To understand the physiology, pathology and the best treatment for broken compensation, it is necessary to study the physics of the circulation under the different conditions. With the mitral valve insufficient, a greater or less amount of blood is regurgitated into the left auricle, which soon becomes dilated. Distention of any hollow muscular organ, if the distention is not to the point of paralysis, means a greater inherent or reflex attempt of that organ to evacuate itself; the muscular tissue begins to grow, and a hypertrophy of the left auricle with the above-named lesion develops. The muscular tissue of the auricle, however, is not sufficient to allow any great hypertrophy. The blood flowing from the pulmonary veins into the left auricle finds this cavity already partly filled with blood regurgitated from the left ventricle. The pulmonary blood, being impeded, tends to flow more slowly, and therefore dams back into the lungs, causing a passive congestion of the lungs. The pulmonary artery thus finds the pressure ahead unusually great, and the right ventricle reflexly learns that it requires a greater force to empty itself than before; in fact, it may not succeed in completely accomplishing this until its distention, by an incomplete evacuation of its contained blood plus the blood coming from the right auricle, has caused the right ventricle also to become hypertrophied. This increased muscular action of the right ventricle relieves the pulmonary congestion, and an increased amount of blood is forced into the left auricle. On account of its hypertrophy, the left auricle is able to send an increased amount of blood into the left ventricle, which in turn becomes hypertrophied and sends enough blood into the aorta to satisfy the requirements of the systemic circulation in spite of the leakage through the mitral valve.
As long as this compensation continues, there are no symptoms. If any dilatation occurs from disease, degeneration or from increased work put on the heart (and it is readily seen how delicate this equilibrium is), signs of broken compensation begin to occur. The left ventricle with its enormous strain is perhaps the first part to dilate, thus enlarging the opening of the defective mitral valve. The left auricle is then unable to cope with the increased amount of regurgitant blood, and there is in consequence congestion in the lungs, and the right ventricle finds the pressure ahead in the lungs greater than it can well overcome. The right ventricle, in its turn being overworked, becomes dilated, and as a result of the inability of the right ventricle to evacuate its contents perfectly, the right auricle is unable to force its venous blood into the right ventricle, and there is then a damming back and sluggish circulation in the superior and inferior venae cavae. The results of these circulatory deficiencies are, in the first place, congestion of the lungs and dyspnea; in the second place, with the impaired force of the left ventricle making the arterial circulation imperfect, and with the impaired return of venous blood to the right auricle making the venous circulation sluggish, passive congestions of various organs occur and are evidenced in headache and venous congestion of the eyes and throat, with perhaps cerebral irritability, sleeplessness, and inability to do good mental work. The sluggish return of the blood in the inferior vena cava causes primarily a sluggish portal circulation with a passive congestion and enlargement of the liver. This causes imperfect bile secretion and an imperfect antidotal action to the various toxins of the body or to any alkaloidal drugs or poisons ingested. This congestion of the liver causes a damming back of the blood in the various veins of the portal system, which causes congestion of the stomach and of the mucous membrane of the bowels, and an imperfect secretion of the digestive fluids of these structures. There is also congestion of the spleen. The imperfect return of the blood through the inferior vena cava also interferes with the return of the blood through the renal veins, and more or less renal congestion occurs, with a concentrated urine and perhaps an albuminuria as the result. The same sluggish flow of the inferior vena cava blood, plus the imperfect tone of the systemic arterial system, means that the circulation at the distal portions of the body—the feet and the legs—is imperfect when the patient is up and about, with the result of causing pendant edemas, which disappear at night when the patient is at rest and the heart more easily accomplishes its work.
The physical signs of such a heart, the increased valvular murmur or murmurs, its irregular action, possibly intermittence or irregular contractions of different parts of the heart, causing diocrotic or intermittent pulse with a lowered blood pressure, are all signs readily found. The quickened respiration is Nature's method of aiding the return circulation in the veins by increasing the negative pressure in the chest. The increased number of pillows the patient requires at night is to aid Nature's need to have a better venous return circulation in the vital centers at the base of the brain.
The dry, troublesome, tickling cough is generally due to a congestion of the blood vessels at the base of the tongue, in the lingual tonsil region, or possibly in the larynx. Later the passive congestion of the lungs may be sufficient to cause a bronchitis, with cough and expectoration.
Sometimes, as indicative of primary cardiac distress, these patients have sharp pains through the heart. Such pains are the exception rather than the rule, and are more likely to occur in chronic myocarditis or in coronary disease: in other words, in true angina pectoris.
If there is considerable venous congestion there may be more or less frequent recurrent venous hemorrhages. This frequently is an epistaxis, or a bleeding from hemorrhoids, or in women profuse menstruation or a metrorrhagia.
It is perfectly understandable from the physics of the condition of broken compensation that anything which improves the tone of the heart and makes it again compensatory removes all of these many disabilities, congestions and subacute inflammations. If, however, these passive congestions are long continued, some organs soon become chronically degenerated. This is especially true of the liver and kidneys.
PHYSICS OF MITRAL STENOSIS
Mitral stenosis, though less common than mitral regurgitation, is a frequent form of disease of the valves, especially in women. Often this condition is associated with regurgitation; but in a simple mitral stenosis the greatest hypertrophy is of necessity in the right ventricle. The left auricle finds it difficult to empty all of its blood into the left ventricle during the ordinary diastole of the heart. This auricle then somewhat hypertrophies, but is unable to prevent more or less damming back of the blood into the lungs through the pulmonary veins. This causes passive congestion of the lungs, and the right ventricle finds that it must labor to overcome the increased resistance in the pulmonary artery, and hypertrophies to overcome this increased amount of work. When this condition has become perfected, compensation is established and the circulation is apparently normal. Nature causes these hearts, when they are disturbed or excited, to pulsate slowly, causing the diastole to be longer than in a heart with mitral regurgitation. This allows more blood to enter the left ventricle, and the left ventricle, acting perfectly on the blood which it receives, causes a good systolic pressure in the aorta and the systemic arteries. The left ventricle in this condition does not become hypertrophied. If the heart does act rapidly and the left ventricle contracts on an insufficient amount of blood, the peripheral pulse is necessarily small and the arterial tension is diminished. Very constant in this condition, and of course noticeable whenever there is pulmonary congestion, is the sharp, accentuated closure of the pulmonary valve. The lungs on the least exertion are always a little overfilled with blood. The pulmonary circulation is always working at a little disadvantage.
The first symptoms of lack of compensation with the lesion of mitral stenosis are lung symptoms—dyspnea, cough, bronchitis, slight cyanosis, sometimes blood streaks in the expectorated mucus and froth, and, if the congestion is considerable, some edema of the posterior part of the lungs, if the patient is in bed. Sooner or later during this failing compensation the right ventricle becomes dilated, and the symptoms of cardiac insufficiency and venous congestion occur, as described above with mitral insufficiency.