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POINT-COUNTERPOINT COMMENTS
University of Pittsburgh
e-mail: pinskymr{at}ccm.upmc.edu
The following letters are in response to the Point:Counterpoint series "The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct" that appears in this issue.
To the Editor: I believe Dr. Brengelmann's (1) criticism of the Guyton model of the interaction between the circulation and the heart in controlling cardiac output (2) is wrong as validated by clinical observation. As initially described by Mitzner and Goldberg (3) using a right heart bypass preparation, cardiac output cannot be increased by increasing the pump speed in patients undergoing cardiopulmonary bypass unless reservoir volume or fluid resuscitation simultaneously occur. Although the "bathtub" analogy of Dr. Magder (4) is overly simplistic in lumping one reservoir and a single outflow circuit, it correctly models the role that cardiac function plays in determining cardiac output. We previously showed that the cyclic change in right atrial pressure induced by positive pressure ventilation alters pulmonary flow and their relation approximates an instantaneous venous return curve (5). Furthermore, venous return physiology explains the development of acute cardiogenic pulmonary edema. If the only thing that happened with myocardial ischemia was decreased contractility, then cardiac output would decrease but filling pressure would not rise greatly because its upstream mean systemic pressure is only 
10 mmHg. What causes the acute increase in filling pressure is the associated increased sympathetic tone decreasing vascular unstressed volume, increasing mean systemic pressure for the same blood volume. This also explains why sympathetolytic agents rapidly improve cardiovascular status (6). Thus the Guyton model of the control of the circulation is strongly supported by real-life examples and explains the pathophysiology of disease and can be used to define appropriate therapy.
REFERENCES
The Johns Hopkins University
To the Editor: The systemic circulation can be viewed as an elastic compartment analogous to the lungs. The respiratory physiologist has no problem in understanding the role of elastic recoil pressure as a determinant of expiratory flow, because expiration typically occurs by the passive recoil of the elastic elements of the lung. It may be difficult to visualize expiratory pressure and flow relations under isovolume conditions, because air cannot move out of the lungs at constant lung volume. It was only with the construction of expiratory pressure-flow relations under isovolume conditions (not a simple exercise!; Refs. 2, 3) that expiratory flow limitation was understood, and this resulted in an appreciation of the role of elastic recoil pressure as a major determinant of maximum expiratory flow (4, 5).
The isovolume venous return curve presents the opposite dilemma to the circulatory physiologist. How can the emptying of a balloon have any relevance in an isovolume system? Thus Brengelmann's inference that "the balloon model has a glaring defect ... because outflow would remove volume from the elastic compartment, prohibiting the isovolume conditions of the venous return curve" (1). The conceptual necessity of continuous replacement of the draining volume of the systemic circulation obscures the role of the simultaneous mechanics of emptying (elastic recoil and resistance to venous return) that determines the maximum attainable cardiac output. The circulatory or respiratory pressure-flow isovolume curves, remarkably similar to each other, arise from the same mechanical principles and clearly reveal how flow may become independent of the activity of the pump.
REFERENCES
Department of Physics
National Taiwan Normal University
To the Editor: Magder (5) depicted arterial inflow as a tap in a bathtub. However, in a circulatory system, there are many bathtubs. Flowing from the heart to any bathtub, blood has to travel a long journey by passing through tubes of decreasing cross sections. How to supply all bathtubs with the appropriate amount of blood becomes an important task for the heart. The heart is designed to provide enough power for blood transportation in an efficient way via pulsatile pumping.
Pulsatile pumping makes blood propagate as a wave not as a direct flow. It is the same strategy as using AC transmission line to replace DC current for long-distance electric power delivery. Pressure gradients and flow in the vasculature develop hand in hand as a consequence of pumping (1). Movement of the blood in artery is governed by a pressure wave equation (3) not by the Poiseuille's Law. In other words, left ventricular output is delivered through pressure wave, offering all bathtubs the sufficient blood and energy source for venous return. Pulse pressure is transmitted deeper into the microcirculation (2). Without a pulsatile pump, only bathtubs near the heart may get enough blood.
Heart rate control is an important regulation for proper blood supply. Frequency-matching rules (4) are the matching relations between heart rate and the natural frequencies of arterial systems or organs. Fulfilling these rules enhances the efficiency of power transportation, and these rules can be used to explain how heart rate and total blood flow change during exercise.
REFERENCES
UTMB
To the Editor: Hydraulic resistance is customarily defined as a pressure drop divided by flow (when gravitational and temperature gradients can be ignored). The entire systemic resistance, (MAP–RAP)/CO, can be split into its serial components (e.g., Rprecap), each defined as the appropriate 
P divided by CO. Guyton's definition of "the resistance to venous return" [Rvr = (MSFP–RAP)/VR] is unconventional because the driving pressure does not exist while blood is flowing and because Rvr cannot be identified with any particular series component of the circuit. MSFP should not be confused with the average pressure in the system or any pressure in the system while blood is flowing. Rvr is not specifically the flow resistance through the venous system. Guyton himself pointed out in his textbook that about one-third of Rvr was in arterioles and small arteries.
The concept of Rvr arose from "venous return curves" where flow increases as RAP decreases below MSFP. The obvious explanation for this relationship is that, in these experiments, the decrease in RAP and increase in VR were both caused by an experimental increase in CO, as discussed by Brengelmann.
The argument that elastic recoil force in vessel walls provides the driving force for VR (aka CO) is specious. Vessel wall tension and blood flow are both maintained by the left ventricle.
As a teacher of cardiovascular physiology, I have always avoided the fussy and misleading concept of Rvr and the notion that MSFP is the driving force. Neither concept is useful.
Indiana University School of Medicine
To the Editor: A careful reading of Guyton's papers (2, 3) related to the mean systemic pressure (Pms) shows that the junction of his "cardiac function curve" with his "venous return curve" at a specific right atrial pressure (Pra; Ref. 3) is valid only at equilibrium conditions. It was not designed to provide the dynamic characteristic of the cardiovascular system during disturbances. Furthermore, a simple "venous resistance" (Rsv) to flow is not part of Guyton's concept. It is the "resistance to venous return," which is a complex combination of systemic resistances and compliances (2). Neither author seems to realize that a simple Rsv must be associated with a systemic peripheral venous pressure (Psv), which cannot currently be measured but can only be assumed to be similar in magnitude to the Pms. Furthermore, the Pms is a fixed pressure at a given total systemic stressed volume and total systemic compliance. The Pms is not changed by a change in cardiac output or venous return. A decrease in flow from the arteries will lead to a passive decrease in systemic venous stressed volume (because inflow is less than outflow) and a decreased Psv (because the volume is less) at a constant Pra. An increase in right ventricular function will lead to a decreased Pra and then an increase in venous return. These changes will lead to redistributions of blood volume based on the integral of inflow minus outflow for each compartment. (The principal of mass balance, see Ref. 6).
In retrospect, I wish that I had been more explicit (5).
REFERENCES
Johns Hopkins University
To the Editor: This is a most curious controversy (1, 2), seemingly so 20th Century. In fact, it is not clear what the controversy really is, because no sane person can argue with the fact that venous return must equal cardiac output in the steady state. So, if we agree to deal exclusively with the steady state, then the only question is what are the hemodynamic relations that exist in the peripheral circulation? In this regard, Dr. Brengelmann seems to have misinterpreted the question. Of course there is no steady-state flow if the heart is dead, but because even the most powerful heart cannot generate blood, in the steady state the heart's ability to pump blood is limited to what comes back to it. The blood flow returning to the heart is driven by the difference between the elastic recoil pressure of the peripheral circulation and the pressure at the input to the heart, i.e., the right atrium. This is fact—hardly something to be debated on expensive journal pages. What can be discussed is how best to model this peripheral circulation, and given the highly nonlinear pressure-volume properties of the peripheral vasculature with its complex parallel vascular pathways, this is still not entirely understood. Nevertheless, the bottom line is the same as it was well before Guyton (or anyone else) even thought about it, that steady-state flow back to the heart is always determined by a mean pressure gradient divided by an effective equivalent resistance, properly designated as the resistance to venous return.
REFERENCES
This article has been cited by other articles:
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  S. Nour, G. Wu, Z. Zhensheng, J. C Chachques, A. Carpentier, and D. Payen The Forgotten Driving Forces in Right Heart Failure: New Concept and Device* Asian Cardiovasc Thorac Ann, October 1, 2009; 17(5): 525 - 530. [Abstract] [Full Text] [PDF]
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 A. F. Corno Systemic venous drainage: can we help Newton? Eur. J. Cardiothorac. Surg., June 1, 2007; 31(6): 1044 - 1051. [Abstract] [Full Text] [PDF]
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