What increases venous return?

Answer 1

According to Starling's law, an increase in venous return (i.e. increase in preload on the ventricles) results in a more effective contraction, hence augmenting cardiac output, as long as the actin and myosin fibrils in the muscle fibers are not overstretched.

In the most simple terms, the more blood the heart collects blood from venous return, the more it is able to distribute through cardiac output. If venous return is poor, cardiac output will be poor- basically like a water pump that is connected to an insufficient supply of water.

Answer 2

If the questioner has in mind a situation when venous return temporarily differs from cardiac output, then this is a situation in which the distribution of volume within the vasculature changes. The only way that the rate of arrival of blood at the right atrium (venous return) can differ from the rate at which blood leaves the left ventricle (cardiac output) when the total volume within the vasculature is constant is for at least some part of the vascular container to be changing volume. For example, the hepatic vasculature changes volume dynamically. When its volume is changing at a certain rate in ml/min then those mls/min are reflected in just that discrepancy between mls/min coming into the hepatic vasculature (a share of the cardiac output) and the mls/min leaving it (a share of the venous return). If you can imagine a sudden fright causing a dynamic change in the hepatic vasculature such that the whole liver shrinks, then recognize that this volume change was due to an increase in the rate of outflow from the hepatic vasculature. That could manifest as a temporary increase in venous return. Diversion of volume from a part of the vasculature to the central vasculature as a temporary increase in venous return will tend to increase pressures at the entrance to the atrium, an increased filling force that, through the Starling mechanism, would tend to increase stroke volume of the right ventricle and, in turn the left ventricle. Things get complicated, though, for the volume dynamic may have been associated with a change in vascular resistance in one or more of the organ vasculatures. To grasp what the overall change might be is beyond the scope of a short answer like this. You'd need to know a lot of cardiovascular physiology. An excellent guide would be the two books on the human CV system by Loring Rowell, two monographs published by Saunders. But, if the questioner has in mind venous return in the context of "venous return curves", a topic typically included in basic texts on the CV system, there's another complication. Some would say that the question could be discussed in terms of the intersection of cardiac output curves and "venous return curves". But if venous return curves are interpreted as showing how right atrial pressure determined venous return in relation to mean circulatory pressure, that's a misconcept. In the isolated peripheral vasculature, right atrial pressure is a variable dependent upon the steady state flow, not vice versa. This is controversial. Again, it gets a bit deep. The questioner might begin with a couple of articles in the literature. A "point-counterpoint" debate on the subject appeared in the 2006 Journal of Applied Physiology (J Appl Physiol 101: 1525-1526, 2006). The present writer's criticism of what he perceives as a misconcept in interpretation of venous return curves appeared in the 2003 Journal of Applied Physiology (J Appl Physiol 94: 849-859, 2003.)

Answer 3

Increase venous returns increases end diastolic volume (EDV)

Answer 4

exhalation, the venous pump - muscle contraction, and sypmpathetic stimulation of the vascular bed