Venous return curve

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Venous return is the rate of blood flow back to the heart. It normally limits cardiac output.

Contents

Superposition of the cardiac function curve and venous return curve is used in one hemodynamic model. [1]

Physiology

Venous return (VR) is the flow of blood back to the heart. Under steady-state conditions, venous return must equal cardiac output (Q), when averaged over time because the cardiovascular system is essentially a closed loop. Otherwise, blood would accumulate in either the systemic or pulmonary circulations. Although cardiac output and venous return are interdependent, each can be independently regulated.

The circulatory system is made up of two circulations (pulmonary and systemic) situated in series between the right ventricle (RV) and left ventricle (LV). Balance is achieved, in large part, by the Frank–Starling mechanism. For example, if systemic venous return is suddenly increased (e.g., changing from upright to supine position), right ventricular preload increases leading to an increase in stroke volume and pulmonary blood flow. The left ventricle experiences an increase in pulmonary venous return, which in turn increases left ventricular preload and stroke volume by the Frank–Starling mechanism. In this way, an increase in venous return can lead to a matched increase in cardiac output.

Hemodynamically, venous return (VR) to the heart from the venous vascular beds is determined by a pressure gradient (venous pressure - right atrial pressure) and venous resistance (RV). Therefore, increases in venous pressure or decreases in right atrial pressure or venous resistance will lead to an increase in venous return, except when changes are brought about by altered body posture. Although the above relationship is true for the hemodynamic factors that determine the flow of blood from the veins back to the heart, it is important not to lose sight of the fact that blood flow through the entire systemic circulation represents both the cardiac output and the venous return, which are equal in the steady-state because the circulatory system is closed. Therefore, one could just as well say that venous return is determined by the mean aortic pressure minus the mean right atrial pressure, divided by the resistance of the entire systemic circulation (i.e., the systemic vascular resistance). [2]

It is often suggested that venous return dictates cardiac output, effected through the Frank Starling mechanism. However, as noted above it is clear that, equally, cardiac output must dictate venous return since over any period of time both must necessarily be equal. Similarly, the concept of mean systemic filling pressure, the hypothetical driving pressure for venous return, is difficult to localise and impossible to measure in the physiological state. Furthermore, the Ohmic formulation used to describe venous return ignores the critical venous parameter, capacitance. It is confusion about these terms that has led some physiologists to suggest that the emphasis on 'venous return' be turned instead to more measurable and direct influences on cardiac output such as end diastolic pressure and volume which can be causally related to cardiac output and through which the influences of volume status, venous capacitance, ventricular compliance and venodilating therapies can be understood. [3]

Factors affecting venous return mechanism

  1. Musculovenous pump: Rhythmical contraction of limb muscles as occurs during normal locomotory activity (walking, running, swimming) promotes venous return by the muscle pump mechanism.
  2. Decreased venous capacitance : Sympathetic activation of veins decreases venous compliance, increases vasomotor tone, increases central venous pressure and promotes venous return indirectly by augmenting cardiac output through the Frank-Starling mechanism, which increases the total blood flow through the circulatory system.
  3. Respiratory pump: During inspiration, the intrathoracic pressure is negative (suction of air into the lungs), and abdominal pressure is positive (compression of abdominal organs by diaphragm). This makes a pressure gradient between the infra- and supradiaphragmatic parts of v. cava inferior, "pulling" the blood towards the right atrium and increasing venous return.
  4. Vena cava compression: An increase in the resistance of the vena cava, as occurs when the thoracic vena cava becomes compressed during a Valsalva maneuver or during late pregnancy, decreases return.
  5. Gravity: The effects of gravity on venous return seem paradoxical because when a person stands up, hydrostatic forces cause the right atrial pressure to decrease and the venous pressure in the dependent limbs to increase. This increases the pressure gradient for venous return from the dependent limbs to the right atrium; however, venous return actually decreases. The reason for this is when a person initially stands, cardiac output and arterial pressure decrease (because right atrial pressure falls). The flow through the entire systemic circulation falls because arterial pressure falls more than right atrial pressure; therefore the pressure gradient driving flow throughout the entire circulatory system is decreased.
  6. Pumping action of the heart: During the cardiac cycle right atrial pressure changes alter central venous pressure (CVP), because there is no valve between the heart's atria and the large veins. CVP reflects right atrial pressure. Therefore, right atrial pressure also alters venous return.

Related Research Articles

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The blood circulatory system is a system of organs that includes the heart, blood vessels, and blood which is circulated throughout the entire body of a human or other vertebrate. It includes the cardiovascular system, or vascular system, that consists of the heart and blood vessels. The circulatory system has two divisions, a systemic circulation or circuit, and a pulmonary circulation or circuit. Some sources use the terms cardiovascular system and vascular system interchangeably with the circulatory system.

<span class="mw-page-title-main">Systole</span> Part of the cardiac cycle when a heart chamber contracts

Systole is the part of the cardiac cycle during which some chambers of the heart contract after refilling with blood. The term originates, via New Latin, from Ancient Greek συστολή (sustolē), from συστέλλειν, and is similar to the use of the English term to squeeze.

Hemodynamics or haemodynamics are the dynamics of blood flow. The circulatory system is controlled by homeostatic mechanisms of autoregulation, just as hydraulic circuits are controlled by control systems. The hemodynamic response continuously monitors and adjusts to conditions in the body and its environment. Hemodynamics explains the physical laws that govern the flow of blood in the blood vessels.

<span class="mw-page-title-main">Diastole</span> Part of the cardiac cycle

Diastole is the relaxed phase of the cardiac cycle when the chambers of the heart are re-filling with blood. The contrasting phase is systole when the heart chambers are contracting. Atrial diastole is the relaxing of the atria, and ventricular diastole the relaxing of the ventricles.

<span class="mw-page-title-main">Mitral stenosis</span> Heart disease with narrowing of valve

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<span class="mw-page-title-main">Atrial septal defect</span> Human heart defect present at birth

Atrial septal defect (ASD) is a congenital heart defect in which blood flows between the atria of the heart. Some flow is a normal condition both pre-birth and immediately post-birth via the foramen ovale; however, when this does not naturally close after birth it is referred to as a patent (open) foramen ovale (PFO). It is common in patients with a congenital atrial septal aneurysm (ASA).

Vascular resistance is the resistance that must be overcome to push blood through the circulatory system and create flow. The resistance offered by the systemic circulation is known as the systemic vascular resistance (SVR) or may sometimes be called by the older term total peripheral resistance (TPR), while the resistance offered by the pulmonary circulation is known as the pulmonary vascular resistance (PVR). Systemic vascular resistance is used in calculations of blood pressure, blood flow, and cardiac function. Vasoconstriction increases SVR, whereas vasodilation decreases SVR.

<span class="mw-page-title-main">Jugular venous pressure</span>

The jugular venous pressure is the indirectly observed pressure over the venous system via visualization of the internal jugular vein. It can be useful in the differentiation of different forms of heart and lung disease. Classically three upward deflections and two downward deflections have been described.

<span class="mw-page-title-main">Fontan procedure</span>

The Fontan procedure or Fontan–Kreutzer procedure is a palliative surgical procedure used in children with univentricular hearts. It involves diverting the venous blood from the inferior vena cava (IVC) and superior vena cava (SVC) to the pulmonary arteries without passing through the morphologic right ventricle; i.e., the systemic and pulmonary circulations are placed in series with the functional single ventricle. The procedure was initially performed in 1968 by Francis Fontan and Eugene Baudet from Bordeaux, France, published in 1971, simultaneously described in 1971 by Guillermo Kreutzer from Buenos Aires, Argentina, and finally published in 1973.

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<span class="mw-page-title-main">Cardiac cycle</span> Performance of the human heart

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Central venous pressure (CVP) is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. CVP is often a good approximation of right atrial pressure (RAP), although the two terms are not identical, as a pressure differential can sometimes exist between the venae cavae and the right atrium. CVP and RAP can differ when arterial tone is altered. This can be graphically depicted as changes in the slope of the venous return plotted against right atrial pressure.

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The bidirectional Glenn (BDG) shunt, or bidirectional cavopulmonary anastomosis, is a surgical technique used in pediatric cardiac surgery procedure used to temporarily improve blood oxygenation for patients with a congenital cardiac defect resulting in a single functional ventricle. Creation of a bidirectional shunt reduces the amount of blood volume that the heart needs to pump at the time of surgical repair with the Fontan procedure.

In medicine, the mean systemic pressure is defined as the mean pressure that exists in the circulatory system when there is no blood motion. A similar term, mean circulatory filling pressure, (MCFP) is defined as the mean pressure that exists in the combined circulatory system & pulmonary system when there is no blood motion. The value of MSP in animal experimental models is approximately 7 mm Hg. It is an indicator of how full the circulatory system is, and is influenced by the volume of circulating blood and the smooth muscle tone in the walls of the venous system .

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

A plot of a system's pressure versus volume has long been used to measure the work done by the system and its efficiency. This analysis can be applied to heat engines and pumps, including the heart. A considerable amount of information on cardiac performance can be determined from the pressure vs. volume plot. A number of methods have been determined for measuring PV-loop values experimentally.

<span class="mw-page-title-main">Pathophysiology of heart failure</span>

The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and cardiac amyloidosis. Over time these increases in workload will produce changes to the heart itself:

References

  1. Brengelmann GL (March 2003). "A critical analysis of the view that right atrial pressure determines venous return". J. Appl. Physiol. 94 (3): 849–59. doi:10.1152/japplphysiol.00868.2002. PMID   12391065.
  2. Klabunde, Richard E. "Venous Return - Hemodynamics". Cardiovascular Physiology Concepts. Retrieved 8 March 2011.
  3. Reddi; Carpenter (2005). "Venous excess: a new approach to cardiovascular control and its teaching". J Appl Physiol. 98 (1): 356–364. doi:10.1152/japplphysiol.00535.2004. PMID   15322065. S2CID   12499872 . Retrieved 10 Dec 2014.