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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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 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.
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.
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.
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.
If the congestion of the lungs is very great, and death seems imminent from cardiac paralysis, if cyanosis is serious, and bloody. frothy mucus is being expectorated, venesection and an intramuscular injection of aseptic ergot may be indicated. Digitalis should also be given, hypodermically perhaps, but its action would be too late if it was not aided by other more quickly acting drugs. The physician may often save life by such radical measures.
This is the most frequent form of valvular disease of the heart, and is due to a shortening or thickening of the valves, or to some adhesion which does not permit the valve, to close properly, and the blood consequently regurgitates from the left ventricle into the left auricle during the contraction of the ventricle. Such regurgitation may occur without valvular disease if for any reason the left ventricle becomes dilated sufficiently to cause the valve to be insufficient. Such a dilatation can generally be cured by rest and treatment. As with mitral stenosis, the most frequent causes are rheumatism and chorea, with the occasional other causes as previously enumerated.
The characteristic murmur of this lesion is a systolic blow, accentuated at the apex, transmitted to the left of the thorax, generally heard in the back, near the lower end of the scapula, and transmitted upward over the precordia.
Of all cardiac lesions, this is the safest one to have. Sudden death is unusual, the compensation of the heart seems to be most readily maintained, and the patient is not so greatly dangered by overexertion or by inflammations in the lungs. As in mitral stenosis, any increase in blood pressure—whether the normal increase after the age of 40, any continued earlier high tension, or increase from occupation or exercise—is serious as causing the left ventricle to act more strenuously, so that more blood is forced back into the left auricle, the lungs become congested, and the right ventricle, sooner or later, becomes incompetent.
When compensation fails with these patients, the first sign is pendent edema of the feet, ankles and legs; subsequently, if there is progressive failure of compensation, the usual symptoms occur.
The treatment is principally rest and digitalis, and the recovery of compensation is often almost phenomenal. Patients with this lesion are likely to be children and young adults, and the heart muscle readily responds as a rule to the treatment inaugurated. Later, in these patients, or if the lesion occurs in older patients, the return to compensation does not occur so readily. If the condition is developed from a myocarditis or from fatty degeneration of the heart, it may be impossible to cause the left ventricle to improve so much as to overcome this relative dilatation or relative insufficiency of the valve. If the dilatation of the left ventricle is due to some poisoning such as nicotin, with proper treatment— stopping the use of tobacco, administration of digitalis, and rest— the heart muscle will generally recover and the valve again properly close.
Valvular disease at the aortic orifice is much less common than at the mitral orifice, and while stenosis or obstruction is less common from rheumatism or acute inflammatory endocarditis than is insufficiency of this valve, a narrowing or at least the clinical sign of narrowing, denoted by a systolic blow at the base of the heart over the aortic opening, is in arteriosclerosis and old age of frequent occurrence. If such narrowing occurs without aortic insufficiency at the age at which it usually occurs, it may not seriously affect the heart. It may follow acute endocarditis, but it most frequently follows chronic endocarditis or atheroma, in which the aortic valves become thickened and more or less rigid; this condition most frequently occurs in men.
Anything that tends to increase arterial tension, as tobacco, lead or hard work, or anything that tends to cause arterial disease, as alcohol or syphilis, is often the cause of this lesion.
At times the edges of the valves may grow together from ulcerative inflammation, and the lumen thus be diminished in size; or projecting vegetations may interfere with the opening of the valve and with the flow of blood. With such narrowing the left ventricle more or less rapidly hypertrophies to overcome its increased work.
The murmur caused by this lesion is a systolic one, either accentuated in the second intercostal space at the right of the sternum, or perhaps heard loudest just to the left of the sternum in this region. The murmur is also transmitted up the arteries into the neck, and may at times be heard in the subclavian arteries. It may also be transmitted downward over the heart. The pulse is slow, the apex of the rise of the sphymographic arterial tracing is more or less sustained and rounded, and the rise is much less than normal.
If this lesion occurs in old age, there is general arterial disease present, and the tension and compressibility of the arteries vary, depending on how much they are hardened. The disturbed circulation is evidenced by imperfect peripheral circulation and capillary sluggishly, with at times pendent edema of the feet and ankles, but, perhaps, little congestion of the lungs. The left ventricle being sufficient, there is no damming back through the left auricle to the lungs. The left ventricle may, however, become weakened, either by some sudden strain or by a chronic myocarditis, and relative insufficiency of the mitral valve may occur. The subsequent symptoms are typically those of loss of compensation.
This lesion may allow a patient to live for years, provided no other serious disturbance of the heart occurs, such as myocarditis or coronary disease; but sooner or later, with the failing force of the blood flow and the lessened aortic pressure, slight attacks of anemia of the brain occur, causing syncope or fainting. Also, sooner or later these patients have little cardiac pains. They begin to "sense" their hearts. There may not be actual anginas, but a little feeling of discomfort, with perhaps pains shooting up into the neck, or a feeling of pressure under the sternum. Little excitements or overexertions are likely to make the heart attempt to contract more rapidly than it is able to drive the blood through the narrowed orifice, and this alone causes cardiac discomfort and the feeling of cardiac oppression.
It is essential, then, that these patients should not hasten and should not become excited; and any drug or stimulant which would cause cardiac excitement is bad for them. On the other hand, these are the very patients in whom, sometimes, alcohol in small doses may be advisable, especially if the patient is old; and a dose of alcohol used medicinally when an attack of cardiac disturbance is present is good treatment. The quick dilatation is valuable. Nitroglycerin will also do good work in these cases, and with high blood tension may be the only safe drug for the patient to have on hand. As soon as his attack occurs, with or without real angina pectoris, let him dissolve in his mouth a nitroglycerin tablet. If he feels faint, he will feel better the moment he lies down, and in this instance he may be improved by a cup of coffee, or a dose of caffein or camphor.
If the left ventricle becomes still weaker and shows signs of serious weakness, or if there is actual dilatation, the question of whether or not digitalis should be used is a subject for careful decision. The left ventricle should not be forced to act too sturdily against this aortic resistance. Consequently the dose of digitalis must be small. On the other hand, it frequently happens, especially in old age, that myocarditis or fatty degeneration has already occurred before this cardiac weakness develops in the presence of aortic narrowing, and digitalis may not be indicated at all. We cannot tell how far degeneration may have gone, however, and small doses of digitalis used tentatively and carefully, perhaps 5 drops of an active tincture two or three times a day, and then the drug carefully increased to a little larger dose to see whether improvement takes place, is the only way to ascertain whether or not digitalis can be used with advantage. If it increases the cardiac pain and distress, it should not be used. Strychnin is then the drug relied on, with such other general medication as is needed, combined with the coincident administration of nitroglycerin, which may also be given in conjunction with digitalis, if deemed advisable. Generally, however, if a heart with aortic stenosis needs stimulation, the blood pressure is generally none too high, although there may be arteriosclerosis present. Therefore when nitroglycerin is indicated to lower blood pressure, digitalis is not usually indicated; when digitalis is indicated to aid the heart, nitroglycerin is generally not indicated. These patients must have high blood pressure to sustain perfect circulation at the base of the brain.
Patients who have this lesion should not use tobacco in large amounts, or sometimes even small amounts, as tobacco raises the blood pressure and thus puts more work on the left ventricle; in the second place, if the left ventricle is failing, much tobacco may hasten its debility. On the other hand, with a failing left ventricle and a long previous use of tobacco, it is no time to prohibit its use absolutely. A failing heart and the sudden stoppage of tobacco may prove a serious combination.
This lesion, though not so common as the mitral lesion, is of not infrequent occurrence in children and young adults as a sequence of acute rheumatic endocarditis. If it occurs later in life it generally is associated with aortic narrowing, and is a part of the general endarteritis and perhaps atheroma of the aorta. Sometimes it is caused by strenuous exertion apparently rupturing the valve.
This form of valvular disease frequently ends in sudden death. On the other hand, it is astonishing how active a person may be with this really terrible cardiac defect. This lesion, from the frequent overdistention of the left ventricle, is one which often causes pain. While the left ventricle enlarges enormously to overcome the extra distention due to the blood entering the ventricle from both directions, the muscle sooner or later becomes degenerated from poor coronary circulation. Unless the left ventricle can do its work well enough to maintain an adequate pressure of blood in the aorta, the coronary circulation is insufficient, and chronic myocarditis is the result. If the left ventricle has maintained this pressure for a long time, edemas are not common unless the cardiac weakness is serious and generally permanently serious: that is, slight weakness, in this lesion, does not give edemas as does slight loss of compensation in mitral disease, and unless the weakness of the ventricle is serious, the lungs are not much affected.
The physical sign of this lesion is the diastolic murmur, which is loudest of the base of the heart, is accentuated over the aortic orifice, and is transmitted up into the neck and the subclavians, and down over the heart and down the sternum with marked pulsation, of the arteries (Corrigan pulse) and often of some of the peripheral veins, notably of the arms and throat.
If the left ventricle becomes dilated the mitral valve may become insufficient, when the usual lung symptoms occur, with hypertrophy of the right ventricle; and if it fails, the usual venous symptoms of loss of compensation follow. This lesion not infrequently causes epistaxis, hemoptysis and hematemesis.
Digitalis is always of value in these cases, but it should not be pushed. If a heart is slowed too much, the regurgitation into the left ventricle is increased. Therefore such hearts should not be slowed to less than eighty beats per minute, or sudden anemia of the brain and sudden death may occur. These patients must not do hard work.
This rarely, if ever, occurs alone; it is generally a sequence of other valvular defects, and represents an overworked, dilated right ventricle. It may, however, occur from lesions of the lungs which impede the blood flow through them. Such are fibroid changes in the lungs, emphysema, prolonged chronic bronchitis, the last stages of pulmonary tuberculosis, old neglected pleurisies with cirrhosis or fibrosis of the lung, and repeated attacks of asthma—anything, whether valvular defect or pulmonary circulatory disturbance, which increases the pressure ahead and the work of this ventricle.
The symptoms are those of loss of compensation as described under other valvular lesions. There may be jugular pulsation, especially evident in the external jugular on the left side. The liver enlarges and may pulsate. There are edemas, dropsies, ascites and perhaps hemorrhages. The heart is enlarged and there is a soft systolic blow heard at the lower end of the sternum. The dyspnea is sometimes very great, and cyanosis may be present, especially during paroxysms of coughing.
This lesion of the heart is always benefited by digitalis, but the continuance of the improvement and its amount depend, of course, on the cause of the dilatation of the ventricle. Strychnin is often of advantage. These patients should rarely receive vasodilators, and hot baths, overheating, overloading the stomach and vigorous purging should never be allowed. Sometimes improvement will not take place until ascitic or pleuritic fluid, if present, has been removed.
This is rare and probably always congenital, and is supposed to be due to an inflammation of the endocardium during intra-uterine life. In early childhood it is possible that it may be associated with left-side endocarditis.
A special treatment of the heart, if any is needed, would probably not be indicated unless there was associated tricuspid insufficiency, when digitalis might be used.
If this rare condition occurs, it is probably congenital. A distinctive murmur of this insufficiency would be diastolic and accentuated in the second intercostal space on the left of the sternum. It should be remembered that aortic murmurs are often more plainly heard at the left of the sternum. Sooner or later, if this lesion is actually present, the right ventricle dilates and cyanosis and dyspnea occur. Digitalis would therefore be indicated.
If stenosis is actually present in this location, the lesion is probably congenital. It might occur after a serious acute infectious endocarditis, but then it would be associated with other lesions of the heart. It has been found to be associated with such congenital lesions of the heart as an open foramen ovale or foramen Botalli, or with an imperfect ventricular septum, and perhaps with tricuspid stenosis—in short, a cardiac congenital defect. The right ventricle becomes hypertrophied, if the child lives to overcome the obstruction.
The physical sign is a systolic blow at the second intercostal space on the left; but as just stated, such a murmur must surely be dissociated from an aortic murmur if found to develop after babyhood, and it should also be diagnosed from the frequently occurring hemic, basic and systolic murmurs; that is, if signs of pulmonary lesions are not heard soon after birth or in early babyhood, the diagnosis of pulmonary defects can be made only by exclusion.
Unless the right ventricle is found later to be in trouble, there is no treatment for this condition. If the right ventricle dilates, digitalis may be of benefit.
It is not proposed here to describe the condition of sudden cardiac failure, or acute dilatation during disease, or after a severe heart strain, but to describe the terrible cardiac agony which occurs, sometimes repeatedly, with many patients who have valvular lesions. These patients may not have the symptoms of loss of compensation. Probably some one or more chambers of the heart become overdistended and act irregularly, or the blood is suddenly dammed up in the lungs, with the oppression and dyspnea caused by such passive congestion, or perhaps it is the right ventricle that is suddenly in serious trouble.
A physician receives an emergency call, and knows, if it is not a patient who has hysteria, that it is his duty to see the patient immediately. The friends of the patient all anxiously await the physician's arrival; front doors are often wide open, and the servants and the whole household are in a great state of excitement and anxiety. The position in which the patient will be found is that which he has learned gives him the greatest comfort. If the physician knows his patient, he will know how he will find him. He may lie sitting up in bed; he may be standing, leaning over a chair; he may be sitting in a chair leaning over a table or leaning over the back of another chair; but he is using every auxiliary muscle he possesses to respire. He is generally bathed in cold perspiration; the extremities are often icy cold; he calls for air, and to stop fanning all in one breath; he wishes the perspiration wiped off his brow, and nearly goes frantic while it is being done; there is agony depicted on his face; his eyes stare; his expirations are often groaning. Sometimes there is even incontinence of urine and feces, often hiccup or short coughs, perhaps vomiting, and possibly sharp pangs of pain in the cardiac region. A patient with these symptoms may die at any moment, and the wonder is that so many times one lives through these paroxysms.
The patient can hardly be questioned, can certainly not be carefully examined; and herein lies the advantage of the family physician who knows the patient and his heart, and in whom the patient has confidence.
In fact, this confidence which such a patient has in the physician who has more or less frequently aided him in weathering these terrible attacks is alone the greatest boon the patient can have.
The immediate conditions to meet are the rapid fluttering heart, the nervous excitation and cardiac anxiety, and perhaps the most important of all, the vasomotor spasm that is often so pronounced. Physically we have, then, a heart with leaking or constricted valves; in either case more blood is entering the chambers of the heart than can be expelled in one contraction, while the peripheral resistance due to the spasm of the blood vessels, because of fear, becomes greater every minute and tends still more to interfere with the peripheral circulation and the complete emptying of the heart of its surplus blood. Owing to the well known stimulus to distention of hollow muscular organs, the heart contracts faster and faster.
Soon, by some disarrangement of the inhibitory apparatus, the pneumogastric nerves, the heart loses its governor, and the beats increase to even 150 a minute, with irregular contractions, the blood being sent through the arteries with irregular force, as evidenced by the varying volume of the pulse. At this time, with or without cardiac pain, which upsets the rhythm of the heart, the patient becomes frightened at the feeling of impending demise, and the cerebral reflexes begin to add to the cardiac difficulty. The breathing becomes nervously rapid, besides that which is due to the rapid heart. The chill of fear is added to the already contracted peripheral vessels, and the surface of the body becomes cold, the extremities sometimes intensely so. Next it seems as if the strongly contracted arterioles begin actually to prevent some of the peripheral circulation, the blood is piled up in the large arteries, and the venous circulation becomes more and more sluggish, while the lips, finger nails and forehead become cyanotic. Respiration becomes more rapid and deep; the inspiration being as strong as possible with every auxiliary muscle taking part, thus making the negative pressure in the chest aid in bringing the blood back through the veins. Part of the extra respiratory stimulus comes from the imperfectly aerated blood reaching the respiratory center.
Two factors may normally, without treatment, stop these paroxysms, and the "bad heart turn" may be cured spontaneously. The first of these is self-control. If the patient does not lose his head, by an effort of the will he saves himself from becoming nervous or frightened and therefore escapes the result of mental excitement; the increased peripheral blood pressure from fear does not occur, and in a shorter or longer time the heart quiets down. The physician recognizes this power, and gives his patient immediate assurance that he will soon be all right; the patient who knows his physician immediately feels this assurance and is quickly improved.
The second factor in spontaneous cure of the heart attack is relaxation. The exhaustion from the respiratory muscular efforts, together with the drowsy condition caused by the cerebral hyperemia and from the imperfectly aerated blood, causes finally a dulling of the mental acuity, and the nervous excitement abates, which, with the exhaustion, gives a relaxation of peripheral arterioles: the resistance to the flow of the blood is removed, the surface of the body becomes warm, the heart quiets down by the equalization of the circulation, and the paroxysm is over.
The part the nervous system plays in this paroxysm is shown by the good result obtained from injections of morphin, even when there is no pain; hence the action of morphin is directly in line with the natural resolution of the symptoms: it quiets the nervous system, causes drowsiness, relaxes spasm, and thus causes increased peripheral circulation; many times this is the only treatment necessary.
During these heart attacks it is more than useless to administer any drug by the stomach, as in this condition there will be no absorption, even if there is no vomiting.
While morphin is generally indicated, as just suggested, a very large dose should not be given, lest the activity of the respiratory center be impaired (it is already in trouble), and undoubtedly death may easily be caused by an overaction of morphin during these heart attacks. The addition of atropin to the morphin will prevent depression from the morphin. Also, atropin sometimes quiets cardiac pain, but it will not steady the heart, may irritate it, and will increase vasomotor tension, although peripheral nerve irritation may be diminished. Hence a fair dose of morphin hypodermicaly with a small dose of atropin, if respiratory depression is feared, is a physiologic method of bettering the condition. In this kind of heart attack a drug which often acts well is nitroglycerin. It may be given hypodermically in a dose of from 1/200 to 1/100 grain, or a tablet may be dissolved on the tongue, and the dose be repeated once or twice at fifteen-minute intervals, until there is throbbing in the forehead, which shows that a sufficient amount of the drug has been administered. This headache will generally not last long. In the meantime the peripheral blood vessels are relaxed, the surface of the body becomes warm, the heart quiets, and the attack is over. To hasten the action of nitroglycerin (that is, to equalize the circulation) a hot foot-bath is often valuable. Amyl nitrite may be inhaled with the same object in view, but the action is very intense, the prostration often severe, and unless there is angina pectoris, nitroglycerin is much better.
The symptoms of a heart attack may not be quite those described above; they may be those of sudden dilatation or semiparalysis of the heart, in which the prostration is intense and the patient is unable to sit up, although he may be leaning against several pillows. There is dyspnea, but the patient cannot aid respiration with the auxiliary muscles by holding the arms and shoulders tense or obtaining support from the aruls; in fact, the arms are almost strengthless. The surface of the body may be warm, and the arms may be warm except the hands; the feet, ankles and legs may be cold. There is generally more or less cyanosis, although the face may be pale. The finger nails often show venous stasis. In these cases the blood pressure is subnormal, the pulse may be hardly perceptible, and there is none of the tension of the body from fear. The patient may be fearful, but lie is completely collapsed. Such an attack may occur suddenly in a heart that is perfectly compensating, or it may accompany general edemas and dropsies.
If the emergency is excessively urgent, the lungs filling up with blood, moist rales beginning to occur, and frothy and blood-tinged sputum being coughed up, venesection may be indicated; combined with proper hypodermic medication it may save life, and does at times. In fact, a patient who shows every sign of fatal cardiac collapse may be saved. (one of the best drugs to administer to such patient is an aseptic ergot, injected intramuscularly.) The drug of all drugs for future action (as it will not act immediately) is digitalis, given hypodermically.
Whether digitalis shall be given at all, or how large the dose shall be depends on whether or not the patient has been taking digitalis in large quantities.
He may already be overpowered with digitalis. In that case it would be contraindicated.
Stroplianthin, especially when given intravenously, has been found to be a quickly acting circulatory stimulant. The dose of strophanthin, Merck, ranges from 1/500 to l/200 grain. The intravenous dose of strophanthin, Thoms, is about 1/130 grain. It should not be repeated within a day or two, if at all. Ampules of strophanthin in solution for intravenous use are now available.
Atropin in a dose of 1/150 grain, and strychnin in a dose of 1/40 or 1/30 grain are valuable aids in stimulating the circulation under these conditions. The atropin should not be repeated. The strychnin may be repeated in three, four or five hours, depending on the size of the previous close.
Of all quickly acting stimulants, none is better than camphor in saturated solution in sterile oil as may be obtained in ampules. Alcohol is absolutely contraindicated in the latter condition. In the former kind of heart attack, vasodilation from a large close of whisky or brandy may be of value. The dose should be large to cause immediate increased peripheral circulation, dilation, and even a little stupefaction of the central nervous system, and it may be effectual in a way not dissimilar to the action of morphiti.
The consideration of this subject will include the following topics:A. Hygiene.B. Diet.C. Elimination.D. Physical measures.E. Medication.1. Cardiac Tonics: Digiralis, strophanthus, caffein, strychnin.2. Cardiac Stimulants: Camphor, alcohol, ammonia.3. Vasodilators: Nitrites, iodids, thyroid extract.4. Cardiac Nutritives: Iron, calcium.5. Cardiac Emergency Drugs: Ergot, suprarenal active principle,pituitary active principle, atropin, morphin, and also someof the drugs already mentioned.
Of all treatment for broken compensation or dilated heart, nothing equals rest in bed. Sometimes it is the only treatment that is needed. The rigidness of this rest, the length of time that it should endure, and the period at which relaxation of such rest should be allowed depend entirely on the individual patient; no rule can be established. Most of the symptoms must disappear before exercise is allowed. Perhaps a not infrequent exception to the rule is when cardiac weakness, generally a inyocarditis, develops in a patient after 50. It is not always wise to keep such a patient in bed; he may be rested and his exercise greatly restricted, but sometimes it is difficult to get him out of bed if he is kept there any length of time.