218 THE CIRCULATION OF THE BLOOD 



be kept constant or altered at will while venous filling, or arterial 

 pressure, was independently altered. But this is no advantage because 

 the same conditions can be fulfilled after vagotomy in otherwise intact 

 animals ; for example, by clamping the aorta in order to raise the arterial 

 resistance, or by injection of saline or clamping of the vena cava in order 

 to vary the venous inflow. Each of these experimental procedures can 

 be maintained for several beats without causing changes that spread suf- 

 ficiently to cause alteration in the other factor and during these few beats, 

 intracardiac pressure curves can be taken by the optical method and the 

 response of the heart precisely analyzed. 



The important pressures to measure are that just before systole (initi;il pressure) 

 and that at the height of systole (maximal pressure). By clamping the vena cava, for 

 example, the initial and maximal pressures in both ventricles were immediately de- 

 creased whereas by injecting saline into the jugular vein both of these were increased. 

 By raising the arterial resistance (clamping the aorta or by causing reflex general 

 vasoconstriction), the initial pressures for a beat or two were not affected at all in 

 the right ventricle and only moderately so in the left, but the maximal pressures 

 were decidedly increased. By measuring the volume changes along with those of 

 pressure it was found that there was always an increase in initial pressure (in the 

 right ventricle) accompanying an increase in initial volume a result which shows 

 that Starling is wrong in concluding that it is only the initial length of the fibers 

 that determines their contractile power. These relationships, moreover, break down 

 entirely both when the initial pressure is excessively elevated (in which case there is 

 a diminished pressure maximum and a lessened discharge) and when the myocardium 

 is depressed, as by poisoning with chloral. While admitting that the initial length 

 of the cardiac muscle is a most important factor in determining the strength of the 

 succeeding contraction, as it is also in skeletal muscle, Wiggers concludes that changes 

 in volume cannot occur without accompanying alteration in initial tension. He there- 

 fore considers the tone of the heart in diastole as an important factor in determining 

 its systolic force. 



The Effect of Alteration in Rate of Heart Beat on Output of Blood 



At this stage it is important to analyze the effect on the output of the heart per 

 minute (the minute volume) brought about ~by inert a.^r in (lie rate of beat. When 

 the venous inflow is slow, the ventricle does not dilate to its full capacity in diastole 

 and acceleration of the beat does not improve the output in a unit of time. The 

 same is true when the inflow is just sufficient to dilate the ventricle to the maximal 

 extent at the moment that systole supervenes, for although more blood is discharged 

 than in the first case, acceleration cannot improve the output. When, on the other 

 hand, the inflow is sufficiently rapid so that the ventricle is practically filled to its 

 limit some time before diastole ends, the output is increased by acceleration. In 

 other words, when there is no so-called period of diastasis following active diastole, 

 acceleration of the beat will not increase the output in a unit of time. 



The condition in which increased heart rate occurs with greatest certainty is mus- 

 cular exercise. The initial quickening is due to impulses travelling to the cardiac 

 centers in the medulla from centers in the cerebrum (see page 229), and it is clear 

 that the acceleration will be of value in increasing the cardiac output in proportion 



