IHE CONTROL OF THE FUNCTION OF THE HEART 497 



250 



1.0' 



-'-, , 



oi- 



FiG. 6. HR = heart rate. A-V O™ = coronary arteriovenous oxygen difference in volumes per 

 cent. 



reoard to the tracins>s shown in figure 5 (lower), it 

 should be noted that, due to the positioning of the 

 aortic flowmeter, the "volume transients" observed 

 were related not to the ventricle alone but to the left 

 atrium and ventricle plus aorta. 



Over a certain range, the work produced by stri- 

 ated muscle which encounters an afterload (an in- 

 creased resistance to shortening at some interval 

 after it has begun to contract from a gi\en initial 

 length) will be greater than when it is not so after- 

 loaded (36, 37). This is an inherent property of mus- 

 cle in any given biochemical state and does not, as 

 far as is known, require an alteration in its state to 

 exhibit this phenomenon. This may, of course, con- 

 tribute to the increased work produced in the first 

 beat after an increased aortic resistance is suddenly 

 applied. Homeometric autoregulation is not meant 

 to encompass this aspect of cardiac muscle perform- 

 ance but rather refers to the increased contractility 

 which develops (phase 2) in the subsec(uent beats 

 after the increased resistance is applied. The rate of 

 development of tension cannot and, in fact, is not 

 increased on the first beat, since the ventricle has no 

 way of sensing that it is to encounter an afterload 

 until the aortic diastolic pressure is at least equaled 

 by that in the ventricle. In subsequent beats the 

 rate of development of tension is increa.sed (fig. 3) 



and it is only then that an increase in contractilitv is 

 said to have taken place. 



2) Heart rate {Bowditch effect). The patterns of re- 

 sponse ob.served after an abrupt change of heart 

 rate without a change in aortic resistance are shown 

 in figure 5 (upper right), and more particularly in 

 figure 6.-1. In the former the heart rate was abruptly 

 changed from 124 to 163 and back to 131 while 

 cardiac output and total coronary flow were held 

 constant. In the latter, shortly after the increase in 

 rate there is, in pha.se i , a rise in LVED pressure as 

 when tlie aortic resistance is increased. The first few 

 beats after the increase in rate are weaker than the 

 subsequent ones as evidenced by the aortic pressure 

 tracing. This pattern indicates a diminished cardiac 

 output while inflow remains constant, thus deinon- 

 strating that the rise in LVED pressure is paralleled 

 by an increase of ventricular volume, .^t the onset of 

 phase 2, L\'ED pressure declines while the aortic 

 pulse is augmented briefly and a new equilibrium 

 state is reached (phase 3), during which there is a 

 slighth higher cardiac inflow and, presumably there- 

 fore, a higher cardiac output. At the onset of pha.se 4, 

 when returning to the initial rate, it is clear, from the 

 lower LVED pressure, wider aortic pulse, and main- 

 tained inflow that an increase in contractility had 

 taken place during the period of increased heart rate. 



