542 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION I 



apt to be limited or restricted by "venous return" 

 in tlie erect than in the recumbent position. One 

 criterion for restriction of cardiac output by inade- 

 quate venous return would be failure of the cardiac 

 output to increase when the heart rate is accelerated 

 (see below). 



Assuming that the erect position reduces ventricular 

 dimensions and stroke volume because venous return 

 is limited by depletion of the preventricular sump, 

 this mechanism would be greatly exaggerated by 

 exposure to positive radial acceleration. When cen- 

 trifugal forces act from head to foot, the increased 

 weight of the blood tends to produce increased accum- 

 ulation of blood in dependent regions. Gauer (14) 

 employed cinefluorographic angiocardiography to 

 study the changes in ventricular volume and stroke 

 volume in monkeys exposed to radial acceleration 

 up to five or six times the force of gravity. At the 

 onset of gravitational stress the diastolic heart size 

 and stroke volume were not reduced for a few heats, 

 but the radiodensity of the lungs was rapidly reduced. 

 Then the diastolic and systolic volumes rapidly 

 diminished in a few beats until the systolic reserve 

 volume was completely depleted, and the ventricles 

 emptied during each stroke. From this point on, 

 the stroke volume was a function solely of diastolic 

 filling. This description conforms very well to the 

 concept that stroke volume directly reflects the venous 

 return when, under the influence of centrifugal forces. 

 the systolic reserve volume and preventricular sumps 

 are maximally depleted. Clearly, the cardiac output 

 may be reduced and be limited by inadequate "'venous 

 return" during positive radial acceleration. 



RELATION OF HEART R.\TE TO C.'^RDI.^C OUTPLIT 



If the heart in an intact dog is accelerated artifici- 

 ally through stimulating electrodes previously applied 

 on the atrial wall, the diastolic and systolic dimensions 

 and the systolic excursions diminish progressively as 

 the heart rate is increased in a stepwise fashion. This 

 observation suggests that cardioacceleration, unac- 

 companied by accelerated blood flow throughout 

 the system, increases cardiac output at the expense 

 of the preventricular sumps and the ventricular 

 systolic reserve volume. However, induced tachy- 

 cardia may indeed produce increased cardiac output, 

 if the preventricular .sumps remain adequately filled. 

 For example, W'eissler el al. (58) produced a tachy- 

 cardia in normal recumbent subjects by administering 

 atropine, and demonstrated a large increase in 



cardiac output accompanied by a fall in central 

 venous pressure. Stroke volume was not significantly 

 altered. Erect subjects displayed a reduction in 

 central venous pressure and central blood volume, 

 greater cardioacceleration produced by atropine, and 

 reduced stroke volume. As a result, cardiac output 

 increased only slightly. Counterpressure, applied by 

 inflating anti-G suits over the legs and abdomen, 

 restored in part the cardiac output and stroke volume 

 in erect subjects. 



Reduction in heart size and stroke volume with 

 tachycardia indicates that blood is pumped out of 

 the ventricles faster than the preventricular sumps 

 are replenished by venous flow. The filling pressure 

 of the heart diminishes, but, at the same time, the 

 pressure gradient along the veins may become steeper 

 and flow toward the heart could be accelerated by 

 this mechanism. The pressure and the capacity of the 

 preventricular sumps are both greater in the recum- 

 bent than in the erect positions. These considerations 

 suggest that an inappropriate tachycardia (such as, 

 paroxysmal tachycardia or anxiety) may produce a 

 large increase in cardiac output in reclining subjects 

 when the sumps are well distended. In the erect 

 position, a similar degree of tachycardia may not 

 increase cardiac output to the same extent. 



In summary, the cardiac responses observed during 

 changes from the recumbent to the erect position 

 conform well to predictions from the Frank-Starling 

 mechanism. These effects are exaggerated by exposure 

 to positive radial acceleration. The variable capacity 

 reservoirs, or preventricular sumps, just upstream 

 from each ventricle, correspond functionally to the 

 venous reservoir employed in the heart-lung prepara- 

 tion. Under the influence of such gravitational forces, 

 a reduction in \enous return may rather direcdy 

 reduce stroke volume and even limit the increase in 

 cardiac output winch can be produced by tachy- 

 cardia. An increase in heart size and stroke volume 

 in the recumbent position occurs in both dogs and 

 men in spite of the differences in the orientation of 

 the long axis of body. A teleologically satisfying 

 rationale for a greater stroke volume and cardiac 

 output at rest than in the erect position is not obvious 

 at present. The role of the Frank-Starling mechanism 

 is not immediately apparent in other spontaneous 

 cardiac adjustments such as eating, startle reactions, 

 alterting responses, walking, running, or jumping, 

 presumably because other control mechanisms play 

 dominant roles. 



