Background: cardiac output curves
Conceptually, venous return curves flourished in soil cultivated by cardiac output curves. Cardiac output curves are straightforward in concept. Pcv is unquestionably a major influence on Qo through the relationship between preload and cardiac fiber shortening known as Starling's Law. This relationship is relatively easy to comprehend in terms of the intrinsic length-tension characteristics of cardiac muscle -- the greater the preload, the greater the shortening. The cardiac output curve reveals the relationship in terms of Pcv, the index of preload or end-diastolic fiber length, and Qo*see footnote 1
Cardiac output curves are a convenient way of describing the influences of other variables. Specifically, afterload and contractility are commonly regarded as independent variables that, together with Pcv, determine stroke volume. A given cardiac output curve must be regarded as the dependence of Qo upon Pcv for particular fixed levels of contractility and afterload. With higher afterload, the curve would be shifted downward; increased contractility shifts it upward. A family of cardiac output curves on the Pcv-Qo plane can represent the influence of one of the other independent variables as contour plots. This way of looking at the performance of the heart, then, has the advantage of making it easy to illustrate interaction of Pcv (preload), afterload, and contractility. For an example of this way of viewing cardiac function, see Herndon and Sagawa (7); an illustration from their paper is included in Levy’s article 8.
Background: moving the focus from the heart to the vasculature
How actual cardiac output curves might be obtained is easy to imagine, though far from easy to accomplish. Guyton and his co-workers and other investigators who studied the influence of Pcv on Qo had to work out a way of altering Qo without regard for or interference from effects on cardiac filling pressure via the peripheral vasculature. They depended on pumps or other interventions to make it possible to set Pcv at desired levels. One could focus on how Qo varied in relation to Pcv and forget about the peripheral vasculature.
Their natural extension from asking how Qo depends on Pcv was to go on to ask how Pcv varies with Qr**see footnote 2, using similar apparatus. The experiments would be designed to make it possible to focus on the vasculature and forget about the heart. This is what Guyton and his colleagues set out to do in the original research on which present views of venous return curves are based; the example selected is the 1957 paper (5).
The fundamental confusion about their experiments derives from the fact that, in their isolated vasculature preparation, Qo and Qr were identical except for brief imbalances during which changes in volume of the compartments of the compliant vasculature make up the difference.
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*
Though the connection is between preload and stroke volume, heart rate is assumed to be constant over the extent of a cardiac output curve or for a family of cardiac output curves. Also, Pcv is the preload for the right heart and thus its direct influence is on right ventricular stroke volume (RVSV). For the present development, assume that it has the identical influence on left ventricular stroke volume (LVSV), i.e., that the effect of Pcv on RVSV produces the change in left ventricular filling pressure that produces the identical effect on LVSV. This is basically what Guyton stated occurred in response to experimentally induced changes in Pcv {5}. Return to footnote callout in text** Some would say that the strictly parallel question is to ask how Pcv varies with Qo (not Qr) in the isolated vasculature, and thus easily arrive at the negative feedback concept, i.e., through its influence on the heart, Pcv sets the Qo that in turn causes exactly that Pcv through the energy dissipation in the peripheral vasculature. The influence of Pcv increase on the heart is to increase Qo. The influence of increased Qo via the vasculature is to decrease Pcv (as we can infer from simple models and learned from Guyton's experiments). Thus the cardiac and vascular effects countervail and can achieve negative feedback-stabilized equilibrium. Guyton and his coinvestigators could have avoided a lot of confusion if that had taken that approach.
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