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Cardiovascular physiology: VENOUS RETURN


Recently, the factors influencing cardiac pumping function have been extensively reviewed. Clinicians now routinely manipulate heart rate, contractility, preload and impedance in the therapy of low cardiac output states. Current emphasis on cardiac function has resulted in a tendency to ignore the important role normally played by the peripheral circulation in the regulation of cardiac output. Normal circulatory function represents an interaction between the peripheral circulation and the heart. This presentation will emphasize the role of the peripheral circulation in the regulation of cardiac output in accordance with principles first elucidated by Guyton and others, t.2
The concept of venous return

Ian R. Thomson MO FRCP(C)

volume is augmented. These examples indicate that

the heart (or roller pump on bypass) does not


normally have access to an unlimited supply of venous blood. In fact, cardiac output is often limited by the amount of blood returning to the heart from the systemic circulation, the v e n o u s r e t u r n

(VR).
The cardiac output curve

The heart performs the work of pumping the blood, and its pumping capacity is controlled by the autonomic nervous system. Therefore one is tempted to conclude that cardiac output (CO) is regulated by aumnomically mediated changes in heart rate (HR) and myocardial contractility. Cardiac output is perceived as a dependent variable resulting from the product of heart rate and stroke volume (SV). CO = HR SV (equation 1)

Implicit in such a "cardiac model" of circulatory regulation is the assumption that the heart always has access to an unlimited supply of venous blood which will not be exhausted if cardiac function is enhanced. This assumption is usually invalid. For example, under normal circumstances increases in heart rate induced by electrical pacing cause little change in cardiac output. J,4 Similarly, during cardiopulmonary bypass when the heart is replaced by a roller pump, it is not possible to arbitrarily increase pump output to any desired level. As roller pump output is increased the blood in the oxygenator reservoir is quickly depleted and pump flow cannot be further increased unless circulating blood CAN ANAESTH SOC J 1984 / 31:3 / ppS31-37

The pumping capability of the heart can be characterized by c a r d i a c o u t p u t c u r v e s which relate cardiac output (CO) to right atrial pressure (Pra). Cardiac output curves graphically illustrate the Frank-Starling mechanism, whereby raising cardiac preload results in increased cardiac output. Cardiac output curves can be measured in dosedchest animals by inserting a large cannula into the fight atrium and varying the height of an attached reservoir of blood. 2 When measured under optimal conditions the curves look like those in Figure 1, which have been extrapolated to man from animal data. The upslope of the normal curve is very steep and CO varies substantially with small changes in Pra. The curves then reach a plateau where CO is independent of Pra. The height of the plateau tells us the maximum cardiac pumping capacity. At a resting level of sympathetic tone the normal heart can pump about 5 L/min at a right atrial pressure of zero. Output increases to a maximum of 10-15 l_/min at a right atrial pressure of 4 mmHg. With intense sympathetic stimulation the maximum pumping capacity increases to 20-30L/rain. Even the unstimulated heart is capable of pumping more than twice the normal cardiac output. Thus, the normal heart has a significant reserve pumping capacity. Since the venous return to the heart is usually

Dr. I.R, Thomson, Department of Anaesthesia, UniverSity of Manitoba, St. Boniface General Hospital, Winnipeg, Manitoba, R2H 2A6.

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FIGURE 2 Schematic diagram of right heart bypass preparat o n used to measure venous return curves. (From Guyton AC, Jones CE, Coleman TG. Circulalory Physiology: Cardiac Outl;ut and its Regulation. Philadelphia, WB Saunders, 1973, Reproduced with permission.)

RIGHT ATRIAL PRESSURE (mm.Hg)

FIGURE 1 Effecton the cardiacoutputcurveof changesin


autonomic tone. (From Guyton AC, Jones CE, Coteman TG. CLnculatory Physiology: Cardiac Output and its Regulation. Philadelphia, WB Sannders, 1973. Reproduced with permission.)

substantially less than maximum cardiac pumping capacity, the heart normally plays a p e r m i s s i v e role in the circulation, using the Frank-Starling mecha nism to adjust its output to match venous return_ In such circumstances, cardiac output is determined by the peripheral circulatory factors which regulate venous return.
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- 1 0 to - 2 0 m m H g at the left hand side of the collapsible tube. Pressure at the right hand side of the tube is then equal to atmospheric. Under these circumstances right atrial pressure (Pra) can be adjusted to any desired level by raising or lowering the segment of collapsible tubing. In this manner the relationships between Pra and venous return can be defined (Figure 3). Such experiments reveal that as Pra is raised, venous return is impeded, and vice versa. In the absence of reflexes, if Pra is raised sufficiently (to about 7 mmHg), venous return falls to zero, the circulation ceases, and pressure equalizes throughout the systemic blood vessels. This

The tendency for blood to return to the heart from the peripheral circulation can be characterized by a venous return c u r v e with the same coordinates as the cardiac function curves in Figure 1. Venous return curves have been measured in experimental animals by Guyton et al. using the elegant right heart bypass preparation illustrated in Figure 2. In this preparation a bypass pump replaces the right ventricle. Blood enters the pump via a segment of collapsible tubing, and is returned to the pulmonary artery. The pump is set to maintain a pressure of

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FIGURE 3 The normal venous return curve. (From Guylon AC, Jones CE, Coleman TG. Circulatory Physiology: Cardiac Output and its Regulation. Philadelphia, WB Sounders, 1973. Reproduced with permission.)

Thomson:

CARDIOVASCULAR

PHYSIOLOGY

$33 15-20 per cent above the value at P r a = 0. The plateau occurs because negative right atrial pressures cause the extrathoracic veins to collapse and act as Starling resistors which prevent any increase in venous return. The pressure in these veins cannot be reduced substantially below - 4 mmHg. Thus, there is a finite limit to the pressure gradient for venous return at any value of Pms. This explains why enhanced pump function, which merely lowers Pro, cannot normally produce a large increase in cardiac output unless there is a simultaneous change in the factors in equation 1 which affect venous return. Such alterations in venous return can result either from changes in Pms or RVR and produce predictable changes in the venous return curve.

occurs because blood collects in the highly compliant venous capacitance vessels. The pressure at which venous return ceases is the mean systemic tiffing pressure (Pms). It is a static measurement of the degree of filling of the systemic circulation and is influenced primarily by btood volume and vascular capacitance. As Pro is reduced below Pms venous return increases progressively to a value of 5 L/rain in humans when Pro equals zero. Figure 3 reveals that the relationship between venous return and Pro is linear for right atrial pressures between zero and Pros. In this region venous return is defined by equation 2. Pms - P r a VR - - RVR (equation 2)

Venous return is proportional to the difference between Pros and Pra. This difference is the hydrostatic pressure gradient promoting venous return. The denominator in equation 1 has units of resistance and is referred to as the resistance to venous return (RVR). The resistance to venous return is not synonymous with the systemic vascular resistance, but i8 a complex term reflecting both the resistance and capacitance of the circulation. Although the relationship in equation 1 has been confirmed experimentally it can also be derived algebraically from theoretical considerations which are beyond the scope of this presentation. ~ Equation 2 is invalid at fight atrial pressures below zero. As Pra becomes more negative, venous return quickly reaches a plateau at a level only

Effect of changes in Pros


Changes in Pros cause a parallel displacement of the venous return curve (Figure 4). Increases in Pros shift the venous return curve to the right and enhance venous return at any given right atrial pressure. Conversely, decreases in Pms shift the curve to the left and decrease venous return. Since Pros reflects the static filling pressure of the systemic circulation it is influenced by changes in blood volume and capacitance. For example, a 15 per cent decrease in blood volume will reduce Pros to zero, whereas a similar increment in blood volume will double Pms. Thus, venous return is critically dependent on blood volume. Sympathetic tone influences Pros through effects on capacitance vessels. Total spinal anaesthesia reduces Pros to 5 mmHg, whereas maximal sympathetic discharge increases Pms to about 17 mmHg. Muscular contraction, especially of the abdominal muscles can also increase Pms very substantially by causing extravascular compression of capacitance vessels. Increases in Pms induced by sympathetic discharge and muscular contraction are important in producing the necessary enhancement of venous return which occurs during muscular exercise, or during compensation for hypovolemia.

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Effect of changes in RVR


Changes in RVR alter the slope of the venous return curve (Figure 5). A decrease in RVR rotates the venous return curve clockwise, enhancing venous return. Increasing RVR rotatcs the venous return curve counter-clockwise, tending to decrease venous

FIGURE 4 A family of venous return curves illustrating the effect of changes in mean systemic pressure (Pros}. (From Guyron AC, Jones CE, Coleman TG. Circulatory Physiology: Cardiac Output and its Regulation. Philadetphia, WB Saunders, 1973. Reproduced with permission).

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cardiac output. These two variables can never differ for more than a few heartbeats before a new equilibrium state is reached. Both cardiac output and venous retum curves have the same coordinates of flow versus pressure, and can be plotted on a single graph as in Figure 6. This graphical analysis of circulatory function allows us to visualize the equilibrium which results from interactions of the heart and peripheral circulation. The point of intersection of the cardiac output and venous return curves, the equilibrium point, defines the state of the circulation. The normal curves illustrated in Figure 6 intersect at Pra = 0 and CO or VR = 5 Limin. Changes in either the cardiac output or venous realm curve will shift the circulation to a new equilibrium point and change Pra and/or CO. The circulatory effects of changes in sympathetic tone, and muscular exercise, provide useful examples of how changes in cardiac function and venous return affect the equilibrium point.
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F/GURE 5 A family of vermus return curves depicting the effect of changes in the resistance to venous return. (l~om Guylon AC, Jones CE, Coleman TG. Circulatory Physiology: Cardiac Output and its Regulation. Philadelphia, WB Saunders, 1973. Reproduced with permission.)

Changes in sympathetic tone


Figure 7 illustrates the circulatory effects of changing sympathetic tone. The figure is based on animal data extrapolated to humans. The normal curves equilibrate at point A (Pra = 0, CO = 5 L/min).

return. Changes in RVR most commonly result from changes in peripheral vascular resistance induced by autoregulatory vasoconstriction or vasodilation in response to changing metabolic needs of body tissues. This probably represents the primary mechanism by which venous return, and thus cardiac output, is adjusted to match total body oxygen consumption. For example, muscular exercise produees marked vasodilation in muscle which reduces RVR and enhances venous return. Pathological decreases in RVR occur with arterial-venous fistulae, beri-beri, or anaemia and the marked increase in venous return in these states can lead to high output cardiac faiture, latrogenic increases in RVR can be produced by administration of a vasoconstrictor, or hy manoeuvres such as infrarenal cross-clamping of the aorta.

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FIGURE 6 The normal cardiac output and venous return cu wes are equated on one graph. The point of inlerse.cfion, the equilibrium point, defines tile normal circulatory stzte. (From Guyton AC, Jones CE, Coleman ILL Circulatory Physiology: Cardiac Output and its Regulation. Philade]phia, WB Saunders, 1973. Reproduced with permission.)

Graphical analysis of the circulation Maintenance of a stable circulatory state demands that an equilibrium exist between venous return and

Thomson: CARDIOVASCULAR PF1YS[OLOGY

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FIGURE 7 The effect of varying degrees of sympathetic tone on the cardiac output and venous return curves. Increasing sympathetic stimulation causes cardiac output to incense markedly as right atrial pressure decreases slightly. (From Guyton AC, Jones CE, Coleman TC. Circulatory Physiology: Cardiac Output and its Regulation. PhiLadelphia, WB Saunders, 1973~ Reproduced wiflapermission.)

Total sympathectomy by high spinal anaesthesia impairs cardiac function, and causes vasodilation o f capacitance vessels. This shifts the cardiac output curve to the right, and the decrease in Pms shifts the venous return curve to the left. The new equilibrium occurs at B, and represents a 40 per cent decrease in CO. Sympathetic stimulation has opposite effects. Cardiac function is enhanced and vasoconstriction in capacitance vessels increases Pms and enhances venous return. The new equilibrium points are at C and D for moderate and maximal sympathetic stimulation respectively. It is apparent that maximal sympathetic stimulation can almost double cardiac output while decreasing right atrial pressure. Interestingly, almost all of the increase in cardiac output results from the shift in the venous return curve caused by vasoconstriction of capacitance vessels, and not from enhanced cardiac function.
Adaptation to exercise The circulatorT adaptation to maxhnal muscular exercise is illustrated in Figure 8. Once again, the

solid curves intersecting at point A represent the normal situation prior to exercise. The onset of exercise is associated with extensive muscular contraction which externally compresses blood vessels, increasing Pms to about 18 mmHg and slightly increasing RVR as well. The new venous return curve intersects the normal cardiac output curve at B, producing an immediate increase in CO of about 70 per cent and a slight rise in right atrial pressure. Next, activation of the sympathetic nervous system causes a further increase in Pros and an improvement in cardiac function. The new cardiac function and venous return curves intersect at C. Cardiac output is now 12.5 L/min and Pra has returned to zero. Finally, increased metabolism in muscle causes extensive vasodilation and a significant decrease in the resistance to venous return. The venous return curve is rotated clockwise and intersects the enhanced cardiac function curve at D. Cardiac output has been increased by four- or fivefold with only a slight increase in Pra. Clearly, changes in both the peripheral circulation and in

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return also explains why malpositioning or kinking of venous lines has such disastrous consequences during bypass. Even a minor obstruction to venous drainage between the patient and the pump-oxygenator will result in an increase in right atrial pressure. Because venous return falls to zero when Pra equals Pms (usually about 7 mmHg) then even minor elevations in Pra will dramatically decrease venous return.

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Spinal anaesthesia
The circulatory effects of total spinal anaesthesia have previously been discussed and are illustrated in Figure 7. Lower levels of spinal anaesthesia which do not result in cardiac denervation, should aftect only the peripheral circulation, primarily decreasing Pros by dilating capacitance vessels. Restoration of Pros by administration of crystalloid and/or alpha-adrenergic agonists should be sufficient therapy to restore venous return and cardiac output to normal levels. Even when a high spinal results in cardiac denervafion, beta-adrenergic agonists shoutd rarely be required if cardiac function was not previously impaired. The normal denervated heart has sufficient reserve pumping capacity to provide a normal cardiac output if preload is restored.

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FIGURE 8 Graphical analysis of the circulatory response to heavy muscularexemon. See text tbr detaiJedexplanation. (From Guyton AC, Jones CE, Coleman TC. Circulatory Physiology: Cardiac Output and its Regulation. Philadelphia, WB Saunders, 1973. Reproduced with permission.)

cardiac function are essential to the auainment of a maximal increase in cardiac output during exercise.

Potential applications
Cardioputmonary bypass
Understanding concepts of venous return is essential to management of cardiopulmonary bypass. During total bypass, venous blood is drained by gravity from the patient to the pump-oxygenator. The siphon effect of gravity drainage normally reduces right atrial pressure to negative values, thus maximizing the pressure gradient for venous return. In this circumstance, if the volume in the oxygenator reservoir is kept constant, the roller pump plays a permissive role in the circulation, pumping whatever venous return it receives back into the aorta. If, under these circumstances, bypass flow is inadequate then venous return must be augmented by either increasing Pros on decreasing RVR. An increase in Pms is accomplished by increasing the patient's circulating blood volume, either by transferring blood from the oxygenator reservoir to the patient, or by adding fluid to the system while reservoir volume is kept constant. If venous return falls in the face of an elevated systemic vascular resistance, then a vasodilator which acts on resistance vessels would be expected to improve venous return by decreasing RVR. The concept of venous

Inhalation anaesthetics
The effects of inhalation anaesthetics on the venous return curve remain to be detertnined. Until such experiments are performed, our understanding of the cardiovascular effects of these agents will be incomplete. Most studies document the effects of inhalation agents on Pra and CO (i.e., on the equilibrium point). ~ However, the pathogenesis of a change in the equilibrium point cannot be clearly understood unless the cardiac output and venous return curves are measured. Inhalation agents probably have clinically relevant effects on venous return. For example, the peripheral venodilation seen clinically with halothane, might be associated with a decrease in Pms. This might be a contributing factor in the dccrcase in cardiac output seen with halothane. The effects of non-anaesthetic drugs, such as nitroprusside, on the venous return curve have recently been investigated. 6 Similar experiments should improve our understanding of anaesthetics

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PHYSIOLOGY

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Summary
Cardiac output is not regulated simply by autonomically mediated changes in heart rate and stroke volume. More often, changes in cardiac output predominantly reflect changes in the peripheral circulation which in turn change venous return. Any attempt to analyze circulatory function without considering the peripheral circulation will be incomplete. The principles discussed above can be fruitfully applied to the analysis of many clinically important derangements of circulatory function. This discussion is only intended as an introduction to concepts which have been exhaustively developed and discussed by Guyton et al. ~ A careful review of this source material will reward the interested reader.

References
1 Guyton AC. Cardiac output, venous return, and their regulation. In: Guyton AC, Textbook of Medical

Physiology. Philadelphia, WB Saunders, 1981, pp. 274-88. 2 Guyton AC, Jones CE, Coleman TG. Circulatory physiology: Cardiac output and its regulation. 2nd Edition. Philadelphia: WB Saunders, 1973.
3 Miller DE, Gleason WL, Whalen RE, Morris JJ, Mclntosh HD. Effect of ventrlcula.r rate on the car-

diac output in the dog with chronic heart block. Circ Res 1962; 10: 658-63. 4 Parker JO, Ledwich JR, West RO, Case RB. Reversible cardiac failure during angina pectoris: Hemodynamic effects of atrial pacing in coronary artery disease. Circulation 1969; 39: 745-57.
5 Eger El lind, Smith NT, Stoelting RK, Cullen DJ, Kadis LB. Whitcher CE. Cardiovascular effects of

halothane in man. Anesthesiology 1970; 32: 396-409.


6 Pouleur H, Covell JW, Ross J Jr. Effects of nitro-

prusside o~ venous return and central blood volume in the absence and presence of heart failure. Circulation 1980; 61: 328-37.

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