246 THE HUMAN BODY. 



more blood out than it did previously, then arterial pressure 

 will rise; while if the heart beats more feebly it will fall. 



Modifications of Arterial Pressure by Changes in the 

 Peripheral Resistance. Let the pump c in Fig. 98 still 

 work steadily sending 10,800 cub. cent. (360 oz.) per minute 

 into B and the resistance increase, it is clear arterial pressure 

 must rise. For B is only stretched enough to squeeze out in 

 a minute the above quantity of liquid against the original re- 

 sistance, and cannot at first send out that quantity against the 

 greater. Liquid will consequently accumulate in it until at 

 last it becomes stretched enough to send out 10,800 cub. 

 cent. (360 cubic oz.) in a minute through the small tubes, in 

 spite of the greater resistance to be overcome. A new mean 

 pressure at a higher level will then be established. If, on the 

 contrary, the resistance diminishes while the pump's work 

 remains the same, then B will at first squeeze out in a minute 

 more than it receives, until finally its elastic pressure is 

 reduced to the point at which its receipts and losses balance, 

 and a new and lower mean pressure will be established in B. 



Similarly in the vascular system, increase of the peripheral 

 resistance by narrowing of the small arteries will increase 

 arterial pressure in all parts nearer the heart, while dilata- 

 tion of the small arteries will have the contrary effect. 



Summary. We find then that arterial pressure at any 

 moment is dependent upon (1) the rate of the heart's beat; 

 (2) the quantity of blood forced into the arteries at each 

 beat; (3) the calibre of the smaller vessels. All of these, 

 and consequently the capillary circulation which depends 

 upon arterial pressure, are under the control of the nervous 

 system (see Chap. XVII.). 



The Pulse. When the left ventricle contracts it forces a 

 certain amount of blood into the aorta, which is already dis- 

 tended and on account of the resistance in front cannot 

 empty itself as fast as the contracting ventricle fills it. As 

 a consequence its elastic walls yield still more it enlarges 

 both transversely and longitudinally and if exposed in a 

 living animal can be seen and felt to pulsate, swelling out at 

 each systole of the heart, and shrinking and getting rid of 

 the excess during the pause. A similar phenomenon can be 

 observed in all the other large arteries, for just as the con- 

 tracting ventricle fills the aorta faster than the latter empties 

 (the whole period of diastole and systole being required by 



