As a rule, if, prior to the endocarditis, the patient were free from valvular lesions, the systolic murmur is not propagated far without the left border of the heart. It is probable that the anatomical changes which generally occur during the progress of the endocarditis rarely involve immediate valvular insufficiency, either at the mitral or aortic orifice. Hence, the mitral murmur may not proceed from an actual regurgitant current from the ventricle to the auricle. It is not, then, strictly correct to call it a mitral regurgitant murmur. It is an intra-ventricular murmur, or it may be called a mitral systolic murmur, this term not implying the occurrence of regurgitation.

The physical evidence of endocarditis is not afforded by the existence of the murmur just named. A mitral murmur exists sufficiently often without denoting existing inflammation. It may proceed from valvular lesions which are to be presently considered. To be evidence of endocarditis, the murmur must be developed under observation; in other words, the practitioner must be satisfied that the murmur which he discovers did not exist on a previous examination. As it is generally in cases of rheumatism that endocarditis occurs, let it be assumed that, on the first examination of a patient affected with rheumatism, a mitral murmur is found. The murmur is not proof of endocarditis, for it is not known that the murmur did not exist prior to the rheumatic attack. The existence of endocarditis is only probable, and the probability of the disease is greater if this be the first attack of rheumatism. But if, on a first examination, no murmur be found, and, subsequently, a mitral murmur become developed, it is evidence of endocarditis. The evidence is strengthened if, at the same time, pain or præcordial distress and excited action of the heart point to the occurrence of a cardiac complication. Reference has been made, thus far, to a mitral murmur only as evidence of endocarditis. The exudation of lymph, and the deposit of fibrin at the aortic orifice, may occur in this disease, giving rise to an aortic murmur. I have been led, however, to think that an aortic and a pulmonic murmur are not infrequently developed in cases of rheumatism without endocarditis, more. especially in females, being due to the condition of the blood; in other words, being inorganic murmurs. Hence, I would not base a positive diagnosis of endocarditis on the development of an aortic murmur alone, certainly unless the symptoms, at the same time, denoted a cardiac complication, and pericarditis did not exist. Irrespective of cases of rheumatism, it is well known that an aortic murmur with the first sound, i. e., systolic, is sufficiently cominon as an inorganic murmur, and, alone, is never proof of endocarditis. It may be doubted if insufficiency of the aortic valve be ever an immediate result of endocarditis; at all events, I have never met with an aortic regurgitant murmur developed in the progress of endocarditis.

In view of the fact that, in the great majority of the cases of endocarditis, it is a complication of articular rheumatism, not only do we seek for the evidence of its development in the course of the latter disease, but the existence of articular rheumatism renders the diagnosis more complete than if this disease did not exist.

An endocardial murmur produced by endocarditis is generally permanent, but I have repeatedly known it to disappear after recovery from rheumatism. In cases of endo-pericarditis, the endocardial exists with an exocardial or friction murmur. In general, the two murmurs may be readily distinguished, and each referred to its source.

PROGNOSIS. The prognosis, in cases of endocarditis, is always favorable. The disease involves far less immediate danger than pericarditis. The danger in endocarditis is, for the most part, remote, and relates to the valvular lesions which are apt to follow. The continuance of inflammation in a

chronic form is, probably, rare. The persistence of an endocardial murmur is no evidence of the continuance of the inflammation; this may simply denote roughening of the endocardial membrane, from lymph or fibrin which remains, and which may never be removed. Possibly the washing away of lymph or fibrin in small particles may give rise to local disturbance in some of the organs into which they are carried with the arterial blood; but, with regard to this, we have no precise knowledge. Vegetations of greater or less size may be detached, and, forming emboli, occasion disturbance of the circulation and nutrition of the brain or other parts by plugging distributing arteries. Of this we have some knowledge, but further researches are desirable. These are accidents incidental to endocarditis in some cases. In general, as occurring in the pathological connection in which it usually occurs, viz., in the course of acute articular rheumatism, and disconnected from pericarditis, it involves no immediate danger, gives rise to no symptoms denoting gravity of disease, is frequently completely latent, and is an important complication chiefly because it may be the foundation for valvular lesions which, after the lapse of many months, or, it may be, many years, occasion serious consequences.

TREATMENT. The inflammation in endocarditis being confined, generally, to one side of the heart, and limited chiefly to the valvular portion of the endocardium, rarely occasions great constitutional disturbance. Following the general principles which are to govern the employment of bloodletting, it will not often be called for. Depletion by means of saline purgatives or laxatives will generally suffice, provided the symptoms do not contraindicate any lowering measures.

Præcordial pain and disturbed action of the heart indicate anodyne remedies and soothing applications to the chest. Blisters, with reference to these symptoms, are of doubtful propriety. Sinapisms and stimulating liniments will probably secure all the advantage to be derived from counter-irritation. Measures addressed to the supposed causative condition of the blood are rationally indicated. Occurring generally in connection with rheumatism, if the local affections, this of course included, depend on the presence of a morbid material in the blood, it is plainly an object either to neutralize or eliminate this material. The means to be employed for this object will be hereafter considered in connection with the subject of rheumatism.

The remote evil consequences of endocarditis proceed from the exudation of lymph beneath, or the deposit of fibrin upon, the valvular portion of the endocardium. It is, therefore, undoubtedly desirable to limit and remove these immediate effects of the inflammation. The fibrin of the blood is increased in acute rheumatism more than in any other disease, and, for this reason, perhaps, fibrinous deposits are apt to take place. With this view, measures to reduce the excess of fibrin, and to favor its liquid state, are rationally indicated. Alkaline remedies and ammonia, there is reason to believe, contribute to the latter of these two ends. Mercury has been supposed to diminish the amount of fibrin in the blood. That it possesses this power, however, has been inferred rather than demonstrated, and the correctness of the inference admits of doubt. It may be doubted whether the fibrin deposited upon the membrane is ever absorbed; it either remains or is washed away either gradually or in mass, by the current of blood. The deposit beneath the membrane, however, it is probable, may be absorbed, and it is an object, if possible, to promote its removal in that way. Mercury has been supposed to be useful by a sorbefacient operation here, as in other diseases in which the exudation of lymph takes place. Its power as a sorbefacient remedy has doubtless been much overrated, but we are not warranted in saying that it is devoid of this

power. If employed, it should be given circumspectly, so as to avoid, as much as possible, its depressing effects. Iodine given internally or applied externally may be employed for the same purpose.

The practitioner should bear in mind that the persistence of an endocardial murmur is not sufficient ground for the continuance of sorbefacient or other remedies. The persistence of the murmur is not evidence that the inflammation continues. The treatment of endocarditis should cease when the local and general symptoms of the disease are no longer present.

MYOCARDITIS.

Inflammation of the muscular structure of the heart is extremely rare. When it occurs it is generally in connection with endocarditis or pericarditis, singly or combined. It may occur, however, irrespective of either of these affections. Suppuration may take place as a result of myocarditis, the pas being either collected in abscesses or infiltrated. The pus may be discharged into the pericardial sac, giving rise to pericarditis, or into one of the cavities of the heart, causing purulent infection of the blood. Rupture of the heart may be a consequence of inflammation and suppuration. An abscess in the inter-ventricular septum may lead to perforation. Induration is another result of inflammation in this structure. Aneurismal dilatation is still another. The inflammation is oftener seated in the walls of the left, than of the right, ventricle.

It is a serious affection, as impairing, in proportion to its extent, the muscalar power of the heart, and as involving a liability to the accidents just. stated. Associated with either endocarditis or pericarditis, or both, it adds, of course to the gravity and danger. Its coexistence with these affections, and its existence without them, cannot be determined during life.

CHAPTER III.

VALVULAR LESIONS WITH ENLARGEMENT OF THE HEART.

Anatomical Characters-Clinical History-Pathological Character-Causation-DiagnosisPrognosis-Treatment.

HAVING considered, in the two preceding chapters, the inflammatory affections of the heart, the structural lesions of this organ next claim attention. The structural lesions relate, in the first place, to the valves and orifices of the heart. These are known commonly as valvular lesions. Other lesions relate to the walls and cavities of the heart. Enlargement of the heart, in the great majority of cases, proceeds from valvular lesions, and the latter, sooner or later, in the great majority of cases, give rise to cardiac enlargement. In considering, therefore, valvular lesions, I shall also consider enlargement as dependent thereon, and, afterward, notice enlargement occurring without valvular lesions.

ANATOMICAL CHARACTERS.-Valvular lesions are situated, in the great majority of cases, in the left side of the heart, that is, at the mitral and aortic orifice. Tricuspid and pulmonic lesions are comparatively rare. The

morbid appearances in different cases are extremely diversified. The valvular curtains and segments are frequently thickened and contracted; or, they may be simply encumbered with vegetations of greater or less size, without being incapacitated for the performance of their function. They are sometimes rendered more or less rigid by calcareous deposit. The mitral curtains are not infrequently united at their sides so as to form a funnel-shaped canal leading from the auricle to the ventricle, the opening consisting of a small slit, called the button-hole contraction of the mitral orifice. The aortic segments, expanded and rigid, in some cases, diminish the size of this orifice to that of a crow's quill, or even much smaller. The valves may become atrophied, and are liable to rupture or perforations. Rupture of one of the valves is an occasional accident without prior disease, when an excessive strain is induced by the violent action of the heart in severe muscular exertions. Under these circumstances, the tendinous cords which unite the extremities of the mitral curtains to the papillary muscles, are especially apt to give way. For a full description of the varied changes which are observed in different cases of valvular lesions, the reader is referred to works on morbid anatomy.

In a clinical point of view, all the diverse alterations of structure embraced under the name of valvular lesions, may be arranged, according to their effects upon the circulation, into the following groups: First, obstructive lesions, that is, lesions which impede the flow of blood by producing contraction of the orifices; second, regurgitant lesions, that is, lesions which interfere with the function of the valves, rendering them incompetent or insufficient, and consequently allowing backward or regurgitant currents; third, lesions which involve both obstruction and regurgitation; and, fourth, lesions which involve neither obstruction nor regurgitation, but give rise to morbid sounds by roughening the surface over which the blood flows. The lesions belonging to the last group are of little or no immediate importance, and, although giving rise to abnormal sounds known as endocardial or bellows murmurs, may be quite innocuous.

The lesions which involve either obstruction or regurgitation, or both, lead to enlargement of the heart. They produce this result by giving rise to over-repletion of certain of the cavities of the organ. Limiting attention to the lesions situated at the mitral and aortic orifice, the primary effect differs according to the situation. Mitral obstructive and regurgitant lesions, as a rule, produce, first, dilatation of the left auricle, because these lesions give rise, as the first effect, to over-repletion of this cavity. Dilatation of the left auricle occasions pulmonary obstruction, because the overrepleted auricle does not offer space for the free admission of the blood returned to the heart from the lungs. As a consequence of pulmonary obstruction, the right ventricle is over-repleted, and hence occurs enlargement of this portion of the heart as the next effect. Over-repletion of the right auricle is the next effect, leading to dilatation of this cavity, and, finally, as a consequence of obstruction of the systemic venous system due to the right auricle being constantly filled, the left ventricle may become enlarged. This is the series of effects caused by mitral lesions which involve either obstruction or regurgitation, or both.

Lesions of the aortic orifice, either obstructive or regurgitant, or both, produce a similar series of effects with a different point of departure. The left ventricle is first over-repleted and becomes enlarged. Dilatation of the left auricle follows, and successively the right ventricle and right auricle are enlarged, if life be sufficiently prolonged. Cases are not infrequent in which obstructive or regurgitant lesions are situated at both the mitral and aortic orifice. The effects of the aortic and mitral lesions are combined in these cases.

Enlargement of the heart, with or without valvular lesions, is of two kinds, viz., first, enlargement due to abnormal growth or hypertrophy, and, second, enlargement due to dilatation. As a rule, in examinations after death, the enlargement is not found to be exclusively by either hypertrophy or dilatation, but the two kinds of enlargement are combined. A marked difference exists in different cases, as regards the symptoms, signs, and the danger, according to the predominance of either hypertrophy or dilatation. As a rule, hypertrophy of the ventricles takes place before dilatation. The overrepletion of the ventricular cavities induces augmented power of muscular action, and this causes byper-nutrition or abnormal growth. The ventricles grow in consequence of long-continued increased power of muscular action, precisely as the voluntary muscles become enlarged as a consequence of exercise.

The hypertrophic growth of the ventricles has its limit, as the enlargement of voluntary muscles is limited. The voluntary muscles cannot increase indefinitely, but after a certain amount of increased growth, it ceases, notwithstanding the exercise of the muscle is continued. So with the heartthe hypertrophy at length reaches a point beyond which no further growth takes place. The extent to which the heart can increase by hypertrophy varies in different persons, as the point at which the increase of the voluntary muscles varies. The enlargement by hypertrophy is represented by the increased weight of the heart. In cases in which a very great amount of hypertrophy takes place, the weight of the heart is found to be four or five times greater than in health.

Dilatation, sooner or later, follows hypertrophy. When nutrition can no longer be excited to canse progressive growth, the continued over-repletion of the cavities causes the walls to yield and dilatation takes place. The dilatation goes on, and at length it predominates over the hypertrophy; that is, in relative amount the former exceeds the latter. The enlargement by hypertrophy is due to a vital process, viz., hyper-nutrition; but the enlargement by dilatation is produced mechanically. Hypertrophy involves augmented power of the muscular walls; dilatation involves diminished power, or weakness, in proportion as the cavities are enlarged. In proportion as dilatation predominates over hypertrophy, the volume of the heart rather than the weight is increased.

Enlargement may be much more marked in one portion of the heart than in another portion, or it may be limited to a part of the organ. The right ventricle, for example, may be chiefly or exclusively the seat of enlargement in connection with mitral valvular lesions, and this may hold true of the left ventricle in connection with aortic valvular lesions. The left ventricle may be enlarged by predominant dilatation while the right ventricle is enlarged by predominant hypertrophy, and vice versa.

CLINICAL HISTORY.-Valvular lesions, so long as they involve neither obstruction nor regurgitation, give rise to no symptoms of disease, and their existence is only ascertained by means of physical signs. Lesions involving obstruction or regurgitation, or both, as a rule, do not occasion much inconvenience until they have led to enlargement of the heart. Moreover, as a rule, lesions occasion suffering and are attended with danger in proportion to the enlargement which they have produced, and chiefly the enlargement due to dilatation.

The first symptoms proceeding from mitral obstructive or regurgitant lesions pertain to the respiratory system. Deficiency of breath on exercise is, for some time, the chief inconvenience. This progressively increases, in proportion as the obstruction to the pulmonary circulation increases. The