Disturbances of the Heart Part 11

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; compet.i.tive 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 pa.s.sive 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 accomplis.h.i.+ng 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, pa.s.sive 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 pa.s.sive 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 alb.u.minuria 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 pa.s.sive 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 pa.s.sive 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 a.s.sociated 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 pa.s.sive 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 pa.s.sages. 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