Increased pulmonary venous return to the left atrium leads to increased filling preload of the left ventricle, which in turn increases left ventricular stroke volume by the Frank-Starling mechanism. In this way, an increase in venous return to the heart leads to an equivalent increase in cardiac output to the systemic circulation. Hemodynamically, venous return VR to the heart from the venous vascular beds is determined by a pressure gradient venous pressure, P V , minus right atrial pressure, P RA divided by the venous vascular resistance R V between the two pressures as shown to the figure.
Therefore, increased venous pressure or decreased right atrial pressure, or decreased venous resistance leads to an increase in venous return.
P RA is normally very low fluctuating a few mmHg around a mean of 0 mmHg and P V in peripheral veins when the body is supine is only a few mmHg higher. Because of this, small changes of only a few mmHg pressure in either P V or P RA can cause a large percent change in the pressure gradient, and therefore significantly alter the return of blood to the right atrium.
For example, during lung expansion inspiration , P RA can transiently fall by several mmHg, whereas the P V in the abdominal compartment may increase by a few mmHg. These changes result in a large increase in the pressure gradient driving venous return from the peripheral circulation to the right atrium.
Although the above relationship is true for the hemodynamic factors that determine the flow of blood from peripheral veins abdominal venous cava in the figure back to the right atrium of the heart, it is important not to lose sight of the fact that blood flow through the entire systemic circulation can be represented by either the cardiac output or the venous return, because these are equal in the steady-state owing to the circulatory system being 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.
There is much confusion about the pressure gradient that determines venous return largely because of different conceptual models that are used to describe venous return.
Furthermore, although transient differences occur between the flow of blood leaving cardiac output and entering the heart venous return , these differences when they occur cause adjustments that rapidly return in a new steady-state in which cardiac output flow out equals venous return flow in.
Transient changes in venous return can occur in response to several factors as listed below:. Increasing right atrial pressure impedes venous return, while lowering this pressure facilitates venous return. Respiratory activity can also affect the diameter of the thoracic vena cava and cardiac chambers, which either directly e.
Pressures in the right atrium and thoracic vena cava are very dependent on intrapleural pressure P pl , which is the pressure within the thoracic space between the organs lungs, heart, vena cava and the chest wall.
During inspiration, the chest wall expands and the diaphragm descends see animated figure. This makes the P pl become more negative, which leads to expansion of the lungs, cardiac chambers right atrium [RA] and right ventricle [RV] , and the thoracic superior and inferior vena cava SVC and IVC, respectively.
This expansion causes the intravascular and intracardiac pressures e. Because the pressure inside the cardiac chambers falls less than the P pl , the transmural pressure pressure inside the heart chamber minus the P pl increases, which leads to cardiac chamber expansion and an increase in cardiac preload and stroke volume through the Frank-Starling mechanism.
Furthermore, as right atrial pressure falls during inspiration, the pressure gradient for venous return to the right ventricle increases. During expiration, the opposite occurs although the dynamics are such that the net effect of respiration is that increasing the rate and depth of ventilation facilitates venous return and ventricular stroke volume.
The left side of the heart responds differently to the respiratory cycle. During inspiration, expansion of the lungs and pulmonary tissues causes pulmonary blood volume to increase, which transiently decreases the flow of blood from the lungs to the left atrium.
Therefore, left ventricular filling actually decreases during inspiration. In contrast, during expiration, lung deflation causes flow to increase from the lungs to the left atrium, which increases left ventricular filling.
The net effect of increased rate and depth of respiration, however, is an increase in left ventricular stroke volume and cardiac output. Cardiovascular Physiology Concepts Richard E.
Klabunde, PhD. Klabunde, all rights reserved Web Design by Jimp Studio.
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