5IO HANDBOOK OF PHYSIOLOGY ^^ CIRCULATION I 



pressure in the heart is produced by the sequential 

 and progressive development of tension in the various 

 segments of the myocardium which comprise the 

 pump chamber while other segments are as yet un- 

 contracted and are readily extensible. When these 

 segments contract independently of any programmed 

 sequence, no external work is accomplished as, for 

 example, with ventricular fibrillation. Conversely, 

 the extent to which the myocardial fibers contract 

 synchronously will influence the external work pro- 

 duced when the over-all stimulus to the contraction of 

 each fiber is constant. A corollary of this is that a 

 greater stimulus to contraction (fiber length) would 

 be required to produce the same external work when 

 the contraction is less synchronous than when it is 

 more so. 



Figure i8 shows the results of an experiment in 

 which the stimulus was abruptly shifted from the 

 atrium to the ventricle. Heart rate and catechol- 

 amine background were not altered. During atrial 

 stimulation (left panel) the duration of ventricular 

 systole (from the beginning of ventricular systole to 

 the aortic incisura) was 1 90 msec, stroke volume 1 1 . i 

 ml, stroke work 18.3 g-m, and the rate of doing work 

 96.4 g-m per systolic second. In contrast, during 

 ventricular stimulation (right panel) the duration of 

 ventricular systole was 220 msec, stroke volume 5.8 

 ml, stroke work 5.8 g-m, and the rate of doing work 

 26.4 g-m per systolic second. These observations are 



consonant with those findings (50) indicating that 

 the conduction velocity in the bundle of His is sub- 

 stantially greater than that in nonspecialized con- 

 ducting tissue (16). The more leisurely and well- 

 defined diastolic interval and the shorter period re- 

 quired for systole (especially in relation to the stroke 

 voluine, stroke work, and stroke power produced), 

 when the ventricle contracts more sNiichronously, are 

 noteworthy. This type of experiment, in which the 

 obser\ed changes were induced without altering the 

 catecholamine background, indicates the extent to 

 which influences which alter synchronicity can modify 

 the external stroke work and stroke power produced 

 from any given end-diastolic pressure as the result of 

 modifying the rate of development of tension in the 

 myocardium. 



If this explanation is correct, nameh', that the 

 degree of synchronicity with wiiich the \entricle 

 contracts can appreciably modify tlie external stroke 

 work and stroke power it produces from any given 

 end diastolic pressure, then these data may aid in the 

 interpretation of the altered ventricular dynamics ob- 

 served when sympathetic stimulation is applied. For, 

 when cardiac sympathetic stimulation results in 

 more external stroke work and power being pro- 

 duced from any gi\-en end diastolic pressure or fiber 

 length, and the rise and fall of ventricular pressure 

 are steeper, the ventricular contraction gives every 

 appearance of being a more synchronous one. In 

 view of the fact that there is a more rapid propagation 

 of the wave of depolarization during catecholamine 

 stimulation (16), it is to be suspected that an increased 

 synchronicity is contributing to the observed findings, 

 making it unwise to consider the altered performance 

 to be due solely to increased contractility of each 

 fiber. From the findings in figure iB it is to be expected 



that the VFC,,- as well as VFC, 



vould be shifted 



to the right when the heart is paced by ventricular 

 rather than by atrial stimulation, and evidence that 

 tills is so has recenth' been obtained (42a). 



B. Influence of Cardiac Sympathetic Xerve 

 Stimulation on the Atrium 



Evidence which indicates that the atrium as well 

 as the ventricle contracts with more vigor during 

 sympathetic stimulation is shown in figure 19. In 

 figure 19 (upper) are left atrial, left ventricular 

 diastolic, and aortic pressure tracings from a dog in 

 which atrioventricular block had been surgically 

 induced. The atrium was paced at a constant rate. 

 The control tracing is the left panel and that during 



