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This softening and some swelling of the lower layers of the endocardium allow the pushing up of these extravasated blood cells which, being covered with fibrin, makes the little vegetations above described; and as just stated, the fibrin may form a more or less permanent cap.
It is often difficult to decide when acute endocarditis has developed; but with the knowledge that the endocardium often becomes inflamed during almost any of the acute infections, the physician should repeatedly examine the heart for murmurs, for muffled closure of the valves, or for other evidences of endocarditis or myocarditis during the acute infective process.
*Effect of Rheumatism.*—The disease which affects the heart more frequently than any other is rheumatism. This attacks the lining membrane, or endocardium, and causes, not infrequently, a shrinkage of the heart valves. The heart is thus rendered defective and, to perform its function in the body, must work harder than if it were in a normal condition.
The gonococcus is carried to the joint in the blood-stream and is first deposited in the synovial membrane, in the tissues of which it can usually be found; it may be impossible to find it in the exudate within the joint. The joint lesions may be the only evidence of metastasis, or they may be part of a general infection involving the endocardium, pleura, and tendon sheaths.
In the ventricles, Lewis states, the Purkinje fibers act as the conducting agent, stimuli being conducted to all portions of the endocardium simultaneously at a rate of from 2,000 to 1,000 mm. per second. The ventricular muscle also aids in the conduction of the stimuli, but at a slower rate, 300 mm. per minute.
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.
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.
The greater the amount of myocarditis, the more doubtful is the heart strength in the near future. The greater the amount of endocarditis, the greater the doubt of freedom from future permanent valvular lesions. This inflammation of the endocardium is generally confined to the region of the valves, and the valves most frequently so inflamed are the mitral and aortic.
All the cavities of the heart are lined with a smooth, delicate membrane, called the endocardium. Semilunar valves. 2. Tricuspid valve. 3. Mitral valve. 4. Right auricle. 5. Left auricle. 6. Right ventricle. 7. Left ventricle. 8. Chordæ tendineæ. 9. Inferior vena cava. 10. Superior vena cava. 11. Pulmonary artery. 12. Aorta. 13. Pulmonary veins.
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.
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