Letter to the editor: Why persist in the fallacy that mean systemic pressure drives venous return?

TO THE EDITOR: The work of Berger et al. (3), recently published in the American Journal of Physiology-Heart and Circulatory Physiology, has at its core the idea that steady-state venous return (F) is driven through the resistance to venous return (Rven) by the difference between mean systemic filling pressure (MSFP) and right atrial pressure (Pra)—what they refer to as “Guyton’s model.” That idea comes from the “venous return curves” introduced in a seminal 1955 article (7). They were plots of steady-state F and Pra data obtained at various levels of total blood volume in dogs, a different plot for each volume. F was recorded as the output of a pump that forced blood collected at the right atrium into the pulmonary artery, never venous return as distinguished from cardiac output since these were equal when data was recorded. Pra at zero F was MSFP (by definition), the greater the volume, the greater the MSFP. With increase in F, Pra fell proportionately until it became close to zero. They elected to plot the data with Pra on the x-axis. Thus plotted, the data fit the pattern that would appear if Pra were the independently variable pressure at the outlet of a resistive outflow tract draining a chamber kept at a constant pressure set at MSFP; in quantitative terms, F (MSFP Pra) divided by a constant with dimensions of resistance. This appearance supported the interpretation that MSFP Pra is the pressure head that drives venous return and that reducing Pra would be the key to increasing venous return. But it was actually the height of a Starling resistor that was the independent variable in the experiments of Guyton et al. (7), not Pra. This variable resistance throttled the pump output to bring F to the level at which the resultant Pra was consistent with the vertical position of the resistor relative to heart level [for exposition of this point, see Brengelmann (5)]. In short, it was F that set Pra, not vice versa. When Levy (8) took the approach of controlling F and recording Pra without the incorporation of a variable resistor in the circuit, he found the same proportionality between Pra and F in the range of Pra between zero and MSFP (8). More recent articles have followed Levy in arguing that what we might call the F (MSFP Pra)/Rven view is a misinterpretation. (1, 2, 4). Nonetheless, the notion expressed in Berger et al. (3) persists. They and other adherents of this view evidently believe that MSFP exists physically within some significant subcompartment at the upstream end of the venous resistance, not just at zero F, but at normal operating levels. But that has an implication inconsistent with seeing MSFP as a “driving pressure.” Region within vasculature at mean systemic pressure a passive conduit. What keeps this compartment within the vasculature at constant pressure, MSFP? The only answer consistent with the steady-state assumption is that its outflow is matched by inflow that keeps its volume and associated distending pressure constant. If the volume and pressure within the vascular compartment at MSFP do not change, that means that the elastic energy stored in the walls of the compartment is not what drives its outflow. It cannot deliver energy to the flow moving through it; that would require shortening of its elastic fibers. Therefore, even if there is such a thing as a compartment that stays at MSFP despite changes in F, it cannot be the source of the work expended in driving F through the venous resistance. It is merely a passive conduit. The elastic energy stored in its walls is untapped. In the absence of other energy sources such as the pumping action of respiration and of contracting skeletal muscle, all the work expended in forcing blood through the vasculature comes from the cardiac pump. Mean systemic pressure in models. But what is really meant by “Guyton’s model”? Not a single compartment at MSFP and single outflow resistance, but a circuit of resistors and capacitors formed the analog of the peripheral vasculature from which Guyton et al. (7) derived their expression relating F, Pra, and the parameter called “impedance to venous return.” Though that electrical analog predicts the decline in Pra from MSFP that accompanies increase in F, none of its capacitors remain at constant voltage. Likewise, in other electrical or hydraulic analogs that quantitatively show the inverse F:Pra relationship, there is no physical representation of a persistent MSFP in any of the elastic components (10, 11). What about the physical models one sees offered as teaching aids that represent MSFP as the hydrostatic pressure in a container (6, 9) from which venous return drains into the heart? For example, in one such conceptual model intended to represent the zero-flow condition with Pra equal to MSFP [Fig. 1A (9)], MSFP is meant, presumably, to be taken as the pressure at the bottom of the container. But the heart is shown positioned at the level of the surface of the liquid, where pressure would be zero, not MSFP. In Fig. 1B (9), the high-flow condition with Pra well below MSFP is illustrated with the heart positioned below the level of the bottom of the container. But there the pressure at the entrance to the heart would be MSFP plus the