Venous return and mean systemic filling pressure: physiology and clinical applications

Abstract

Venous return is the flow of blood from the systemic venous network towards the right heart. At steady state, venous return equals cardiac output, as the venous and arterial systems operate in series. However, unlike the arterial one, the venous network is a capacitive system with a high compliance. It includes a part of unstressed blood, which is a reservoir that can be recruited via sympathetic endogenous or exogenous stimulation. Guyton's model describes the three determinants of venous return: the mean systemic filling pressure, the right atrial pressure and the resistance to venous return. Recently, new methods have been developed to explore such determinants at the bedside. In this narrative review, after a reminder about Guyton's model and current methods used to investigate it, we emphasize how Guyton's physiology helps understand the effects on cardiac output of common treatments used in critically ill patients.

Keywords: Fluid therapy; Guyton; Heart–lung interactions; Mean systemic filling pressure; Norepinephrine.

Fig. 1

The three determinants of venous return. At equilibrium, cardiac output (CO) and venous return (VR) are similar. Venous return is the inflow of the right heart. Its three determinants are the mean systemic filling pressure (Pmsf), the right atrial pressure (RAP) and the resistance to venous return (RVr) according to the formula: venous return = (Pmsf–RAP)/RVr. LV: left ventricle, RV: right ventricle

Fig. 2

Overlaying of cardiac function curve and venous return curve. The venous return curve (in blue) indicates that venous return decreases when right atrial pressure (RAP) increases. Mean systemic filling pressure (Pmsf) is the pressure at the x-intercept of the venous return curve. Resistance to venous return (RVr) is represented by the inverse of the slope. At the intersection of the venous return curve and the cardiac function curve (in red) stands the point of equilibrium, whose coordinates reflect the haemodynamic conditions

Fig. 3

Example of a venous return curve obtained by the heart–lung interactions method. In this example, end-expiratory and end-inspiratory holds were performed. The 4 pairs of values of central venous pressure and cardiac output obtained during these holds were plotted on a graph, with cardiac output on the y-axis and central venous pressure on the x-axis. The regression line of these points could be equated to the venous return curve. The mean systemic filling pressure (Pmsf) was estimated as the pressure corresponding to the x-intercept of the extrapolated regression line. The resistance to venous return (RVr) was estimated as the inverse of the slope of the regression line

Fig. 4

Effects on venous return and its determinants of typical clinical situations. A Hypovolaemic shock. Hypovolaemia decreases the stressed volume and therefore the mean systemic filling pressure (Pmsf). Then, the gradient between Pmsf and right atrial pressure (RAP) decreases, while the resistance to venous return (RVr) is not modified. As a consequence, the equilibrium point is shifted to the bottom left, and cardiac output (CO) and venous return decrease. B Cardiogenic shock. The slope of the Frank–Starling curve decreases. The equilibrium point is shifted to the bottom right, following the new, flattened, Frank–Starling curve. Right atrial pressure (RAP) increases, whereas mean systemic filling pressure (Pmsf) and resistance to venous return (RVr) are not modified. The (Pmsf–RAP) gradient decreases, reducing venous return and cardiac output (CO). C Septic shock. Vasodilation increases the venous capacitance, which decreases mean systemic filling pressure (Pmsf). Consequently, the gradient between Pmsf and right atrial pressure (RAP) decreases. Resistance to venous return (RVr) may also decrease. As a consequence, venous return and cardiac output (CO) decrease. A “hyperdynamic state”, with increased cardiac contractility, may steepen the Frank–Starling curve, while septic myocardial dysfunction may flatten it. Dashed lines and the index “1” indicate the normal state. Solid lines and the index “2” correspond to the pathological state

Fig. 5

Effects of volume expansion on venous return and its determinants depending on the degree of preload responsiveness. Volume expansion increases the stressed blood volume and, then, increases mean systemic filling pressure (Pmsf). The equilibrium point is shifted to the upper right. A In the case of preload responsiveness (PR), Pmsf increases to a larger extent than right atrial pressure (RAP), inducing an increase in the (Pmsf–RAP) gradient. Venous return and cardiac output (CO) increase. B In the case of preload non-responsiveness (PNR), RAP increases to a similar extent as Pmsf, the (Pmsf–RAP) gradient remains unchanged and CO does not increase significantly