FUNCTIONAL ANATOMY OF CARDIAC PUMPING 



787 



ventricular ejection (see atrial volume curve in 

 fig. 16 and superior vena cava flow curve in fig. 22). 

 In Chapter 1 7, vol. I, of this Handbook, evidence is 

 given that in normal man the venous stream toward 

 the heart pulsates reciprocally to the aortic stream 

 leaving the chest. The exactitude of the reciprocal 

 relationship is said to be measured by the very small 

 volume equivalent of the cyclic changes (cardiac) in 

 intrathoracic pressure after making allowance for 

 the elasticity of the chest walls (60, 64). 



In conclusion, the filling of the atrium during ven- 

 tricular systole depends not only upon the pressure 

 of blood in the venous reservoir which is available 

 for passive filling from behind; it depends also on 

 the vigor with which ventricular systole moves the 

 atrioventricular junction. Thus a more forceful con- 

 traction (commonly associated with a larger stroke 

 volume) ensures additional inflow into the atrium 

 and therefore facilitates the next ventricular ejection 

 without the need for further decreasing the systolic 

 reserve volume to maintain a large stroke volume. 

 The increase in ventricular outflow and in atrial 

 inflow are mediated by the same force, ventricular 

 contraction, and both favor a more thorough filling 

 of the ventricle during the next diastole. 



The central veins are most suitable for this reser- 

 voir function because through partial collapse of 

 their walls, their content can change rapidly without 

 much change of pressure. They form a collapse 

 chamber which is the functional counterpart of 

 the aortic compression chamber (18). On the ar- 

 terial side, the compression chamber based on the 

 elastic distensibility of the walls assures the trans- 

 formation of the discontinuous cardiac ejections into 

 steady flow to the tissues. On the venous side, the 

 collapse chamber based on the pliability of the walls 

 assures at the atrial entrance the transformation 

 of the steady flow from the tissues into the pulsatile 

 flow which is needed for the discontinuous cardiac 

 filling [see also Irisawa et al. (83)]. 



The filling of the venous collapse chamber is in 

 turn aided by the atrial systole. From a hemodynamic 

 standpoint the function of atrial contraction is two- 

 fold: /) It ejects some blood into the ventricular 

 cavity, a well-established fact, and 2) it passively 

 enlarges the central venous reservoir by briefly- 

 slowing down or stopping atrial inflow. The small 

 amount of backflow which is often recorded during 

 atrial systole at the caval-atrial junction normally 

 does not extend far into the periphery (18). It is 

 readily taken up by a widening of the collapse 

 chamber and, together with the continued inflow 



from the periphery, creates the pool from which the 

 next ventricular filling derives its supply. 



Any force which lowers pressure in a region toward 

 which flow occurs, is called suction, whether or not 

 the pressure developed in that region drops below 

 atmospheric zero. Physically "suction" is the same 

 as pressure (force per area). It is a reduction of pres- 

 sure at some point in a system by the application of a 

 force which results from an energy conversion proc- 

 ess, e.g. muscular contraction, elastic recoil, pulling 

 of a plunger. Since blood is attracted into the atrium 

 by ventricular contraction, one may therefore state 

 that atrial filling is at least in part brought about 

 by suction upon the venous blood mediated through a 

 stretching and enlargement of the atrial cavity by 

 the contracting ventricular muscles which cause a 

 descent of the atrioventricular junction. This phe- 

 nomenon can be termed ''ventricular systolic suction" 

 upon the atrial content. 



[A semantically more rigid definition of the concept of 

 "suction" holds that suction can be thought of only in locations 

 where the transmural pressure is negative (142). Accordingly 

 suction cannot be transmitted through viscera (atria, veins) 

 which have collapsible walls. As long as these viscera contain 

 blood at a greater pressure (including equivalent kinetic energy) 

 than the extra visceral pressure, the dominant force is "pressure" 

 from upstream rather than "suction" from downstream. This 

 pressure maintains the walls of the atria and intrathoracic veins 

 under elastic tension during the entire cardiac cycle. Ed.] 



When the atrioventricular valves open during 

 ventricular diastole, there is another decrease in 

 atrial pressure (Y wave), which results once more 

 in an acceleration of venous blood inflow into the 

 atrium. This second acceleration is more pronounced 

 at slow heart rates and is usually greater in closed- 

 chest than in open-chest animals. Apparently the 

 expansion of all the cardiac cavities through the 

 pulling force of the lungs [Pfuhl (129, 130)] helps 

 to make the atrial inflow during ventricular diastole 

 slightly greater than during ventricular systole. The 

 increase in atrial inflow during ventricular diastole 

 may also be a consequence of the attraction of atrial 

 blood into the ventricle through the forces which 

 expand the ventricle during diastole (ventricular 

 diastolic suction, see following section). These forces 

 not only affect the blood contained in the atrium 

 but in turn even affect the adjoining veins by lowering 

 the atrial pressure, particularly during the phase of 

 rapid ventricular filling. Figure 22 illustrates the 

 phasic increases in superior vena caval flow during 

 ventricular systole (S) and during ventricular diastole 

 (D) in an anesthetized closed-chest dog. 



