Interface III: Venous Return
Venous Return
If we return to the simple model of the circulatory system we introduced earlier, we can assume that, blood pumped from the heart moves through the arterial circulation into a reservoir. The reservoir represents both the total volume of blood contained within circulatory system and the elastic properties (compliance) of the involved vessels.
Blood volume in the reservoir is classified in two ways, stressed and unstressed volume. The unstressed volume is the blood required to fill (but not distend) the walls of vessels within the circulatory system. Unstressed volume does not support blood flow back to the heart. Stressed volume is the volume that distends vessel walls once a vessel is filled. The distending pressure created by stressed volume in the reservoir is called the mean systemic pressure (Pms) and is a primary determinant of blood flow toward the heart. Pms, represents the mean blood pressure within the systemic circulation. Since the majority of blood volume in the body is contained within the venous system, Pms is actually quite low (~8-10mmHg).
Adapting the Hagen-Poiseuille Law to Venous Circulation
Blood flow from the reservoir toward the heart is passively driven by the pressure gradient between the mean systemic pressure (Pms) and the downstream right atrial pressure (PRA), in accordance with the principles of the Hagen–Poiseuille law, which describes laminar flow through cylindrical tubes (see equation below). In this context, the venous return from the reservoir to the heart can be expressed as the pressure gradient between the upstream Pms and the downstream PRA, divided by the resistance to flow (Rv) within the venous circuit. This relationship mirrors the structure of Ohm’s law in electrical circuits, where the flow (analogous to current) is driven by the pressure difference (analogous to voltage) and is inversely proportional to the resistance within the circuit. However, the fundamental origin of the equation lies in the Hagen–Poiseuille law, which governs fluid dynamics in this scenario.
Pressure : Flow Relationship
- An adaptation of Hagen- Poiseuille and Ohm's Laws
The Guyton Curve
In the 1950’s, Arthur Guyton demonstrated the determinants of venous return graphically in what are now called a Guyton curve or venous return curve. The Guyton curve demonstrates the relationship between venous return (Flow) on the Y-axis and right atrial pressure (PRA) on the X-axis. The slope of this curve represents the resistance to venous return. Understanding the curve and how manipulations to Pms, PRA, or Rv influences it is important to fully understanding hemodynamic physiology.
Let's explore the Guyton curve further.
Mean Systemic Filling Pressure (Pmsf):
Based on the Pressure:Flow equation above, when the right atrial pressure (RAP) and the mean systemic filling pressure (Pmsf) are equal (no pressure gradient), flow will cease. This point corresponds is represented by the x-intercept of the venous return curve on the pressure axis where venous return equals zero.
Manipulating the Pmsf
Pmsf can be altered in two distinct ways:
Way #1: The total volume of the reservoir could be changed (Fig. A). This occurs with the addition or removal of fluids.
Fig. A: Assuming favorable venous compliance, the addition of intravascular volume leads to an increase in Pmsf by expanding the stressed volume compartment.
The net effect of changes to stressed volume (PMS) is to move the x-intercept of the venous return curve left or right.
This illustrates the effect a fluid bolus has on venous hemodynamics. As we can see, a rightward shift of the curve (higher Pms) would yeild a greater flow (venous return) for a given PRA
Way #2: The compliance (or diameter) of the reservoir can be altered in such a way that the proportion of stressed to unstressed volume is shifted (Fig. C). Systemic vasodilation or constriction from changes in neural tone, catecholamine responses, or the use of exogenous vasoactive medications all have the potential to modify vascular compliance. When Pms increased by this method, the effect on the venous return curve is identical to above; it shifts to the right and the result is that a higher flow rate will result at a given Pra.
Fig. C: Systemic vasoconstriction decreases overall venous compliance, shifting fluid from unstressed volume to stressed volume, despite no net addition of fluid. When a vasopressor with venular tropism is administered, venous compliance decreases, converting unstressed volume into stressed volume and thereby increasing mean systemic filling pressure (Pmsf).
Clinical Pearl:
Interestingly, profound inflammatory states may impair cardiovascular performance, even when cardiac output appears relatively high. This apparent paradox is often explained by a significant reduction in systemic vascular resistance. In such scenarios, the use of a vasopressor with β₁-adrenergic properties (such as norepinephrine or epinephrine) can provide a beneficial positive inotropic effect. When combined with a reduction in venular compliance, the result is a synergistic enhancement of venous return, cardiac contractility, and ultimately, a net increase in cardiac output.
Right Atrial Pressure
Right Atrial Pressure (PRA) or Central Venous Pressure (CVP) is a fascinating parameter with significant physiological meaning. It is readily measurable in any patient with a central venous catheter. Yet, its clinical utility has been frequently questioned, often unfairly. Much of this criticism arises from a misunderstanding of what CVP truly represents.
In simple terms, CVP is not an isolated variable. Rather, it is the point of equilibrium between two curves:
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The venous return function, which describes how blood flows back to the heart, and
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The right and left ventricular function curve, which represents the heart’s ability to pump forward.
Because CVP is the result of this interaction, it cannot be interpreted independently. It is not merely a "volume status number," but a dynamic reflection of the cardiovascular system’s balance between venous return and right heart permissive performance.
Determinants of CVP
1. Cardiac Function: Cardiac function (both right ventricular permissive function and left ventricular restorative function) moves blood away from the right heart. Increased cardiac output raises arterial pressure and, consequently, lowers PRA. Most of the blood volume, however, remains stored in high-capacitance systemic veins (the stressed reservoir), so cardiac function has little effect on mean systemic filling pressure (Pmsf). Lowering PRA increases the pressure gradient between Pmsf and PRA, which drives venous return upward.
2. Intravascular Reflected Pressure: Because the heart lies within the thoracic cavity and the right atrial wall is thin, pleural pressure changes are transmitted almost directly to the right atrium. This means that respiratory mechanics, mechanical ventilation, and intrathoracic pressure shifts can significantly affect measured PRA.
Let us now delve deeper into two key physiological principles that govern the venous return function:
REFERENCES
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Norepinephrine exerts an inotropic effect during the early phase of human septic shock. Hamzaoui O, Jozwiak M, Geffriaud T, Sztrymf B, Prat D, Jacobs F, Monnet X, Trouiller P, Richard C, Teboul JL. Br J Anaesth. 2018 Mar;120(3):517-524. doi: 10.1016/j.bja.2017.11.065. Epub 2017 Nov 21. PMID: 29452808.
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