Venous Return, Mean Systemic Filling Pressure, and Stressed Volume

Giving fluid can increase cardiac output, but it can also raise venous pressure without producing useful additional flow. A vasopressor can sometimes improve cardiac filling without adding fluid. These effects become easier to understand when the venous circulation is treated as an active part of the system.

To understand the response, follow blood from the systemic veins to the right atrium. Establish what pressure drives it, what opposes its passage, and whether the heart can eject the blood that arrives.

7.1 Venous Return: Flow Back to the Heart

Venous return is the flow of blood from the systemic circulation into the right atrium. In a steady state, it equals effective cardiac output when there is no significant shunt or other abnormal flow pathway.

The heart and veins adjust together. If more blood returns than the heart ejects, blood accumulates upstream of the heart and filling pressure rises. If the heart briefly ejects more than returns, the volume supplying it falls. These volume and pressure changes move the circulation toward a state in which return and output match. This is the shared operating point.

A simplified model expresses venous return as:

Mean systemic filling pressure, abbreviated Pmsf, represents the upstream filling pressure in this model. Right atrial pressure, Pra, is the downstream pressure. Subtract Pra from Pmsf to obtain the pressure difference supporting return. Divide that difference by resistance to venous return, Rvr, to calculate flow. With pressures in mm Hg and resistance in mm Hg·min/L, the result is in L/min.

Guyton and colleagues experimentally characterized venous-return curves in dogs. Their work showed that return decreased as right atrial pressure approached the upstream filling pressure. At sufficiently low right atrial pressures, return reached a plateau rather than increasing without limit. These experiments provided a foundational model, but their numerical values are not treatment targets for human patients. 1

The equation helps explain a response by identifying which pressure or resistance changed. A rise in Pmsf can increase return if Pra and Rvr stay unchanged. A rise in Pra can reduce return if the other terms stay unchanged. In a patient, fluid, vasoactive drugs, or ventilation may change several terms at once. Interpret the combined response rather than assuming that an intervention changes only one.

7.2 Stressed and Unstressed Volume

Blood volume fills a vascular system that can change its capacity. Veins and venules contain a large reservoir of blood, and their walls can accommodate substantial volume changes.

Unstressed volume is the theoretical volume that fills the vascular system without stretching it enough to generate positive distending pressure in the model. Stressed volume is the additional volume that stretches the vessel walls. Those stretched walls recoil against the contained blood and generate pressure.

These terms describe the pressure–volume relationship, not two separate collections of blood. The same blood can contribute differently when venous tone changes. We cannot identify a set of blood cells as permanently belonging to the stressed or unstressed component.

When veins dilate, they can hold more blood without generating much recoil pressure. At the same total blood volume, the modeled stressed component may therefore fall. When veins constrict and hold less blood at low pressure, more of the existing volume generates recoil pressure. Return may increase if that pressure increase enlarges the gradient to the right atrium.

This explains one component of relative hypovolemia during vasodilation. The vessels hold more blood at low pressure, so the available volume may generate too little pressure to support return. No blood loss is required for this mechanism. Actual blood loss or movement of plasma out of vessels can still coexist with it; the mechanism does not establish that total blood volume is normal.

The simple distinction also has limits. Real pressure–volume relationships are nonlinear and vary between vascular regions. Surrounding pressure affects distension. The model is most useful when it clarifies a mechanism without being mistaken for a direct measurement of two separate blood compartments.

7.3 Mean Systemic Filling Pressure

Mean systemic filling pressure is the equilibrium pressure of the systemic vascular compartment under defined no-flow conditions. Imagine interrupting flow while preserving the vascular conditions specified by the model. Pressure differences within the systemic compartment would dissipate as blood redistributed. The remaining equilibrium pressure reflects the recoil of the filled vessels.

During ongoing circulation, arteries, capillaries, and veins have different pressures because blood is moving through resistances. A routine venous catheter measures local pressure within that flowing system. It does not directly measure the no-flow equilibrium pressure. Pmsf therefore represents an upstream model pressure rather than a single accessible location for a transducer.

Mean circulatory filling pressure is a related term that refers to the entire circulation, including the pulmonary compartment and heart. The terms are sometimes used loosely, but the distinction matters when comparing definitions and measurement methods.

For a simplified linear systemic pressure–volume relationship:

In this simplified relationship, compliance describes the volume change per unit increase in distending pressure. More stressed volume produces more recoil pressure if compliance stays unchanged. Greater compliance produces less pressure for the same stressed volume. Changes in venous tone can also shift the volume at which pressure begins to rise. The approximation therefore requires a specified pressure reference and vascular state.

For a hypothetical stressed volume of 1,000 mL and compliance of 100 mL/mm Hg, each 100 mL corresponds to a 1 mm Hg increase in pressure within the linear model. Divide volume by compliance:

1,000 ÷ 100 = 10 mm Hg

These assumed values illustrate the calculation. A routine examination cannot assign this stressed volume or compliance to a patient.

As blood leaves a distended vascular compartment, vessel recoil releases stored elastic energy. Without continuing cardiac work, this pressure difference would decline as blood redistributed. The heart continually returns blood to the arterial system and maintains circulation. Vascular recoil can support return, but it cannot sustain unlimited flow without the pump.

The pressure is also not a target to maximize. A higher Pmsf may support return if the pressure gradient increases and the heart can handle the additional filling. If right atrial pressure rises similarly, the useful gradient may change little. High filling pressures can then coexist with inadequate flow.

7.4 Resistance to Venous Return and the Shape of the Curve

Resistance to venous return describes the effective opposition to flow from the systemic vascular reservoir to the right atrium. It is a property of the distributed circulation within the model.

Rvr and systemic vascular resistance use different upstream pressures. Systemic vascular resistance is calculated from mean arterial pressure minus Pra, divided by cardiac output. Rvr uses Pmsf minus Pra, divided by venous return. Even though output and return match at steady state, the pressure differences are different. The two resistance values are therefore not interchangeable.

Guyton and colleagues experimentally examined the contribution of arterial and venous resistance to venous return and output. Their work demonstrated that the location of a resistance change matters in a system containing compliant vascular regions. A resistance change cannot be interpreted solely from its effect on a global resistance calculation. 2

A venous-return curve plots return on the vertical axis against Pra on the horizontal axis. On its approximately linear part, return falls as Pra rises. If Rvr increases, a change in pressure produces a smaller change in flow, so the line becomes less steep. A larger gradient is then needed for the same return. If Pmsf rises while Rvr stays unchanged, return is greater at the same Pra.

At sufficiently low Pra, a compliant venous segment may narrow or collapse because its surrounding pressure exceeds its internal pressure. That segment then limits flow. Further lowering Pra beyond it may fail to increase return. The relevant pressure difference is now limited by the pressure at the collapsible segment, so the simple linear relationship no longer applies.

This is why “lower right atrial pressure” cannot be treated as an unlimited strategy for increasing return. The pressure reference, external pressure, vessel behavior, and cardiac function must all be considered.

7.5 Right Atrial Pressure Is Both an Operating Pressure and a Result

Pra rises or falls according to how much blood arrives and how effectively the heart moves it onward. It forms the downstream term in the return equation, but it is also a result of the heart and circulation working together. It cannot usually be changed independently of the other determinants.

An improvement in cardiac performance can increase output while lowering right atrial pressure. The heart transfers blood out of the venous compartment more effectively, and the circulation settles at a new operating point. Conversely, impaired right ventricular ejection can raise right atrial pressure while output falls.

This does not justify treating right atrial pressure as an independently adjustable knob. A pressure change after fluid, a vasopressor, or ventilation may occur because several parts of the system have changed together.

Pressure around the right atrium also affects the reading. The pressure that distends the chamber is its transmural pressure: pressure inside minus pressure outside. Positive intrathoracic pressure can raise measured central venous pressure without producing the same increase in distension. Compare ventilation and surrounding pressure before assuming that two identical central venous pressures represent identical cardiac filling.

Central venous pressure is often used as an estimate of right atrial pressure. Its interpretation requires correct leveling and zeroing, a suitable catheter location, and an interpretable waveform. A mean number can conceal large waves or respiratory variation that contribute to the physiological explanation.

The practical task is to interpret pressure and flow together. A rise in venous pressure with improved output has a different meaning from the same pressure rise with unchanged or falling output.

7.6 Why Fluid Can Raise Pressure Without Raising Output

Fluid can increase stressed volume and Pmsf. Whether output rises depends on the simultaneous response of right atrial pressure, resistance, and cardiac performance.

Consider illustrative values of Pmsf 12 mm Hg, Pra 4 mm Hg, and Rvr 2 mm Hg·min/L. First calculate the pressure difference:

12 − 4 = 8 mm Hg

Then divide it by resistance:

8 ÷ 2 = 4 L/min

The modeled return, and thus steady-state output, is 4 L/min.

Now suppose fluid raises Pmsf to 16 mm Hg while Pra rises only to 5 mm Hg. The new gradient is:

16 − 5 = 11 mm Hg

With Rvr still 2 mm Hg·min/L:

11 ÷ 2 = 5.5 L/min

The gradient has increased from 8 to 11 mm Hg, and flow has risen from 4 to 5.5 L/min. Upstream pressure increased more than downstream pressure, allowing more blood to return.

Return to the starting values and consider a different response to the same rise in Pmsf. This time Pra rises to 8 mm Hg:

16 − 8 = 8 mm Hg

At unchanged resistance:

8 ÷ 2 = 4 L/min

Both pressures have risen, but the difference between them has not changed. The model therefore predicts no flow increase.

Cecconi and colleagues examined fluid challenges in postsurgical ICU patients using a Pmsf analogue. The estimated upstream pressure increased in responders and nonresponders. In nonresponders, central venous pressure rose along with it, limiting the increase in the calculated venous-return gradient. This was an observational study using a model-derived pressure, so its findings must be interpreted with those dependencies in mind. 3

The examples show why higher filling pressures do not establish successful treatment. Check whether flow increased, whether perfusion improved, and whether the pressure rise worsened congestion. If fluid mainly raises Pra without improving flow, further loading may cause harm without correcting the perfusion problem.

7.7 Venous Tone: Recruiting Existing Volume

Sympathetic activity and vasoactive drugs can constrict veins. The constricted vessels hold less blood at low pressure. More of the existing volume then stretches the vessel walls and generates recoil pressure. This can increase the modeled stressed volume without adding blood.

This is one reason norepinephrine can increase cardiac filling. It can also change resistance along the return pathway, stimulate the myocardium, and increase arterial ejection load. These effects occur together. The final flow response depends on their balance rather than on venous recruitment alone.

Persichini and colleagues reduced norepinephrine in 16 patients with septic shock. Estimated mean systemic pressure and Rvr both fell. Lower resistance would favor return at the same gradient, but the fall in upstream pressure reduced the gradient enough that return fell overall. The study demonstrates effects beyond arterial pressure. Its selected patients and physiological design do not establish the same output response in every shock state. 4

Recruitment of existing volume is not the same as replacing lost blood. A patient with hemorrhage still requires treatment of the bleeding and the consequences of actual volume loss. Likewise, a patient with poor right ventricular function may not convert additional filling pressure into useful flow.

Withdrawal of a vasoactive drug can change this balance again. Falling venous tone may reduce the pressure supporting return even if total blood volume has not changed. A new fall in output should therefore prompt reassessment rather than an automatic conclusion that the patient has developed a new fluid deficit.

The net effect of a vasoactive adjustment should be judged through arterial pressure, flow, perfusion, and congestion. The direction of any one measurement cannot capture the entire response.

7.8 Ventilation and External Pressure

Positive-pressure ventilation changes pressure around the right atrium and thoracic veins. It can increase the atrial pressure measured relative to atmosphere and alter the gradient supporting return.

Upstream pressure can change as well. Positive airway pressure may be transmitted to the abdomen or redistribute venous blood. Either can alter the pressure supporting return. A fall in output therefore cannot always be explained by assuming an unchanged Pmsf and a higher Pra.

Jellinek and colleagues studied ten patients undergoing defibrillator implantation. Positive airway pressure increased both right atrial pressure and the estimated upstream filling pressure. The measured pressure gradient remained similar even though stroke volume fell. This selected physiological study illustrates why changes in return cannot always be explained by a downstream pressure rise alone. 5

At the same time, lung inflation can change right ventricular afterload. A fall in output after increasing PEEP may therefore involve impaired venous return, increased right ventricular load, or both. Improved oxygenation does not exclude an adverse circulatory response.

During spontaneous inspiration, falling intrathoracic pressure can lower Pra relative to the systemic venous compartment and favor return. The additional blood must still pass through the right ventricle and lungs. Strong negative pressure also increases left ventricular transmural ejection pressure. Greater inspiratory effort can therefore increase filling while making left ventricular ejection harder. It does not guarantee a sustained rise in useful output.

Rising abdominal pressure can squeeze blood from abdominal veins toward the thorax. It can also compress the veins through which that blood must travel and raise pressure opposing organ drainage. Whether flow increases depends on which effect predominates and whether the heart can handle the extra return.

These interactions explain why pressure measurements must be compared under documented respiratory and positional conditions. A change in central venous pressure after intubation should not automatically be interpreted as an increase in blood volume or improved preload.

7.9 Estimating Mean Systemic Filling Pressure at the Bedside

Pmsf cannot ordinarily be measured by directly stopping the whole systemic circulation in a living patient. Bedside approaches therefore estimate the pressure using maneuvers or mathematical models.

One bedside method uses several inspiratory holds to change Pra and measures flow during each hold. Each pressure–flow pair becomes a point on an estimated venous-return curve. A line is fitted through these points and extended to where it would cross zero flow. The pressure at that intercept estimates Pmsf. The method projects toward zero flow; it does not actually stop the patient’s circulation.

Maas and colleagues used inspiratory-hold maneuvers in postoperative cardiac surgery patients to estimate venous-return curves and Pmsf. Their work demonstrated the feasibility of studying these relationships with an intact circulation. It also depended on the assumptions that the measured flow and pressure pairs adequately represented the modeled relationship. 6

The method requires suitable ventilation, stable conditions, and reliable pressure and flow measurements. Pressure transmission, venous redistribution, and the time taken to reach a new state can affect the estimate. It should not be treated as a universally applicable direct measurement.

Another method briefly isolates an arm from the flowing circulation and allows local arterial and venous pressures to approach equilibrium. It uses that local equilibrium pressure as an estimate. A third method calculates a mathematical analogue from arterial pressure, central venous pressure, cardiac output, and assumed vascular properties. These methods obtain their values differently and can therefore produce different estimates.

Maas and colleagues compared these approaches in a small postoperative cardiac surgery population. The methods tracked some changes in the same direction, but absolute estimates differed, particularly for the mathematical analogue. Their study illustrates why numerical estimates must retain the name and assumptions of the method used. Agreement observed in one selected population does not establish interchangeability everywhere. 7

A mathematical estimate that includes cardiac output partly changes because the entered output changes. Finding an association between that estimate and output may therefore reflect their shared input as well as physiology. Such a calculation does not independently confirm the output measurement. Identify the method and its assumptions before using an estimated Pmsf to support a clinical interpretation.

7.10 Venous Congestion and Organ Function

A circulation can contain substantial volume and high filling pressures while delivering inadequate useful flow. In that setting, a further increase in pressure may worsen organ function.

High venous pressure raises the downstream pressure against which an organ drains. If arterial pressure stays unchanged, the pressure difference across the organ narrows and flow may fall. Higher venous pressure can also raise microvascular pressure and increase filtration into tissue. Edema develops if filtration exceeds lymphatic removal. The consequences depend on the organ and its surrounding pressures.

The kidney is an important example. Renal arterial pressure is only one side of its perfusion environment. Venous pressure and pressure within the abdomen and kidney can also affect function. Low urine output therefore does not prove that the kidney requires additional intravascular volume.

Mullens and colleagues found an association between venous congestion and worsening renal function in patients with advanced decompensated heart failure. This observational study supports attention to the venous side of the circulation. It does not establish a universal central venous pressure target or prove that every episode of kidney dysfunction will respond to fluid removal. 8

The appropriate assessment integrates venous pressure with cardiac function, pulmonary findings, organ perfusion, and the response to prior interventions. A high pressure may partly reflect external pressure, so the measured number alone is insufficient.

Fluid removal can reduce venous pressure and congestion. It can also reduce stressed volume and the upstream pressure supporting return. The aim is therefore to relieve congestion while maintaining enough flow for perfusion. Follow output and organ function as removal proceeds instead of assuming that a lower venous pressure is always beneficial.

7.11 Applying the Venous-Return Model at the Bedside

Consider an illustrative patient with persistent shock and rising venous pressure after fluid. Cardiac output has changed little. Echocardiography shows impaired right ventricular ejection, and peripheral perfusion remains poor.

The first interpretation should not be that the circulation simply needs a higher upstream filling pressure. The heart may be unable to move additional return through the pulmonary circulation. Further loading could raise right atrial pressure and congestion without producing useful additional output.

Use assumed values to illustrate the mechanism. Let Pmsf be 18 mm Hg, Pra 10 mm Hg, and Rvr 2 mm Hg·min/L:

Return = (18 − 10) ÷ 2 = 4 L/min

If loading raises Pmsf to 22 mm Hg and Pra to 14 mm Hg:

Return = (22 − 14) ÷ 2 = 4 L/min

Both pressures have risen by 4 mm Hg. Their difference remains 8 mm Hg, so modeled flow remains 4 L/min. The example does not assign measured Pmsf or Rvr to this patient; it explains how venous pressure can rise without a flow increase.

The next assessment must identify what is limiting right ventricular output. Pulmonary vascular load, ventilation, ischemia, rhythm, valve function, and mechanical obstruction may be relevant. The role of systemic vascular tone also requires assessment. No single component of the venous-return equation selects the treatment.

In a different patient, vasodilation with preserved cardiac reserve may reduce the pressure supporting return. A vasoactive adjustment could recruit existing venous volume and improve flow. That mechanism must be checked against the actual response rather than assumed from the arterial pressure increase.

Use the model to explain the observed response. Additional volume helps flow only if it changes the pressure–resistance relationship in a way the heart can use. Check the gradient, the return pathway, and ventricular ejection together. Then judge treatment by perfusion and congestion as well as flow.

References

1. Guyton AC, Lindsey AW, Abernathy B, Richardson T. Venous return at various right atrial pressures and the normal venous return curve. American Journal of Physiology. 1957;189(3):609–615. doi:10.1152/ajplegacy.1957.189.3.609.

2. Guyton AC, Abernathy B, Langston JB, Kaufmann BN, Fairchild HM. Relative importance of venous and arterial resistances in controlling venous return and cardiac output. American Journal of Physiology. 1959;196(5):1008–1014. doi:10.1152/ajplegacy.1959.196.5.1008.

3. Cecconi M, Aya HD, Geisen M, et al. Changes in the mean systemic filling pressure during a fluid challenge in postsurgical intensive care patients. Intensive Care Medicine. 2013;39(7):1299–1305. doi:10.1007/s00134-013-2928-6.

4. Persichini R, Silva S, Teboul JL, et al. Effects of norepinephrine on mean systemic pressure and venous return in human septic shock. Critical Care Medicine. 2012;40(12):3146–3153. doi:10.1097/CCM.0b013e318260c6c3.

5. Jellinek H, Krenn H, Oczenski W, Veit F, Schwarz S, Fitzgerald RD. Influence of positive airway pressure on the pressure gradient for venous return in humans. Journal of Applied Physiology. 2000;88(3):926–932. doi:10.1152/jappl.2000.88.3.926.

6. Maas JJ, Geerts BF, van den Berg PCM, Pinsky MR, Jansen JRC. Assessment of venous return curve and mean systemic filling pressure in postoperative cardiac surgery patients. Critical Care Medicine. 2009;37(3):912–918. doi:10.1097/CCM.0b013e3181961481.

7. Maas JJ, Pinsky MR, Geerts BF, de Wilde RB, Jansen JR. Estimation of mean systemic filling pressure in postoperative cardiac surgery patients with three methods. Intensive Care Medicine. 2012;38(9):1452–1460. doi:10.1007/s00134-012-2586-0.

8. Mullens W, Abrahams Z, Francis GS, et al. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. Journal of the American College of Cardiology. 2009;53(7):589–596. doi:10.1016/j.jacc.2008.05.068.