A system of practical medicine. By American authors. Vol. 3

by Unknown

In some instances lime salts and large masses of chalky matter are found imbedded in the indurated valves. In such cases the surface and edges of the valves are so rough and jagged that more or less obstruction accompanies the regurgitation.

All these changes, except calcification, may also occur in the chordæ tendineæ and columnæ carneæ. The valves may also become adherent to the walls of the ventricles, or as a result of the shrinking and shortening of the chordæ tendineæ the valve-flaps may not pass back to the plane of the orifice.

Again, the valves or the chordæ tendineæ may be ruptured, so that the valves are pressed during the cardiac systole back into the auricle. If the chordæ tendineæ which are inserted nearest the centre of the valve become lengthened, that part of the flap will be bent upon itself, having evidently yielded to the blood-pressure, and this allows of regurgitation. Sometimes, when the valves appear perfectly healthy, by the application of the water test they will be found to be insufficient.

The first effect of mitral regurgitation is dilatation of the left auricle, due to the pressure of the two blood-currents during its diastole—one from the lungs, and the other from the left ventricle. This dilatation leads to thickening and hypertrophy of the left auricular walls. Following this, the pulmonary circulation is impeded, the pulmonary vessels enlarge, and they may undergo degeneration as a result of the continued regurgitant pressure.

Passive congestion of the lungs with brown or pigment induration is an early pathological sequel of mitral regurgitation. The constant interference with the return circulation from the lungs obstructs more or less the outward current of blood to the lungs from the right ventricle. As the obstruction is a gradual one, the right ventricle becomes so hypertrophied as to overcome it. Consequently, the hypertrophied right ventricle compensates at first for the mitral regurgitation, and as long as the right ventricle is able to fully overcome the abnormal pressure of the blood in the lungs from the mitral regurgitation, so long the patients are comfortable. Sooner or later, however, the compensatory hypertrophy of the right ventricle ceases, and a secondary dilatation occurs which admits of no compensation.

This final dilatation of the right ventricle is favored by the myocardial degeneration, which occurs as a result of defective nutrition of the heart-walls; when this condition is reached the veins throughout the body are placed in a similar condition to those in the lungs.

This general venous congestion is indicated by passive hyperæmia of the abdominal viscera and by cyanosis of the surface during active physical exercise.

The liver is the organ first affected, on account of its great vascularity and from the fact that the hepatic veins do not collapse readily and possess no valves. Thus the liver becomes enlarged and stony (the nutmeg liver) as a result of the obstruction to the emptying of the hepatic vein, and when there is coexistent obstruction of the bile-ducts jaundice will be present.

This portal obstruction induces passive hyperæmia of the intestines and stomach, enlargement of the spleen, and large and painful hemorrhoidal tumors. The impediment to the return of blood from the brain causes cerebral congestion; from the kidney, renal congestion; and, finally, the obstruction to the systemic venous return leads to the accumulation of fluid in the areolar tissue and in the cavities. This dropsy generally begins in the feet and extends upward. In females the obstruction in the vena cava inferior induces derangements of the menstrual functions. Ascites, hydrothorax, hydro-pericardium, and pulmonary oedema may subsequently develop.

In addition to these changes, the dilated and hypertrophied left auricle throws an abnormal quantity of blood with abnormal force into the left ventricle during its diastole, which leads to dilatation of its cavity and necessitates a compensatory hypertrophy of the left ventricular walls. This hypertrophy of the left ventricle increases the force of the reflux current, so that during excitement and active physical exertion pulmonary congestion, oedema, and cerebral apoplexy are liable to occur. In many cases of mitral regurgitation, when the venous engorgement is excessive, general dropsy is favored by the anæmia produced by the obstruction of the thoracic duct.