Venous return curve - Wikipedia
THE CARDIAC OUT PUT AND VENOUS RETURN. The vascular function ( venous return) curve depicts the relationship between blood flow. Changes in cardiac output without changes in stressed volume occur because of changes in arterial and venous resistances which redistribute. Under steady-state conditions, venous return must equal cardiac output (CO) when Although the above relationship is true for the hemodynamic factors that .
They could also augment flow into the atrium from a reservoir, thereby increasing right atrial pressure. Some of the experiments were conducted with closed chest animals that were breathing again negative pressure as low as —10 mm Hg, lowering the intrathoracic and right atrial pressures to the lowest physiological levels. These extensive series of experiments laid the groundwork for an in-depth understanding of the basic factors controlling venous return.
Determinants of Venous Return Everywhere in the body, pressure gradients and resistances determine blood flow rate. When considering venous return, the pressure gradient is mean systemic pressure minus the right atrial pressure, and resistance is the total peripheral vascular resistance.
It is probable that some of the difficulties associated with conceptualizing and measuring mean systemic pressure have contributed to the challenges in understanding venous return.
Mean systemic pressure is affected by blood volume and vascular tone. When blood volume is normal, mean systemic pressure is approximately 7 mm Hg [ 34 ]. If mean systemic pressure is measured after blood volume has been changed rapidly in steps above and below normal while sympathetic nervous system activity has been blocked, a volume—pressure relationship is obtained. An example of such a curve is illustrated by the solid line in Figure 2. Several of its characteristics are significant: The blood volume at which mean systemic pressure is 0 mm Hg is termed the unstressed vascular volume of the system.
Reducing blood volume below the unstressed vascular volume does not result in further reduction in mean systemic pressure. The sympathetic nervous system and locally acting and circulating vasoactive hormones affect vascular smooth muscle tone. Increasing vascular tone shifts the volume—pressure curve to the left without significantly affecting the slope. When vascular tone increases, unstressed volume decreases and mean systemic pressure increases for each level of blood volume.
Conversely, totally blocking the sympathetic nervous system or otherwise reducing vasomotor tone has been shown to shift the curve to the right in a parallel manner. The vessels on the arterial side have much less capacity and are much less distensible than the veins, and consequently, the characteristics of their volume—pressure relationship differ markedly from those of the venous side; the unstressed arterial vascular volume is approximately 0.
In addition, the arterial vessel wall is more responsive to sympathetic nervous system innervation and vasoactive hormones. Several sites in the vascular system have large reservoir capacities. Portions of the vascular system have a large capacitance, that is, they can gain or lose large volumes of blood with little change in pressure.
Therefore, as pressure within other portions of the venous system increases or decreases, large volumes of blood can move into or out of these reservoirs, buffering changes in pressure throughout the vascular system.
Smooth muscle of the vascular walls of some of the vessels in these sites can contract in response to sympathetic stimulation and circulating vasoconstrictor substances, significantly decreasing their capacitance and causing additional blood to be translocated to other portions of the circulation.
Large veins in the abdomen and thorax are especially effective reservoirs, as are the sinuses of the spleen and liver. The vascular plexuses of the skin can also function as reservoirs.
Blood flow into the skin is highly responsive to catecholamines released from the sympathetic nerves innervating the resistance vessels of the skin, the constriction of which decreases blood volume stored in the veins of the skin.
All of these reservoir functions can significantly affect mean systemic pressure, as their effective capacitance is altered, and blood is transferred to or from other portions of the vascular system. The vasopressor hormone angiotensin II is implicated as a causative factor in many forms of hypertension. The renal sodium-retaining effects of angiotensin II are the primary mechanisms contributing to sustained blood pressure elevation, although the peptide has other significant vascular actions.
Its effects on mean systemic pressure were analyzed in a series of studies in dogs in which angiotensin II was infused intravenously for 7 days, raising mean arterial blood pressure from the normal level of to mm Hg [ 5 ].
Blood volume remained unchanged, while mean systemic pressure rose from 9. The effect of the hormone was to increase the vascular tone, causing an increase in filling pressure at a constant blood volume. Right atrial pressure is normally approximately 0 mm Hg or atmospheric pressure. At a normal level of right atrial pressure, venous return will be normal as long as mean systemic pressure and resistance are normal.
Each additional 1 mm Hg increase resulted in a similar decrease in venous return, until atrial pressure reached 7 mm Hg, the mean systemic pressure, at which point flow into the heart ceased. The results of their study are plotted in Figure 2. As atrial pressure is raised from the normal value of 0 to 7 mm Hg, venous return falls from the normal level to 0.
Venous return curve
The slope of the relationship is the inverse of the more When right atrial pressure is reduced below the normal value of 0 mm Hg, a different venous return response pattern is observed. But with subsequent 1 mm Hg increments in pressure reduction, the rate of rise in venous return falls progressively less until it reaches a steady level at pressures below —4 mm Hg.
Further right atrial pressure reductions below —4 mm Hg will not increase venous return further. The negative right atrial pressure and venous return data are presented in Figure 2. The relationship becomes curved as pressure falls to approximately —2 to —3 mm Hg as the slope decreases progressively with additional reductions in atrial pressure.
At approximately —4 mm Hg, the slope becomes 0, and further reductions do not cause additional increases in venous return. The relationship is curvilinear between —2 and —4 mm Hg due to progressively increasing resistance to venous return resulting from collapse of more The explanation for the nonlinear nature of the relationship in the negative pressure range of the right atrial pressure and the plateau below —4 mm Hg is the progressive collapse of veins as the luminal pressure falls below extramural pressure.
Within the chest, the pressure averages approximately —4 mm Hg but cycles between values more negative during inspiration to slightly positive during expiration. As right atrial pressure, which is equal to venous pressure anywhere within the thorax, falls below atmospheric pressure, some veins just outside their point of entry into the thorax may collapse during inspiration, as their intraluminal pressure falls below atmospheric pressure. As central venous pressure falls lower, more veins may collapse for longer portions of the respiratory cycle, while below —4 mm Hg, essentially, all veins in the chest remain collapsed until the buildup of upstream blood increases their intraluminal pressure to —4 mm Hg or greater.
The collapse of the veins increases resistance to venous return, which is the inverse of the slope of the relationship between flow and right atrial pressure.
Ultimately, resistance becomes infinite below —4 mm Hg, preventing any increase in flow above that present at —4 mm Hg. The resistance increases progressively as right atrial pressure falls from approximately —2 to —4 mm Hg, causing the plotted relationship between pressure and flow to be curvilinear in this range. The pulsations of the right atrium cause a retrograde pressure wave that may progress through the central veins to varying distances. These pulses contribute to the fluctuations in venous closure that occur in the negative right atrial pressure range that are reflected in the curve or splay of the pressure—flow relationship.
Changes in arterial as well as venous resistances affect venous return. In Chapter 1the progressive blood pressure reductions throughout the vascular system were presented in Table 1.The Cardiovascular System and Venous Return
The greatest segmental pressure reduction occurs at the arterioles, indicating that arterioles contribute the largest portion of total systemic vascular resistance. Furthermore, the resistance of the arterioles is highly dynamic, capable of increasing or decreasing several folds in a few seconds.
The smooth muscle in the arteriole walls responds rapidly to changes in concentrations of circulating vasoactive hormones, local metabolically linked mediators, and input from fibers of the sympathetic nervous system. Angiotensin II and catecholamines in the blood and locally produced endothelin are powerful arteriolar smooth muscle agonists, significantly affecting resistance to venous return. In the experiment referred to above, in which angiotensin II was infused into dogs for 7 days, venous return remained unchanged while mean systemic pressure increased from 9.
During this period, right atrial pressure increased slightly from 1. Calculating resistance to venous return during the control period from the pressure gradient for venous return mean systemic pressure—right atrial pressure and the rate of venous return cardiac output yields a value of 2.
After 7 days of angiotensin infusion, resistance to venous return increased to 3. In a study on dogs, after a 7-day control period, angiotensin II was infused intravenously for an additional 7 days. Locally produced and circulating nitric oxide, prostacyclin, and prostaglandin E2 are vascular smooth muscle antagonists, producing arteriolar dilation and reduction of resistance to venous return.
Local tissue metabolism, in particular, aerobic metabolism, strongly affects arteriolar resistance. Activity that reduces tissue pO2 especially elicits significant arteriolar dilation and reduction in resistance to venous return. The linkage between total body tissue oxygen demand and resistance to venous return is a fundamental mechanism governing control of cardiac output. This is the basic mechanism by which the cardiovascular system responds to changes in demand for cardiac output as metabolic rate changes.
Other means of cardiovascular control may take part in responses to metabolic changes, but this connection of tissue oxygen demand to resistance to venous return is of overriding significance. Oxygen demand is a strong determinant of resistance to venous return over periods ranging from seconds to hours and in long-term and steady-state conditions.
If demand is elevated for extended periods of days or weeks, new microvascular vessels grow through the tissue in need, decreasing local vascular resistance and increasing blood flow. Conversely, if blood flow exceeds demand for periods of several days or more, microvascular vessels will degenerate, reducing vascular density and increasing resistance. This process is termed rarifaction and normally normally takes place in tissues whose use and metabolic activity are reduced.
Rarifaction also may occur if arterial blood pressure increases. For example, in the angiotensin II infusion experiment, the infusion resulted in a steady-state increase in arterial blood pressure of 60 mm Hg by affecting renal function, and the peptide had an immediate direct constrictor effect on the arterioles throughout the body. But during the 7-day course of the study, the sustained increase in arterial pressure may have induced microvascular rarifaction throughout the body.
The immediate and delayed increases in tissue resistance throughout the body may both have contributed to the increase in observed resistance to venous return during the infusion period. The relatively large diameter of central veins presents little resistance to flowing blood, although they are easily compressed and flattened by surrounding tissue. When they are compressed, they create significant resistance. For example, many veins entering the thorax over the first ribs are partially compressed by the sharp angle of the path over the bone.
In the abdomen, the weight of the viscera may flatten the great veins, and in the neck, atmospheric pressure prevents the jugular veins from assuming a rounded shape when a person is upright. Within the thorax, the veins may collapse if central venous pressure falls much lower than the atmospheric pressure. Even considering these impediments to blood flow, venous resistance is a relatively minor component of resistance to venous return.
Arterial resistance, especially that portion resulting from the arterioles, makes up the greatest portion of total vascular resistance. It is this portion that is most actively regulated in response to changes in demand of the circulatory system. 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.
Rhythmical contraction of limb muscles as occurs during normal locomotory activity walking, running, swimming promotes venous return by the muscle pump mechanism. Sympathetic activation of veins decreases venous compliance, increases venomotor 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.
During inspiration, the intrathoracic pressure is negative suction of air into the lungsand abdominal pressure is positive compression of abdominal organs by diaphragm. This makes a pressure gradient between the infra- and supradiaphragmatic parts of v.
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.
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.
CV Physiology | Venous Return - Hemodynamics
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.
Pumping action of the heart: During the cardiac cycle right atrial pressure changes alter central venous pressure CVPbecause 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.