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HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



in figures 16 and 17. The left atrial volume is greatest 

 during isovolumetric relaxation of the left ventricle. 

 During the rapid ventricular inflow* phase the atrial 

 volume decreases rapidly, but not so fast as the 

 ventricle fills. This indicates that some blood enters 

 the atrium from the veins while at the same time a 

 greater amount leaves it toward the ventricle. During 

 the phase of slow ventricular inflow (diastasis) the 

 atrial volume remains practically unchanged, point- 

 ing out that inflow from the veins and outflow toward 

 the ventricle are approximately in balance. Inci- 

 dentally, this gives a measure of the rate of venous 

 return to the atrium during this phase by simply 

 calculating the increase in ventricular volume. 

 During atrial systole (approximately end of P wave 

 of electrocardiogram, fig. 1 7) the atrial volume 

 decreases precipitously. The rate at which the atrial 

 volume decreases and the ventricular volume simul- 

 taneously increases speaks in favor of a negligible 

 backflow of atrial blood into the veins during atrial 

 systole. At the peak of atrial systole the volume of 

 blood contained in the atrium is minimal, but still 

 amounts to approximately 4 ml in dogs. During the 

 phase of isovolumetric ventricular contraction, the 

 atrial volume already begins to increase owing to 

 an accelerated venous inflow. It continues to increase 

 at a rather fast rate during rapid ventricular ejection 

 and at a slower rate during the phase of reduced 

 ventricular ejection. Whereas the ventricular stroke 

 volume of the 1 2-kg dog amounts to about 8 ml, 

 the difference between the largest and smallest 

 atrial volume amounts to only 5 ml. This indicates 

 that during the ventricular rapid and slow filling 

 phases approximately 3 ml passes from the veins 

 through the atrium into the ventricle without being 

 recorded as an atrial volume increase. It further 

 indicates that during ventricular isovolumetric con- 

 traction, rapid and reduced ventricular ejection, 

 about 5 ml pass from the veins into the atrium 

 while the atrioventricular valves are closed. 



Obviously, one expects during exercise a greater 

 accommodation of blood in the atrium during ven- 

 tricular ejection and a greater outflow of blood from 

 the atrium into the ventricle during the ventricular 

 rapid and slow filling phase. There are still no meas- 

 urements available concerning such physiological 

 adaptations. It appears reasonable to suggest that 

 in exercise the atrium ejects during its own systole a 

 greater volume, thereby drawing upon the amount 

 of blood usually remaining at rest in the atrium at 

 the end of atrial systole. This might be termed the 

 "atrial systolic reserve volume." 



ATRIAL FILLING 



The phasic changes of venous return which bring 

 about atrial filling are still a subject of debate. It is 

 often stated that venous blood returns to the heart 

 solely as a result of the force imparted to it on the 

 arterial side of the circulation (vis a tergo). Yet there 

 are reasons to believe that the systolic contraction 

 of the ventricular myocardium also contributes to 

 atrial filling by causing an expansion of the atria 

 [see also Hamilton (60) and Holzlohner (79)]. 

 This view- was originally advocated by Purkinje 

 (132) who observed that during ventricular systole 

 the atrioventricular junction (the plane of the heart 

 valves) descends toward the apex and pulls on the 

 atrial walls. The atrial cavity is then passively ex- 

 panded and the pressure in it drops, causing an 

 acceleration of blood from the veins into the atria. 

 Among functional anatomists, the concept of the 

 attraction of blood into the atrium by the descent of 

 the valvular plane toward the apex during ventric- 

 ular systole has gained great favor. By injecting 

 drops of radiopaque contrast material into peripheral 

 veins and taking X-ray cinematographic pictures, 

 Bohme (14) could demonstrate a remarkable acceler- 

 ation of central venous flow during ventricular sys- 

 tole. Records obtained from direct measurements 

 of blood flow in the superior and inferior venae cavae 

 with a high fidelity flowmeter by Brecher & Praglin 

 (25) and by Brecher (19) confirmed Bohme's ob- 

 servations. It appears now that ventricular contrac- 

 tion does cause a sudden expansion of the atrium. 

 This mechanism lowers the pressure in the atrium 

 and produces the X wave, much as a plunger with- 

 drawn in the barrel of a syringe lowers the pressure 

 therein. The expansion of the atrium probably begins 

 with the asynchronous contraction of the papillary 

 muscles during the early part of the isovolumetric 

 phase and continues during rapid ventricular ejec- 

 tion. In the hands of Rushmer (136, 139) the lipiodol 

 injection technique indicated only a moderate accel- 

 eration of caval blood flow during early ventricular 

 systole [see also Lynch (107)]. However, Rushmer's 

 findings can be reconciled with those of Bohme and 

 Brecher, if one considers the differences in the various 

 experimental conditions (open or closed chest, 

 anesthetized or awake animals, slow or fast heart 

 rate, inspiration, expiration, volemic status, etc.). 

 The measurements of Gribbe (56, 57) in intact closed- 

 chest animals definitely indicate an increased atrial 

 inflow beginning at isovolumetric ventricular con- 

 traction and continuing during the rapid phase of 



