Cardiac Variations in Venous Return Studied With a New Bristle Flowmeter

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Abstract
Cardiac factors influencing venous return were studied in acute dog expts. with a new bristle flowmeter of high fidelity. Directly measured blood flow in the superior vena cava is greatly accelerated during ventricular systole when the tricuspid valves are closed. Simultaneously recorded blood pressure and flow curves indicate that this acceleration is caused by the contraction of the myocardium which expands the atrium through a piston-like descent of the atrioventricular junction. Thus, each ventricular contraction ejects not only blood into the arteries but also attracts blood from the veins into the atrium. Venous return is only slightly, if at all, accelerated during ventricular diastole. Conclusive exptl. evidence is furnished supporting the view that venous return is augmented during ventricular diastole by the direct sucking action of increased negative intrathoracic pressure on the walls of the atrioventricular cavity. During atrial contraction, flow in the central vein is briefly stopped or even reversed. In the open chest this flow reversal is accentuated by positive pressure lung inflation. The total amt. of superior cava flow per unit time remains constant at different heart rates. With bradycardia the larger portion of blood enters the atrium during ventricular diastole, whereas with tachycardia 80% of the atrial inflow occurs during ventricular systole. Thus, the heart possesses a self-regulatory mechanism by shifting its atrial filling from a largely passive inflow during the long diastole at slow heart rates to an active systolic attraction of venous blood with tachycardia. It is emphasized that through this fundamental mechanism the heart assures its own venous return upon which the maintenance of cardiac output depends.

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