of the causes, by measures addressed to the morbid conditions of the blood belonging to these affections. This part of the treatment, however, will be more appropriately considered, in connection with rheumatism and renal disease, hereafter. The importance of measures to prevent the development of pericarditis, in the course of these diseases, will also be then considered. If the disease end in recovery without becoming chronic, adhesion of the pericardial surfaces, to a greater or less extent, may be expected to take place. This result was formerly supposed, by Hope and others, to lead to progressive enlargement of the heart, and therefore pericarditis was regarded as a highly serious disease with reference to its remote effects. This is an error which arose from imputing to pericardial adhesion the consequences of the valvular lesions, which often coexist. It may be doubted if adhesion alone tends to produce enlargement, and there is reason to believe that, if not associated with valvular lesions, it may give rise to little or no inconvenience. The pericardial surfaces are not infrequently found, in autopsical examinations, universally adherent, as a result of ancient pericarditis, without any other evidence of cardiac disease, and when no symptoms referable to the heart had existed during life.

CHRONIC PERICARDITIS.

Chronic pericarditis may be subacute from the beginning, or it may follow the acute form of the disease. If acute pericarditis do not end in convalescence after the lapse of from two to three weeks, it becomes a chronic affection. As regards anatomical characters, cases differ. In some cases of chronic pericarditis, there is no liquid effusion, but the pericardial surfaces are agglutinated by several layers of lymph, which collectively may be half an inch or more in thickness. Under these circumstances, the lymph is not absorbed, a low grade of inflammation continues, and the disease ends fatally after a variable duration.

In other cases, liquid effusion remains and progressively accumulates, the pericardial sac becomes more or less dilated, and it is sometimes so much enlarged as to depress the diaphragm and occupy the greater part of the thoracic space. The amount of liquid which has been known to accumulate in the pericardium is enormous, amounting to eight or ten pints.

In chronic pericarditis without liquid effusion, pain is rarely prominent. The symptoms are those dependent on feebleness of the circulation, due to the impaired muscular power of the heart, and on constitutional irritation. In the cases in which large effusion exists, the heart is weakened by compression, and the patient suffers from dyspnoea caused by interference with the respiratory function. The dyspnoea may amount to orthopnoea if the accumulation of liquid be very large. Pain under these circumstances is rarely a prominent symptom.

The diagnosis, if liquid effusion be not present, must often be inferential, being based mainly on the knowledge of the existence of antecedent acute pericarditis. Creaking friction murmur exists in some cases, notwithstanding the agglutination of the pericardial surfaces. If friction-murmur be not present, and acute pericarditis be not known to have existed, a positive diagnosis is extremely difficult, if not impossible. The heart is found to be more or less enlarged, but there are no means of determining that the enlargement proceeds from the deposit of lymph. If liquid effusion be present, the physical signs render the diagnosis easy and positive. Flatness on percussion exists on the anterior surface of the chest, extending on either side of the sternum toward the axillary region, in proportion as the pericardial sac is dilated. Obliteration of the intercostal depressions and even bulging may

be observed. Fluctuation in the intercostal spaces is sometimes felt. Laterally, beyond the limit of the flatness on each side, resonance on percussion and the respiratory murmur show the presence of lung. The heart's impulse is suppressed, but a shock communicated by the action of the heart may be felt. A friction murmur is sometimes heard, even when the quantity of effused liquid is very large. The sounds of the heart are feeble, the first sound being more weakened than the second, and short and valvular like the second sound. These signs render the diagnosis sufficiently clear.

The prognosis in cases of chronic pericarditis is always extremely unfavorable. The disease ends fatally after a duration varying much in differ

ent cases.

The indications for treatment are to improve the tone of the system and impart vigor to the heart by tonic remedies, with nutritious diet and other hygienic measures. The propriety of much counter-irritation is doubtful. Everything which tends, directly or indirectly, to weaken the heart or the vital powers is to be avoided. In this point of view mercurialization is objectionable. If there be much liquid effusion, diuretic remedies may be tried, and small blisters. Hydragogue cathartics, in these cases, if the patient be feeble, are to be employed with great circumspection. In a case not long since under my observation, elaterium given in small doses and producing but a moderate effect, appeared to hasten the fatal termination. Iodine may be employed as a sorbefacient, externally and internally. Puncture of the pericardial sac is admissible, if the effusion be large and other measures fail to diminish it. Clinical data for determining the value of the operation of paracentesis, are wanting.

PNEUMO-PERICARDITIS.

This name denotes the presence of air or gas within the pericardial sac in cases of pericarditis. Air or gas may find its way into this situation through a wound of the thoracic walls, or of the oesophagus, and through a fistulous communication between the lungs or the stomach and the pericardial cavity. Air may get access into this cavity through a wound of the chest, and pericarditis not be developed. The condition, then, is expressed by the term pneumo-pericardium. It is possible that gas may be generated by decomposition of the products of inflammation within this cavity, but examples must be exceedingly rare.

The presence of air and liquid gives rise to splashing and sometimes metallic sounds, with the movements of the heart, which are heard on auscultation; and percussion over the præcordia elicits a tympanitic resonance. These cases belong among the curiosities of clinical experience. The treatment of pneumo-pericarditis involves the same principles as the treatment of pericarditis without the presence of air or gas.

CHAPTER II.

Endocarditis-Anatomical Characters-Clinical History-Pathological Character-Causation

-Diagnosis-Prognosis-Treatment-Myocarditis.

INFLAMMATION of the membrane lining the cavities of the heart, or the endocardium, is called endocarditis. Our knowledge of the existence of this disease is one of the developments of modern pathological research. It

is a highly important disease considered more especially in its relation to structural lesions of the valves and orifices of the heart.

The inflammation is doubtless in some cases acute, and in other cases subacute or chronic, but as the symptoms and signs do not enable us to determine clinically the grade of inflammatory action, a division of the disease into the acute and chronic form is unnecessary.

ANATOMICAL CHARACTERS.-The disease very rarely proves fatal during its progress, and, therefore, the opportunity of observing the morbid appearances is seldom offered. On this account the observations of Dr. Richardson in cases of endocarditis produced, artificially, in inferior animals, by the introduction into the blood of lactic acid injected into the peritoneal cavity, are valuable. These observations show arborescent redness from congestion of the vessels beneath the membrane, and considerable swelling of the valves, especially the auricular valves, from the exudation, beneath the membrane, of lymph with serum. More or less exudation also takes place on the free surface of the membrane covering the valves and tendinous cords. Much of this exudation must be washed away with the currents of blood; that which remains sometimes assumes the form of patches of false membrane, but it is oftener disposed in the form of small masses, or beads, situated especially at the base or near the extremities of the valvular curtains and segments. These small masses are often observed, in greater or less number, varying in size from that of a pin's head to a millet seed, oftenest in the auricular aspect of the mitral curtains, and the ventricular aspect of the aortic segments. Roughening the surface of the membrane, they become the nuclei of the so-called warty excrescences or vegetations, their size being increased by the deposit of fibrin from the blood within the cavities of the heart. In this way they may attain to a considerable size. It is not uncommon to find, attached to the valves, vegetations as large as a pea, a bean, a filbert, and even still larger. They may be loosely attached to the endocardium, so that but little force is required to detach them, or they may adhere with considerable firmness. They are liable to be separated during life, giving rise to emboli, to which reference has already been made, and which will be again referred to in other connections.

Aside from these products of inflammation, the membrane in certain situ ations, especially over the valves, loses its smooth, polished appearance, becoming rough and velvety. It is more easily separated than in health, owing to brittleness of the areolar tissue beneath it. Ulcerations or erosions, perforation of the valves, laceration, and morbid adhesions of the valvular curtains or segments, are occasionally incident to the progress of endocarditis. These and other changes, however, are oftener remote than immediate effects of inflammation, and they will be considered, under the head of valvular lesions, in another chapter. In examinations of the heart after death, redness of the endocardial membrane and of the lining membrane of the vessels near the heart, is frequently found, which is due to staining with hematine dissolved out of the red corpuscles, and occurs after death. This appearance is no evidence of disease of the endocardium.

The anatomical characters of endocarditis are generally limited to the left side of the heart, that is, the left ventricle and auricle. The right cavities are very rarely the seat of endocardial inflammation, and never without inflammation of the left cavities. This statement, of course, applies to the disease as occurring after birth. There is reason to believe that endocarditis may occur during foetal life, and that the reverse of the statement

1 Vide Prize Essay on Coagulation of the Blood, by B. W. Richardson, M. D.

just made then takes place, viz., the right cavities, and not the left, are the seat of the inflammation. The inflammation is either limited to or is especially marked in the valvular portions of the endocardial membrane. This is probably owing partly to the presence of fibrous tissue beneath the endocardium in these situations, and in part to the strain which falls upon the valves in the performance of their functions.

CLINICAL HISTORY.-Authenticated cases of endocarditis disconnected from other diseases which serve to mask its symptoms to a greater or less extent are wanting. The clinical history of the disease, therefore, so far as it is at present known, will require but brief space. Our knowledge of the disease is confined chiefly to the cases in which it occurs in connection with acute articular rheumatism, and in a certain proportion of these cases it is associated with pericarditis. Pain referable to the præcordia is not a constant, and is rarely a prominent symptom. The pain, when present, is dull, not sharp or lancinating like the pain in pericarditis or pleuritis. The patient may complain of an obscure sense of distress in the præcordia, not amounting to pain. The action of the heart is morbidly excited. The organ beats with abnormal force, and its action is sometimes irregular. The action of the heart may be found to be out of proportion to the force of the pulse. The local symptoms, in short, as regards the action of the heart, are those of palpitation. In proportion to the acuteness of the inflammation, doubtless, febrile movement is induced, together with the symptoms of constitutional disturbance which accompany fever symptomatic of inflammation in other situations. The local and general symptoms, however, are often not prominent, and, so far as these are concerned, the disease is not infrequently latent. Hence the existence of the disease was unknown prior to the last quarter of a century.

PATHOLOGICAL CHARACTER.-The morbid changes which belong to endocarditis are, in many respects, the same as in serous inflammations. But the inflammatory products in this situation are not retained to be removed by absorption, but are, in a great measure, carried by the currents of blood directly into the circulation.

It may be doubted whether suppuration often takes place upon the endocardial surface. Newly-formed tissue, giving rise to morbid growths, is a result of inflammation in this situation. The warty vegetations which have been referred to are sometimes in part organized. Adhesion of parts in contact, viz., of the mitral curtains to each other, and the aortic segments to the walls of the aorta, is an occasional result of inflammation. It is stated by Bouillaud that the valves may become gangrenous as a result of inflammation; this must be exceedingly rare.

CAUSATION-Endocarditis, in the great majority of eases, is not a primary disease. There is reason, however, to believe that it occurs as an idiopathic affection not very infrequently, and is overlooked in consequence of its latency as regards cardiac symptoms. This may be inferred from the number of cases in which valvular lesions referable to inflammation are found in persons who have never experienced the disease in the course of which endocarditis is apt to be developed, viz., articular rheumatism. As met with in practice, it is generally incidental to the disease just named. It is supposed to occur in a large proportion of the cases of acute articular rheumatism; statistics appear to show that the proportion is not far from one-half. There is room, however, for the suspicion that the existence of the disease has been sometimes assumed on insufficient evidence. The ground for this suspicion will be stated in connection with the consideration of the diagnosis. It is not

to be doubted that the disease is frequently developed in the course of rheu matism. Endocarditis, like pericarditis, may perhaps in some cases precede the affection of the joints. It may occur at any time in the course of a rheumatic attack, but it is usually developed in the early or middle period.

When developed in the course of rheumatism, it is not from the transference of the affection of the joints to the endocardial membrane; that is, not by a metastasis, but, like pericarditis developed in the same connection, it is produced by the internal causative condition which gives rise to the articular affection. That this causative condition consists of a morbid material in the blood is probable, and the fact of the endocarditis being generally limited to the left side of the heart would seem to render it probable that the morbific agent is generated within the blood during its passage through the pulmonary organs. If the agent in the blood exerted its effect upon the endocardium by means of the vessels distributed to the heart, there is no apparent reason why the right side should not be affected as well as the left; but assuming that the agent in the blood acts by being brought into direct contact with the endocardium, it is intelligible that this agent existing in the blood received into the left cavities from the pulmonary cir cuit should act upon the membrane lining these cavities, and that it should be eliminated, neutralized, or decomposed before the blood has passed through the systemic circuit, and reached the right cavities of the heart. This is the view taken by Dr. Richardson, and it is sustained by the fact that in his experiments of injecting lactic acid into the peritoneal cavity, endocarditis was produced not in the left, but in the right cavities of the heart, the acid being destroyed in these experiments before the blood passes through the pulmonary circuit and reaches the left cavities. Moreover, these experiments render it probable that the morbific agent which gives rise to the affections of the heart and joints in rheumatism is lactic acid, produced in the blood during its passage through the lungs.

Endocarditis and pericarditis are not infrequently associated in cases of rheumatism, and this compound affection is denominated endo-pericarditis. Rheumatic pericarditis very rarely, if ever, exists without endocarditis. The reverse of this, however, does not hold good; endocarditis is not infrequently developed without pericarditis.

Endocarditis, either with or without pericarditis, is developed in a certain proportion of cases in the course of Bright's disease. It is stated, also, to occur occasionally in the eruptive and continued fevers, and in cases of pyæmia. It may possibly be produced by contusions of the chest. It may be associated with pleuritis or pneumonitis, when it occurs in rheumatism or in other pathological connections. The most rational view in these cases is to attribute the coexisting affections to a common causative condition.

DIAGNOSIS.-The symptoms in cases of endocarditis are insufficient for a positive diagnosis. The symptoms are even less diagnostic than those which belong to the clinical history of pericarditis, and the disease is oftener latent. The diagnosis of this disease, as well as of pericarditis, must rest on physical evidence. The exudation of lymph, or the deposit of fibrin upon the endocardium, gives rise to an endocardial murmur, and the diagnosis is to be based on the development of this murmur, taken in connection with the symptoms. The murmur is due to the roughening of the endocardial surface, and, as the anatomical changes are especially situated upon the curtains of the mitral valve, at least in cases of rheumatic endocarditis, the murmur is usually of mitral origin. The murmur is of a soft or bellows character. It accompanies the first sound of the heart; that is, it is systolic. It is heard loudest at or near the apex of the heart, and may be limited to this situation.