No cardiac debilitating drug should be administered when myocarditis has been surmised or diagnosed. The safest hypnotic, if one is needed, is morphin in small doses. If there are weakening perspirations, atropin should be given, especially as it is also a circulatory stimulant. Calcium in almost any form seems to be of value in the majority of heart conditions. It is a sedative to the nervous system, and is certainly indicated in acute myocarditis. Calcium lactate is perhaps the best salt to administer, in doses of 0.25 gm. (4 grains), three or four times in twenty-four hours. Calcium glycerophosphate may be used, in powder form or in capsule, in doses of 0.30 gm. (5 grains) three or four times in twenty-four hours; or lime-water may be given.

An exact prognosis of this inflammation is impossible. We do not know how far an acute myocarditis may progress and entire recovery take place; we do not know how slight a myocarditis may cause serious symptoms. Clinically we know that many patients after serious illness never again have perfect circulatory strength. Other patients almost die of heart failure and yet apparently absolutely recover their ability to do hard physical work.

CHRONIC MYOCARDITIS: FIBROUS

Chronic myocarditis may develop on an acute myocarditis, but is generally a slowly progressive chronic process from the beginning; it occurs mostly in persons past middle life, and as a rule is not primarily associated with rheumatism or valvular disease of the heart. Perhaps generally the term "chronic myocarditis" is incorrect, as a real inflammatory condition is not present and has not been present; it is really a degenerative process with the development of connective tissue, a fibrosis and more or less hardening of the arterioles, a cardiosclerosis. In many instances this fibrosis is associated with fat deposits or fatty degeneration. The disease is often caused by a narrowing or obstruction or calcareous degeneration of the coronary arteries, thus diminishing the blood supply to the heart muscle. This chronic myocardial degeneration is often a part of the general arteriosclerosis, and is an important factor in what is termed cardiovascular-renal disease. In simple chronic renal diseases the heart first normally hypertrophies to overcome the increased blood tension and increased resistance.

The principal causes of this degeneration are normal old age, or premature age caused by various conditions. In other words, anything which hastens arteriosclerosis will cause myocardial degeneration. The causes recognized as most frequently producing this condition are syphilis; gout; repeated attacks of rheumatism; excess in the use of alcohol (meaning repeated daily too large amounts, as well as actual dipsomania); the overuse of tobacco; excess in drinking tea or coffee; general overeating, and excessive eating of meat in particular, if the organs of elimination do not work perfectly and if such eating causes or allows putrefactive changes in the intestines; and progressive, prolonged wasting diseases, such as tuberculosis and cancer. It has also seemed in some cases that the only cause was excessive, hard physical labor, including excessive athletic work, and in other cases that prolonged anxiety and worry have been causes of cardiac degeneration and actual cardiac failure. Prolonged absorption of toxins from mouth and tonsil infections may be a not infrequent cause.

These myocardial changes are sometimes associated with chronic pericarditis and chronic endocarditis, and may accompany or follow valvular disease of the heart. Failure of compensation in valvular disease and dilatation of the heart are sequences which occur sooner or later.

SYMPTOMS AND SIGNS

The symptoms of chronic myocardial degeneration are progressive weakness, slight at first, noticeable on exertion (and what was not considered exertion becomes such), as evidenced by slight palpitation, slight shortness of breath, leg weariness and mental tire. The heart frequently becomes more rapid, not only with exertion and change of position to the erect, but even after eating. Slight cardiac stimulants, as coffee, affect the heart more than previously; there is some sleeplessness, more or less troublesome, and more or less indigestion. There may be mental irritability and some mental deterioration, as shown in various ways. There are likely to be slight edemas of the lower extremities toward night. The amount of urine may diminish. A previously high blood pressure becomes lower. The pulse may be occasionally intermittent, and later actually irregular.

The physical signs often show an enlargement of the heart, with increased activity at first, from irritability of the heart and a lack of perfect coordination; later the heart may show typical signs of weakness. Not infrequently a heart suffering from fibrosis acts perfectly until some sudden exertion, as lifting, running or serious illness causes it suddenly to become weak. Such a heart rarely regains its former strength. This occurs frequently to those who have supposed themselves to be in perfect physical health. Some sudden strain which they have previously been able to endure without injury, such as carrying a weight upstairs, cranking a refractory engine, pumping up a series of tires, or walking rapidly with a younger or more active companion, will suddenly give cardiac distress signals, serious exhaustion and more or less lengthy prostration, perhaps for an hour or so, or perhaps for several days. Permanent cardiac weakness may follow, or compensation may again occur, to be more easily broken later. Slight cardiac pains and sensations referred to the cardiac region become frequent. Disliking to lie on the left side, when previously the patient has been able to sleep on this side without discomfort, is an evidence of cardiac disturbance. There may be no real pains, but the patient becomes conscious of his heart, perhaps for the first time in his life. This alone is an indication of coming trouble.

If these signs and symptoms develop late in life, or at any age with other symptoms of sclerosis or senility, little can be done therapeutically except to afford temporary relief and to prevent the occurrence of acute attacks of cardiac distress or dyspnea. If the disturbance is really due to chronic cardiac degeneration, the sooner the patient learns that his ability is restricted, that his life is narrowed, the better for his future.

MANAGEMENT

The advice he should receive is well understood: to avoid physical efforts; to avoid mental tire; to avoid overeating or overdrinking of any foods or liquids; to reduce or abstain from alcohol, coffee, tea and tobacco, depending on what seems advisable in the individual case; to reduce the amount of meat eaten, especially if there is intestinal indigestion; to relieve intestinal indigestion; to cause free daily movements of the bowels; to abstain from any food which tends to cause gastric or intestinal flatulence; to abstain from such foods as contain nucleins, if the patient is gouty; to take frequent warm baths (not too hot) to promote the secretions and the circulation in the skin, and to take such daily exercise as seems advisable. If the patient cannot take exercise, simple calisthenics or massage should be instituted.

Whether nitroglycerin or other nitrite is advisable depends on the peripheral blood pressure. If the blood pressure is low, or not higher than is best for the patient, such treatment would be inadvisable. If, from the supposed cause, iodid seems to be indicated, it should be given in small doses and continued for some time. It is often wise, however, to give small doses, as 0.10 or 0.20 gm. (2 or 3 grains) once or twice in twenty-four hours, for a long period, to any patient who leas fibrosis or selerosis in any form. Iodid tends to prevent the progress of connective tissue formation. It is quite possible that some of its value is in activating a sluggish or imperfectly acting thyroid gland. If the patient is old, his thyroid is subinvoluting, and a little more of its activity will be of advantage. Many diseases which cause chronic myocarditis also cause, later, subactivity of the thyroid. Thyroid extract may be indicated if the patient is obese.

If, in spite of this management and treatment, the patient has cardiac asthma attacks, with or without pain, especially if there are pendent edemas, the question arises as to whether or not digitalis should be given. In such cases one cannot tell without trying whether digitalis will be of benefit or will cause more discomfort. 11 small dose of an active preparation should be given at first twice in twenty-four hours, and after a week once in twenty-four hours, its action being carefully watched and the decision as to whether the dose is too large or too small arrived at. It may do a great amount of good; it can cause increased cardiac pains. If used carefully and stopped when it appears not to be acting well, it will do no harm.

Chilling of the surface of the body should be avoided; sudden cold or sustained severe cold, which increases the contraction of the peripheral blood vessels and puts more strain on the heart muscle, is to be avoided if possible. More hours in bed at night and lying down after the heavier meals of the day will tend to give the heart the kind of rest it needs. Also complete rest for one day a week, or a rest of several days at a time, and a rest, both mental and physical, with such walking, golfing or riding as seems advisable, for at least one month every year, will prolong the lives of these patients, and may make an imperfect heart act well for months and years. If the patient is anemic he should, of course, receive some nonastringent iron; a. tablet of saccharated ferric oxid (Eisenzucker), in small doses, 0.20 gm. (3 grains), once or twice in twenty-four hours, is sufficient.

The prognosis of a case diagnosed as chronic myocarditis or chronic degeneration of the heart is doubtful, as one cannot tell until several weeks or months of observation whether this particular heart also has fatty degeneration or not. If there is fatty degeneration, the prognosis is bad. If there is no serious fatty degeneration, the patient, with the modified life outlined, may live for a long time. Acute dilatation from any serious strain on the heart may occur, and if there is fatty degeneration it is liable to occur at any time. Attacks of cardiac asthma are always serious, and always damage the heart a little more.

FATTY DEGENERATION

Fatty degeneration of the heart muscle may be caused by acute poisoning (as phosphorus, arsenic, etc.), by serious infections, or it may follow fibrosis of the heart or coronary artery disease. The symptoms are those of serious circulatory weaicnens, which does not seem to improve under any ordinary management. It is difficult, if the heart is enlarged, to determine whether there is more or less serious acute dilatation or whether the heart muscle has suffered fatty degenration.

The treatment of such a patient requires the best of judgment as to the amount of food and liquid that should be given, the regulation of the administration of laxatives, the sponging of the body, the means of producing sleep if there is insomnia, how much reading, conversation or amusements should be allowed, how much stimulation by stryclmin or other stimulating drug should be given, and whether or not very small doses of digitalis should he tried. These are all matters for individualizing, and for the best medical judgment which we are called on to give. How much repair can take place in a heart muscle when fatty degeneration has started we do not know. Such treatment will give the heart the only chance it has to recuperate, but the prognosis is bad.

FATTY HEART

The cause of deposits of fat around the heart or in between its chambers is the same as the cause of general obesity. These patients are likely to be obese, or at least to have large abdomens with large deposits of fat around the abdomen. This fat in itself will interfere somewhat with abdominal respiration. This tends to cause dyspnea, and the heart tends to be disturbed from these causes, if much fat is not really in the pericardium. The symptoms are those of imperfect heart action; the patient is dyspneic on exertion or in leaning over, the heart acts rapidly on such exertion, the patient puffs, perspires easily, and becomes leg weary, sedentary in his habits, and more or less incapacitated for work. He may not be a large eater; if he is, and his eating habit is corrected, the prognosis is better than if he is putting on weight in spite of eating sparingly.

The general treatment is that for obesity, and if the heart muscle is intact, various depletion methods may be inaugurated. More and more exercise, sweatings from Turkish baths, electric-light baths, body baking, vigorous massage and more or less purging are all valuable. Anything which reduces the general weight will help the heart. The prognosis is often good.



ENDOCARDITIS

It should be understood that especially in acute conditions a positive separation of endocarditis from myocarditis is incorrect. Acute endocarditis can probably not occur without some inyocarditis, and myocarditis probably does not occur without some endocardial disturbance and perhaps some pericardial irritation. This is especially true in endocarditis which occurs during any acute infection, even in rheumatism. The greater the amount of pericarditis, the more serious is the acute condition. The greater the amount of myocarditis, the more doubtful is the heart strength in the near future. The greater the amount of endocarditis, the greater the doubt of freedom from future permanent valvular lesions.

Endocarditis may be divided into: acute mild (simple) endocarditis, acute malignant (ulcerative, infective) endocarditis, chronic endocarditis and valvular disease.

ACUTE MILD ENDOCARDITIS

This inflammation of the endocardium is generally confined to the region of the valves, and the valves most frequently so inflamed are the mitral and aortic. There may be a slight inflammation or actual ulceration and loss of tissue. Vegetations more or less constantly occur on the inflamed surfaces, with more or less danger of particles becoming loosened and moving free in the blood stream, causing embolic obstruction in different parts of the body. There is also more or less probability of serious adhesions or contractions occurring from the healing of the ulcerated surfaces. The future health and welfare of the valves depend on the fact that the inflammation has healed without contractions or adhesions.

It is often difficult to decide when acute endocarditis has developed; but with the knowledge that the endocardium often becomes inflamed during almost any of the acute infections, the physician should repeatedly examine the heart for murmurs, for muffled closure of the valves, or for other evidences of endocarditis or myocarditis during the acute infective process.

It has been shown positively that acute endocarditis is due to micro-organisms, generally streptococci, staphylococci or pneumococci, and, more frequently than once believed, gonococci. The most frequent causes are acute rheumatic fever, diphtheria, pneumonia, cerebrospinal meningitis, scarlet fever, erysipelas, influenza, chorea, gonorrhea, sepsis and typhoid fever. It may also follow a follicular tonsillitis or some infection of the mouth or throat with or without arthritis. Tuberculosis may also occasionally cause an endocarditis. Organisms may be found in a terminal simple endocarditis due to a chronic disease, as tuberculosis or cancer; such inflammations may have been caused by circulating toxins.

It will be noticed by the foregoing classification that the terms "mild" and "malignant" endocarditis are used. The purpose is to convey the fact that there may be no etiologic distinction between the two forms, and it is impossible to decide clinically in the beginning of an endocardial inflammation which form is present. In the malignant form the infection is probably more serious or the infective germs are more active, the ulcerations deeper, and the likelihood of emboli and the seriousness of such embolic infarcts more serious and more dangerous. The differences in inflammation in the two cases is really one of degree, and the classification is made to coincide with this probable fact. it is, of course, clinically recognized that endocarditis following certain diseases, especially rheumatism, is of the simple or mild type, while that termed ulcerative endocarditis may occur apparently as a primary or general infection, and the causative bacteria, as a rule, are readily discovered in the blood. The Streptococcus viridans is one of the most dangerous of these bacteria.

A SECONDARY AFFECTION

Mild endocarditis is rarely a primary affection, and is almost invariably secondary to one of the diseases named above. Nearly 75 percent of secondary endocarditis occurs as a complication of acute articular rheumatism and chorea, or subsequently. On the other hand, about 40 percent of all patients with acute articular rheumatism develop endocarditis, sometimes perhaps so mild as to be hardly discoverable. This complication is most likely to occur during the second or third week of rheumatic fever. It is not sufficiently recognized that a subacute arthritis, recurring tonsillitis, open and concealed infections in the mouth, and even a condition of the system with acute, changeable and varying joint and muscle pains may all develop a mild endocarditis, even with subsequent valvular lesions. Therefore in all of these conditions the decision can be made only as to how much rest the patient must have or how serious the condition is to be considered by careful examination of the heart in every instance.

Children are more liable than adults to this complication, especially with rheumatism. Therefore, acute mild endocarditis with future valvular lesions occurs most frequently during childhood and adolescence, and if one attack has occurred, a subsequent infection, especially of rheumatism, is liable to cause another acute endocarditis.

PATHOLOGY

The part of the heart most affected is the part which has the most work to do—the left side of the heart—and of this side the left ventricle and therefore the mitral and aortic valves; the most frequent valve to be inflamed and to stiffer permanent disability is the a mitral valve, the valve which in its inflamed condition is subjected to the greatest amount of pressure and therefore irritation. Not infrequently soft systolic murmurs are heard at the pulmonary and tricuspid valves during acute endocarditis. It is rare, however, that these valves are so affected during childhood or adult life as to be permanently disabled.

Whether a diminished alkalinity of the blood in rheumatism has anything to do with the cause of the frequent complication of endocarditis has not been determined. Whether the administration of alkalies to the point of increasing the alkalinity of the blood is any protection against the complication of endocarditis has also not been positively demonstrated, although clinically such treatment is believed by a large number of practitioners to be wise.

A chronic endocarditis with permanent lesions of the valves may become an acute inflammation with an infectious provocation.

It has been shown that even in a few hours after endocarditis has started, little vegetations composed of fibrin, with white blood cells, red blood pigment and platelets, may develop. Practically in all instances such vegetations develop, and later become more or less organized into connective tissue. These little vegetations, generally minute, perhaps not exceeding 4 mm. in height, are irregular in contour like a wart. Some of these may have small pedicles, and as such, of course, are more likely to become loosened and fly off into the blood stream. It is of interest to note that these little vegetations are more likely to be on the left side of the heart than the right; on the valves than any other part, and on the mitral valve than on the aortic. The consequence is a more frequent permanent disability of the valves of the left side of the heart, and of these more frequently the mitral. Although these little vegetations and excrescences sooner or later become mostly connective tissue, still fibrin and white blood cells may form thin layers over them, more or less permanent. In this fibrin are frequently found bacteria, even when there has been no recent acute inflammation. The deeper layers of the endocardium during acute inflammation may become infiltrated with young cells, with resultant softening and destruction of the intercellular substance. This softening and some swelling of the lower layers of the endocardium allow the pushing up of these extravasated blood cells which, being covered with fibrin, makes the little vegetations above described; and as just stated, the fibrin may form a more or less permanent cap. If this cap is disintegrated or lost and the cells under it washed away in the blood stream, ulceration takes place, which may be more or less serious, even to the perforation of a valve or actual erosion of one of its cusps, and the parts of the valves most seriously affected are the parts which strike against each other on closure; as previously stated, the parts subjected to the greatest strain and the greatest amount of friction during the inflammation are the parts most seriously affected afterward.

If a perforation has occurred, it may make a permanent leak. If an erosion of the edge of the valve has occurred, it may make permanent insufficient closure. If the valve has become thickened and stiffened during the cicatricial healing, it may not only be incompetent, but may not open perfectly, and a narrowed orifice may be the consequence. During the healing of these granulating ulcers there may be thickening of the part or shrinking of the tissue, and the valve may become shortened by adhesion to the wall, or the cusps of the valve may adhere together so that the valve becomes permanently unable to open properly or to close properly, or to do either.

Not infrequently and probably more frequently than we recognize, recovery without any of the pathologic lesions just described follows mild endocarditis. The occurrence of simple endocarditis is undoubtedly frequent during acute disease, and is unrecognized because there are no lesions of the heart at the time or subsequently; but valvular lesions only too frequently follow the endocarditis which occurs with rheumatism. Occasionally the ulcerations become serious, and ulcerative endocarditis or malignant endocarditis develops on the mild inflammation. In this form the little vegetations are liable to become loosened, fly off into the blood stream, and cause emboli in different parts of the body.

Recently Fraenkel [Footnote: Fraenkel: Beitr. z. path. Anat. u. z. allg. Path., 1912, iii, 597.] concluded that the microscopic nodules which occur in endocarditis in the myocardium, and which consist of the several varieties of white blood corpuscles first referred to by Aschoff in 1904, are characteristic only of acute rheumatism. Fraenkel found these nodules in the myocardium in a case of chorea, showing the close relationship between it and rheumatism.

While repeated careful examination of the heart during acute infections will generally show signs of endocarditis if it is present, even if there are no subjective symptoms, the disease may be so insidious as not to be noted until a valvular lesion occurs. Often, however, during the course of the disease, especially in rheumatism, there is a slight increase in fever and there is a discomfort complained of in the region of the heart, frequently accompanied by slight dyspnea. Real pain is seldom present unless the pericardium is affected. If the myocardium is much inflamed at the same time, the heart becomes more rapid and the blood tension lowered, and the apex beat diminished in intensity and perhaps not palpable. If there is pain, with or without pericarditis, it is often referred to the epigastrium, especially in children. The patient is often nervous, restless and sleepless. In simple endocarditis emboli rarely occur. If they do, of course the signs will be in the part in which the infarct occurs. Besides the diminished intensity of the apex beat and its greater diffusion, the valve sounds may be muffled, and sooner or later there may be systolic murmurs over the different orifices. Of course systolic murmurs may be due to a disturbed condition of the blood, but if they occur with the above-mentioned symptoms and signs, endocarditis should be diagnosed. If the heart becomes seriously weak and the patient suffers much dyspnea, myocarditis should be known to be present with the endocarditis. If there is a diastolic murmur, there can be no question of serious endocarditis having occurred. Unexplainable palpation during acute illness liar been thought to be a distinct symptom of endocarditis.

TREATMENT OF ENDOCARDITIS

As mild endocarditis rarely occurs primarily but is almost always secondary to some acute disease, its immediate treatment is only a slight modification of that of the disease which is causing it. A complication which is so frequent should always be expected, and consequently warded off or prevented, if possible. Knowledge of the diseases which are most liable to cause endocarditis makes frequent heart examinations a necessity, to note when it arrives. While an extra heart tire, sleeplessness, and the circulation of unnecessary toxins from a bad condition of the bowels and from improperly selected food all make this complication more liable, its occurrence is, nevertheless, often unpreventable.

The most efficacious preventive pleasures are sleep, rest, the stopping of pain, prevention of exertion, proper food which does not cause flatulence or other indigestion, good, sufficient daily movements of the bowels, the prevention of intestinal distention, and maintenance of a clean, moist surface of the body, produced by such sponging and bathing as the temperature demands.

The disease having developed, the indications for treatment are really few; in fact, the treatment is mostly negative. There is generally but little local pain; the temperature from simple endocarditis alone is not high and the acute symptoms tend to abate.

Local Treatment.—Endocarditis having been diagnosed, especially if there is palpation or pain, an ice bag over the heart is often of considerable value, but not so efficient as in pericarditis. It often tends to quiet the heart, and may be of some value reflexly in slowing the inflammation. If it causes restlessness, however, and does not lessen the pain (which in some instances it may increase), it certainly should be stopped. Children, in whom this complication so frequently occurs, generally do not bear the ice bag well. Sometimes it may be advisable to substitute warm applications, and often a great deal of comfort is derived from them, the patient soon going to sleep. One of the greatest values of either cold or hot applications is diminution of the discomfort from the cardiac disturbance, and the stopping of any pain which may be present. If they do not do this, there is no object in using either cold or heat.

The discomfort from blisters over the heart during the acute stage of endocarditis is greater than any good which they can do. In adults a few small blisters may be used intermittently around the borders of the heart, after the acute symptoms are over, to act reflexly on the heart and possibly aid absorption of inflammatory products. Sometimes improvement seems to follow such treatment; it certainly can do no harm.

During convalescence, the skin over the heart may be painted with iodin, repeated often enough to cause stimulation without injuring the skin; it seems at times to be of value. Various iodin or iodid ointments have been used, but they probably have no more value than the administration of small doses of iodid.

Systemic Treatment.—As this complication most frequently occurs during acute rheumatism, the question arises as to the value or harmfulness of salicylates and alkaline drugs. With our recent better understanding of the action on the heart of pure salicylates (either natural or synthetic saliclic acid, which have been shown to act identically, if equally pure), we must believe that in any ordinary dosage they will injure the heart but rarely. While salicylic acid will not prevent endocarditis, it should he continued, if it is of benefit with regard to the arthritis. The indication for its use depends on its effect on the joints. As it acts at times almost as a specific in rheumatism, it would seem that it should be of value in the endocarditis caused by rheumatism. On the other hand, the endocarditis occurs during the second or third week of acute rheumatism, after the blood has been thoroughly saturated with salicylic acid. Therefore it certainly does not tend to prevent rheumatic endocarditis; hence for this complication alone salicylic acid is not indicated.

ALKALIES

Anything which tends to increase the acidity of the tissues and to diminish the alkalinity of the blood, whether from starvation or outer causes, seems to pro-duce endocardial and myocardial irritation, if not actual inflammation. Therefore in a disease like rheumatism, which seems to be made worse by anything which increases the acidity, alkalies are obviously indicated, and it is probable that an increased alkalinity of the blood tends to prevent endocardial irritation, and may soothe an inflammation already present. Until we have some positive knowledge to the contrary, alkalies should be freely administered during endocarditis, especially during rheumatic endocarditis. Potassium citrate in 2 gm. (30 grain) closes, in wintergreen water, should be given every three to six hours, depending on how readily the urine is made alkaline. This may be given with the salicylic acid treatment, and also when the salicylic acid has been stopped. It may be well, if sodium salicylate is being used, to give also sodium bicarbonate, the sodium bicarbonate often preventing irritation of the stomach from the sodium salicylate, the dose being equal parts of the sodium salicylate and the sodium bicarbonate administered in plenty of water. If some other form of salicylic acid is preferred, novaspirin, which is methylene-citryl-salicylic acid and contains 62 percent of salicylic acid, is perhaps the least irritant to the stomach of the salicylic preparations. This drug is decomposed in the intestine into its component parts, salicylic acid and methylene-citric acid. If this drug is combined with sodium bicarbonate, the disintegration into its component parts would be likely to occur in the stomach.

IRON

It is essential for the welfare of the patient, especially after a long illness before the complication of endocarditis could occur, and in rheumatic fever, in which all meat and meat extractives have been kept from the diet, that small doses of iron should be administered daily. Not only the fever process, but also the salicylic acid tends to prevent the healthy normal growth of red corpuscles. and such patients suffering from rheumatism are often seriously anemic after the aente inflammation has ceased. The iron administered may be 5 drops of the tincture of the chlorid, in lemonade or orangeade, twice in twenty-four hours (and it should be remembered that lemon and orange burn to alkalies in the system and do not act as acids); or 0.1 gm. (1 1/2 grains) of reduced iron in capsule twice in twenty-four hours, or a 3 grain tablet of saccharated ferric oxid (Eisenzucker) twice in twenty-four hours.

OPIUM

As so many times repeated, real pain must be stopped, and morphin, either by the mouth or hypodermically, should be used to the point of stopping such pain. If the patient is a young child, codein sulphate or the deodorized tincture of opium may be used in the dose found sufficient, and either one will act satisfactorily. The dose given should be small but repeated sufficiently often to stop the pain. The dose necessary for the given individual will soon be learned, and that dose may be repeated at such intervals as the condition may require. Sometimes the hypnotic selected, if one is needed, will be sufficient to quiet the cardiac aches or pains.

BROMIDS AND CHLORAL

If there is much restlessness and the circulation is good, that is, if myocarditis is probably not present, the bromids may be of great value, especially in children. The dose should be sufficient to quiet the nervous system. The drug may be discontinued after a few days, if the conditions improve. If the bromid, except in large doses, will not cause sleep, a sufficient dose of chloral should be given. Chloral is one of the most satisfactorily acting drugs which we have to produce sleep and to cause cardiac rest. While it should not be given if there is real cardiac weakness, the good which it does is so much greater than the possible bad effect on the heart, that it should not be forgotten for some newer hypnotic. The worst part of this drug is its taste, and the best way to administer it is to have it in solution in water and the dose given on cracked ice with a little lemon juice to be followed by a good drink of water and a piece of orange pulp for the patient to chew. Ordinarily a bad-tasting drug such as chloral is well administered in effervescing water, but effeverscing waters are generally inadvisable when there is any kind of inflammation of the heart, as they are liable to cause distention of the stomach and pressure on the heart. Some physicians prefer chloralamid as a less disagreeable drug and one which acts almost as efficiently as chloral. As the close of this must be larger than the dose of chloral, it is a question of doubt as to which is the better drug to use. Of the newer hypnotics, veronal=sodium (sodium-diethyl-barbiturate) is among the best. It acts quickly, is less depressant and is a safer salt than most of the other newer hypnotics. It is the readily soluble sodium salt of veronal (diethyl-barbituric acid). When combined with any active drug, sodium seems to make it less toxic and less depressant. The dose of this drug is from 0.2 to 0.3 gm. (3 to 5 grains).

PREVENTION

If the patient is weak, the circulation depressed, the blood pressure low, and the heart rapid, the drug advisable to produce rest and sleep is almost always morphin or some other form of opium. Morphin, with few exceptions, is a cardiac tonic and a cardiac stimulant, unless the dose is much too large. As long as the bowels are daily moved and the food is not given at the time of the full action of the morphin, when digestion might be delayed or interfered with, in most patients the action of this drug during serious illness is entirely for good. The greatest mistake in using morphin for the production of sleep, or for physical and mental rest and comfort when there is not severe pain, is in giving too large a dose. If pain is not severe, or due to inflammatory distention of some undilatable part, to pressure on some nerve, to distention of some tube by a calculus or to some serious injury to the nerves, large doses of morphin are not needed. Small doses will act much more efficiently. It is excessively rare that a hypodermic of one- fourth grain of morphin sulphate is needed, except for the conditions enumerated. It is often a fact that so small a dose as one-eighth grain of morphin or even one-sixth grain will cause sufficient stimulation of a nervous patient, because its primary stimulant effect on the spinal cord is greater than its depressant effect on the brain, to require another dose (one-fourth grain altogether) to give such a patient rest. On the other hand, this patient may many times be quieted by one-tenth grain of morphin sulphate on account of the size of the dose being not sufficient to stimulate the spinal cord. Many a time clinically when one-eighth grain has failed, a dose of one-fourth grain having been apparently necessary, a change to one-tenth grain has proved entirely and perfectly satisfactory.

DIET

As intimated in the preceding paragraph, the diet during endocarditis must be carefully regulated. It must be sufficient, and appropriate for the disease in which the complication occurs, but it must be in such dosage and administered with such frequency as to cause the least possible indigestion. Large amounts of milk are rarely advisable. Too much milk is certainly given, even in rheumatism. While pretty well tolerated by children, it is often badly tolerated as far as digestive symptoms are concerned, by adults. The amount of liquid given should be governed by the amount of urine passed and by the amount of perspiration. The patient should not be overloaded with liquid if he does not need it. Enough carbohydrate must be given.

LAXATIVES

If the bowels are known to be in excellent condition and not loaded with fecal matters, brisk catharsis is not needed simply because endocarditis has developed. If the bowels have been neglected, a small dose of calomel, aided by a compound aloin tablet, is necessary and good treatment. Subsequent movements of the bowels should be daily obtained by vegetable laxatives with occasional enemas, as needed. With all inflammation of the heart and the possibility of myocarditis developing or being actually present, it is not advisable to use salines freely or often.

CARDIAC DRUGS

Whether any drug should be used which acts directly on the heart is often a question for decision. As endocarditis is generally secondary to some acute disease, the patient has become weakened already, and the circulation is not sturdy; therefore such a drug as aconite is probably never indicated. The necessary diminished diet, catharsis, hypnotic, salicylic acid and alkalies all tend to quiet the circulation and diminish any strenuosity of the heart that may be present. Unfortunately, during fever processes, digitalis in ordinary doses rarely slows the heart; and while it might slow the heart if given in large doses, it would also cause too powerful contractions of the ventricles. Digitalis is inadvisable if there is much endocardial inflammation, and especially if there is supposed or presumed to be acute myocardial inflammation. If a patient had already valvular disease from a previous endocarditis, and during this attack insufficiency of the heart was evidenced by pendent edemas, digitalis Should be administered; but it probably should not be given to other patients during the acute period of inflammation.

BATHS

During rheumatism the peripheral blood vessels are generally dilated and the skin perspires profusely. This is caused not only by the rheumatism, but also by the salicylates. The surface of the body should be sponged with cold, lukewarm or hot water, depending on the temperature, especially of the skin. The cold water will reduce the temperature and tone the peripheral blood vessels; the hot water, if the temperature is low and the skin moist and flabby, will cleanse it and also tone the peripheral blood vessels. If the blood vessels are dilated and the perspiration profuse, atropin is indicated, both as a cardiac stimulant and contractor of the blood vessels and as a preventer of too profuse sweating. The dose should be from 1/200 to 1/100 grain for an adult, given two or three times in twenty-four hours, depending on its action and the indications. It should be remembered that atropin is not a sleep-producer; it may stimulate the cerebrum. Therefore at night it might well be combined with a possible necessary hypodermic injection of morphin.

STRYCHNIN

The question of the advisability of strychnin is a constant subject for discussion. Strychnin is overused in the cases of most patients who are seriously ill. In a patient in whom we are trying to cause nervous and muscular rest, strychnin is certainly contraindicated. On the other hand, if the heart is acting sluggishly, the peripheral circulation is imperfect, and atropin is not acting well, it is advisable to give strychnin in a dose not too large and not too frequently repeated. Strychnin should be avoided, if possible, in the evening in order that the patient may sleep. Whether it should be given by the mouth or hypodermically would depend entirely on the seriousness of the condition. Once in six hours is generally often enough for strychnin to be administered unless the dose is very small.

ALCOHOL

It is rarely, if ever, advisable to use alcohol. In certain instances, however, especially in older patients who are accustomed to alcohol, a little whisky administered several times a day may act only for good, both as a food and as a peripheral dilator. But it must be remembered that alcohol is not a cardiac stimulant, and that a large dose will be followed by more cardiac depression. Nitroglycerin may act as well as whisky in the kind of cases mentioned. Caffein stimulation in any form is generally inadvisable during inflammation of the heart.

PROGNOSIS AND CONVALESCENCE

The duration of acute endocarditis varies greatly; it may be two or three weeks, or the inflammation may become subacute and last for several months. Although mild endocarditis rarely causes death of itself, it may develop into an ulcerative endocarditis, and then be serious per se. On the other hand, it may add its last quota of disability to a patient already seriously ill, and death may occur from the combination of disturbances. As soon as all acute symptoms have ceased, rheumatic or otherwise, and the temperature is normal, the amount of food should be increased; the strongly acting drugs should be stopped; the alkalies, especially, should not be given too long, and the salicylates should be given only intermittently, if at all; iron should be continued, massage should be started, and iodid should be administered, best in the form of the sodium iodid, from 0.1 to 0.2 gm. (1 1/2 to 3 grains), twice in twenty-four hours, with the belief that it does some good toward promoting the resorption of the endocardial inflammatory products and can never do any harm. Prolonged bed rest must be continued, visitors must still be proscribed, long conversations must not be allowed, and the return to active mental and physical life must be most deliberate.

No clinician could state the extent to which the valvular inflammation will improve or how much disability of the valves must be permanent. It is even stated by some clinicians that a rest in bed for three months is advisable. While this is of course excessive, certainly, when the future health and ability of the patient are under consideration, and especially when the patient is a child or an adolescent, time is no object compared with the future welfare of the person's heart. It is one of the greatest pleasures of a the clinician to note such a previously inflamed heart gradually diminish in size and the murmurs at the valves affected gradually disappear. Although they may have disappeared while the patient is in bed, he is not safe from the occurrence of a valvular lesion for several months after he is up and about.

While the discussion of hygiene would naturally be confined to the hygiene of the disease of which the endocarditis is a complication, still the hygiene of its most frequent cause, rheumatism, should be referred to. Fresh air and plenty of it, and dry air if possible, is what is needed in rheumatism, and a shut-up, over-heated and especially a damp room will continue rheumatism indefinitely. It is almost as serious for rheumatism as it is for pneumonia. Sunlight and the action of the sun's rays in a rheumatic patient's bedroom are essential, if possibly obtainable.

As so many rheumatic germs are absorbed from diseased or inflamed tonsils or from other parts of the mouth and throat, proper gargling or swashing of the mouth and throat should be continued as much as possible, even during an endocarditis. The prevention of mouth infections will be the prevention of rheumatism and of endocarditis.

MALIGNANT ENDOCARDITIS: ULCERATIVE ENDOCARDITIS

Since we have learned that bacteria are probably at the bottom of almost any endocarditis, the terms suggested under the classification of endocarditis as "mild" and "malignant" really represent a better understanding of this disease. They are not separate entities, and a mild endocarditis may become an ulcerative endocarditis with malignant symptoms. On the other hand, malignant endocarditis may apparently develop de novo. Still, if the cause is carefully sought there will generally be found a source of infection, a septic process somewhere, possibly a gonorrhea, a septic tonsil or even a pyorrhea alveolaris. Septic uterine disturbances have long been known to be a source of this disease. Meningitis, pneumonia, diphtheria, typhoid fever and rarely rheumatism may all cause this severe form of endocarditis.

Ulcerative endocarditis was first described by Kirkes in 1851, was later shown to be a distinctive type of endocarditis by Charcot and Virchow, and finally was thoroughly described by Osler in 1885.

Ulcerative endocarditis was for a long time believed to be inevitably fatal; it is now known that a small proportion of patients with this disease recover. Children occasionally suffer from it, but it is generally a disease of middle adult life. Chorea may bear an apparent causal relation to it in rare instances.

Ulcerative endocarditis may develop on a mild endocarditis, with disintegration of tissue and deep points of erosion, and there may be little pockets of pus or little abscesses in the muscle tissue. If such a process advances far, of course the prognosis is absolutely dire. If the ulcerations, though formed, soon begin to heal, especially in rheumatism, the prognosis may be good, as far as the immediate future is concerned. If the process becomes septic, or if there is a serious septic reason for the endocarditis, the outlook is hopeless. This form of endocarditis is generally accompanied by a bacteremia, and the causative germs may be recovered from the blood. One of the most frequent is the Streptococcus viridans.

DIAGNOSIS

If a more malignant form of endocarditis develops on a mild endocarditis, the diagnosis is generally not difficult. If, without a definite known septic process, malignant endocarditis develops, localized symptoms of heart disturbance and cardiac signs may be very indefinite.

If there is no previous disease with fever, the temperature from this endocarditis is generally intermittent, accompanied by chills, with high rises of temperature, even with a return to normal temperature at times. There may be prostration and profuse sweats. Even without emboli there may be meningeal symptoms: headache, restlessness, delirium, dislike of light and noise, and stupor; even convulsions may occur. The urine generally soon shows albumin; there may be joint pains; the spleen is enlarged and the liver congested. Some definite cardiac symptoms are soon in evidence, with more or less progressive cardiac weakness. Occasionally there are no symptoms other than the cardiac.

Characteristic of this inflammation is the development of ecchymotic spots on the surface of the body, especially on the feet and lower extremities. Sooner or later, in most instances of the severe form of this disease, emboli from the ulcerations in the heart reach the different organs of the body, and of course the symptoms will depend on the place in which the emboli locate. If in the abdomen, there are colicky pains with disturbances, depending on the organs affected; if in the brain, there may be paralysis, more or less complete. In all infaret occurs in one of the organs of the body there must of necessity occur a necrosis of the part and an added focus of infection. If a peripheral artery is plugged, gangrene of the part will generally occur, if the patient lives long enough.

TREATMENT

If pneumonia or gonorrhea is supposed to be the cause of the endocarditis, injections of stock vaccines should perhaps be used. If the form of sepsis is not determinable, streptococcic or staphylococcic vaccines might be administered. It is still a question whether such "shotgun" medication with bacteria is advisable. Patients recover at times from almost anything, and the interpretation of the success of such injection treatment is difficult. Exactly how much harm such injections of unnecessary vaccines can produce in a patient is a question that has not been definitely decided. Theoretically an autogenous vaccine is the only vaccine which should be successful. The vaccine treatment of ulcerative endocarditis was not shown to be very successful by Dr. Frank Billings [Footnote: Billings, Frank: Chronic Infectious Endocarditis, Arch. Int. Med., November, 1909, p. 409.] in his investigation, and more recent treatment of this disease, when caused by the Streptococcus viridons, by antogenous vaccines has confirmed his opinion.

Other treatment of malignant endocarditis includes treatment of the condition which caused it plus treatment of "mild" endocarditis, as previously described, with meeting of all other indications as they occur. As in all septic processes, the nutrition must be pushed to the full extent to which it can be tolerated by the patient, namely, small amounts of a nutritious, varied diet given at three-hour intervals.

Whether milk or any other substance containing lime makes fibrin deposits on the ulcerative surfaces more likely or more profuse, and therefore emboli more liable to occur, is perhaps an undeterminable question. In instances in which hemorrhages so frequently occur, as they do in this form of endocarditis, calcium is theoretically of benefit. Quinin has not been shown to be of value, and salicylic acid is rarely of value unless the cause is rheumatism.

Alcohol has been used in large doses, as it has been so frequently used in all septic processes. If the patient is unable to take nourishment in any amount, small doses of alcohol may be of benefit. It is probably of no other value. It is doubtful whether ammonium carbonate tends to prevent fibrin deposits or clots in the heart, as so long supposed. In fact, whenever the nutrition is low and the patient is likely to have cerebral irritation from acidemia, whenever the kidneys are affected, or whenever a disease may tend to cause irritation of the brain and convulsions, it is doubtful if ammonium carbonate or aromatic spirit of ammonia is ever indicated. Ammonium compounds have been shown to be a cause of cerebral irritation. Salvarsan has not been proved of value.

Intestinal antisepsis may be attained more or less successfully by the administration of yeast or of lactic acid ferments together with suitable diet. The nuclein of yeast may be of some value in promoting a leukocytosis. It has not been shown, however, that the polymorphonuclear leukocyte increase caused by nuclein has made phagocytosis more active.

Malignant endocarditis may prove fatal in a few days, or may continue in a slow subacute process for weeks or even months.

CHRONIC ENDOCARDITIS

It is not easy to decide just whew all acute endocarditis has entirely subsided and a chronic, slow-going inflammation is substituted. It would perhaps be better to consider a slow-going inflammatory process subsequent to acute endocarditis as a subacute endocarditis; and an infective process may persist in the endocardium, especially in the region of the valves, for many weeks or perhaps months, with some fever, occasional chills, gradually increasing valvular lesions and more or less general debility and systemic symptoms. Such a subacute endocarditis may develop insidiously on a previously presumably healed endocardial lesion and cause symptoms which would not be associated with the heart, if an examination were not made. Sometimes such a slow-going inflammatory process will be associated with irregular and intangible chest pains, with some cough or with many symptoms referred to the stomach, so that the stomach may be considered the organ which is at fault. There may be dizziness, headache, feelings of faintness, sleeplessness, progressive debility and a persistent cough, with some bronchial irritation and with occasional expectoration of streaks of blood, which may cause the diagnosis of incipient tuberculosis to be made. The need of a careful general examination must be emphasized again before a decision is made as to what ails the patient, or before cough mixtures are given unnecessarily, quinin is prescribed for supposed malarial chills, or various diets and digestants are recommended for a supposed gastric disturbance.

The term "chronic endocarditis" should be reserved for a slowly developing sclerosis of the vavles. This may occur in a previous rheumatic heart and in a heart which has suffered endocarditis and has valvular lesions, or it may occur from valvular strain or heart strain from various causes; it is typically a part of the arteriosclerotic process of age, and is then mostly manifested at the aortic valve.

ETIOLOGY

Rheumatism is the cause of most instances of cardiac disease which date back to childhood or youth, while arteriosclerosis and chronic infection cause most cardiac diseases in the adult. In the former case it is the mitral valve which is the most frequently affected, while in the latter it is the aortic valve. Any cause which tends to induce arteriosclerosis may be a cause of chronic endocarditis, such as gout, syphilis, chronic nephritis, alcoholism, excessive use of tobacco, excessive muscular labor and hard athletic work. Lead is also another, now rather infrequent, cause. Severe infections may tend to make not only an arteriosclerosis occur early in life, but also a chronic endocarditis. Heart strain may also be a cause of chronic endocarditis, especially at the aortic valve. Forced marches of soldiers, competitive athletic feats, and occupations which call for repeated hard physical strain may all cause aortic valve disease. Tobacco, besides increasing the blood tension and thus perhaps injuring the aortic valve, may weaken the heart muscle and cause disturbance and irritation and perhaps inflammation of the mitral valve.

There is no age which is exempt from valvular disease, but the age determines the valve most liable to be affected. If endocarditis occurs in the fetus, it is the right side of the heart that is affected; in children and during adolescence it is most frequently the mitral valve that is involved; while in the adult or in old age it is the aortic valve that is most liable to become diseased. Statistics have shown that the valves of the left side of the heart are diseased nearly twenty times as frequently as those of the right side of the heart. They also show that the mitral valve is diseased more than one and one-half times as frequently as the aortic valve. Early in life probably the two sexes are equally affected with valvular disease, with perhaps a slight preponderance among females, because of their greater tendency to chorea. Females also show a greater frequency to mitral stenosis than do males. Aortic disease, on the other hand, from the very fact of their strenuous life and occupations, is nearly three times more frequent in men than in women.

PATHOLOGY

If a chronic endocarditis has followed an acute condition, some slight permanent papillomas or warty growths may he left from the healed granulating or ulcerated surfaces. Sometimes these little elevations on the valves become inflamed and then adhere together, or adhere to the wall of the heart, and thus incapacitate a valve. Sometimes these excrescences undergo partial fatty degeneration, or may take on calcareous changes and thus stiffen a valve.

If the chronic inflammation is not superimposed on an acute endocarditis there may be no cell infiltration and therefore no softening, but there is a tendency to develop a fibrillated structure, and a fibroid thickening of the endocardium occurs, especially around the valves. This induration causes contraction and narrowing of the orifices with shortening and thickening of the chordae tendineae, and the valves imperfectly open, or no longer close. Fatty degeneration may occur in the papillary growths with necrotic changes, and this may lead to the formation of atheromatous ulcers which may later become covered with lime deposits, and then a hard calcareous ring may form. Fibrin readily deposits on this calcareous substance and may form a permanent capping, or may slowly disintegrate and allow fragments to fly off into the blood stream and cause more or less serious embolic obstruction. If this chronic endocarditis develops with a general arteriosclerosis, the wine inflammation soon occurs in the aorta, and, following the endarteritis in the aorta, atheromatous deposits may also occur there. Chronic endocarditis of the walls of the heart, not in immediate continuity with endocarditis of the valves, is perhaps not liable to occur, except with myocarditis.

TREATMENT

A subacute or a chronic infective endocarditis should be treated on the same plan as an acute endocarditis, which means rest in bed and whatever medication seems advisable, depending on the supposed cause of the condition.

A chronic endocarditis which is part of a general arteriosclerosis requires no special treatment except that directed toward preventing the advance of the general disease.



CHRONIC DISEASES OF THE VALVES

PATHOLOGIC PHYSIOLOGY

The development of permanent injury to one or more valves of the heart may have been watched by the physician who cares for a patient with acute endocarditis, or it may have been noted early during the progress of arteriosclerosis or other conditions of hypertension. On the other hand, many instances of valvular lesions may be found during a life-insurance examination, or are discovered by the physician making a general physical examination for an indefinable general disturbance or for local symptoms. without the patient ever having known that he had a damaged heart. The previous history of such a patient will generally disclose the pathologic cause or the physical excuse.

As soon as a valve has become injured the heart muscle hypertrophies to force the blood through a narrowed orifice or to evacuate the blood coming into a compartment of the heart from two directions instead of one, as occurs in regurgitation or insufficiency of a valve. The heart muscle becomes hypertrophied, like any other muscle which is compelled to do extra work. Which part or parts of the heart will become most enlarged depends on the particular valvular lesion. In some instances this enlargement is enormous, increasing a heart which normally weighs from 10 to 12 ounces to a weight of 20 or even 25 ounces, and extreme weights of from 40 to 50 ounces and even more are recorded.

As long as the heart remains in this hypertrophied condition, which may be called normal hypertrophy since it is needed for the work which has to be done in overcoming the defect in the valve, there are no symptoms, the pulmonary and systemic circulation is sufficient, and the patient does not know that he is incapacitated. Sooner or later, however, the nutrition of the heart, especially in atheromatous conditions, becomes impaired, and the lack of a proper blood supply to the heart muscle causes myocardial disturbance, either a chronic myocarditis or fatty degeneration. If there is no atheromatous condition of the coronary arteries, and arterial disease is not a cause of the valvular lesion, compensation may be broken by some sudden extra strain put on the heart, either muscular or by some acute sickness or a necessary anesthetic and operation. From any of these causes the muscle again becomes impaired, and the heart, especially the part which is the weakest and has the most work to do relatively to its strength, becomes dilated, compensation is broken, and all of the various circulatory disturbances resulting from an insufficient heart strength develop.

PRECAUTIONS TO BE OBSERVED

As long as compensation is complete, there are no medication and physical treatment necessary for the damaged heart. The patient, however, should be told of his disability, and restrictions in his habits and life should be urged on him. The most important are that all strenuous physical exercise should be interdicted; competitive athletics should be absolutely prohibited; prolonged muscular effort must never be attempted, whether running, rowing, wrestling, bicycle riding, carrying a heavy weight upstairs or overlifting in any form. The patient should be taught that he should never rush upstairs, and that he should never run rapidly for a car or a train or for any other reason; he should not pump up a tire, or repeatedly attempt to crank a refractory engine; even the prolonged tension of steering a car for a long distance is inadvisable. He should be told that after a large meal he is less capacitated for exertion than a man who has not a damaged heart. It is better if he drinks no tea or coffee; it is much better if he absolutely refrains from tobacco and alcohol. Prolonged mental worry, business frets and mental depression are all injurious to his heart. Anything which seriously excites him, whether anger or a stimulating drug, is harmful. Any disease which he may acquire, especially lung disturbances, as pneumonia or even a serious cough, requires that he take better care of himself and be more carefully treated and take more rest in bed than a patient who has not a damaged heart. Anything which raises the blood pressure is of course more serious for his heart than for a perfect heart; therefore drinking large amounts of liquid, even water, is inadvisable. It simply means so much more work for the heart to do. Such patients should rarely be given any drug that causes cardiac debility, and should never take one without advice. This applies to all the coal-tar drugs, acetylsalicylic acid (aspirin), etc.

One other fact should be impressed on the person with a valvular lesion and compensation, and that is that he has but little, if any, reserve circulatory power. While he is in apparently perfect health, it takes little circulatory strain to push his heart to the point of danger or insufficiency. As nothing keeps this reserve so good or increases it more than rest, he should expect to have a restful day at least once a week, and a good rest of at least two or three weeks once or twice a year.

A patient with these restrictions may live for years with a serious valvular defect and may die of some intercurrent disease which has nothing to do with the circulatory system.

It is easily recognizable that as the majority of acute lesions of the valves occur in children, it is impossible to prevent them from taking more or less strenuous exercise, and this is probably the reason that we have so many serious broken compensations during youth or early adolescence.

As referred to under the subject of myocarditis, many symptoms for which a patient consults his physician are indefinite and intangible, though due to cardiac weakness. If a patient with a damaged heart has a sudden dilatation, of course his symptoms are so serious that the physician is immediately summoned. If, however, he has a slowly developing insufficiency of the heart muscle, his first symptoms are more or less indefinite cardiac pains, slight shortness of breath, slight attacks of palpitation, a dry, tickling, short cough occurring after the least exertion, some digestive disturbances, often sluggishness of the bowels, gastric flatulence, possibly nosebleeds, and sooner or later some edema of the lower extremities at the end of the day.

DECOMPENSATION

To understand the physiology, pathology and the best treatment for broken compensation, it is necessary to study the physics of the circulation under the different conditions. With the mitral valve insufficient, a greater or less amount of blood is regurgitated into the left auricle, which soon becomes dilated. Distention of any hollow muscular organ, if the distention is not to the point of paralysis, means a greater inherent or reflex attempt of that organ to evacuate itself; the muscular tissue begins to grow, and a hypertrophy of the left auricle with the above-named lesion develops. The muscular tissue of the auricle, however, is not sufficient to allow any great hypertrophy. The blood flowing from the pulmonary veins into the left auricle finds this cavity already partly filled with blood regurgitated from the left ventricle. The pulmonary blood, being impeded, tends to flow more slowly, and therefore dams back into the lungs, causing a passive congestion of the lungs. The pulmonary artery thus finds the pressure ahead unusually great, and the right ventricle reflexly learns that it requires a greater force to empty itself than before; in fact, it may not succeed in completely accomplishing this until its distention, by an incomplete evacuation of its contained blood plus the blood coming from the right auricle, has caused the right ventricle also to become hypertrophied. This increased muscular action of the right ventricle relieves the pulmonary congestion, and an increased amount of blood is forced into the left auricle. On account of its hypertrophy, the left auricle is able to send an increased amount of blood into the left ventricle, which in turn becomes hypertrophied and sends enough blood into the aorta to satisfy the requirements of the systemic circulation in spite of the leakage through the mitral valve.

As long as this compensation continues, there are no symptoms. If any dilatation occurs from disease, degeneration or from increased work put on the heart (and it is readily seen how delicate this equilibrium is), signs of broken compensation begin to occur. The left ventricle with its enormous strain is perhaps the first part to dilate, thus enlarging the opening of the defective mitral valve. The left auricle is then unable to cope with the increased amount of regurgitant blood, and there is in consequence congestion in the lungs, and the right ventricle finds the pressure ahead in the lungs greater than it can well overcome. The right ventricle, in its turn being overworked, becomes dilated, and as a result of the inability of the right ventricle to evacuate its contents perfectly, the right auricle is unable to force its venous blood into the right ventricle, and there is then a damming back and sluggish circulation in the superior and inferior venae cavae. The results of these circulatory deficiencies are, in the first place, congestion of the lungs and dyspnea; in the second place, with the impaired force of the left ventricle making the arterial circulation imperfect, and with the impaired return of venous blood to the right auricle making the venous circulation sluggish, passive congestions of various organs occur and are evidenced in headache and venous congestion of the eyes and throat, with perhaps cerebral irritability, sleeplessness, and inability to do good mental work. The sluggish return of the blood in the inferior vena cava causes primarily a sluggish portal circulation with a passive congestion and enlargement of the liver. This causes imperfect bile secretion and an imperfect antidotal action to the various toxins of the body or to any alkaloidal drugs or poisons ingested. This congestion of the liver causes a damming back of the blood in the various veins of the portal system, which causes congestion of the stomach and of the mucous membrane of the bowels, and an imperfect secretion of the digestive fluids of these structures. There is also congestion of the spleen. The imperfect return of the blood through the inferior vena cava also interferes with the return of the blood through the renal veins, and more or less renal congestion occurs, with a concentrated urine and perhaps an albuminuria as the result. The same sluggish flow of the inferior vena cava blood, plus the imperfect tone of the systemic arterial system, means that the circulation at the distal portions of the body—the feet and the legs—is imperfect when the patient is up and about, with the result of causing pendant edemas, which disappear at night when the patient is at rest and the heart more easily accomplishes its work.

The physical signs of such a heart, the increased valvular murmur or murmurs, its irregular action, possibly intermittence or irregular contractions of different parts of the heart, causing diocrotic or intermittent pulse with a lowered blood pressure, are all signs readily found. The quickened respiration is Nature's method of aiding the return circulation in the veins by increasing the negative pressure in the chest. The increased number of pillows the patient requires at night is to aid Nature's need to have a better venous return circulation in the vital centers at the base of the brain.

The dry, troublesome, tickling cough is generally due to a congestion of the blood vessels at the base of the tongue, in the lingual tonsil region, or possibly in the larynx. Later the passive congestion of the lungs may be sufficient to cause a bronchitis, with cough and expectoration.

Sometimes, as indicative of primary cardiac distress, these patients have sharp pains through the heart. Such pains are the exception rather than the rule, and are more likely to occur in chronic myocarditis or in coronary disease: in other words, in true angina pectoris.

If there is considerable venous congestion there may be more or less frequent recurrent venous hemorrhages. This frequently is an epistaxis, or a bleeding from hemorrhoids, or in women profuse menstruation or a metrorrhagia.

It is perfectly understandable from the physics of the condition of broken compensation that anything which improves the tone of the heart and makes it again compensatory removes all of these many disabilities, congestions and subacute inflammations. If, however, these passive congestions are long continued, some organs soon become chronically degenerated. This is especially true of the liver and kidneys.

PHYSICS OF MITRAL STENOSIS

Mitral stenosis, though less common than mitral regurgitation, is a frequent form of disease of the valves, especially in women. Often this condition is associated with regurgitation; but in a simple mitral stenosis the greatest hypertrophy is of necessity in the right ventricle. The left auricle finds it difficult to empty all of its blood into the left ventricle during the ordinary diastole of the heart. This auricle then somewhat hypertrophies, but is unable to prevent more or less damming back of the blood into the lungs through the pulmonary veins. This causes passive congestion of the lungs, and the right ventricle finds that it must labor to overcome the increased resistance in the pulmonary artery, and hypertrophies to overcome this increased amount of work. When this condition has become perfected, compensation is established and the circulation is apparently normal. Nature causes these hearts, when they are disturbed or excited, to pulsate slowly, causing the diastole to be longer than in a heart with mitral regurgitation. This allows more blood to enter the left ventricle, and the left ventricle, acting perfectly on the blood which it receives, causes a good systolic pressure in the aorta and the systemic arteries. The left ventricle in this condition does not become hypertrophied. If the heart does act rapidly and the left ventricle contracts on an insufficient amount of blood, the peripheral pulse is necessarily small and the arterial tension is diminished. Very constant in this condition, and of course noticeable whenever there is pulmonary congestion, is the sharp, accentuated closure of the pulmonary valve. The lungs on the least exertion are always a little overfilled with blood. The pulmonary circulation is always working at a little disadvantage.

The first symptoms of lack of compensation with the lesion of mitral stenosis are lung symptoms—dyspnea, cough, bronchitis, slight cyanosis, sometimes blood streaks in the expectorated mucus and froth, and, if the congestion is considerable, some edema of the posterior part of the lungs, if the patient is in bed. Sooner or later during this failing compensation the right ventricle becomes dilated, and the symptoms of cardiac insufficiency and venous congestion occur, as described above with mitral insufficiency.

Again, as in mitral insufficiency, if compensation is restored in mitral stenosis, these symptoms are improved. These patients, however, are never quite free from dyspnea on exertion. Any inflammation of the lungs, even a severe bronchitis, is more or less serious for the patients and their hearts. The mucous membrane of their bronchial tubes and air vesicles is always hyperemic, and it takes little more congestion to all but close up some of the passages. and dyspnea or asthma, or suffocating, difficult cough is the consequence.

PHYSICS OF AORTIC LESIONS

Next in frequency to mitral insufficiency is aortic insufficiency, which occurs most frequently in men. The cavity of the heart that is most affected by this lesion is the left ventricle, which receives blood both from the left auricle, and regurgitantly from the aorta. This part of the heart, being the strongest muscular portion, is the part most adapted to hypertrophy, and the hypertrophy with this lesion is often enormous. For a long time this large muscular section of the heart can overcome all difficulties of the aortic insufficiency. The pulse, however, will always show the quickly lost arterial pressure of every beat on account of the aorta losing its pressure through the regurgitant flow of blood. Sooner or later, from the impaired aortic tension causing a diminished or imperfect flow of blood through the coronary arteries, impaired nutrition of the heart muscle occurs. In other words, an intestinal or chronic myocarditis or fibrosis develops, with perhaps later a fatty degeneration. When this condition occurs, of course, the repair of the heart is impossible.

This form of valvular lesion is the one that is most likely to cause sudden death. In aortic regurgitation Nature causes the heart to beat rapidly. Such a heart must never beat slowly, as the longer the diastole prevails the more blood will regurgitate into the left ventricle, and death may occur from sudden anemia of the base of the brain. Such a heart may, of course, receive a sudden strain, or the left ventricle may dilate, and yet serious myocarditis or fatty degeneration may not have occurred.

The signs of lack of compensation are generally cardiac distress, rapid heart, insufficiency of the systolic force of the left ventricle, and therefore impaired peripheral circulation, a sluggish return circulation, pendent edemas, and soon, with the left auricle finding the left ventricle. insufficiently emptied, the damming back of the blood is in broken compensation with the mitral lesions.

AORTIC STENOSIS

Aortic narrowing or stenosis is a frequent occurrence in the aged and in arteriosclerosis when the aorta is involved. It is not a frequent single lesion in the young. If it occurs in children or young adults, it is likely to be combined with aortic regurgitation, meaning that the valve hay been seriously injured by an endocarditis.

The first effect of this narrowing is to cause hypertrophy of the left ventricle, and as long as this ventricle is able to force the blood through the narrowed opening at the aortic valve, the general circulation is perfect. Nature again steps in to cause such a heart to heat deliberately, allowing time for the contracting ventricle to force the blood through the narrowed orifice. The blood pressure may be sufficient, or even increased if arteriosclerosis is present, although the rise of the sphygmograph tracing is not so high as normal. If the pressure in the aorta is sufficient from the amount of blood forced into it, the coronary arteries receive enough blood to keep up the nutrition of the heart muscle. Sooner or later, however, the left ventricle will become weakened, especially when there is arteriosclerosis or other hypertension, and chronic endocarditis and fatty degeneration result. If the left ventricle becomes sufficiently weakened or dilated, the same damming back of the blood through the lungs and right heart occurs, and more or less serious signs of broken compensation develop. The main danger, however, with a heart with this lesion, occurring coincidently with arteriosclerosis, is a progressive chronic myocarditis.

OTHER LESIONS

Tricuspid insufficiency, except as rarely found in the fetus, is generally due to a relative insufficiency rather than to an actual disease of the tricuspid valve. In other words, if the right ventricle dilates the valve may be insufficient. Tricuspid stenosis, pulmonary stenosis and pulmonary insufficiency are rare, and are probably nearly always congenital.

The diagnosis as to whether the murmurs heard in the heart are hemic, functional, accidental, or indicative of valvular lesions would be without the scope of this book. It is always presumed that a correct diagnosis has been made, or at least a presumptively correct diagnosis. Frequently more than one murmur and more than one lesion in a heart are present. Often one murmur denotes a permanent lesion, and another may be one that will become corrected when compensation is improved.

SYMPTOMATOLOGY AND TREATMENT OF CHRONIC VALVULAR LESIONS

Before discussing the treatment of broken compensation in general, it may be well to describe briefly the differences in the symptoms and treatment of the various valvular lesions.

MITRAL STENOSIS: MITRAL NARROWING

This particular valvular defect occurs more frequently in women than in men, and between the ages of 10 and 30, and is generally the result of rheumatic endocarditis or chorea, perhaps 60 percent of mitral stenosis having this origin. Other causes are various infections or chronic disease, such as nephritis. Of course, like any valvular lesion, it may be associated with other lesions, and sooner or later in many instances, when the left ventricle becomes dilated or weakened, mitral insufficiency also occurs.

It has sometimes seemed that high blood pressure has caused the left ventricle to act with such force as to irritate this mitral valve, and later develop from such irritation a sclerosis or narrowing, and stenosis occurs. It has been suggested that, though lime may be of advantage in heart weakness, as will be stated later, if the blood is overfull of calcium ions the valvular irritations may more readily have deposits of calcium, in other words, become calcareous, and therefore cause more obstruction. It is quite likely, however, that this sort of deposit is only a piece of the general calcification of tissue in arteriosclerosis and old age, and could not be caused by the administration of calcium to a younger patient, and might then occur in older patients even if substances containing much calcium were kept out of the dict. Calcium metabolisim in arteriosclerosis and in softening of the bones is not well understood.

Patients with this lesion are seriously handicapped when any congestion of the lungs occurs, such as pneumonia, pleurisy, or even bronchitis. Asthma is especially serious in these cases, and these patients rarely live to old age.

The pulse is generally slow, unless broken compensation occurs; dyspnea on exertion is a prominent symptom; the increased secretion of mucus in the bronchial tubes and throat is often troublesome, and there is liable to be considerable cough. If these patients have an acute heart attack, a feeling of suffocation is their worst symptom and the dyspnea may be great, although there may be no tachycardia, these hearts often acting slowly even when there is serious discomfort. When compensation fails, there is an occurrence of all the usual symptoms, as previously described.

The distinctive diagnostic physical sign of this lesion is the diastolic and perhaps presystolic murmur heard over the left ventricle, accentuated at the apex and transmitted some distance to the left of the heart. There is also an accentuated pulmonary closure. To palpation this lesion often gives a characteristic presystolic thrill at and around the apex.

The first symptoms of weakening of the compensation are irregularity in the beat and venous congestion of the head and face, causing bluing of the lips, often nosebleed, and sometimes hemoptysis and insomnia. Later the usual series of disturbances from dilatation of the right ventricle occurs. As previously stated, with the absence of good coronary circulation and the consequent impaired nutrition, the left ventricle may also dilate and the mitral valve may become insufficient. Sudden death from heart failure may occur with this lesion more frequently than with mitral insufficiency but less frequently than with aortic insufficiency.

A particularly dangerous period for women with this lesion is when the blood pressure rises after the menopause and the patients become full-blooded and begin to put on weight. Also, these patients always suffer more or less from cold extremities. In most cases they sleep best and with least disturbance with the head higher than one pillow.

Besides the usual treatment for broken compensation in patients with this lesion, digitalis is of the greatest value, and the slowing of the heart by it, allowing the left ventricle to be more completely filled with the blood coming through the narrowed mitral opening during the diastole, is the object desired. This drug acts similarly on both the right and left ventricles, and though there is no real occasion for stimulation of the left ventricle, and it is the right ventricle that is in trouble, dilated and failing, still a greater force of left ventricle contraction helps the peripheral circulation. The action on the right ventricle contributes greatly to the relief of the patient by sending the blood through the lungs and into the left auricle more forcibly. and the left ventricle receives an increased amount of blood, the congestion in the lungs is relieved, and the dyspnea improves. Perhaps there is no class of cardiac diseases in which more frequent striking relief can be obtained than in these cases of mitral stenosis.