scholarly journals The Guytonian Equation: Established Physiological Law?

2020 ◽  
Vol 5 (2) ◽  
Author(s):  
George L Brengelmann

The present collection of papers is meant to focus on old and new concepts about venous return. This essay argues that one widely held old concept is wrong. The misconception would be perpetuated by those who speak of “repurposing the systemic venous return model”. The model in question describes systemic venous return as driven through a “resistance to venous return” in proportion to the difference between mean systemic pressure and right atrial pressure. It arose from experiments in which right atrial pressure (Pra) was recorded while flow was forced through the peripheral vasculature by a pump, with data points taken after pressures equilibrated to each new level of flow. The steady-state flow (F) set by the pump could be taken interchangeably as cardiac output (CO) or venous return (VR). Pra at the zero-flow level settled at what is defined as “mean systemic pressure” (Pms), understood as the pressure at which all the elastic segments of the peripheral vasculature equilibrate in the absence of pressure differences associated with flow. Total circulating volume was kept constant, independent of flow level. The data were approximated by the equation Pra = Pms – F*RVR, alternatively written as F = (Pms – Pra)/RVR. From the point of view of the first formulation, we see Pra falling in proportion to F, starting from Pms at zero flow, a concise statement of the actual experimental procedure and findings. The second formulation has been seen from a different perspective; that F is proportional to the net driving pressure, i.e., (Pms – Pra), in which Pra is seen as a back pressure opposing venous return. From this point of view, adopted by a leading researcher of his time, A.C. Guyton, comes the idea that, to increase VR, the heart must somehow reduce Pra. Re-examining the model that Guyton and his coworkers developed reveals that the appearance of Pms in their equation does not identify this variable as a pressure that exists physically at the upstream end of the pathway for venous return. At best, the model offers a way of looking at the factors that determine the equilibrium between the Pra that results in the peripheral vasculature at a particular steady-state level of flow that is consistent with the influence of Pra on the output of the heart. It has nothing to offer for the advancement of understanding of the pathophysiology of real, dynamic flow within vascular segments.

2003 ◽  
Vol 94 (3) ◽  
pp. 849-859 ◽  
Author(s):  
George L. Brengelmann

A. C. Guyton pioneered major advances in understanding cardiovascular equilibrium. He superimposed venous return curves on cardiac output curves to reveal their intersection at the one level of right atrial pressure (Pra) and flow simultaneously consistent with independent properties of the heart and vasculature. He showed how this point would change with altered properties of the heart (e.g., contractility, sensitivity to preload) and/or of the vasculature (e.g., resistance, total volume). In such graphical representations of negative feedback between two subdivisions of a system, one input/output relationship is necessarily plotted backward, i.e., with the input variable on the y-axis (here, the venous return curve). Unfortunately, this format encourages mistaken ideas about the role of Pra as a “back pressure,” such as the assertion that elevating Pra to the level of mean systemic pressure would stop venous return. These concepts are reexamined through review of the original experiments on venous return, presentation of a hypothetical alternative way for obtaining the same data, and analysis of a simple model.


2011 ◽  
pp. 48-54
Author(s):  
James R. Munis

By its nature, circulatory physiology is also susceptible to circular reasoning because every part of an interconnected system is affected by, and affects, every other part. If we're not careful, we end up saying things like ‘venous return equals cardiac output’ when, in the steady state, that is true by definition and nothing new is gained. If we grant that right atrial pressure (PRA) is the ‘downstream’ pressure for venous return, then it follows that PRA should be inversely related to venous return (and therefore, to cardiac output). If we simply apply Ohm's law to the cardiovascular system, we forget that the mean arterial pressure not only contributes to venous return but also is sustained by venous return. If venous return fails for any other reason (unrelated to arterial pressure), so too will mean arterial pressure eventually fail.


2017 ◽  
Vol 313 (2) ◽  
pp. H408-H420 ◽  
Author(s):  
Per W. Moller ◽  
Bernhard Winkler ◽  
Samuel Hurni ◽  
Paul Philipp Heinisch ◽  
Andreas Bloch ◽  
...  

The relevance of right atrial pressure (RAP) as the backpressure for venous return (QVR) and mean systemic filling pressure as upstream pressure is controversial during dynamic changes of circulation. To examine the immediate response of QVR (sum of caval vein flows) to changes in RAP and pump function, we used a closed-chest, central cannulation, heart bypass porcine preparation ( n = 10) with venoarterial extracorporeal membrane oxygenation. Mean systemic filling pressure was determined by clamping extracorporeal membrane oxygenation tubing with open or closed arteriovenous shunt at euvolemia, volume expansion (9.75 ml/kg hydroxyethyl starch), and hypovolemia (bleeding 19.5 ml/kg after volume expansion). The responses of RAP and QVR were studied using variable pump speed at constant airway pressure (PAW) and constant pump speed at variable PAW. Within each volume state, the immediate changes in QVR and RAP could be described with a single linear regression, regardless of whether RAP was altered by pump speed or PAW ( r2 = 0.586–0.984). RAP was inversely proportional to pump speed from zero to maximum flow ( r2 = 0.859–0.999). Changing PAW caused immediate, transient, directionally opposite changes in RAP and QVR (RAP: P ≤ 0.002 and QVR: P ≤ 0.001), where the initial response was proportional to the change in QVR driving pressure. Changes in PAW generated volume shifts into and out of the right atrium, but their effect on upstream pressure was negligible. Our findings support the concept that RAP acts as backpressure to QVR and that Guyton’s model of circulatory equilibrium qualitatively predicts the dynamic response from changing RAP. NEW & NOTEWORTHY Venous return responds immediately to changes in right atrial pressure. Concomitant volume shifts within the systemic circulation due to an imbalance between cardiac output and venous return have negligible effects on mean systemic filling pressure. Guyton’s model of circulatory equilibrium can qualitatively predict the resulting changes in dynamic conditions with right atrial pressure as backpressure to venous return.


2019 ◽  
Vol 317 (5) ◽  
pp. H939-H953 ◽  
Author(s):  
George L. Brengelmann

More than sixty years ago, Guyton and coworkers related their observations of venous return to a mathematical model. Showing steady-state flow (F) as proportional to the difference between mean systemic pressure (Pms) and right atrial pressure (Pra), the model fit their data. The parameter defined by the ratio (Pms − Pra)/F, first called an “impedance,” came to be called the “resistance to venous return.” The interpretation that Pra opposes Pms and that, to increase output, the heart must act to reduce back pressure at the right atrium was widely accepted. Today, the perceived importance of Pms is evident in the efforts to find reliable ways to estimate it in patients. This article reviews concepts about venous return, criticizing some as inconsistent with elementary physical principles. After review of basic background topics—the steady-state vascular compliance; stressed versus unstressed volume—simulations from a multicompartment model based on data and definitions from Rothe’s classical review of the venous system are presented. They illustrate the obligatory connection between flow-dependent compartment pressures and the distribution of volume among vascular compartments. An appendix shows that the pressure profile can be expressed either as decrements relative to arterial pressure or as increments relative to Pra (the option taken in the original model). Conclusion: The (Pms − Pra)/F formulation was never about Pms physically driving venous return; it was about how intravascular volume distributes among compliant compartments in accordance with their flow-dependent distending pressures, arbitrarily expressed relative to Pra rather than arterial pressure.


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