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Am J Physiol Heart Circ Physiol 304: H489, 2013;
doi:10.1152/ajpheart.00886.2012.
Letter To The Editor
Reply to “Letter to the editor: A return to the venous return controversy:
a visual aid for combatants’”
Daniel A. Beard1 and Eric O. Feigl2
1
Department of Physiology, Biotechnology and Bioengineering Center, Medical College of Wisconsin, Milwaukee, Wisconsin;
and 2Department of Physiology and Biophysics, University of Washington, Seattle, Washington
Flow ⫽ (50 mmHg ⫺ PRA) ⁄ R50⫺RA
F ⫽ (PMS ⫺ PRA) ⁄ RVR
(1)
is a correct mathematical statement following from the Guyton
model but has been misinterpreted to mean that it is the cause
of cardiac output. As a counter example, choose an arbitrary
pressure between aortic pressure and right atrial pressure, say
50 mmHg. One may then define a statement of Ohm’s law:
Address for reprint requests and other correspondence: D. A. Beard, Medical
College of Wisconsin, Biotechnology and Bioengineering Ctr., 8701 Watertown Plank Rd., Milwaukee, WI 53226 (e-mail: [email protected]).
http://www.ajpheart.org
(2)
where R50-RA is the associated effective resistance. This statement is mathematically correct and serves as a definition for
R50-RA, just as Eq. 1 serves as the definition of RVR. However,
neither Eq. 1 nor Eq. 2 illustrates the cause of cardiac output,
which is determined by the pressure and flow the left ventricle
develops that results in a cardiac output via the input impedance of the systemic circulation.
Dr. Munis equates peripheral venous pressure with PMS in the
last sentences of his letter (2) and in his Eq. 2. This is also the
claim in his clinical paper where he suggests that venous pressure
measured in the hand or arm is proposed as a substitute for PMS
[Munis et al. (3)]. For all the reasons given above, neither the
Guyton nor the Munis model justifies equating peripheral venous
pressure with PMS. While it is true that clinicians may use the
height of the jugular venous pulse as an indication of the blood
volume status of the patient, this needs to be used with other
observations and judgment. The height of the jugular pulse may
vary without an alteration in blood volume, notably by a change
in cardiac output. (An elevated jugular venous pulse is often an
indication of low cardiac output).
In summary, most students, physiologists, and physicians intuitively understand that in heart failure, blood tends to dam up at
the right atrial inlet side of the cardiac pump. It only takes a little
more thought to recognize the opposite; that is, right atrial pressure will tend to fall if cardiac output increases. What actually
happens during exercise, postural changes, heat stress, hemorrhage, etc., is more complicated than simple series models of the
systemic circulation can reveal.
Many commentaries over several decades have demonstrated
that the Guyton model generates more confusion than clarity. It is
time to stop teaching the Guyton model with its associated
misinterpretations.
DISCLOSURES
No conflicts of interest, financial or otherwise, are declared by the author(s).
AUTHOR CONTRIBUTIONS
D.A.B. and E.O.F. drafted, edited, and revised manuscript, and E.O.F.
approved final version of manuscript.
REFERENCES
1. Beard DA, Feigl EO. Understanding Guyton’s venous return curves. Am J
Physiol Heart Circ Physiol 301: H629 –H633, 2011.
2. Munis J. Letter to the editor: “A return to the venous return controversy: a
visual aid for combatants.” Am J Physiol Heart Circ Physiol. doi:10.1152/
ajpheart.00762.2012.
3. Munis JR, Bhatia S, Lozada LJ. Peripheral venous pressure as a hemodynamic variable in neurosurgical patients. Anesth Analg 92: 172–179,
2001.
0363-6135/13 Copyright © 2013 the American Physiological Society
H489
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We thank Dr. Munis for his letter (2) concerning interpreting Guyton’s model of the circulation. In our opinion, when
considering Guyton’s model, it is useful to distinguish three types
of questions: 1) Are the statements concerning the model mathematically correct?, 2) Are the interpretations of the model legitimate?, and 3) Is the model adequate to represent the cardiovascular system during hemorrhage, exercise, heart failure, etc.? We
agree with much of the content of Dr. Munis’s analysis, particularly his clarifications that right atrial pressure does not act to
impede cardiac output. However, we take issue with his application of the concept of mean systemic pressure (PMS). This is a
concept that is accurately defined by Guyton’s model but was
illegitimately interpreted by Guyton to represent a driving pressure for cardiac output.
In Guyton’s model, PMS is the imaginary constant pressure
that would exist after cardiac pumping has ceased and flow
becomes zero everywhere in the circulation without a change
in resistance or capacitance anywhere in the circuit. When
there is blood flow, the PMS pressure cannot be measured and
exists only as an artifact of a mathematical model. It is an
indication of how tightly the blood volume fills the capacitance
of the systemic circulation. Simple manipulations of its definition allow us to derive equally valid mathematical expressions where flow is proportional to either ⫹PMS or ⫺PMS. [See
Eqs. A2 and A3 in Beard and Feigl (1)]. It therefore is an error
to infer from either of these expressions that PMS is a physical
force driving or impeding flow in the circuit.
We agree with Dr. Munis when he writes “PMS does not change
in an isovolumic situation.” However, we find his statement,
“Similarly, the locus of PMS in the veins remains isometric during
steady-state flow and is constrained from moving blood,” difficult
to interpret. There is no locus of PMS when blood is flowing. It
cannot be associated with a physical entity or force when blood is
flowing.
Remember that the Guyton model only pertains to the steady
state when by definition venous return equals cardiac output.
The famous Guyton equation for cardiac output flow (F) during
steady state [Eq. A2 in Beard and Feigl (1)]
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