io8 Disturbances of Circulation. 



pressure still higher. (Powerful muscular contractious force 

 larger amounts of blood into the right heart ; the ventricles become 

 engorged and the hsemic pressure rises.) Eventually the heart 

 loses its force as a pathological hypertrophy is not, as might be sup- 

 posed from the thickness of the walls, capable of indefinite response 

 to increased functional demands, but on the contrary, is often 

 unable to accomplish even the more moderate requirements made 

 upon the strength of the heart. Perhaps the reason for this is that the 

 influences which give rise to cardiac hypertrophy at the same time 

 harm the myocardium in other respects. For example, valvular 

 lesions, causing the heart to become hj'pertrophied in their train," 

 are frequently caused by infectious substances. Such agencies may 

 also cause a myocarditis; and if the inflammation be protracted and 

 of low grade, it causes considerable reduction in the efficiency of 

 the muscle. Moreover, the conditions which cause pathological 

 cardiac hypertrophy are typically not stationary, but on the con- 

 trary the circulatory difficulties are apt to progress (the stenosed 

 orifices are likely to become still more narrowed, thrombi which 

 interfere with the vascular lumen become larger, capillary areas 

 become contracted) ; and from such extra demands upon its ability 

 the heart becomes fatigued. There must eventually, therefore, suc- 

 ceed upon compensatory hypertrophy a period of failure of com- 

 pensation, a period of broken compensation. [There are numer- 

 ous influences which combine to limit cardiac hypertrophy* and to 

 determine its eventual loss of compensatory power, and so certain 

 and uniform are these results that it might well be declared a law 

 that every pathological hypertrophy of the heart must necessarily 

 reach a limit to its enlargement and must thereafter fail in its power 

 of compensation and undergo degenerative changes. The limita- 

 tions, aside from those set by the age of the muscle and its inher- 

 ent power of increase, depend mainly upon the amount of proper 

 blood which the coronary vessels are able to supply. In a 

 great measure this is determined by the original size and construc- 

 tion of these vessels, although doubtless there is a possibility of 

 true hypertrophy in these so as to accommodate the growing needs 

 of the enlarging organ ; yet if the original cause of the hypertrophy 

 were a widespread arteriosclerosis the coronary arteries would 

 be extremely likely to have been involved. Even were this not 

 true, the mechanical influence of a hypertrophied left ventricle 

 upon the walls of these vessels in close functional and topograph- 

 ical relation with the pumping action, and the similar influences 



