What’s wrong with stating that central venous pressure controls venous return?
Does pressure at the entrance to the right atrium act as a "back pressure" that exerts an independent influence on venous return? Is venous return driven by the pressure gradient between mean systemic pressure and central venous pressure, against the resistance of the venous system? Those who would say yes to these questions support their assertion on interpretations of the "venous return curves" in the seminal papers by Arthur Guyton and his coworkers (2, 3, 5, 6). That these are misinterpretations was shown in the critical analysis by Matthew Levy published in 1979 (8). Yet they are perpetuated in present day cardiovascular lore including textbook treatments of the control of cardiac output. This paper is intended to reinforce and extend Levy’s effort in terms of the elementary view of the venous system mechanics shown in Figure 1.
Figure 1. Physical model. The peripheral venous system represented by two compliant compartments connected by a segment with fixed resistance. Pressure inside the peripheral and central venous compartments are designated Ppv and Pcv, respectively. The difference between them, the pressure gradient associated with flow, is determined by the product of the resistance between them and the flow. In steady states, this flow is cardiac output (Qo in the text), identical to venous return (Qr in the text). When the pressures are changing dynamically, Qo and Qr differ while volume is displaced from one compartment to the other.
Lumped properties of the venous system
The schematic arrangement in Figure 1 illustrates a mechanical model of the venous system that is, at least implicitly, widely taken as an acceptable first approximation. The two bulges are intended to represent the elasticity of the venous system, lumped into two separate compartments, peripheral and central. Within these compartments, pressure and volume are related through the compliance of the compartment. The peripheral venous compartment is shown as a larger bulge because most of the venous compliance is in the small peripheral segments of the venous system. It may be thought of as the parallel combination, i.e. sum, of the compliances of the venular segments of the individual organ vasculatures. The central compartment corresponds, roughly, to the aggregate compliance of the collecting veins in which pressure is nearly identical to pressure at the entrance to the right atrium. For an introduction to properties of the venous system, see Rowell (9).
The segment between these two compliant compartments represents the lumped resistance property of the venous system. The pressure gradient between the two compartments develops across this resistance, in proportion to the flow passing through it. In general, when the flow changes, pressure changes in both compartments and their individual volumes adjust in proportion to their compliances.
This is a perfectly appropriate and useful conceptual model. For example, we can see that Qr might temporarily exceed Qo after a sudden reduction in Qo through discharge of volume from both compartments. With the addition of a third compliant compartment and a resistance to represent the arterial system, and suitable parameters for the resistances and capacitances, this simple model correctly predicts the important features of the relationships known as venous return curves (better named as vascular function curves as Levy pointed out (8)) as will be shown below.
But fundamental errors in interpretation coexist with this physical model, specifically:
Confusion of Ppv with mean circulatory pressure (Pmc).
Interpretation of the linear sloped portion of venous return curves as revealing the resistance of the vascular tree that connects the peripheral and central venous compartments.
Above all, regarding Pcv as an independent variable that controls venous return.
I believe that these errors arise through confusion about the experiments in which the data plotted as venous return curves were obtained and that the confusion was deepened by subsequent discussion of what the curves showed. The next sections point out that all the "venous return" data points were obtained at times when cardiac output and venous return were identical, and that the central venous pressure regarded as the independent variable was obtained through manipulation of cardiac output.
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