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Letter to the Editor

Continuing the Debate: Branko Furst’s Alternative Model And the Role of the Heart

Rafael Dalmau MD

To the Editor:

As a young practicing anesthesiologist—and only a bystander in the progress related to the subject of cardiac output regulation, circulatory equilibrium, heart–lung–vasculature interactions, and clinical hemodynamics—I believe I have some arguments that may enrich the interesting debate started by “Branko Furst’s Radical Alternative—Is the Heart Moved by the Blood, Rather Than Vice Versa?” which appeared in the January issue of P&T,1 and then continued with Dr. George L. Brengelmann’s “Debating the Role of the Heart” letter to the editor in May.2

Guyton’s Model: The Source of Blood Propulsion and the Role of the Heart

The problem and controversy surrounding Guyton’s model of systemic circulation have been especially active since the beginning of the 21st century. As anyone interested in the topic must know, this model is centered on the concept of systemic “venous return” and a group of hemodynamic parameters that govern this phenomenon, such as mean systemic filling pressure, right atrial pressure, venous resistance, stressed and unstressed blood volume, and vascular compliance. Furthermore, the model deals directly with the subject brought up by Walter Alexander in his January P&T article,1 and, of course, by Dr. Furst in his own work: the energy source for blood propulsion or the question of “what makes the blood go around.” 3 While my objective here is not to thoroughly review this controversy and the arguments put forward by the opposing views, I do nevertheless consider this letter an opportunity to point to a rather subtle misconception about an apparent “priority” of Guyton’s model suggested by Furst’s biological model and in Alexander’s review.

Cognizant of the ambiguity and inconsistency of Guyton’s theory, Alexander nevertheless seems to favor the latter on the basis that it “more closely matches the observed phenomena,” 1 referring to the role of right atrial pressure as a “back-pressure” to venous return (reminiscent of the heart as an “organ of impedance”), and probably also to the idea of “autonomous venous return” developed by physiologists Solbert Permutt and Paolo Caldini in the 1980s.4 On the other hand, Alexander recognizes that Guyton’s model “sees the left ventricle as central,” 1 and Dr. Furst puts forth that “the ultimate source for blood propulsion can be traced to the hydrodynamic equivalent of Ohm’s Law,” 5 so both Guyton’s model and its polar opponent (the so-called “left ventricular model” of the circulation) would “differ only on the surface but not in essence.” 5

It is important to clarify that Guyton’s model does not conceive of the heart as having a central role, but a secondary (“permissive”) role (as Dr. Furst also acknowledges5,6), which is lowering right atrial pressure, allowing steady venous return to drain from a lumped vascular compartment at mean systemic pressure; in other words, in Guyton’s model, the heart is part of the scheme, but the “propulsion center” in the circuit (functioning as a pressure head) consists of an abstract and algebraically artifactual pressure–energy source located in the systemic peripheral venous segment, which can be represented by “hydrostatic analogs.” So, Guyton’s model, indeed, is a version of an Ohmic/Poiseuillian circuit (the “pressure gradient for venous return”) and a “pressure–propulsion” model, though physically and physiologically inconsistent with the dynamics of the circulation710 and the conservation of energy.810 So, it is safe to say that is fallacious.10 Guyton’s model by no means represents a step toward the overcoming of the pure and classical left ventricular model, but…

What Is Meant by the Left Ventricular Model?

The idea that the pressure gradient from the aorta to the right atrium determines the flow,3 that the heart is both responsible for this gradient and the only one regulator of cardiac output,5 and that practically no important role is played by the peripheral vasculature has been labeled as the left ventricular view or model (also known as “cardiocentrism”). In addition, defenders of Matthew N. Levy’s interpretation11 (and Fred S. Grodins’ before that12,13) of the essential dynamics of the circulatory system and the interaction between heart and vasculature have been considered adherents to this left ventricular model.3,5,6,14 It has been articulated in the prior paragraph that the left ventricular model and Guyton’s model boil down to a pressure gradient responsible for blood flow to occur. Dr. Brengelmann has stressed the nature of this profound misconception in hydrodynamics—the rather informal notion that pressure gradients are somehow primary to fluid flow—at many opportunities; one serious implication being the misinterpretation that the role of the heart is to “raise the arterial pressure which then drives the flow through the system” 14—an assertion that has erroneously been attributed to Guyton’s model critics (especially to Dr. Brengelmann) ever since the beginning of the debate.

This mistaken and biased attribution has distorted and obscured the important contributions achieved by contemporary Guyton’s model critics, which aimed for a better and more direct understanding of the human circulatory system: the unbreakable interaction between cardiac output, blood volume distribution, and vascular transmural pressures, along with the clarification of Guyton’s experimental procedures and findings, and the true nature and significance of heart–vasculature interaction and Guyton’s model itself;7 the focus on the pressure–volume relation at the level of the peripheral vasculatures and its fundamental role in determining the preload of the heart through the “veno-ventricular coupling”;15,16 the “venous excess” approach and the strong emphasis on the problem behind the conception of venous return as an “Ohmic” flow;17,18 the formal demonstration of the algebraic manipulation in Guyton’s venous return equation, and the design of a simplified but coherent model of the cardiovascular system.7,19,20

This, of course, is a reductionist and incomplete summary of Guyton’s model critics’ work, but the message I’d like to get across is that their focus has been nothing at all similar to a “cardiocentric” view of human circulation. Instead, the emphasis on the peripheral circulation by these authors is crucial and realistic. The left ventricular paradigm ruled for the most part of the modern discoveries in hemodynamics,21 with a radical turn by the second half of the 19th century after the contributions of Weber and then Starling; but the left ventricular model and Guyton’s model are “two sides of the same coin,” so it is suggested that Guyton’s model critics would no longer be considered adherents to this view.

Classical Models and the Problem of Translation to Clinical Hemodynamics

The current understanding and approach to human circulation in certain medical specialties, along with the assessment of hemodynamic parameters to guide hemodynamic management, moves among three classical standpoints, all of which are model-based and sometimes in deep conflict with each other. These groups are: 1) Poiseuille: in which the main focus is made on the measurement of cardiac output (flow), vascular pressures, and resistance—as the approach to a system driven by a pressure gradient; 2) Guyton: estimation of the “mean systemic filling pressure” by various methods, vascular compliance, and the “stressed blood volume,” as well as the “pressure gradient for venous return” (although, the latter is distinctly “Poiseuillian”); and 3) Starling: assessment of the “stroke volume variation” through a group of surrogates known as “dynamic parameters” that indicate the preload dependence of the ventricles—also referred to as “the position in Starling’s cardiac function curve”—which informs about the “fluid responsiveness.”

It is paradoxical and contradictory that, being one of the main and central goals to determine the “volume status” and to guide fluid therapy, none of these approaches contemplates blood volume as an effective hemodynamic variable. Instead, they fundamentally dismiss the possibility for considering blood volume a “target” variable, and so to assess it directly. Thus, it is my personal conviction that the framework opened by the authors mentioned above as “Guyton’s model critics” altogether would set the basis and rationale for a novel and realistic approach to clinical hemodynamics, based on blood volume as an effective fundamental hemodynamic variable, the reinterpretation of the meaning of classical hemodynamic parameters, and for the definitive overcoming of the Poiseuillian view of human circulation, which seems to be, by far, the prevailing picture in clinical practice and teaching.

Finally, I applaud the passionate struggle and intellectual efforts devoted by all debaters who strive relentlessly for making sense of a complex system and physiology, helping and guiding medical research scientists and practitioners, and extend special thanks to Dr. George Brengelmann.

References

  1. Alexander W. Branko Furst’s radical alternative. Is the heart moved by the blood, rather than vice versa?. P T 2017;42;(1):33–39.
  2. Brengelmann G. Letter to the editor: debating the role of the heart. P T 2017;42;(5):306
  3. Magder S. Point: the classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct. J Appl Physiol (1985) 2006;101;(5):1523–1525.
  4. Permutt S, Caldini P. Regulation of cardiac output by the circuit: venous return. In: Boan J, Noordegraff A, Raines J. Cardiovascular System Dynamics Cambridge, Massachusetts: MIT Press. 1987;465–479.
  5. Furst B. The heart: pressure-propulsion pump or organ of impedance?. J Cardiothorac Vasc Anesth 2015;29;(6):1688–1701.
  6. Furst B, O’Leary AM. Is the heart a pressure or flow generator? Possible implications and suggestions for cardiovascular pedagogy. Adv Physiol Educ 2016;40;(2):200
  7. Brengelmann GL. A critical analysis of the view that right atrial pressure determines venous return. J Appl Physiol (1985) 2003;94;(3):849–859.
  8. Brengelmann GL. Counterpoint: The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is not correct. J Appl Physiol (1985) 2006;101;(5):1525–1526. discussion 1526–1527
  9. Brengelmann GL. Letter to the editor: comments on “Value and determinants of the mean systemic filling pressure in critically ill patients”. Am J Physiol Heart Circ Physiol 2015;309;(8):H1370–H1371.
  10. Brengelmann GL. Letter to the editor: why persist in the fallacy that mean systemic pressure drives venous return?. Am J Physiol Heart Circ Physiol 2016;311;(5):H1333–H1335.
  11. Levy MN. The cardiac and vascular factors that determine systemic blood flow. Circ Res 1979;44;(6):739–747.
  12. Grodins FS. Integrative cardiovascular physiology: A mathematical synthesis of cardiac and blood vessel hemodynamics. Q Rev Biol 1959;34;(2):93–116.
  13. Grodins FS, Stuart WH, Veenstra RL. Performance characteristics of the right heart bypass preparation. Am J Physiol 1960;198:552–560.
  14. Magder S. Volume and its relationship to cardiac output and venous return. Crit Care 2016;20:271 Erratum in: Crit Care 2017;21(1):16
  15. Tyberg JV. Venous modulation of ventricular preload. Am Heart J 1992;123;(4 pt 1):1098–1104.
  16. Tyberg JV. How changes in venous capacitance modulate cardiac output. Pflugers Arch 2002;445;(1):10–17.
  17. Reddi BA, Carpenter RH. Venous excess: a new approach to cardiovascular control and its teaching. J Appl Physiol (1985) 2005;98;(1):356–364.
  18. Reddi BA, Carpenter RH. Venous return: cardiomythology?. Clin Med (Lond) 2007;7;(1):35–36.
  19. Brengelmann GL. Learning opportunities in the study of Curran-Everett’s exploration of a classic paper on venous return. Adv Physiol Educ 2008;32;(3):242–243.
  20. Beard DA, Feigl EO. Understanding Guyton’s venous return curves. Am J Physiol Heart Circ Physiol 2011;301;(3):H629–H633.
  21. Parker KH. A brief history of arterial wave mechanics. Med Biol Eng Comput 2009;47;(2):111–118.