FUNCTION OF THE VASCULAR SYSTEM
The amount of blood flow needed by body tissues constantly changes. The percentage of blood flow received by individual or-gans or tissues is determined by the rate of tissue metabolism, the availability of oxygen, and the function of the tissues (Table 31-1). When metabolic requirements increase, blood vessels dilate to in-crease the flow of oxygen and nutrients to the tissues. When metabolic needs decrease, vessels constrict, and blood flow to the tissues decreases. Metabolic demands of tissues increase with physical activity or exercise, local heat application, fever, and in-fection. Reduced metabolic requirements of tissues accompany rest or decreased physical activity, local cold application, and cooling of the body. If the blood vessels fail to dilate in response to the need for increased blood flow, tissue ischemia (ie, deficient blood supply to a body part) results. The mechanism by which blood vessels dilate and constrict to adjust for metabolic changes ensures that normal arterial pressure is maintained.
As blood passes through tissue capillaries, oxygen is removed, and carbon dioxide is added. The amount of oxygen extracted by each tissue differs. For example, the myocardium tends to extract about 50% of the oxygen from arterial blood in one pass through its capillary bed, whereas the kidneys extract only about 7% of the oxygen from the blood that passes through them. The aver-age amount of oxygen removed collectively by all of the body tis-sues is about 25%. This means that the blood in the vena cavae contains about 25% less oxygen than aortic blood. This is known as the systemic arteriovenous oxygen difference. The value increases when the amount of oxygen delivered to the tissues is decreased relative to their metabolic needs (see Table 31-1).
Blood flow through the cardiovascular system always proceeds in the same direction: left side of the heart to the aorta, arteries, ar-terioles, capillaries, venules, veins, vena cavae, and right side of the heart. This unidirectional flow is caused by a pressure differ-ence that exists between the arterial and venous systems. Because arterial pressure (approximately 100 mm Hg) is greater than ve-nous pressure (approximately 4 mm Hg) and fluid always flows from an area of high pressure to an area of lower pressure, blood flows from the arterial to the venous system.
The pressure difference (∆P) between the two ends of the ves-sel provides the impetus for the forward propulsion of blood. Im-pediments to blood flow offer the opposing force, which is known as resistance (R). The rate of blood flow is determined by dividing the pressure difference by the resistance:
Flow rate =∆P/R
This equation clearly shows that, when resistance increases, a greater driving pressure is required to maintain the same degree of flow. In the body, an increase in driving pressure is accom-plished by an increase in the force of contraction of the heart. If arterial resistance is chronically elevated, the myocardium hyper-trophies (enlarges) to sustain the greater contractile force.
In most long smooth blood vessels, flow is laminar or stream-lined, with blood in the center of the vessel moving slightly faster than the blood near the vessel walls. Laminar flow becomes tur-bulent when the blood flow rate increases, when blood viscosity increases, when the diameter of the vessel becomes greater than normal, or when segments of the vessel are narrowed or con-stricted. Turbulent blood flow creates a sound, called a bruit, that can be auscultated with a stethoscope.
Fluid exchange across the capillary wall is continuous. This fluid, which has the same composition as plasma without the proteins, forms the interstitial fluid. The equilibrium between hydrostatic and osmotic forces of the blood and interstitium, as well as cap-illary permeability, governs the amount and direction of fluid movement across the capillary. Hydrostatic force is a driving pres-sure that is generated by the blood pressure. Osmotic pressure is the pulling force created by plasma proteins. Normally, the hy-drostatic pressure at the arterial end of the capillary is relatively high compared with that at the venous end. This high pressure at the arterial end of the capillaries tends to drive fluid out of the capillary and into the tissue space. Osmotic pressure tends to pull fluid back into the capillary from the tissue space, but this os-motic force cannot overcome the high hydrostatic pressure at the arterial end of the capillary. At the venous end of the capillary, however, the osmotic force predominates over the low hydro-static pressure, and there is a net reabsorption of fluid from the tissue space back into the capillary.
Except for a very small amount, fluid that is filtered out at the arterial end of the capillary bed is reabsorbed at the venous end. The excess filtered fluid enters the lymphatic circulation. These processes of filtration, reabsorption, and lymph formation aid in maintaining tissue fluid volume and removing tissue waste and debris. Under normal conditions, capillary permeability remains constant.
Under certain abnormal conditions, the fluid filtered out of the capillaries may greatly exceed the amounts reabsorbed and car ried away by the lymphatic vessels. This imbalance can result from damage to capillary walls and subsequent increased permeability, obstruction of lymphatic drainage, elevation of venous pressure, or decrease in plasma protein osmotic force. The accumulation of fluid that results from these processes is known as edema.
The most important factor that determines resistance in the vas-cular system is the vessel radius. Small changes in vessel radius lead to large changes in resistance. The predominant sites of change in the caliber or width of blood vessels, and therefore in resistance, are the arterioles and the precapillary sphincter. Pe-ripheral vascular resistance is the opposition to blood flow pro-vided by the blood vessels. Poiseuille’s law provides the method by which resistance can be calculated:
R = 8θL/πr4
where R = resistance, r = radius of the vessel, L = length of the vessel, θ = viscosity of the blood, and 8/π = a constant. This equa-tion shows that the resistance is proportional to the viscosity or thickness of the blood and the length of the vessel but is inversely proportional to the fourth power of the vessel radius.
Under normal conditions, blood viscosity and vessel length do not change significantly, and these factors do not usually play an important role in blood flow. A large increase in hematocrit, how-ever, may increase blood viscosity and reduce capillary blood flow.
Because the metabolic needs of body tissues, even at rest, are con-tinuously changing, an integrated and coordinated regulatory sys-tem is necessary so that blood flow to individual areas is maintained in proportion to the needs of that area. As might be expected, this regulatory mechanism is complex and consists of central nervous system influences, circulating hormones and chemicals, and inde-pendent activity of the arterial wall itself.
Sympathetic (adrenergic) nervous system activity, mediated by the hypothalamus, is the most important factor in regulating the caliber and therefore the blood flow of peripheral blood vessels. All vessels are innervated by the sympathetic nervous system except the capillary and precapillary sphincters. Stimulation of the sympa-thetic nervous system causes vasoconstriction. The neurotransmit-ter responsible for sympathetic vasoconstriction is norepinephrine. Sympathetic activation occurs in response to physiologic and psy-chological stressors. Diminution of sympathetic activity by med-ications or sympathectomy results in vasodilation.
Other hormonal substances affect peripheral vascular resis-tance. Epinephrine, released from the adrenal medulla, acts like norepinephrine in constricting peripheral blood vessels in most tissue beds. In low concentrations, however, epinephrine causes vasodilation in skeletal muscles, the heart, and the brain. Angio-tensin, a potent substance formed from the interaction of renin (synthesized by the kidney) and a circulating serum protein, stim-ulates arterial constriction. Although the amount of angiotensin concentrated in the blood is usually small, its profound vasocon-strictor effects are important in certain abnormal states, such as heart failure and hypovolemia.
Alterations in local blood flow are influenced by various circu-lating substances that have vasoactive properties. Potent vaso-dilators include histamine, bradykinin, prostaglandin, and certain muscle metabolites. A reduction in available oxygen and nutrients and changes in local pH also affect local blood flow. Serotonin, a substance liberated from platelets that aggregate at the site of ves-sel wall damage, constricts arterioles. The application of heat to parts of the body surface causes local vasodilation, whereas the application of cold causes vasoconstriction.
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