HEART 417 



the force of contraction varies with the length of the 

 fibres. 



For increased work the heart muscle requires more 

 oxygen, and the increased supply is secured by the increased 

 arterial pressure driving more blood into the coronary 

 arteries. This has been demonstrated by actual experiment. 



The output of the heart is thus not controlled by the 

 arterial pressure. 



(3) It is controlled by the inflow from the veins, as may 

 be shown by loosening the clamp on the venous tube, and 

 allowing more blood to enter the heart (fig. 180). The in- 

 creased inflow leads to a distension of the ventricles, and so 

 to an increased force of contraction. This depends upon the 

 lengthening of the ventricular fibres. The normal heart 

 drives out just as much blood as it receives from the veins. 



The way in which the heart adjusts itself may be seen 

 in a man or animal startincf to run. 



(1) The muscular movements pump more blood into the 

 heart from the veins. 



(2) The heart is distended, and pumps more blood into 

 the arteries. 



(3) The pressure in these is further raised, in spite of 

 the dilatation of the arterioles to the muscles, by the con- 

 traction of the abdominal vessels. 



In discussing the rapid adaptation of the heart to the 

 varied requirements, the possibility of the production of a 

 chronic dilatation has been discussed. 



When, as the result of some obstruction to the flow of 

 blood, the heart is called upon to perform continuously an 

 increased amount of work, it is found that the muscle of 

 the ventricular walls increases or hypertrophies. In this 

 way the prejudicial effects of grave valvular disease of the 

 heart may be compensated for. But this compensation is apt 

 to be disturbed and heart-failure to be induced by any 

 interference with the flow of blood through the coronary 

 arteries. 



The self-regulation of the heart is itself insufiicient to 

 maintain the necessary distribution of pressure throughout 



