Letter to the Editor Debating the Role of the Heart To the Editor: In your January issue, an article by Walter Alexander (“Branko Furst’s Radical Alternative. Is the Heart Moved by the Blood, Rather Than Vice Versa?”) argues against the conventional idea that the heart is the energy source for driving blood through the peripheral and pulmonary vasculatures.1 It would have us believe that the important function of the heart is its valving, enabling it to function like a water ram pump (never mind the fact that a water ram pump depends upon an inexhaustible energy source—gravity—that’s not part of the author’s scheme for moving blood). I wonder if the implication has been taken that, if true, this notion suggests a radical new treatment for heart failure: remove the heart and make a low-resistance, valved connection between the connected outflow of the inferior and superior vena cavae and the pulmonary artery, and another between the pulmonary veins and the aorta. This would eliminate that troublesome impedance offered by the heart and allow the purported energy sources within the pulmonary and peripheral microvasculatures shown in Figure 5 to do their job of driving blood flow. As an alternative, perhaps consider the points raised in my letter to the editor of the American Journal of Physiology, Heart and Circulation2 and by others cited in that letter that support the alternative view that the left ventricle supplies the energy that drives blood through the peripheral vasculature and that a residual portion of this energy is what supplies the work done in expansion of the right ventricle during diastole? Thanks to Rafael Dalmau, MD, for bringing this article to my attention. George Brengelmann, PhD Professor Emeritus Department of Physiology and Biophysics University of Washington Seattle, Washington
metabolism and respiration. This interplay is based on dynamic sensing of the state of the metabolism by red blood cells and polar-opposite autoregulatory responses between the pulmonary and peripheral circulations. In this model, blood flow is primary, and pressure secondary. The rhythmic functioning of the muscular ventricles and the valves driven by them sustain a pulsatile, pressurized conjoining of pulmonary and systemic circulations. This is essential for normal physiology, and in heart failure it is collapsing. Dr. Brengelmann states wryly that in Dr. Furst’s model the heart could be removed altogether and replaced with valved pipes to treat heart failure. But in this model, removing the heart to treat heart failure would not work. Why? The experience with totally artificial hearts is instructive, because behind their failure is not a lack of pressure-generating power, but rather an inability to sense and match output with the metabolic requirements of organs and tissues.2 Even terminally failing hearts fulfill this sensing function better than totally artificial ones, which at best serve as a bridge to transplant. This likely explains the greater success experienced when the failing heart is left in situ, as with axial and centrifugal flow ventricular assist devices. My article briefly and Dr. Furst’s book exhaustively detail evidence for autonomous blood movement. He cites primitive organisms and embryonic stages where blood flow occurs either without or preceding heart formation and functioning. In mammals he describes experimental paradoxical increases in cardiac output during aortic occlusion, the counterintuitive success of Fontan repair for univentricular hearts,3 doubled and tripled cardiac output in septic shock, cardiac output increasing well beyond the pumping capacity of the heart during aerobic exercise, and one to two hour persistent blood movement at the level of the microcirculation after cardiac arrest. In the face of languishing progress in treatment of heart failure, thorough examination of Dr. Furst’s model and its implications for therapy is warranted. Walter Alexander
REFERENCES
REFERENCES
1.
1.
2.
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. 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. doi: 10.1152/ajpheart.00536.2016.
Author’s Response
Dr. Brengelmann has persistently supported a mechanical engineering model of circulation, holding left ventricular contractions as the sole power behind the movement of blood. He describes as “a fallacy”1 the prevailing Guyton model, which, while also seeing the left ventricle as central, credits mean systemic pressure as the driver behind venous return, with relative independence for the arterial and venous circulation limbs. Dr. Brengelmann has challenged Dr. Guyton’s experimental proofs as logically invalid. In Dr. Furst’s model, the difficult task of explaining venous return vanishes, because the source of the moving circulation is the dynamic biochemical/biomechanical interplay between
306 P&T • ®
May 2017 • Vol. 42 No. 5
2. 3.
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. doi: 10.1152/ajpheart.00536.2016. DeVries WC. The permanent artificial heart. JAMA 1988;259(6):849–859. Furst B. Fontan physiology revisited. Anesth Analg 2016;122(2): 578–579.
metabolism and respiration. This interplay is based on dynamic sensing of the state of the metabolism by red blood cells and polar-opposite autoregulatory responses between the pulmonary and peripheral circulations. In this model, blood flow is primary, and pressure secondary. The rhythmic functioning of the muscular ventricles and the valves driven by them sustain a pulsatile, pressurized conjoining of pulmonary and systemic circulations. This is essential for normal physiology, and in heart failure it is collapsing. Dr. Brengelmann states wryly that in Dr. Furst’s model the heart could be removed altogether and replaced with valved pipes to treat heart failure. But in this model, removing the heart to treat heart failure would not work. Why? The experience with totally artificial hearts is instructive, because behind their failure is not a lack of pressure-generating power, but rather an inability to sense and match output with the metabolic requirements of organs and tissues.2 Even terminally failing hearts fulfill this sensing function better than totally artificial ones, which at best serve as a bridge to transplant. This likely explains the greater success experienced when the failing heart is left in situ, as with axial and centrifugal flow ventricular assist devices. My article briefly and Dr. Furst’s book exhaustively detail evidence for autonomous blood movement. He cites primitive organisms and embryonic stages where blood flow occurs either without or preceding heart formation and functioning. In mammals he describes experimental paradoxical increases in cardiac output during aortic occlusion, the counterintuitive success of Fontan repair for univentricular hearts,3 doubled and tripled cardiac output in septic shock, cardiac output increasing well beyond the pumping capacity of the heart during aerobic exercise, and one to two hour persistent blood movement at the level of the microcirculation after cardiac arrest. In the face of languishing progress in treatment of heart failure, thorough examination of Dr. Furst’s model and its implications for therapy is warranted. Walter Alexander
REFERENCES
REFERENCES
1.
1.
2.
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. 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. doi: 10.1152/ajpheart.00536.2016.
Author’s Response
Dr. Brengelmann has persistently supported a mechanical engineering model of circulation, holding left ventricular contractions as the sole power behind the movement of blood. He describes as “a fallacy”1 the prevailing Guyton model, which, while also seeing the left ventricle as central, credits mean systemic pressure as the driver behind venous return, with relative independence for the arterial and venous circulation limbs. Dr. Brengelmann has challenged Dr. Guyton’s experimental proofs as logically invalid. In Dr. Furst’s model, the difficult task of explaining venous return vanishes, because the source of the moving circulation is the dynamic biochemical/biomechanical interplay between
306 P&T • ®
May 2017 • Vol. 42 No. 5
2. 3.
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. doi: 10.1152/ajpheart.00536.2016. DeVries WC. The permanent artificial heart. JAMA 1988;259(6):849–859. Furst B. Fontan physiology revisited. Anesth Analg 2016;122(2): 578–579.
