FUNCTIONAL ANATOMY OF CARDIAC PUMPING 



793 



approximately the same pressure rise as initially 

 recorded upon the first infusion. 



The pressure-volume relationships of the peri- 

 cardial sac without the heart were recently studied by 

 Holt et al. (78) in experiments which emphasize the 

 relatively nondistensible nature of the pericardium. 

 The curve in figure 25 illustrates that, as the fluid 

 volume in a dog's pericardial cavity increases, the 

 pressure remains at zero until the volume has reached 

 about 200 ml. Further volume increments cause a 

 rather steep rise in pericardial pressure. The results 

 of these and other experiments [Isaacs et al. (84), 

 Berglund et al. (11)] point to an important function 

 of the pericardium, i.e., to restrain the heart's cav- 

 ities from overdistention. 



In 1 91 4, Henderson & Prince (71) showed that 

 the filling-force relationships which later became 

 known as Starling's law were such in the right and 

 left ventricles as to prevent the engorgement or de- 

 pletion of the lung blood. The lungs were further 

 safeguarded against congestion by the fact that a 

 sudden dilation of the left ventricle within the peri- 

 cardium would prevent the filling of the right heart, 

 limit the amount of blood that could be pumped into 

 the lungs and thus prevent their engorgement. 



There has been much debate as to whether during 

 diastole the heart normally fills the entire pericardial 

 sac [see also Wilson & Meek (162)]. Nelemans 

 (118) concluded that the heart fills the pericardium 

 completely during diastole and that the sac has a 

 restraining influence upon the expansion of the heart. 

 However, this question has not been studied ex- 

 tensively until modern recording techniques enabled 

 Holt et al. (78) to follow the phasic changes of intra- 

 cardiac and intrapericardial pressures during the 

 cardiac cycle under various filling conditions ranging 

 from hypovolemia to plethora. It was found that in 

 an open-chest dog any increase in ventricular end- 

 diastolic pressure above approximately 1 mm Hg 

 causes a nearly equal rise in pericardial pressure. 

 Since end-diastolic pressures of this order of magni- 

 tude are found under normal circulatory conditions, 

 it appears that the ventricle does occupy the peri- 

 cardial sac completely and even stretches it slightly 

 at the end of the filling phase. Since under conditions 

 of plethora a positive pressure is maintained in the 

 pericardial space throughout the cardiac cycle, the 

 transmural ventricular or transmural atrial pressure 

 must then be taken as the difference between intra- 

 cardiac and pericardial pressures rather than as the 

 difference between intracardiac and intrapleural 

 pressures. 



In comparing the phasic changes in intra-atrial, 

 intraventricular, and pericardial pressures, Holt et al. 

 (78) also made observations which cast light on the 

 contribution of the pericardium to the pumping 

 action of the heart by facilitating atrial filling. The 

 pericardial pressure drops markedly during the early 

 part of ventricular systole. "Since the atria are lo- 

 cated within the pericardial sac . . . , the pressure 

 in the right atrium decreases in early systole and 

 the atrium becomes distended by blood rushing 

 into it from the great veins. A measure of the degree 

 of this atrial 'filling pressure' is the difference be- 

 tween right atrial end diastolic pressure and the 

 pericardial pressure in early systole." When the atrial 

 pressure drops, "the pressure gradient from the 

 great thoracic veins to the right atrium is markedly 

 increased. This appears to be a mechanism by which 

 blood is drawn into the atrium during ventricular 

 systole, and in this way blood is ready to fill the ven- 

 tricles immediately on cessation of ventricular systole. 

 Thus, with the pericardium intact, the act of ven- 

 tricular systole draws blood to the ventricle [sic] and 

 insures ventricular filling in early diastole. These 

 results are in agreement with those of Bohme and 

 Brecher who showed that there was a large sudden 

 flow of blood through the superior vena cava toward 

 the heart during early ventricular systole. This 

 has been attributed by several investigators, and 

 most recently by Brecher, to the sudden piston-like 

 downward movement of the atrioventricular junction 

 attracting blood from the central veins into the right 

 atrium. Our data indicate that the increased flow 

 into the right atrium is caused by the sudden de- 

 crease in pericardial pressure with ventricular sys- 

 tolic ejection, and that this factor becomes greater 

 with higher ventricular diastolic pressures. Confirma- 

 tion of the importance of the pericardium in this 

 connection is the observation of Brecher that the 

 acceleration of venous flow toward the right atrium 

 during ventricular systole is decreased by opening 

 the pericardium. It would appear that the increased 

 flow into the right atrium during ventricular systole 

 was caused in large part by the decrease in peri- 

 cardial pressure during early ventricular systole. 

 The question as to how much of this flow is caused 

 by a downward movement of the atrioventricular 

 junction remains unanswered. Quantitative data on 

 this point could be obtained by measuring the flow 

 into the right atrium in the open-chest dog, with 

 the pericardium intact and after complete removal of 

 the pericardium" (78). 



Obviously, both the piston-like downward move- 



