Volume and its relationship to cardiac output and venous return

Abstract

Volume infusions are one of the commonest clinical interventions in critically ill patients yet the relationship of volume to cardiac output is not well understood. Blood volume has a stressed and unstressed component but only the stressed component determines flow. It is usually about 30 % of total volume. Stressed volume is relatively constant under steady state conditions. It creates an elastic recoil pressure that is an important factor in the generation of blood flow. The heart creates circulatory flow by lowering the right atrial pressure and allowing the recoil pressure in veins and venules to drain blood back to the heart. The heart then puts the volume back into the systemic circulation so that stroke return equals stroke volume. The heart cannot pump out more volume than comes back. Changes in cardiac output without changes in stressed volume occur because of changes in arterial and venous resistances which redistribute blood volume and change pressure gradients throughout the vasculature. Stressed volume also can be increased by decreasing vascular capacitance, which means recruiting unstressed volume into stressed volume. This is the equivalent of an auto-transfusion. It is worth noting that during exercise in normal young males, cardiac output can increase five-fold with only small changes in stressed blood volume. The mechanical characteristics of the cardiac chambers and the circulation thus ultimately determine the relationship between volume and cardiac output and are the subject of this review.

Keywords: Capacitance; Cardiac output; Circulatory filling pressure; Compliance; Mean systemic filling pressure; Stressed volume; Time constants; Venous return.

Figures

Fig. 1

The importance of a compliant region in the circulation. a A bellows trying to pump fluid around a system with stiff pipes and no compliance. Flow is not possible because pressing on the bellows instantly raises the pressure everywhere and there is no pressure gradient for flow. b An open compliant region which allows changes in volume for changes in pressure. Flow can occur and there are pulsations throughout. c The compliant region is much large than in (b). The pulsations are markedly dampened and only produce ripples on the surface of the compliant region

Fig. 2

Cardiac output is determined by the interaction of a cardiac function and a return function. MSFP is mean systemic filling pressure, Rv is the resistance to venous return, and Pra is right atrial pressure

Fig. 3

Guyton’s graphical analysis of the return function. a When right atrial pressure (Pra) equals MSFP, flow in the system is zero. b Flow occurs when the cardiac function lowers Pra with a linear relationship between flow and Pra. The slope is minus one over the resistance to venous return (Rv)

Fig. 4

Guyton’s approach to solving the intersection of the return function (venous return curve) and cardiac function curve. Since these two functions have the same axes, they can be plotted on the same graph. Where they intersect gives the working right atrial pressure (Pra), cardiac output, and venous return for the two functions

Fig. 5

Limit of the return function. When the pressure inside the great veins is less than the surrounding pressure (which is zero when breathing at atmospheric pressure), the vessels collapse and there is flow limitation. Lowering right atrial pressure (Pra) further does not increase flow. Maximum venous return (VRmax) is then dependent upon MSFP and venous resistance (Rv). The heart cannot create a flow higher than this value

Fig. 6

Change in cardiac output and venous return with an increase in capacitance. An increase in capacitance is the same as lowering the opening on the side of a tub for it allows more volume to flow out, which is the equivalent of more volume being stressed. Graphically it results in a leftward shift of the volume–pressure relationship of the vasculature (upper left). This shifts the venous return curve to the right and increases cardiac output through the Starling mechanism (lower left). This effect is identical to giving volume to expand stressed volume. Pra right atrial pressure

Fig. 7

The two-compartment Krogh model. In this model the systemic circulation has a large compliant region (such as the splanchnic vasculature) in parallel with a low-compliance region (equivalent of the peripheral vasculature). A shift in the fractional flow to the low-compliance region by decreasing the arterial resistance (Ra-p) into this region decreases venous resistance (upward shift of the slope in b compared with a) but does not change MCFP. Rv-s is splanchnic venous resistance, Rv-p is peripheral venous resistance. (Used with permission from reference [5])