Bench-to-bedside review: An approach to hemodynamic monitoring--Guyton at the bedside

Sheldon Magder, Sheldon Magder

Abstract

Hemodynamic monitoring is used to identify deviations from hemodynamic goals and to assess responses to therapy. To accomplish these goals one must understand how the circulation is regulated. In this review I begin with an historical review of the work of Arthur Guyton and his conceptual understanding of the circulation and then present an approach by which Guyton's concepts can be applied at the bedside. Guyton argued that cardiac output and central venous pressure are determined by the interaction of two functions: cardiac function, which is determined by cardiac performance; and a return function, which is determined by the return of blood to the heart. This means that changes in cardiac output are dependent upon changes of one of these two functions or of both. I start with an approach based on the approximation that blood pressure is determined by the product of cardiac output and systemic vascular resistance and that cardiac output is determined by cardiac function and venous return. A fall in blood pressure with no change in or a rise in cardiac output indicates that a decrease in vascular resistance is the dominant factor. If the fall in blood pressure is due to a fall in cardiac output then the role of a change in the return function and cardiac function can be separated by the patterns of changes in central venous pressure and cardiac output. Measurement of cardiac output is a central component to this approach but until recently it was not easy to obtain and was estimated from surrogates. However, there are now a number of non-invasive devices that can give measures of cardiac output and permit the use of physiological principles to more rapidly appreciate the primary pathophysiology behind hemodynamic abnormalities and to provide directed therapy.

Figures

Figure 1
Figure 1
Arthur Guyton's graphical approach to the factors regulating cardiac output. Upper left: venous return curve. At zero flow (cardiac output (Q)), the right atrial pressure (Pra) is equal to the mean circulatory filling pressure. (MCFP) The lower Pra, the greater Q up to a maximum (flat line), in which case the flow is limited. Upper right: cardiac function curve (Starling curve). The greater Pra, the greater Q up to a plateau, in which case flow is limited by cardiac function. Lower: Since both graphs have the same axes, they can be put together with the working cardiac output and working Pra (or central venous pressure (CVP)) given by the intersection.
Figure 2
Figure 2
Central venous pressure can be low with different cardiac outputs. Venous return cardiac function curves indicating three ways in which central venous pressure can be low with different cardiac outputs. See text for more details. Q, cardiac output; Pra, right atrial pressure.
Figure 3
Figure 3
Approach to management of hypotension. Blood pressure is determined by cardiac output (Q) and systemic vascular resistance (SVR). If Q is normal, the primary reason for a low Q is a decrease in SVR. If Q is decreased, this is the primary problem and Q could be decreased because of a decrease in cardiac function or a decrease in return function. These can be separated by examining the central venous pressure (CVP). Potential therapies are also shown. NE, norepinephrine. Pra, right atrial pressure.
Figure 4
Figure 4
Three ways in which central venous pressure can increase with different cardiac output responses. See text for more details. Q, cardiac output; Pra, right atrial pressure.
Figure 5
Figure 5
Inspiratory variations in central venous pressure predict response of cardiac output to a volume infusion. Patients who have an inspiratory (insp.) fall in central venous pressure (CVP) (left side) can have an increase in cardiac output (Q) with a volume infusion, but not always because it depends how close to the plateau of the cardiac function the venous return intersects. Patients who do not have an inspiratory fall in CVP are unlikely to respond to a volume infusion because this indicates that the venous return curve is intersecting the flat part of the cardiac function curve. Pra, right atrial pressure.

References

    1. Rushmer RF, Smith OA Jr. Cardiac control. Physiol Rev. 1959;16:41–68.
    1. Guyton AC. Determination of cardiac output by equating venous return curves with cardiac response curves. Physiol Rev. 1955;16:123–129.
    1. Guyton AC, Lindsey AW, Bernathy B, Richardson T. Venous return at various right atrial pressures and the normal venous return curve. Am J Physiol. 1957;16:609–615.
    1. Guyton AC, Polizo D, Armstrong GG. Mean circulatory filling pressure measured immediately after cessation of heart pumping. Am J Physiol. 1954;16:261–267.
    1. Coleman TG, Manning RD Jr, Norman RA Jr, Guyton AC. Control of cardiac output by regional blood flow distribution. Ann Biomed Eng. 1974;16:149–163. doi: 10.1007/BF02368487.
    1. Magder S. The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct. J Appl Physiol. 2006;16:1523–1525. doi: 10.1152/japplphysiol.00698.2006.
    1. Magder S, De Varennes B. Clinical death and the measurement of stressed vascular volume. Crit Care Med. 1998;16:1061–1104. doi: 10.1097/00003246-199806000-00028.
    1. Rothe CF. Reflex control of veins and vascular capacitance. Physiol Rev. 1983;16:1281–1295.
    1. Deschamps A, Magder S. Baroreflex control of regional capacitance and blood flow distribution with or without alpha adrenergic blockade. J Appl Physiol. 1992;16:H1755–H1763.
    1. Magder S, Veerassamy S, Bates JH. A further analysis of why pulmonary venous pressure rises after the onset of LV dysfunction. J Appl Physiol. 2009;16:81–90.
    1. Thiele RH, Nemergut EC, Lynch C 3rd. The physiologic implications of isolated alpha(1) adrenergic stimulation. Anesth Anal. 2011;16:284–296. doi: 10.1213/ANE.0b013e3182124c0e.
    1. Thiele RH, Nemergut EC, Lynch C III. The clinical implications of isolated α1 adrenergic stimulation. Anesth Analg. 2011;16:297–304. doi: 10.1213/ANE.0b013e3182120ca5.
    1. Magder S. Phenylephrine and tangible bias. Anesth Analg. 2011;16:211–213. doi: 10.1213/ANE.0b013e318220406a.
    1. 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. 2006;16:1525–1526. doi: 10.1152/japplphysiol.00698a.2006.
    1. Brengelmann GL. A critical analysis of the view that right atrial pressure determines venous return. J Appl Physiol. 2003;16:849–859.
    1. Burkhoff D, Tyberg JV. Why does pulmonary venous pressure rise after onset of left ventricular dysfunction: a theoretical analysis. Am J Physiol. 1993;16:H1819–H1828.
    1. Lindsey AW, Guyton AC. Continuous recording of pulmonary blood volume: pulmonary pressure and volume changes. Am J Physiol. 1959;16:959–962.
    1. Pouleur H, Covell JW, Ross J Jr. Effects of nitroprusside on venous return and central blood volume in the absence and presence of acute heart failure. Circulation. 1980;16:328–337. doi: 10.1161/01.CIR.61.2.328.
    1. Ogilvie RI. Effect of nitroglycerin on peripheral blood flow distribution and venous return. J Pharmacol Exp Ther. 1978;16:372–380.
    1. Green JF. Mechanism of action of isoproterenol on venous return. Am J Physiol. 1977;16:H152–H156.
    1. Permutt S, Riley S. Hemodynamics of collapsible vessels with tone: the vascular waterfall. J Appl Physiol. 1963;16:924–932.
    1. Magder S, Bafaqeeh F. The clinical role of central venous pressure measurements. J Intensive Care Med. 2007;16:44–51. doi: 10.1177/0885066606295303.
    1. Magder S, Potter BJ, Varennes BD, Doucette S, Fergusson D. Fluids after cardiac surgery: a pilot study of the use of colloids versus crystalloids. Crit Care Med. 2010;16:2117–2124. doi: 10.1097/CCM.0b013e3181f3e08c.
    1. de Waal EE, Wappler F, Buhre WF. Cardiac output monitoring. Curr Opin Anaesthesiol. 2009;16:71–77. doi: 10.1097/ACO.0b013e32831f44d0.
    1. Vincent JL, Rhodes A, Perel A, Martin GS, Della Rocca G, Vallet B, Pinsky MR, Hofer CK, Teboul JL, de Boode WP, Scolletta S, Vieillard-Baron A, De Backer D, Walley KR, Maggiorini M, Singer M. Clinical review: Update on hemodynamic monitoring - a consensus of 16. Crit Care. 2011;16:229. doi: 10.1186/cc10291.
    1. Magder SA, Georgiadis G, Cheong T. Respiratory variations in right atrial pressure predict response to fluid challenge. J Crit Care. 1992;16:76–85. doi: 10.1016/0883-9441(92)90032-3.
    1. Magder S. Central venous pressure: a useful but not so simple measurement. Crit Care Med. 2006;16:2224–2227. doi: 10.1097/01.CCM.0000227646.98423.98.
    1. Magder S, Lagonidis D, Erice F. The use of respiratory variations in right atrial pressure to predict the cardiac output response to PEEP. J Crit Care. 2001;16:108–114. doi: 10.1053/jcrc.2001.28194.
    1. Nanas S, Magder S. Adaptations of the peripheral circulation to PEEP. Am Rev Respir Dis. 1992;16:688–693.
    1. Fessler HE, Brower RG, Wise RA, Permutt S. Effects of positive end-expiratory pressure on the gradient for venous return. Am Rev Respir Dis. 1992;16:4–10.

Source: PubMed

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