Cardiac Hypertrophy. 107 



system, of excessive blood pressure and of unusual quantities 

 of blood within the organ. Such 'Svork-hypertrophy" of the gen- 

 eral organ is met in connection with epicardial adhesion to the 

 parietal pericardium, compression of the base of the heart from 

 pleuritic adhesion, tumors or similar conditions, because in such 

 cases the propulsive effort of the entire organ has a greater oppo- 

 sition to overcome. 



Hypertrophy of one side of the heart is seen especially in case 

 of valvular lesions. These valvular lesions involve irregularities 

 in the closure of the orifices of the heart and its great vessels ; 

 they are of two types, either narrowing of the orifices from pro- 

 liferative changes, bloods clots, etc. (stenosis), or incompleteness 

 of closure of the orifices by the valves {valvular insufficiency). 

 Stenosis at the aortic opening increases the work of the left ven- 

 tricle in order that the blood may be forced through the narrowed 

 orifice, and in proportion there ensues a work-hypertrophy of the 

 left ventricular wall. Following stenosis at the origin of the pul- 

 monary artery there occurs a work-hypertrophy of the right heart 

 (sometimes dilatation after special preceding strain). X'alvular 

 insufficiency also leads to hypertrophy, because where the valves 

 are incompletely closed there first occurs a tendency to stasis 

 because of the back pressure of the blood (regurgitation), which is 

 likely to induce ventricular or auricular dilatation, and therefore 

 the heart is required to work the harder in order to propel the larger 

 quantity of blood. Although the so-called compensatory hyper- 

 trophy of the heart does in some measure contribute to the regula- 

 tion of the blood distribution and is of some service, yet in reality 

 it is only the expression of an increased blood-pressure in one of 

 the ventricles or auricles or in the aft'erent or efferent vessels, and 

 the compensation which it induces is only a relative one. As a 

 matter of fact, the increase of pressure persists and the circulation 

 does not become normal (Krehl). Even when the animal is 

 at rest the continued heightened blood pressure causes the develop- 

 ment of dilatation of the capillaries, pulmonary passive congestion 

 and distension with consequent diminution in the pulmonary excur- 

 sion, together with difficulty in breathing. The arteries show dis- 

 tinct changes of the pulse, the vessels being unusually tense and 

 distended ; they eventually lose their elasticity and may rupture. 

 A very large heart may in addition mechanically interfere with 

 the lungs. These consequences are still more evident if the indi- 

 vidual exercises physically, the muscular exertion raising the blood 



