Venous return

The most distensible vessels in the circulatory system are the veins. As with arteries, this feature of the veins also has important physiological implications because it allows them to serve as blood reservoirs. The veins are so distensible that they are capable of holding large volumes of blood at very low pressures. In fact, under resting conditions, 64% of the blood volume is contained within these vessels. 

Compliance (C) in the circulatory system describes the relationship between vascular blood volume (V) and intravascular pressure (P)  

In other words, it is a measure of the inherent distensibility of the blood vessels. The more compliant the vessel is, then the greater the volume of blood that it is capable of accommodating. As mentioned, all blood vessels are compliant. However, the marked difference in distensibility between arteries and veins is illustrated by the following  

Due to the significant amount of elastic connective tissue and smooth muscle in their walls, arteries tend to recoil rather powerfully, which keeps the pressure within them high. In contrast, veins contain less elastic connective tissue and smooth muscle so the tendency to recoil is significantly less and the pressure remains low. 

In addition to serving as blood reservoirs, veins help to regulate cardiac output (CO) by way of changes in venous return (VR). Venous return is defined as the volume of blood that flows from the systemic veins into the right atrium per minute. As discussed in Chapter 14 (cardiac output), a healthy heart pumps all of the blood returned to it. Therefore, CO is equal to VR  

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Both vasoconstrictors and vasodilators have been used in the treatment of priapism. Vasoconstrictors are thought to work by forcing blood out of the cavernosum and into the venous return. Aspiration of the penile blood followed by intracavenous irrigation with epinephrine (1 1,000,000 solution) has been effective with minimal complications.37 In severe cases, surgical intervention to place penile shunts has been used, but there is a high failure rate, and the risk of complications, from skin sloughing to fistulas, limits its use. 

Frank-Starling mechanism The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return. 

Figure 3 Possible blood circulation connections in a physiologically based pharmacokinetic model. (A) Venous return incorporated into lung mass balance equation (B) separate venous blood compartment. See text for definition of symbols.

Length of diastole Venous return (preload) Contractility of the myocardium Afterload Heart rate... 

Hypertension (blood pressure >140/90 mmHg) may be caused by an elevation in cardiac output or excessive vasoconstriction. Diuretics are used in these patients to reduce cardiac output. Assume that the hearts of these individuals are operating on the ascending portion of the cardiac function curve. As the plasma volume is reduced in response to treatment with diuretic drugs, venous return and preload are reduced, as are ventricular filling and stroke volume, and cardiac output, thus bringing blood pressure back within the normal range. 

Explain how blood volume, sympathetic stimulation of the veins, skeletal muscle activity, and respiratory activity influence venous return... 

The sympathetic system also innervates vascular smooth muscle and regulates the radius of the blood vessels. All types of blood vessels except capillaries are innervated however, the most densely innervated vessels include arterioles and veins. An increase in sympathetic stimulation of vascular smooth muscle causes vasoconstriction and a decrease in stimulation causes vasodilation. Constriction of arterioles causes an increase in TPR and therefore MAP. Constriction of veins causes an increase in venous return (VR) which increases end-diastolic volume (EDV), SV (Frank-Starling law of the heart), CO, and MAP. 

Notes CO cardiac output VR venous return HR heart rate SV stroke volume EDV end-diastolic volume ESV end-systolic volume O blood flow AP pressure gradient R resistance r vessel radius P systolic pressure Piiastoik- diastolic pressure MAP mean arterial pressure TPR total peripheral resistance, P venous pressure Era- right atrial pressure Rv venous resistance. 

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

Low-pressure receptors. The low-pressure receptors are located in the walls of the atria and the pulmonary arteries. Similar to baroreceptors, low-pressure receptors are also stretch receptors however, stimulation of these receptors is caused by changes in blood volume in these low-pressure areas. An overall increase in blood volume results in an increase in venous return an increase in the blood volume in the atria and the pulmonary arteries and stimulation of the low-pressure receptors. These receptors then elicit reflexes by way of the vasomotor center that parallel those of baroreceptors. Because an increase in blood volume will initially increase MAP, sympathetic discharge decreases and parasympathetic discharge increases so that MAP decreases toward its normal value. The simultaneous activity of baroreceptors and low-pressure receptors makes the total reflex system more effective in the control of MAP. 

Baroreceptors are sensitive to changes in MAP. As VR, CO, and MAP decrease, baroreceptor excitation is diminished. Consequently, the frequency of nerve impulses transmitted from these receptors to the vasomotor center in the brainstem is reduced. This elicits a reflex that will increase HR, increase contractility of the heart, and cause vasoconstriction of arterioles and veins. The increase in CO and TPR effectively increases MAP and therefore cerebral blood flow. Constriction of the veins assists in forcing blood toward the heart and enhances venous return. Skeletal muscle activity associated with simply walking decreases venous pressure in the lower extremities significantly. Contraction of the skeletal muscles in the legs compresses the veins and blood is forced toward the heart. 

In other words, the increase in cardiac output occurs by extrinsic (sympathetic stimulation) and intrinsic (increased VR and the Frank-Starling law of the heart) mechanisms. Venous return is also markedly increased by the compression of blood vessels in the working muscles. TTie increase in CO causes an increase in MAP, and the increase in MAP contributes to an increase in muscle blood flow. 

Another condition that can impair venous return is pregnancy. As the uterus enlarges during gestation, it may cause compression of the veins draining the lower extremities. Once again, venous and capillary pressures are increased. Filtration is enhanced, reabsorption is inhibited, and edema develops in the lower extremities. 

The liver is a large and distensible organ. As such, large quantities of blood may be stored in its blood vessels providing a blood reservoir function. Under normal physiological conditions, the hepatic veins and hepatic sinuses contain approximately 450 ml of blood, or almost 10% of blood volume. When needed, this blood may be mobilized to increase venous return and cardiac output. 

Dilation, pooling of blood, decreased venous return, decreased cardiac output... 

Bolus diuretic administration decreases preload by functional venodilation within 5 to 15 minutes and later (>20 min) via sodium and water excretion, thereby improving pulmonary congestion. However, acute reductions in venous return may severely compromise effective preload in patients with significant diastolic dysfunction or intravascular depletion. 

The inhibition of sympathetic tone to the venous system (capacitance vessels) results in increased pooling of blood in the venous vascular bed with consequent decreased venous return to the heart and decreased cardiac output. This phenomenon is more pronounced in upright positions because of the effect of gravity. The hemodynamic effects of ganglionic blockers include decreases in cardiac output, renal blood flow, cerebral blood flow and orthostatic hypotension(20,21). 

The curve flattens at very high Po2 as the whole protein reaches saturation point . At rest, haemoglobin in the blood which enters the general circulation from the left side of the heart is about 98% saturated with oxygen and the venous return is approximately 75% saturated with oxygen. 

Venous return will depend on pressure relations ... 

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