency to overstep the limit of dilatation.

We have no definite information as to the nature of the change in the heart which occurs in the process of training, but it must be in the direction of increased vigor, muscular and nervous. The large hearts often noted in athletes may be due, as already mentioned, to the prolonged use of their muscles; but probably no one can become a great runner or oarsman who has not naturally a large and capable heart. Master McGrath, the celebrated greyhound, and Eclipse, the race-horse, both famous for endurance rather than speed, had very large hearts.

Over-training and heart-strain are closely connected with this question of excessive dilatation during severe muscular effort. Both mean the same thing in many cases. A man, perhaps not in very good condition, calls upon his heart for much extra work during a race or the ascent of a very steep mountain, and is seized with cardiac pain and a feeling of distension in the epigastrium, and the rapid breathing continues an unusual time, but the symptoms pass off after a night's quiet. An attempt to repeat the exercise is followed by another attack, or indeed an attack of cardiac dyspnoea may come on while he is at rest.⁶² For months such a man may be unfitted for severe exertion, or may be permanently incapacitated. He has overstrained his heart and has become broken-winded. We see the same thing sometimes in horses. What exactly has taken place in these hearts we cannot say, but their reserve force is lost, and with it the power of meeting the demands exacted in maintaining the circulation during severe exertion.⁶³ The heart-shock of Latham⁶⁴ includes cases of this nature—sudden cardiac breakdown during exertion and not due to rupture of a valve. It seems probable that some cases of sudden death in men and animals during long-continued violent efforts, as in a race, are due to over-distension and paralysis of the heart.

⁶² In St. George's Hospital Reports, 1872, Clifford Albutt gives his own experience.

⁶³ H. C. Wood tells me he believes that wind in athletes is in large part a question of vagus control, and that he has noticed in races of dogs used in hunting and other violent exercise the vagi are more sensitive and powerful than in sedentary breeds. He thinks that a similar difference exists between tame and wild rabbits.

⁶⁴ Diseases of the Heart, New Sydenham Soc. ed.

In the various forms of valvular disease we meet with numerous examples of dilatation. In aortic incompetency during diastole blood enters the left ventricle from the unguarded aorta and from the left auricle, and the amount of blood at the termination of diastole subjects the walls to an extreme degree of pressure, under which they inevitably yield: in time they augment in thickness, and we have the typical eccentric hypertrophy of this condition.

In mitral regurgitation a certain quantity of the blood which should have been driven into the aorta is forced into the auricle from which it came, dilating it; and then in the diastole of the ventricle a larger amount is returned from the auricle, and with increased force, by the hypertrophied walls of this chamber. In mitral stenosis the left auricle is the seat of greatly-increased tension during systole, and dilates as well as hypertrophies; the distension too may be enormous. Dilatation of the right chamber is very common, and is produced by a number of conditions, which were considered under Hypertrophy. All circumstances which permanently increase the tension of the blood in the pulmonary vessels will cause it—mitral stenosis, emphysema, etc. The dilatation seems easily produced, but the accompanying hypertrophy may hold it in check for years. We may here refer to the extreme distension of the right chambers in pneumonia, particularly when the consolidation is extensive. The passive dilatation may be very great and the walls much thinned, and we see the same in states of asphyxia. Valvular lesions of the right heart are not frequent causes of dilatation. When the causes which bring about the dilatation act suddenly, the degree of distension may be great, and there is much more difficulty in the establishment of compensation, as in rupture of an aortic cusp.

2. Impaired nutrition of the heart-walls from degeneration or inflammation may lead to such a diminution of the resisting power that dilatation readily occurs.

In fevers the loss of tone due to parenchymatous degeneration or myocarditis may lead to a condition of acute dilatation which may prove fatal. It is a well-recognized cause of death in scarlatinal dropsy,⁶⁵ and may occur in rheumatic fever,⁶⁶ typhus, typhoid, erysipelas, etc. The myocarditis accompanying acute endo- or pericarditis may lead to dilatation, especially in the latter disease. The cavities are usually large in fatty degeneration or infiltration from the relaxed and atonic state of the walls. In anæmia, leukæmia, and chlorosis the dilatation of the chambers may be considerable. In fibroid degeneration the wall generally yields where the process is most advanced, as at the left apex. The impaired nutrition in coronary disease may lead to dilatation. Under any of these circumstances the walls may yield with normal blood-pressure, or if increased tension is present the effect is the more readily produced.

⁶⁵ Goodhart, Guy's Hospital Reports, Series iii. vol. xxiv.

⁶⁶ Samuel West, Barth. Hospital Reports, xiv.

Pericardial adhesions are usually spoken of as a cause of dilatation, acting by traction from without, and we generally find in a case of extensive and firm union considerable hypertrophy and dilatation. In this condition there is usually some impairment of the superficial layer of muscle which may permit of over-distension.

MORBID ANATOMY.—Usually the condition exists in two or more chambers, and is associated with hypertrophy, the appearances of which have already been described. It is more common on the right side than on the left. Perhaps the most general dilatation which we see is in cases of aortic incompetency, in which all the cavities may be enormously distended. In mitral stenosis the left auricle is often trebled in capacity, and the right auricle and ventricle also are very capacious. The former may contain eighteen to twenty ounces of blood. In many chronic affections of the lungs the right chambers are chiefly affected. Dilatation with thinning is often the result of an acute process met with in the fevers. The walls may be very much thinner than normal, almost membranous, and the dark color of the blood may show through with distinctness. When the distension of one ventricle is very great, there may be a distinct bulging of the septum toward the other side. The shape of the organ is altered, and when the right chambers are chiefly affected it is more globular in shape. Distension of the left auricle may render it visible in the front of the heart, and the appendix may be prominent. The right auricle when enormously enlarged, as in some cases of pneumonia, in emphysema, and in leukæmia, may form a large mass occupying a considerable space in the antero-lateral part of the thorax. The walls in dilatation with thinning are flabby and relaxed, and collapse at once when cut, but in dilatation with hypertrophy they are firm, especially those of the right ventricle.

The auriculo-ventricular rings are often dilated, and there may be an inch and a half, or even two inches, of increase in the circumference. Thus, the tricuspid orifice, the circumference of which is about four and a half inches, may admit freely a graduated heart-cone of over six inches, and the mitral orifice, which is about three and a half inches normally, may admit the cone to five and a half inches or even more. Great dilatation is always accompanied with relative incompetence of the valves, so that free regurgitation into the auricles is permitted. The orifices of the cavæ and of the pulmonary veins may be greatly dilated.

The muscle-substance varies much in appearance according to the presence or absence of degenerations. The endocardium is often opaque, particularly in the auricles. The microscopical examination may show marked fatty or parenchymatous change, but in other instances of dilatation and heart failure in eccentric hypertrophy there may be no special alteration noticeable. I fully agree with Niemeyer's assertion, "that it is not possible by means of the microscope to recognize all the alterations of the muscular fibrillæ which diminish the functional power of the heart."⁶⁷ We know too little as yet of the changes in the ganglia of the heart in these conditions: as centres of control they probably have more to do with cardiac atony and breakdown than we generally admit. Degeneration of them has been noted by Putjakin⁶⁸ and others.

⁶⁷ Textbook of Medicine, vol. i., Am. ed.

⁶⁸ Virchow's Archiv, lxxiv.

SYMPTOMS AND PHYSICAL SIGNS.—Dilatation produces weakness of the cardiac walls, diminishes the vigor of their contractions, and is thus the very reverse of hypertrophy. So long as compensation is maintained the enlargement of a cavity may be considerable: the limit is reached when the hypertrophied walls can no longer in the systole expel all the contents, part of which remain, so that at each diastole the chamber is abnormally full. Thus in aortic incompetency blood enters the left ventricle from the aorta as well as the auricle, dilatation ensues, and also hypertrophy as a direct effect of the increased pressure and increased amount of blood to move. But if from any cause the hypertrophy weakens, and the ventricle during systole does not empty itself completely, a still larger amount is in it at the end of each diastole, and the dilatation becomes greater. The amount remaining after systole is a cause of obstruction, preventing the blood entering freely from the auricle. Incompetency of the auriculo-ventricular valves follows with dilatation of the auricle and impeded blood-flow in the pulmonary veins. Dilatation and hypertrophy of the right heart may compensate for a time, but when this fails stasis occurs in the venous system, with dropsy. The consideration of the symptoms of chronic valvular lesions is largely that of dilatation and its effects. Acute dilatation, such as we see in fevers or in sudden failure of an hypertrophied heart, is accompanied by three chief symptoms—weak usually rapid impulse, dyspnoea, and signs of obstructed venous circulation. Cardiac pain may be present, but it is often absent.

The physical signs of dilatation are those of a weak and enlarged organ. The impulse is diffuse, often undulatory, and is felt over a wide area, and an apex-beat or a point of maximum intensity may not exist. When it does it may be visible, and yet cannot be felt—an observation of Walshe's which is very valuable. An extensive area of impulse with a quick, weak maximum apex-beat may be present. When the right heart is chiefly dilated the left may be pushed over so as to occupy a much less extensive area in the front of the heart, and the true apex-beat is not felt; but the chief impulse is just below or to the right of the xiphoid cartilage, and there is a wavy pulsation in the fourth, fifth, and sixth interspaces to the left of the sternum. In extreme dilatation of the right auricle a pulsation can sometimes be seen in the third right interspace close to the sternum, and with free tricuspid regurgitation this may be systolic in character. Whether the pulsation frequently seen in the second left interspace is ever due to a dilated left auricle is not satisfactorily determined. I have sometimes thought it was presystolic in rhythm, though it may be distinctly systolic. Post-mortem, it is rare in the most extreme distension to see the auricular appendix so far forward as to warrant the belief that it could beat against the second interspace. The area of dulness is increased, but an emphysematous lung or the full distended organ in a state of brown induration may cover over the heart and limit greatly the extent. The directions of increase were considered when speaking of Hypertrophy with dilatation.

The first sound is shorter, sharper, and more valvular in character, and more like the second. As the dilatation becomes excessive it gets weaker. Reduplication is not common, but occasionally differences may be heard in the joint sound over the right and left hearts. Murmurs very frequently obscure the sounds; they are produced by incompetency of the valves due to the great dilatation, or are associated with the chronic valve disease on which the condition depends. The aortic second sound is replaced by a murmur in aortic regurgitation; the pulmonary is accentuated in mitral regurgitation and pulmonary congestion, but with extreme dilatation it may be much weakened. The heart's action is irregular and intermittent, and the pulse is small, weak, and quick.

The DIAGNOSIS is generally easy when the physical signs, the history, and the general condition are taken into account. In a case of valvular disease with hypertrophy the onset of dyspnoea and venous stasis with dropsy tell unmistakably of cardiac dilatation. Increased præcordial dulness, with a weak, diffuse impulse, is not simulated by many conditions, and one only, pericardial effusion, need be specially mentioned. This may present very serious difficulties, and indeed a dilated heart has been aspirated under the belief that effusion was present. The points to be attended to are—the greater lateral dulness in dilatation and the wavy impulse which may extend over a great part of it; in effusion the dulness extends upward and is more pear-shaped, the impulse is not so extensive, and may be tilted up an interspace or may not be visible. The sounds in pericardial effusion are muffled and distant over the dull region, but at its upper limit may be clear. The absence of friction is an important negative sign. In some cases it is extremely difficult to determine between the conditions, and I have known a weak, feeble, irregular heart, with cyanosis, and oedema lead to the diagnosis of dilatation when effusion was present.

The PROGNOSIS depends upon the cause of the dilatation. In anæmia and fevers the temporary dilatation may undoubtedly pass away with the improvement of health; but when the cause is not remediable the danger must be measured by the presence or absence of compensation. In the majority of the cases which we see the dilatation occurs in valve disease, and no symptoms of importance arise so long as the compensation is perfect. Failure of this, which may result from many causes, as already mentioned, is always serious. It may be only temporary, and with care the compensation can be re-established and the symptoms pass away. We constantly see this in the eccentric hypertrophy of the right heart from mitral disease; an attack of bronchitis suffices to disturb the compensation, and with the relief of the catarrhal trouble the dyspnoea and heart symptoms disappear.

The TREATMENT of dilatation is virtually that of chronic valvular disease, and we shall only refer to general indications. With the earliest symptoms of failure the work of the heart should be reduced to a minimum by placing the patient at rest. This in itself may suffice without any other measures. Time and again I have seen, particularly in cases of aortic insufficiency, the dyspnoea relieved and the oedema of the feet disappear and the compensation re-established by placing the patient in bed, enjoining absolute quiet and carefully regulating the diet. The importance of rest in the early stages of heart failure cannot be too much insisted upon.⁶⁹ Quiet and careful dieting may suffice for the milder attacks, but we have usually even in these to resort to heart tonics. Digitalis is the most powerful remedy we possess in restoring and maintaining compensation. Under its use the irregular, feeble, and frequent contraction becomes regular and stronger, and the embarrassed circulation is relieved. In hospital practice the same chronic heart cases may return year after year with attacks of cardiac failure, dyspnoea, dropsy, etc., and each time the rest in bed and digitalis may suffice to restore compensation. A fourth or fifth, even a sixth, attack may be safely weathered, and then the final breakdown occurs when nothing avails to combat the dilatation. Of substitutes for digitalis, caffeine and convallaria have been much used of late. Caffeine in some cases acts more promptly, which is an advantage, but its action is not so certain and not so enduring. Convallaria is very variable in its action; it has succeeded in some instances in which digitalis has failed, and in others has been quite without effect. In extreme cardiac failure with great dilatation, lividity, orthopnoea, and feeble pulse, stimulants must be freely given; ether may be employed hypodermically. In this condition of final asystolism digitalis seems to have lost its influence. In the heart failure of pneumonia I have found camphor a valuable adjuvant to the diffusible stimulants. To improve the general nutrition, and with it that of the heart-muscle, iron and arsenic are most valuable adjuvants, especially in the dilatation of anæmia. The treatment of special symptoms, dropsy, dyspnoea, etc., is considered under Valvular Affections.

⁶⁹ In Ortel's system (Ziemssen's Handbuch der Allgemeine Therapie, Bd. iv.) of treating heart disease exercise, particularly climbing, forms a very important part, but an analysis of his cases shows that most of them were instances of fatty heart in obese persons. It would scarcely be applicable to valvular disease. The severe exercise, he thinks, stimulates the heart-muscle and helps in the restoration of the hypertrophy. His other suggestion, the reduction of the liquids ingested, seems much more reasonable, as in this way the volume of blood to be circulated may be considerably reduced.

Aneurism of the Heart.

This term is now restricted to local or partial dilatations of the wall of one of the cardiac cavities. Formerly, dilatation of the heart or of one of its chambers was spoken of as aneurism. This rare condition⁷⁰ is most frequently associated with fibroid degeneration, but other causes of local weakness of the walls, as ulcer, acute myocarditis, and fatty degeneration, have been present in a few cases. An instance is on record where the aneurism followed a stabbing wound of the chest.⁷¹ The left ventricle is usually involved; very few cases occur in the other chambers. The condition may be acute or chronic.

⁷⁰ In the index catalogue there are references to only 18 cases by American authors. In the museums of Philadelphia there are only 5 specimens—3 in the museum of the College of Physicians; 1 each in the University and Pennsylvania Hospital cabinets.

⁷¹ Quoted by Legg, Bradshawe Lecture on Cardiac Aneurisms, London, 1883.

Acute aneurism is met with occasionally in ulcerative endocarditis, more rarely as the result of local softening due to myocarditis or plugging of a branch of a coronary artery. In severe endocarditis perforation is, I think, more common than the production of aneurism. In one case I saw a deep excavation at the upper part of the septum produce a bulging the size of a marble in the wall of the left auricle, and in another ulceration in one sinus of Valsalva had extended into the septum, the upper part of which presented an aneurismal dilatation which had ruptured into the left ventricle. Legg considers the production of acute aneurism by the rupture of abscesses or cysts as doubtful.

Chronic aneurism is almost confined to the left ventricle, and, as Cruveilhier pointed out,⁷² is the result of fibroid degeneration of the muscle. In a few instances fatty degeneration appears to have been the cause. The monographs of Thurnam,⁷³ Pelvet,⁷⁴ and Legg⁷⁵ give the most complete account of the disease. They are more common in men than in women, and the majority of the cases occur after middle life.

⁷² Anatomie pathologique, Paris, 1835–42.

⁷³ Medico-Chirurgical Transactions, vol. xxi., 1838.

⁷⁴ Des Aneurysmes du Coeur, Paris, 1867.

⁷⁵ Loc. cit.

The situation of the aneurism is most frequently at the apex—59 of 90 cases collected by Legg. They are usually rounded in shape, and may vary in size from a marble to a cocoanut. The sac may be double, as in a case described by Janeway,⁷⁶ or, as in a specimen in Guy's Hospital Museum, the whole wall of the ventricle may be covered with aneurismal bulgings. In the simplest form there is a rounded dilatation at the apex, and the lower part of the septum is lined with thrombi. Often the tumor is distinctly sacculated, and communicates with the ventricle by a very small orifice. The pericardium is usually thickened, and calcification may occur in the walls. Rupture seems rarely to occur—in only 7 of the 90 cases collected by Legg. Of other parts of the ventricle, the septum and the undefended space at the highest part of the septum just below the aortic ring are most often involved. This latter situation is sometimes the seat of a congenital dilatation, usually a small, thin, smooth sac without thrombi, which has no pathological significance.

⁷⁶ N.Y. Med. Journ., 1875, xxi.

Cardiac aneurisms rarely produce any symptoms, and in the majority of cases have been found accompanying other conditions which have proved fatal. At the left apex the increase in dulness and area of pulsation could scarcely be distinguished from hypertrophy unless associated with marked bulging. They seldom perforate the chest-wall. Berthold (quoted by Legg) has described one connected with the right auricle which produced a pulsating tumor beneath the skin, the region of the second and third ribs.

Adventitious Products in the Heart.

Tubercle.—In general tuberculosis and in tuberculous pericarditis there may be nodules in the heart-substance, but, as a rule, this organ is very rarely the seat of tubercle. Large caseous masses sometimes occur, but unless associated with tubercle in other organs they are not to be regarded as necessarily tuberculous. Miliary granulations have been seen on the valves.

Cancer and sarcoma rarely are primary, and are not often met with as secondary growths. Sometimes a mediastinal sarcoma penetrates along the veins and involves the auricle, with or without great involvement of the pericardium. The secondary tumors may be single or multiple. In a case of cancer of the uterus I found a large mass in the wall of the right ventricle, involving also the anterior segment of the tricuspid, and partially blocking the orifice. The surface was eroded, and the pulmonary arteries contained numerous cancerous emboli. In another instance the heart was considerably enlarged by the presence of many rounded masses of colloid cancer throughout the walls. In a remarkable case of sudden death in a child I found the tricuspid orifice firmly blocked with a sarcomatous mass which I thought at first had originated in the heart, but dissection showed to have come from the renal vein, which was filled with sarcoma extending from a large tumor of the kidney. Melanotic cancer, fibromata, and myomata have occasionally been seen, and a secondary epithelial growth has been described by Paget.

Syphilis of the heart is met with in the form of gummata or as a specific arteritis leading to patches of fibroid induration. The gummous growths form tumors of variable size, which usually occupy the septum or the ventricles. Possibly many of the caseous and calcified masses not infrequently met represent obsolete gummata. The syphilitic myocarditis probably originates in an affection of the arteries, and leads to patches of fibroid induration more or less extensive. Many authors hold that syphilis plays a very important rôle in the production of fibroid heart.

Cysts.—Simple cysts are rare in the heart. I have met with two instances—one, the size of a marble, situated in the wall of the right auricle near the septum, was filled with a brownish fluid; the other, the size of a small walnut, occupied the base of the posterior segment of the mitral, and was filled with a clear fluid. Blood-cysts occasionally occur.

Parasites.—The Cysticercus cellulosæ, the larva of Tænia solium, and the hydatid or echinococcus, the larva of Tænia echinococcus of the dog, are sometimes found in the heart. The former, usually single, is extremely rare; in the hog and calf the measles, as the cysts are called, very often exist in the heart-muscle. In the recent paper by Mosler⁷⁷ references are given to 13 cases of cysticerci in the heart. The greatest number present was 19. The hydatid is more common: 25 instances are mentioned in the statistics of Devaine and Cobbold, and Mosler's more recent figures only give 29. They occur in the right ventricle more frequently than in the left. Occasionally they attain a larger size and compress the heart and push back the lungs. The cyst may burst and the contents be discharged into the pulmonary artery or aorta, as in a case given by Osterlen,⁷⁸ in which gangrene of the right leg followed the plugging of the femoral by hydatid vesicles discharged into the blood by the bursting of a cyst in the left auricle.

⁷⁷ Zeitschrift für klinische Medicin, Berlin, Bd. vi., 1883.

⁷⁸ Virchow's Archiv, xlii.

ENDOCARDITIS AND CARDIAC VALVULAR DISEASES.

BY ALFRED L. LOOMIS, M.D.

Endocarditis.

DEFINITION.—Endocarditis is an inflammation of the endocardium, and may be either exudative, neoplastic, or ulcerative in character. While its different varieties are closely connected in their etiology, they are distinct in the extent, duration, character, and course of their pathological changes. They cannot be classified as acute and chronic in the ordinary acceptation of these terms, for they often so merge into each other as to render it difficult, if not impossible, to determine when they cease to be acute and become chronic; and some cases are at no time acute. It has been claimed that an acute endocarditis becomes chronic when its course is prolonged, but the advanced changes are only a stage of the acute process.

So-called acute endocarditis is accompanied by a fibro-cellular exudation into the substance of, and underneath, the endocardium, causing elevations of its surface. The better term for this variety is exudative endocarditis, it being borne in mind that the exudation does not take place upon the free surface of the membrane, but into its substance and underneath it. This form of endocarditis may be entirely recovered from, or it may lead to interstitial changes in the endocardial and myocardial tissue which will correspond to the changes usually described as those of chronic endocarditis.

Interstitial endocarditis is a better term for these changes. The disease may be the sequela of exudative endocarditis, or may be interstitial from its commencement, for the valvular changes of interstitial endocarditis are often found in those who never have had either acute articular rheumatism or exudative endocarditis, but have been the subjects of chronic rheumatism or gout.

Acute exudative endocarditis may, in certain cases, be stamped with an ulcerative process, the result of septic infection, giving rise to those pathological changes which have been described as acute ulcerative endocarditis.

HISTORY.—The history of endocarditis is restricted to modern pathology. It is not spoken of by the older medical writers. Before the sixteenth century knowledge of the structure and functions of the heart was imperfect and scanty, and its diseased conditions were altogether unknown.

The history of the pathology of cardiac disease commenced with Harvey, Lancisi, Vesalius, and Vieussens. They investigated not only the normal structure of the heart and the mechanism of the circulation, but accurately described a few of its valvular diseases.

There is little doubt but that Laennec, Senac, and Morgagni were quite familiar with the valvular diseases of the heart, but Kreisig first traced the relationship between valvular diseases and inflammation of the lining membrane of the heart.

The term endocarditis was first used by Bouillaud, who had the advantage of Laennec's discovery of auscultation. Corrigan first discovered the physical signs of aortic insufficiency. The most important advance in the pathology of endocarditis is due to the investigations of Virchow and Luschka, the former developing its sequelæ or results, the latter its histological changes. Ulcerative endocarditis is of modern date, and its literature scarcely extends back twenty years. The labors of Kirk, Virchow, Charcot et Vulpian, Moxon, Eberth, and Lancereaux are all connected with the etiology and anatomical changes of ulcerative endocarditis.

The relationship of interstitial endocarditis to valvular diseases of the heart and to cardiac murmurs is a subject which at present is engaging the attention of many medical observers.

I shall describe endocarditis under three heads: 1st, Exudative endocarditis; 2d, Ulcerative endocarditis; 3d, Interstitial endocarditis.

That the pathological changes which I shall describe may be readily appreciated, I will briefly review the anatomical structure of the endocardium.

The endocardium consists of connective tissue, with numerous elastic fibrils, covered by and continuous with a layer of flattened cells. Upon this lies the endothelial layer, which disappears in twenty-four hours after death.

Luschka regards the endocardium as continuous with all the arterial tissues, but the majority of histologists consider it a continuation of the internal membrane. Some regard the endocardium and inner coat of the arteries as analogous, since both are non-vascular and have an endothelial covering upon a connective-tissue base. As endocarditis is, for the most part, limited to the valves of the heart, a knowledge of their anatomical arrangement is important.

A transverse section of a segment of an auriculo-ventricular valve shows that upon the superior or auricular surface and upon the inferior or ventricular surface there are flattened cells and endothelium, and that next to each lies a fibro-elastic layer, the superior being the thicker. These two layers are separated by connective tissue.

The layer of flat cells is thickest on the ventricular surface. The fibro-elastic tissue is thickest at the base of the valve. The semi-lunar valves have endocardium on one side and the tunica intima on the other.

Although the endocardium has no vessels of its own, the capillaries upon the cardiac walls are in contact with it. The arrangement in the valves is different, as only a few vessels ramify between the layers of the mitral valve, and none are found, normally, in the sigmoid valves.

Acute Exudative Endocarditis.

This variety of endocarditis is met with most frequently in connection with acute articular rheumatism.

In adults it usually has its seat in the left heart; in intra-uterine life it occurs in the right heart. The inflammation commences in, and seldom extends beyond, the valves and the valvular orifices, but it may involve the whole or any part of the ventricular or auricular portions of the endocardium.

MORBID ANATOMY.—The endocardium becomes infiltrated with young cells, the process beginning in the layer of flat cells. The new formative cells are developed not only from the cells of the layer immediately underneath the endocardium, but also from leucocytes. This hyperplasia, this heaping up of embryo-plastic cells, is accompanied by softening of the deeper layers of the intercellular structure, and as the softening goes on the intercellular substance is destroyed.

The endothelial elements also play an active part in the processes. The masses of new cells push out the endocardium, and papillary elevations are formed, filled with a fluid whose chemical properties resemble those of mucin, since it coagulates into threads when acetic acid is added. The cone-like vegetation is surrounded in the deeper layers of the endocardium by a zone of proliferation which is never distinctly limited, but which exhibits progressive hyperplasia from the periphery toward the centre.

All these changes may have taken place in non-vascular tissue. Where the capillaries are most numerous a punctuate or arborescent vascularity is seen, and this is followed by opacity of the part which is the seat of the inflammation. After death the endocardium and lining membrane of the vessels are often stained; this staining is produced by the coloring matter from the red corpuscles, and is the result of post-mortem change.

There is no exudation upon the villous projections; the coagula found upon them are a deposit of fibrin from the blood, the projections acting as foreign bodies in the blood-current. The fibrinous deposits occur chiefly on the surface which is opposed to the current of the circulation, and sometimes they are distinctly conical; at others they have the shape of a raspberry. They occupy the parts most exposed to the friction of the blood, and are arranged on the borders of the aortic valves at a little distance from their edges, the seat being determined by the limit of the vascular network. The band of tissue which passes from the attached border of the valve to the Arantian body in the centre shows the inflammatory granulations most distinctly. They consist of a cauliflower-like bulbous extremity, connected by a constricted neck with a firm, hard base that is intimately blended with the subjacent tissue. A thin hyaline layer covers each mass. At first these granulations or vegetations are very small and numerous, so that the membrane presents a granular appearance. Later, they become larger, reaching oftentimes the size of a small pea.

Near the insertion of the tendons upon the auricular surface of the mitral valve are found irregular wreaths of vegetations which enclose the attachments of the chordæ tendineæ. Moxon has shown that the friction of the vegetations or of fibrinous clots that gather upon the vegetations may, by the irritation it produces, excite endocarditis at points remote from the valves.

The tendon of the mitral valve may show the effects of endocarditis by becoming soft and friable, and even rupturing, or the chordæ tendineæ may adhere to one another. When such adhesions occur either with agglutinations of the flaps to each other or to the heart-walls, stenosis or regurgitation may result.

In connection with these changes new vessels are developed in the substance of the mitral valve, or those that already exist become more apparent. In the semilunar valves new vessels are formed or neighboring capillaries send out prolongations into the parts destitute of vessels. This, according to Charcot, is one way in which arborescent vascularity occurs. These changes are most marked in those forms of exudative endocarditis which run an acute course.

In some instances the hyperplasia is so extensive as to interfere with nutrition, and may lead to fatty metamorphosis. A cavity is then formed filled with granular fat-cells, discrete fat-globules, and blood-pigment, whose endocardial covering ruptures, and the contents are carried into remote capillaries to cause capillary embolism and septicæmia. This has been called ulcerative endocarditis.

Ulcerative Endocarditis.

Ulcerative endocarditis occurs in those diseases where there is great vital depression. It is met with oftenest in pyæmia, puerperal fever, scarlatina, and diphtheria. It has been called septic, diphtheritic, and infectious endocarditis.¹

¹ Jaccoud, Klebs.

MORBID ANATOMY.—Ulcers may form in endocarditis in either one of three ways: 1st. The exudative process may be so rapid and extensive as to cut off the nutrition of the endocardium covering the apices of the papillary elevations, and ulcers result in non-septic inflammation. 2d. Degeneration of the neoplastic tissue, due either to deficient blood-supply or other causes of impaired nutrition, may so soften the villi or efflorescences that their apices will be swept away by the blood-current and ulcers thus be formed. Charcot especially insists that the ulceration of these elevations is the consequence of granular degeneration, and not of fatty metamorphosis, with which it is often confounded. 3d. The exudative process may be purulent in character, and form minute abscesses in the substance of the valves beneath the endocardium, which, rupturing, leave comparatively deep ulcers. Acute multiple abscesses in the aortic valves are of frequent occurrence in ulcerative endocarditis.

The margins of the ulcers are irregular, but well defined; the edges are swollen and thick, and their floor (the muscular substance of the heart or the fibrous layer of the valve) is infiltrated with pus.

Where there is extensive loss of substance perforation of the valve may occur. These perforations are sometimes closed or hidden by a fibrinous exudation.

The soft and friable vegetations may be torn into long shreds by a forcible blood-current, and subsequently may excite endocardial inflammation where they come in contact with the walls of the heart-cavity, or they may break off and form emboli. A fibrinous string upon a flap of the aortic valve is not infrequently driven down and back by a regurgitant current, so as to excite endocarditis in the mitral valve.

Some observers state that micrococci and bacteria are found in ulcerative endocarditis of a septic or diphtheritic origin, and they have given to it the name of mycosis endocardii. It is probable that these minute organisms are developed by the septic ulcerative process rather than that they are the cause of such processes. They appear as spheres, highly refractive, motionless, cohering in groups, without any stroma. Acids, alkalies, ether, and chloroform have no effect on them, so that they are not to be regarded as vegetable products.

The valvular ulcerations in this form of endocarditis give rise to the most diverse lesions. Masses may be detached from the diseased cardiac orifices, either from the fibrinous deposits on the valves or from ulcerations of the valves themselves, and, having entered the circulation, they will produce various symptoms in the organs and tissues to which they are carried.

It is important to make a distinction between the results produced by displacements into the blood-current of large masses and those arising from the entrance of molecular fragments. It is also to be remembered that the masses from the vegetations or ulcerated valves in ulcerative endocarditis are often stamped with a septic element which leads to the development of suppurative infarctions in different organs.

The size and site of the emboli are important, for they may be so large as to obstruct vessels of large size.

The femoral and even the external iliac may suddenly become impervious to the circulatory currents, on account of the presence of a large embolus from the heart.

When the arteries in the limbs are thus plugged, the result is generally an ischæmia, terminating often in gangrene. Capillary embolism may occur in a number of organs at the same instant, and give rise to a variety of lesions. When the cutaneous capillaries are obstructed ecchymotic spots are produced, followed by cellulitis. When the cerebral vessels are obstructed softening may occur, which, if the vessels are very small, may be developed without any evidence of obstruction to the cerebral circulation. If the obstructed artery is of large size, instantaneous hemiplegia and secondary softening will result.

Capillary emboli may have their seat in the vessels of the spleen, giving rise to infarctions and suppuration.

The kidneys may also undergo analogous changes. Rayer, without knowing the origin of these changes, has given an excellent description of them under the name of rheumatic nephritis.

In addition to the local lesions arising from these arterial or capillary emboli, the septic phenomena are most important. When typhoid symptoms, deep jaundice, and symptomatic intermittent fever are associated with acute endocarditis, it establishes its ulcerative character. In acute exudative as well as in ulcerative endocarditis, when the inflammation progresses rapidly, the valves soften and become less resistant than normal. As a result, they are stretched, bulged, or torn by the stream of the circulating blood-current.

A rupture of the mitral valves will open into the auricular, and that of the aortic into the ventricular, cavity. The reason for this is to be found in the fact that when the valves are closed the blood-pressure is exerted from the left ventricle toward the mitral valve, and from the aorta toward the semilunar valves. If the blood penetrates a rent in a flap of the valves, the endocardium is puffed out, and a valvular aneurism is formed, and round or funnel-shaped aneurismal sacs may project from the valves. The bottom of one of these sacs may be perforated, and long, ragged, gray shreds, covered with fibrin, may be found hanging in the ventricular cavity.

Microscopically, the torn shreds from a valvular aneurism, the result of acute endocarditis, consist of nuclei and round cells imbedded in a mass of granular matter. There is neither connective fibrilla nor elastic tissue. When the ulceration is localized in the ventricle, the pressure of the blood may bulge out the heart-wall, and thus give rise to a so-called partial cardiac aneurism. By rupture of such aneurism communication between the different heart-cavities may be established, which will vary with the seat of the ulceration.

Acute exudative endocarditis may involve the muscular structure of the heart. Such myocarditis (or carditis) may involve the deeper structures, weaken them, and so alter their consistence that bulging and the formation of a ventricular aneurism may result. Usually such myocarditis is so slight that incomplete organization of the new embryo-plastic cells occurs and the tissue undergoes fatty changes. The results of all forms of acute endocarditis are best studied in connection with the morbid changes of interstitial endocarditis, into which they so often gradually merge.

Interstitial Endocarditis.

MORBID ANATOMY.—Interstitial (or chronic) endocarditis may be a continuation of a process which commenced in an acute exudative endocarditis, or it may be interstitial from its commencement, and be so insidiously evolved as to escape notice. The anatomical changes may sometimes be confined to the edges of the valves, at others to their base, or they may involve the entire valves, which become thickened, indurated, contracted, degenerated, and adherent. It is more closely allied to rheumatism, gout, and chronic interstitial changes in other organs than either of the other varieties.

There is no part of the endocardium which is exempt from interstitial inflammation. The favorite place for its development is the endocardium of the valves and that at the apex of the left ventricle. The thickening at first may be either translucent or opaque, and the valves may become three or four times thicker than normal. In some instances, although the valves are thickened and indurated, their functional activity is not interfered with, and they offer no obstruction to the blood-current.

White, thickened, opaque spots are often irregularly scattered over the internal wall of the heart. The vegetations met with in interstitial endocarditis differ from those of the acute exudative variety in that they are less prominent and firmer. They rest upon an indurated base. Their cartilaginous consistency is due to the fact that their cellular elements are not round (as in acute exudative endocarditis), but elongated and flattened, possessing an abundant intercellular fibrillated tissue.

In and underneath the endocardium there is an increase of tissue, and upon any prominence arising from the thickening of the endocardium occur fibrin deposits. These fibrinous efflorescences assume a variety of forms, and sometimes string out into the adjacent vessels and cavities for half an inch or more. Their usual form is globular or wart-like, and their seat is on the ventricular surface of the aortic and upon the auricular surface of the mitral and tricuspid valves.

In interstitial endocarditis the cell-development is far less rapid and abundant than in the acute exudative form, and this very slowness accounts for the greater induration and thickening.

A microscopical examination of a cross-section of an indurated valve shows a number of flat cells arranged in irregular layers, having between them a fibrinous material which has in it here and there a few elastic fibres. The new formations always originate in the layer of flat cells. These changes are best marked in the fibrous zone at the valvular orifices, upon the surfaces of the valves themselves, and in the chordæ tendineæ. The new tissue, whether developed rapidly as in acute exudative, or slowly as in interstitial endocarditis, becomes fibroid and contracts, and this contraction is progressive.

As a consequence, the rigid valves, whose edges are round and hard, are drawn toward their base, and thus are made to assume a puckered appearance. A similar process in the chordæ tendineæ causes them to become hypertrophied, rigid, and cartilaginous, while they are diminished in length. In this way the valves are not only diminished in depth, but not infrequently have their free edges approximated to the cardiac walls, so that extensive valvular insufficiency is the result. This, however, does not always happen, for a thickened cartilaginous valve may have such abundant fibrinous or papillary excrescences upon it that the onward current is obstructed and extensive stenosis results.

As the thickening and rigidity of the flaps of a valve increase, their mobility is diminished, and adhesions take place between their edges which begin at their bases and progress toward their apices: so thoroughly do they become adherent that in some cases all evidence of a valvular outline is lost, and a fibrinous diaphragm is formed across the valvular orifice having only a small slit at its centre, looking and feeling like a buttonhole; hence the term buttonhole slit. The mitral opening, which will usually admit the ends of three fingers, may be so narrowed that the end of the little finger will scarcely pass through it, and the aortic opening may become so diminished as not to admit a small quill. These retractions and adhesions cause the mitral valves, with their columns and cords, to assume the form of a perforated cone.

Long stringy masses of fibrin, when located on the aortic valve, sometimes form adhesions with the aortic walls, and thus is induced a sudden and extensive regurgitation.

Insufficiency and stenosis are often found at the same valvular orifice as the result of the thickening, adhesion, and retraction.

Changes at the aortic orifice usually occur after middle life, and induce more insufficiency, retraction, and adhesion than those which are limited to the mitral valve. The mitral valves are the most frequent seat of interstitial endocardial changes in early and adult life. These lesions are analogous to those characteristic of endarteritis deformans. The tendency of the lowly-organized tissue which results from interstitial endocarditis is to undergo fatty and calcareous changes.

The minute patches of fatty degeneration in the imperfectly organized tissue underneath the endocardium sometimes form atheromatous masses containing more or less granular débris. The endocardium over these patches may be destroyed, or the patches may soften and ulcerate and cause extensive destruction of the valves. Valvular aneurism may form in the same manner as has been described in exudative endocarditis. The formation of calcareous granules and plates is a very frequent termination of interstitial endocarditis.

The aortic orifice is the most frequent seat of calcareous degeneration. It is rarely associated with mitral stenosis. So extensive may this process be that little beads of chalky material may be seen studding the free edges of the valve and even extending into the cardiac cavities.

When interstitial endocarditis has its seat in the endocardium of the cardiac cavities, the endocardium will undergo changes similar to those of the valves, and the muscular walls of the heart will be the seat of interstitial myocarditis. As a result, the walls of the heart become thinner and less resistant than normal, and depressions are formed on its inner surface. The process is in reality a fibrous overgrowth, which occurs in spots varying in size from half an inch to one inch in diameter. When it extends through the entire heart-wall the columns and cords may be so shortened as to cause valvular insufficiency.

If the cardiac walls yield so that a well-defined pouch is produced, a condition results which is called aneurism of the heart. Cardiac aneurism, thus induced, is usually seated at the apex of the left ventricle; the aneurismal sac may vary in size from that of a marble to that of a closed fist, and may communicate with the ventricle by a funnel-shaped or ring-like aperture. The walls of the sac are solid and rigid; the internal surface is smooth, but it may be anfractuous. In the latter case clots adhere to its wall. Cardiac muscular fibres are found here and there in the aneurismal walls. They are mostly, however, made up of layers of flat cells, their flatness being the result of pressure.

Aneurisms at the base and in the inter-ventricular septum may result from the extension of a valvular aneurism.

ETIOLOGY.—In most instances endocarditis depends upon a constitutional dyscrasia characterized by alterations in the vital, physical, or chemical properties of the blood.

Acute exudative endocarditis rarely, if ever, occurs as a primary or idiopathic affection. It seems to have a direct connection with those diseases and dyscrasiæ in which the blood is altered either in the relative proportions of its constituents or in its physiological elements. So frequently is acute exudative endocarditis associated with acute articular rheumatism that they have often been described as one disease.

It is generally stated that acute endocarditis occurs in 50 per cent. of those who suffer with acute articular rheumatism, but the statistics of Bellevue Hospital show that endocarditis complicates rheumatism in only 33 per cent. of the cases. From these statistics it is evident that a majority of the cases of acute rheumatism run their course without endocardial complication.

The irritant action of the blood, the salts of which are changed or which contains excrementitious products or a specific poison, is shown most markedly upon the valvular surface of the endocardium; and it is for this reason that the parts which are most exposed to friction of the blood-current are those which first and most extensively exhibit the pathological changes of endocarditis.

Charcot records a large number of observations in which endocarditis developed in patients with chronic rheumatism and in which it never assumed an acute form. It therefore seems evident that organic lesions of the valves from endocarditis may occur in the course of chronic as well as of acute rheumatism.

There is no disease in which a morbid blood-state exists in which endocarditis may not occur. The essential fevers, the exanthemata, diphtheria, septicæmia, pyæmia, and Bright's disease, are all conditions in connection with which endocarditis is frequently exhibited. It is met with occasionally in secondary syphilis.

Acute and chronic Bright's disease are often complicated by it. When an individual who is already the subject of valvular disease of the heart is attacked with acute rheumatism, the liability to endocarditis is much increased.

Even when rheumatism and chorea are absent, endocarditis is liable to occur when valvular disease exists. Some regard myocarditis, pericarditis, pleurisy, and pneumonia as capable of exciting endocarditis by the extension of the inflammatory process from the surface of the heart; it is questionable if it ever results from such extension. That it can be the result of traumatism is possible: Bamberger records two cases of traumatic endocarditis. Wunderlich ranks measles, next to rheumatism, as a cause of endocarditis.

In estimating the etiological importance that any disease bears in the production of endocarditis, we must remember that not every blowing sound or murmur is indicative of an inflamed endocardium. Bamberger and Niemeyer think that the excited and irregular action of the heart in children, by inducing irregular tension of the valves, may bring about a blowing sound during the course of acute rheumatism.

Acute ulcerative endocarditis is met with in pyæmia, puerperal fever, and endometritis, scarlatina, and diphtheria: it may occur as a secondary affection to some inflammatory focus located in the body—septic endocarditis.

Again, this form of endocarditis may appear without obvious cause—spontaneously or in connection with some specific form of inflammatory disease, as croupous pneumonia. Wilks calls it then arterial pyæmia. Primary ulcerative endocarditis is a name recently and perhaps more aptly given it.

Finally, ulcerative endocarditis may appear as a graft (recurrent endocarditis) upon a valve the seat of interstitial endocarditis, and have all the pathological appearances of the septic form, but none of its clinical aspects.

The majority of cases of interstitial endocarditis are the sequelæ of the exudative form. It is far more frequently associated with articular rheumatism than with any other condition. In a certain proportion of cases the process is interstitial from its onset, especially when it occurs with gout, chronic rheumatism, in alcohol-drinkers, or in the aged.

SYMPTOMS.—The subjective symptoms of acute exudative endocarditis are more obscure than those of any other disease. They are not only few and ill-defined, but they have no regular order of development. When the muscular tissue of the heart is not involved the disease may run its entire course without exhibiting a single subjective symptom.

The urgent symptoms of acute rheumatism, the different phases assumed by the dyscrasiæ and acute infectious diseases in which this condition is liable to occur, so mask those of the endocardial inflammation that they are often overlooked.

When the endocardial inflammation is extensive and the muscular tissue of the heart is involved, the patient will complain of palpitation and a sense of discomfort in the region of the heart; not infrequently cardiac palpitation is accompanied by dyspnoea, and decubitus on the left side is noticed. In a small percentage of cases the palpitation is appreciable to the physician. The heart may beat with great force and its action be tumultuous, and yet the pulse not be altered in character.

The pulse, at first, is usually strong and forcible; later, it becomes rapid, small, feeble, and irregular. In some cases it is very frequent from the onset of the disease. As a rule, the force of the pulse will not correspond to the cardiac activity; for, as the muscular fibres of the heart become involved, its propelling power is diminished, and the pulse is correspondingly feeble and compressible. It may be dicrotic. The respirations are more or less accelerated, and sometimes labored, and there may be paroxysmal dyspnoea. The face may be flushed and covered with a profuse perspiration, or it may assume a dusky, pallid, ashy-gray, or slightly cyanotic hue. In rare cases there may be sleeplessness or nocturnal delirium of a typhoid type. If the muscular tissue of the heart is extensively involved, nausea, vomiting, giddiness, and syncope may be present.

When there is pain in the cardiac region, especially if it is augmented by pressure, pericarditis is usually present, and slight pain or tightness in the cardiac region is not an infrequent symptom, and is quite common when endocarditis occurs in those who are the subjects of chronic valvular disease.

The temperature in acute exudative endocarditis seldom exceeds 103° F.

When ulcerative endocarditis complicates septicæmia and a rupture of a valve occurs, a typhoid state rapidly supervenes. The patient is forced to assume the sitting position on account of the intensity of the dyspnoea, cyanosis is sudden and extreme, and the symptoms of multiple embolism make their appearance. The febrile symptoms are marked; the temperature may reach 106–107° F.; the patient becomes jaundiced; and there are frequent rigors, which, with the paroxysmal febrile attacks, simulate the icteric form of malarial fever. The spleen becomes enlarged and tender, the urine becomes scanty, dark-colored, albuminous, and of high specific gravity, and in severe cases delirium and coma occur.

Some cases of endocarditis putrida (as some German pathologists call it) are attended with nausea, vomiting, and diarrhoea. The frequency with which this form of endocarditis is associated with pneumonia certainly suggests a blood-poison of great intensity. Although it is rarely met with except in septic conditions, it may occur late in severe forms of rheumatic and traumatic endocarditis or when there has been pre-existing suppurative disease of the bones.

The symptoms which attend embolism from detachment of the fibrinous efflorescences upon the valves are due to the arrest of such a plug in an artery whose calibre is too small to admit of its passage. Beyond the obstruction the circulation is arrested; hence results either an infarction or necrosis of the part whose blood-supply is thus shut off. The organ most liable to be the seat of such emboli is the spleen, and after this the kidney and the brain. Hence the occurrence of hemiplegia with aphasia or marked cerebral symptoms in the course of acute endocarditis is indicative of cerebral embolism.

There are no positive subjective symptoms of interstitial endocarditis. There may be palpitation and a sense of uneasiness, sometimes amounting to pain at the præcordial region, with irregularity in the action of the heart, but all of these, when taken together, are not sufficient for a diagnosis. This can be made only from changes in the heart-sounds produced by changes in the valves and valvular orifices.

PHYSICAL SIGNS of exudative endocarditis.—Inspection.—Upon inspection it will sometimes be noticed that the area of the cardiac impulse exceeds the normal—that it is irregular and often tumultuous. As the disease advances, the apex-beat and the impulse grow more indistinct, but never to the same extent or so suddenly as in pericarditis. In children the vessels of the neck exhibit venous stasis far more frequently than in adults.

Palpation.—At the onset of an endocarditis the cardiac impulse is more forceful than normal, and the heart-action is frequently irregular. In some instances the heart thumps violently against the chest-walls. The force of the cardiac impulse varies from day to day. The impulse is stronger when pain is present over the præcordial space. If during the entire course of the disease there is no decrease in the force of the apex-beat, it may be inferred that there is no deficiency in the muscular power of the heart. When acute endocarditis supervenes upon long-standing valvular disease, there will be an alternate increase and diminution in the area and force of the impulse. When the walls of the heart become weakened by subsequent myocarditis, or when the endocardial inflammation is itself very extensive, the force of the apex-beat is diminished. An endocardial thrill is frequently present in acute exudative endocarditis.

Percussion.—The area of cardiac dulness in endocarditis is normal, unless changes at the valvular orifice retard the outflow of blood from the lungs, and then the right-heart cavities become engorged and the area of dulness will extend beyond the normal limits. But it is to be remembered that the increase is always slight, except in those few cases where the heart-cavities are both suddenly and extensively distended with blood or masses of fibrin. Extensive myo- or endocardial inflammation may so weaken the heart-walls that they will dilate, and then percussion will reveal an enlargement in the area of cardiac dulness.

Auscultation.—On auscultation a murmur or murmurs can be heard over the various cardiac orifices. The fact that valvular disease may have previously existed makes it important, at the first visit to a patient who is suffering from acute articular rheumatism, chorea, Bright's disease, etc., to carefully examine the heart. When cardiac hypertrophy exists and valvular disease has pre-existed, it is difficult, if not impossible, to recognize acute exudative endocarditis or to determine the time of its advent if it exist. The most important and constant sign of endocarditis is a systolic murmur, its greatest intensity being over the apex; but this murmur, which is soft and blowing in character, the so-called bellows murmur, may be either ventricular or valvular. In all cases it is due to roughening or thickening of the endocardium. It often changes its point of maximum intensity during the acute period of the disease. It is developed at the onset of the disease, and when one is on the lookout for endocarditis, this will be the first evidence of its occurrence. And yet in some instances no murmur may be present during the entire course of an endocarditis.

A mitral murmur alone occurs in about 50 per cent. of cases of rheumatic endocarditis. It is usually developed early, and before it becomes distinct it is preceded by prolongation of the first sound. This is a transition sound between a normal heart-sound and a murmur. It is a feeble, wavering sound, extending over the slight interval which normally exists between the first and second sounds.

Other changes that are not murmurs, but which frequently precede them, are loud, ringing normal sounds, muffled first sound, feeble first and intensified second sound, doubling of the first sound, roughness of the first sound, and a humming over the right heart.

Complete absence of the heart-sounds is a rare but possible antecedent of an endocardial murmur. A mitral murmur in acute endocarditis is usually audible over a limited area. It is the exception to hear it both in front and at the back. Very frequently it is heard most distinctly over the stomach.

When the blood becomes dammed back into the lungs, there is an extra strain upon the pulmonary semi-lunar valves, and then the second sound will be accentuated over these valves on account of the sharp shock which they sustain during diastole. With this accentuation of the second sound over the pulmonary orifice, the first pulmonic sound may be feeble or absent. A subdued or absent first sound shows tension of the artery.

Reduplication of the second sound in a mitral endocarditis is probably due to the difference in time occupied by the ventricles in emptying themselves. A tricuspid murmur occurs in 50 per cent. of the cases of acute mitral endocarditis—a pulmonic in about one-third of the cases. They are superficial and scratchy in character, and indicate a relaxed condition of the vessels and a thin condition of the blood. These murmurs are never permanent. Mitral endocarditis is accompanied by aortic murmurs in about 16 per cent. of cases. Acute mitral endocarditis occurring with chorea is as apt to become interstitial as when it is of rheumatic origin.

Aortic murmurs are usually soft and blowing, but they may be musical, whistling, or twangy. In aortic endocarditis the second sound is usually lost over the carotids. Incompetency of the aortic valves is met with only in the interstitial form of endocarditis.

In about 12 per cent. of the cases of exudative endocarditis arising from rheumatism a regurgitant murmur will be heard at the tricuspid orifice, but such murmurs are not the result of endocarditis of the right heart.

Tricuspid murmurs are present in 50 per cent. of all cases of recent mitral murmurs, in about 40 per cent. of recent aortic murmurs, and in about one-fourth of mitro-aortic murmurs. Such tricuspid murmurs are due to an increase in the slight normal insufficiency existing at the tricuspid orifice. They are of short duration, and are heard over the body of the heart over the right ventricle. Sometimes they are vibrating in character.

In children aortic endocarditis is rare; at this period obstruction at and regurgitation through the mitral orifice commonly occur together.

The physical signs of interstitial endocarditis are such as are due to those changes in the valves which will be considered under the head of Cardiac Murmurs, and their Relations to Valvular Diseases.

DIFFERENTIAL DIAGNOSIS.—Acute exudative endocarditis may be mistaken for pericarditis, and its murmur may be mistaken for the murmur produced by aortitis and for those that develop during the course of fevers.

The friction sounds of pericarditis are superficial in character, and are limited to the præcordial space, while the murmurs of endocarditis are distant, and each murmur will have its area of diffusion beyond the præcordial space. A pericardial sound is distinctly a friction, creaking, or rubbing sound; it has a to-and-fro character, while the murmur of endocarditis is soft and blowing.

Endocardial murmurs accompany the heart-sounds, while pericardial friction sounds are not always rhythmical with the heart-sounds.

The intensity of a pericardial friction is increased when the patient bends forward at the end of a full inspiration or when the stethoscope is pressed firmly over the præcordial region; and in the last-named case it becomes distinctly grazing and rubbing in character. In endocarditis these methods produce no difference in either the intensity or the character of the murmur. There is an endocardial thrill in endocarditis not present in pericarditis.

As soon as effusion occurs in pericarditis the absence of pain, the alteration in the character of the pulse, the great increase in dulness, and the disappearance of the adventitious sounds will decide the diagnosis.

Aortitis has most of the symptoms of endocarditis, but in addition the pulse is more rapid, the respirations are more hurried, and pain which shoots down the spine and is increased by motion is present in the præcordial region. Not infrequently aortitis is accompanied by cutaneous hyperæsthesia.

Acute inflammation of the aorta is exceedingly rare, and in the few cases observed has been complicated by very grave diseases. Indeed, Powell, Lebert, and Rindfleisch doubt its existence.

In the Medico-Chirurgical Transactions (vol. xlvii. p. 129) Moore gives a case where rigors, fever, intense and painful throbbing of the aorta, and embolic infarction of distant organs occurred, with symptoms so resembling those of endocarditis that few would venture to favor a diagnosis of aortitis during life.

The functional cardiac murmurs which occur in fevers are usually heard only at the base of the heart, while those of endocarditis are most frequent and distinct at the apex. There are no symptoms of obstruction present with febrile murmurs, while they are frequently present in endocarditis.

It is often difficult to determine whether an endocardial murmur is of old or recent origin: if during an attack of acute rheumatism an endocardial murmur is developed under daily examination, it is a certain index of acute exudative endocarditis. If a murmur exists at the first examination which is systolic, soft, and blowing in character, and not accompanied by the evidences of cardiac hypertrophy, there is good reason to believe that it is produced by an acute endocardial inflammation.

If, on the other hand, the murmur is rough in quality, diastolic, and cardiac hypertrophy exists, it cannot be regarded as a sign of acute endocarditis.

The rules for distinguishing murmurs due to interstitial endocarditis from functional murmurs will be given under the head of Cardiac Murmurs.

PROGNOSIS.—Exudative endocarditis is rarely a direct cause of death, but it seldom results in complete recovery. Acute mitral endocarditis terminates in permanent valvular disease in over 25 per cent. of the cases. The elements that will render the prognosis immediately unfavorable in any case are the symptoms of embolism or of metastasis. Sudden splenic enlargement, with tenderness over its site, albuminuria or hemiplegia, when accompanied by the physical signs of acute insufficiency or perforation of a valve with cyanosis, dyspnoea, and disturbance of the heart-rhythm, will render the prognosis exceedingly unfavorable. All these symptoms are diagnostic of acute ulcerative endocarditis, and therefore when the signs of endocarditis appear during the course of pyæmia, diphtheria, or other septic condition, the liability to these conditions must be considered.

When even exudative endocarditis is accompanied or followed by typhoid symptoms its prognosis is unfavorable. In children bronchial complications, catarrhal pneumonia, and intercurrent diarrhoea may lead to a fatal issue. Death may result from acute insufficiency of the heart or from complications.

The prognosis in interstitial endocarditis will depend upon the seat and extent of the valvular lesions which it produces. It will be more fully considered under the head of Valvular Diseases.

In cardiac aneurism death may result from rupture of the aneurismal sac, from apoplexy, or from secondary diseases in other organs.

TREATMENT.—Acute exudative endocarditis is rarely, if ever, idiopathic. It is so constantly associated with certain infectious diseases, and especially with acute articular rheumatism, that its treatment must be determined by the condition under which it occurs.

In every case the patient must have absolute rest in bed in a room whose temperature should never be below 70° or 75° F. The præcordial region should be covered with flannel, and care exercised not to expose the surface when physical examination of the heart is made. Some authorities claim that an ice-bag applied to the præcordial space during the active period of an acute endocarditis will arrest and limit the inflammatory process. My own experience does not sustain the results claimed for this plan of treatment.

In rheumatic endocarditis antirheumatic remedies are indicated, the joints must be kept absolutely at rest, and such local treatment should be resorted to as will relieve pain and give the greatest comfort to the patient.

If the blood is kept alkaline, as indicated by the urine, the liability to endocarditis is diminished.

To ensure rest small doses of opium are often required; but opium cannot be administered as freely in endocarditis as in pericarditis.

During the whole course of acute endocarditis the strength of the patient must be maintained by the judicious use of concentrated nutriment, with some preparation of iron.

When endocarditis occurs with septic diseases and is attended by typhoid symptoms, or when it assumes the ulcerative form, alcoholic stimulants, quinine, and iron must be freely administered.

In endocarditis complicating Bright's disease the rapid elimination of the urea must be established. The severe pain over the præcordial space may be relieved in many subjects by the application of a few leeches to the region.

Experience proved that the employment of mercury (internally) and blue ointment (externally) to lessen the plasticity of the blood, and the internal use of iodide of potassium (for the absorption of fibrinous exudation), were harmful, before it was demonstrated that the theory on which their use was based had no foundation.

Cardiac Murmurs, and their Relations to Valvular Diseases of the Heart.

DEFINITION.—A cardiac murmur is an adventitious or abnormal sound produced within the heart or blood-vessels, either by obstruction to the blood-current, an abnormal direction of the blood-current, or by a change in the blood-constituents.

HISTORY.—The systematic study of cardiac murmurs and valvular diseases dates from the discovery of auscultation by Laennec. Previous to his discovery there are a few recorded cases where observers during the seventeenth and eighteenth centuries described forms of valvular diseases. One of the first to describe a valvular lesion of the heart was Vieussens in 1716. At the close of the seventeenth century Willis and Riverius published cases of valvular disease. In all these instances it was the aortic valves that were diseased, and the discovery of their condition was undoubtedly due to the peculiarity of the radial pulse which is so marked and striking in aortic disease.

In Friedreich's article in Virchow's Handbuch, "Krankheiten des Herzens," Meckel's essay of 1756 is given as the first paper on endocardial disease.

John Hunter² in 1794 gives a lengthened account of a most interesting case of aortic valvular disease. Senac³ gives an account of disease of the auriculo-ventricular valves; and Allan Burns, whose work was published in 1809, describes aortic regurgitation and obstruction, and supposes that "a reflux current can produce a hissing noise, something like what is described as audible palpitation in some diseases of the heart."⁴

² Treatise on the Blood, etc.

³ Treatise on the Heart, 1783.

⁴ Obs. on some of the most Frequent and Important Dis. of the Heart, Allan Burns, Edinburgh, 1809.

The subject of vegetations upon the valves was very fully considered by Corvisart in 1806. Corvisart was the first to mention the importance of what is now called the purring thrill. He stated that "it probably came from a difficulty experienced by the blood in going through an orifice disproportionate to the amount of fluid." Laennec regarded murmurs or bruits as the result of spasmodic contraction of the heart or arteries. Corrigan in 1829 defined murmurs as "the result of the development of currents and the intrinsic collision of the moving liquid."

In 1842, Gendrin gave cardiac murmurs as bruits de frottement endocardiaques, and established the friction theory. He also called attention to the fact that alteration in the constituents of the blood will produce murmurs which are heard in arteries of medium calibre.

Bouillaud describes a murmur as an exaggeration of the normal bruit caused by blood-friction against the segments of the heart, and he says that according to the size or condition of the orifice the murmur will be rasping, sawing, or blowing.

Chauveau states that bruit de souffle is produced by the vibration of a nei e fluide, always formed when blood rushes through a part of the circulatory system actually or relatively dilated.

This nei e fluide has its best development in anæmia, when it is termed the bruit du diable, for the jugular veins do not collapse and the volume of blood in anæmia is diminished. Chauveau's theory is applicable to anæmic murmurs, but not to all cardiac murmurs.

Hope states that "valve murmurs are produced by collision of the blood-particles against one another, or that either the liquid alone or the liquids and solids conjointly may develop murmurs."

There are many who have advocated the tension theory—viz. that an increase in tension and force can so exaggerate a normal sound as to produce a murmur. This theory has no clinical foundation. Often, however, valve-lesions may exist, and the blood-current be so weak, the propulsive force so feeble, that no murmurs are audible.

Some observers are of the opinion that spasm of the papillary muscles and chordæ tendineæ and weakening of these structures through fatty degeneration can cause temporary murmurs.

The conditions that determine the character of a cardiac murmur, its pitch, quality, and intensity, are subject to the same physical laws as govern the formation and quality of sound elsewhere. They are the rapidity and force of the moving body, the obstructions which it meets, and the physical properties of the media of conveyance. The same vibration that produces a murmur may produce an endocardial thrill, called sometimes purring thrill.

Far more important, however, than loudness, pitch, or quality of a murmur are its rhythm, its point of maximum intensity, and the area of its diffusion, all of which can best be considered in connection with the physical signs of each valvular lesion.

During a cardiac diastole the heart-cavities are all filling; just before the commencement of the cardiac systole the blood is forced from the lungs and the cavæ through the auricles into the ventricles, while the mitral and tricuspid valves are pressed against the walls of the ventricles, and no obstruction is offered to the blood-current. If, as the result of disease, any obstruction exists at either one of the auriculo-ventricular orifices, the blood as it passes through the opening will impinge on such obstruction and cause a presystolic murmur.

During a cardiac systole the filled ventricles contract; blood is thrown through the semi-lunar openings, the flaps of whose valves are pressed against the walls of the vessels, so that no obstruction is offered to the outgoing current. At the same instant the auriculo-ventricular valves close their orifices, so that blood may not be forced back into the auricles.

If, as a result of disease, the semi-lunar valves should obstruct the outgoing current, or the mitral or tricuspid valves should not wholly close the auriculo-ventricular orifices, then in the one case the direct blood-current, as it passes over the obstruction at the semi-lunar orifices, would produce a systolic murmur, and in the other the backward current through the abnormal opening at the auriculo-ventricular orifice would also produce a systolic murmur.

Again, if the lungs and the aortic system (when filled at the systole) have, back of them, a semi-lunar valve that does not completely close that end of the circuit, the blood will regurgitate into the ventricles during the period of cardiac rest, so that semi-lunar incompetence will cause a diastolic murmur.

ENDOCARDIAL MURMURS.

Rhythm. Situation. Orifice. Nature.

Systolic 1 Basic, Aortic, Obstructive.

" 2 " Pulmonary, "

" 3 Apical, Mitral, Regurgitant.

" 4 " Tricuspid, "

Diastolic 1 Basic, Aortic, "

Presystolic 1 Apical, Mitral, Obstructive.⁵

⁵ Pulmonary regurgitant murmur (diastolic) and tricuspid obstructive murmur (presystolic) are so rarely met with that, clinically, they may be disregarded.

The following is the order of relative frequency of cardiac murmurs: 1. Mitral regurgitation; 2. Aortic obstruction; 3. Aortic regurgitation; 4. Mitral obstruction; 5. Tricuspid regurgitation; 6. Tricuspid obstruction; 7. Pulmonary obstruction; 8. Pulmonary regurgitation. The most frequent combinations of murmurs are—1. Aortic obstruction and regurgitation; 2. Mitral obstruction and regurgitation; 3. Mitral obstruction and tricuspid regurgitation; 4. Aortic obstruction and mitral regurgitation; 5. Double valvular disease at aortic and mitral orifices (four murmurs).

It is often difficult, after having satisfied ourselves of its existence, to determine the rhythm of an endocardial murmur. To resolve this difficulty it is necessary to determine which is the first and which the second sound of the heart.

The first sound of the heart is synchronous with the carotid pulse, the radial pulse, and the apex-beat. It may be wholly replaced by a systolic murmur, but the second sound is always heard following the apex-beat, for the pulmonic and the aortic valves are never diseased at the same time.

Having determined the existence of a murmur, its rhythm, pitch, intensity, and quality, we next determine its point of maximum intensity. These points of maximum intensity for murmurs at the four valvular orifices of the heart may be briefly summarized as follows: Murmurs arising at the mitral valve are loudest at the apex of the heart or immediately above it; tricuspid murmurs are loudest over the lower part of the sternum; pulmonary murmurs, in the second left intercostal space close to the sternum; and aortic murmurs, in the second right intercostal space at the edge of the sternum and over the whole length of the body of that bone.