ENDOCARDITIS. 



Definition. Pathology and lesions, congestion of the endocardium cover- 

 ing the valves, valves liable through friction and strain, exudation in or on 

 the serosa rendering it opaque, coagula of fibrine on the surface, secondary 

 endocarditis, mycotic, microbes, changes in serosa, distortions and degenera- 

 tions of valves. Symptoms, as in pericarditis, with violent heart impulse 

 of varying force, irregular, intermittent, absence of local tenderness, 

 no fric ion sound, no increase in area of dulness, if lesions are in right 

 heart — venous pulse, venous congestion, dropsies. Valve lesions, in mitral 

 valve — general heart symptoms and murmur with ist heart sound, 2d sound 

 may be repeated and exceptionally a venous pulse — in tricuspid valve — 

 same with constant venous pulse, venous congestion and dropsy ; narrow- 

 ing of the mitral orifice — general heart symptoms and blowing murmur 

 before the ist sound ; narrowing of the tricuspid orifice — same with mur- 

 mur sometimes audible on the right side ; insufficiency of aortic valves — 

 general heart symptoms and murmur with 2d heart sound, double rushing 

 sound in arteries and delay of pulse-beat at jaw ; lesions in pulmonary 

 valves — same but without double rush in arteries, or delay of pulse-beat at 

 jaw. Loose coagula. Embolism. Causes, as in pericarditis and strain on 

 valves, and poisons and microbes in the blood. Prognosis grave. Treat- 

 ment, as in the early stages of pericarditis, antirheumatics and germicides 

 more, and diuretics less desirable. For clots iodides, alkalies. 



Definition. Inflammation of the serous membrane lining the 

 chambers and covering the valves of the heart. 



Pathology and Morbid Anatomy. All cases become complicated 

 by microbian invasion and this infection may be considered as 

 the essential factor in the disease, yet accessory and predisposing 

 causes are hardly less important, as on these depend the suscepti- 

 bility which renders the microbian invasion effective. The acces- 

 sory causes and symptoms will be better understood after the^ 

 diseased conditions have been comprehended. The earliest 

 changes are the reddening and thickening of the lining mem- 

 brane of the heart but above all, of that covering the valves. 

 The valves are particularly exposed to inflammation by reason 

 of the friction of the blood when violently forced through 

 the narrow opening in excited conditions of the heart, by 

 the strain thrown upon them from the violent contractions of 

 the heart, or the recoil of blood in the arteries, and by their 

 susceptibility in common with all other fibrous structures to 



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