Venous return curve

{Refimprove|date=October 2007} Venous return is the rate of blood flow back to the [heart]. It normally limits [cardiac output]

Superposition of the cardiac function curve and venous return curve is used in one hemodynamic model.

Venous return (VR) is the flow of blood back to the heart. Under steady-state conditions, venous return must equal cardiac output (Q), when averaged over time because the cardiovascular system is essentially a closed loop. Otherwise, blood would accumulate in either the systemic or pulmonary circulations. Although cardiac output and venous return are interdependent, each can be independently regulated.

The circulatory system is made up of two circulations (pulmonary and systemic) situated in series between the right ventricle (RV) and left ventricle (LV). Balance is achieved, in large part, by the Frank–Starling mechanism. For example, if systemic venous return is suddenly increased (e.g., changing from upright to supine position), right ventricular preload increases leading to an increase in stroke volume and pulmonary blood flow. The left ventricle experiences an increase in pulmonary venous return, which in turn increases left ventricular preload and stroke volume by the Frank–Starling mechanism. In this way, an increase in venous return can lead to a matched increase in cardiac output.

Hemodynamically, venous return (VR) to the heart from the venous vascular beds is determined by a pressure gradient (venous pressure - right atrial pressure) and venous resistance (RV). Therefore, increases in venous pressure or decreases in right atrial pressure or venous resistance will lead to an increase in venous return, except when changes are brought about by altered body posture (see below). Although the above relationship is true for the hemodynamic factors that determine the flow of blood from the veins back to the heart, it is important not to lose sight of the fact that blood flow through the entire systemic circulation represents both the cardiac output and the venous return, which are equal in the steady-state because the circulatory system is closed. Therefore, one could just as well say that venous return is determined by the mean aortic pressure minus the mean right atrial pressure, divided by the resistance of the entire systemic circulation (i.e., the systemic vascular resistance).

It is often suggested that venous return dictates cardiac output, effected through the Frank Starling mechanism. However, as noted above it is clear that, equally, cardiac output must dictate venous return since over any period of time both must necessarily be equal. Similarly, the concept of mean systemic filling pressure, the hypothetical driving pressure for venous return, is difficult to localise and impossible to measure in the physiological state. Furthermore, the Ohmic formulation used to describe venous return ignores the critical venous parameter, capacitance. It is confusion about these terms that has led some physiologists to suggest that the emphasis on 'venous return' be turned instead to more measurable and direct influences on cardiac output such as end diastolic pressure and volume which can be causally related to cardiac output and through which the influences of volume status, venous capacitance, ventricular compliance and venodilating therapies can be understood.

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