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Rebuttal from Philip Andrew

Beard & Feigl's call for the removal of Guyton's venous return curve from teaching materials (referred to here as the Guyton–Levy venous pressure curve, VPC), is not based on any deficiency of the VPC itself but purely on Guyton's own conceptual misinterpretations thereof (Beard & Feigl, 2013). Levy resolved these misinterpretations in 1979 (Levy, 1979) and there is today no valid remaining misinterpretation. Yet Beard & Feigl, evidently unaware of the full power of the VPC when combined with the Frank-Starling cardiac output (CO) curve to form Guyton's Graphical Analysis (GGA; Guyton et al. 1973), to this day unsurpassed in its ability to model the central haemodynamics of any circulatory state, would have the baby (GGA) thrown out with the bathwater (Guyton's misinterpretations). 
 
Hoping not to put too fine a point on the matter, Beard & Feigl assert that in Guyton's original VPC experiment (Guyton et al. 1957) the artificial pump was the independent variable. In fact, the pump was downstream to the Starling resistor (SR) thus rendering pump output dependent on the hydrostatic height of the SR relative to the canine surrogate mid right atrium. The pump was adjusted manually simply to insure quantitative transfer to the canine left heart of whatever flow emerged through the SR; how much flow was entirely dependent on the throttling effect of the SR. Accordingly, the SR, not the pump, was the true independent variable governing the experiment. This in no way alters the reality that CO was the independent variable controlling right atrial pressure (RAP). As cited (Beard & Feigl, 2013), Grodins and Levy used preparations essentially identical to Guyton's (the SR was excluded) and they varied CO by simply changing the pump rate. Their VPC was similar. This not only supported the validity of Guyton's experiment and the VPC itself, but it also helped disprove Guyton's backpressure premise – if the VPC is the same with or without a SR (which is a simulated tricuspid stenosis intuitively implying backpressure), then RAP must vary due to something other than backpressure. 
 
Beard & Feigl imply the VPC and GGA are deficient for their failure to model peripheral tissue–organ haemodynamics. The VPC/GGA are models of the central circulation. Irrespective of the sundry nuances of peripheral perfusion, spent blood is presented back to the heart by the vasculature in aggregate, not in particular, and this is faithfully represented by the VPC/GGA. 
 
GGA, properly understood, exposes clinical decision making based on considerations of ‘venous return’ as the conceptual distraction it is. GGA accurately provides all the central circulatory information needed to optimally comprehend and manage clinical cardiovascular disorders. There is no clinical circumstance compelling considerations of venous return in lieu of venous pressure as all changes in venous return translate into proportionate changes in venous pressure.