The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct

2006 ◽  
Vol 101 (5) ◽  
pp. 1533-1533 ◽  
Author(s):  
S. Magder
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.


1980 ◽  
Vol 238 (1) ◽  
pp. H80-H86 ◽  
Author(s):  
R. D. Gilbert

Changes in cardiac output (Qco), heart rate, right atrial pressure, (Pra), and mean systemic pressure (Pms) in response to blood volume changes were measured in chronically prepared fetal sheep. With a 10% decrease in blood volume, fetal cardiac output, measured with the microsphere technique, decreased significantly from 592 +/- 28 to 471 +/- 32 ml . min-1 . kg-1. Heart rate changed little from control animals (163 +/- 5) to those with decreased volume (161 +/- 10 beats/min). Right atrial pressure decreased significantly from 5.4 +/- 0.4 to 4.2 +/- 0.6 mmHg. Mean systemic pressure decreased from 13.8 +/- 0.3 to 10.5 +/- 0.6 mmHg. With a 10% increase in fetal blood volume, cardiac output rose insignificantly to 632 +/- 38 ml . min-1 . kg-1. However, right atrial pressure increased significantly to 8.9 +/- 0.6 mmHg and mean systemic pressure increased significantly to 16.5 +/- 0.8 mmHg with the increased volume. Heart rate again changed little (153 +/- 9 beats/min). The fact that cardiac output rose only a small amount, whereas right atrial pressure rose sharply with an increased blood volume, suggests that the fetal heart is operating near the upper limit of its Starling function curve. As a result, there is very limited cardiac reserve for increases in fetal cardiac output.


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.


1957 ◽  
Vol 189 (3) ◽  
pp. 609-615 ◽  
Author(s):  
Arthur C. Guyton ◽  
Arthur W. Lindsey ◽  
Berry Abernathy ◽  
Travis Richardson

The normal venous return curve has been determined in 12 open-chest dogs with intact circulatory reflexes and in 14 open-chest areflex dogs. These curves show that venous return reaches a maximum value when the right atrial pressure falls to –2 to –4 mm Hg and remains at this maximum value down to infinitely low negative pressures. As the right atrial pressure rises to positive values venous return falls and reaches zero when the right atrial pressure has risen to equal the mean circulatory pressure. A venous return curve for the normal, intact dog has been tentatively formulated on the basis of these studies and previous studies in which individual points on the venous return curves of intact dogs have been measured.


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