Similarly, as blood volume decreases, pressure and flow decrease. As blood volume increases, pressure and flow increase. Under normal circumstances, blood volume varies little. Low blood volume, called hypovolemia, may be caused by bleeding, dehydration, vomiting, severe burns, or some medications used to treat hypertension.
It is important to recognize that other regulatory mechanisms in the body are so effective at maintaining blood pressure that an individual may be asymptomatic until 10—20 percent of the blood volume has been lost. Treatment typically includes intravenous fluid replacement. Hypervolemia, excessive fluid volume, may be caused by retention of water and sodium, as seen in patients with heart failure, liver cirrhosis, some forms of kidney disease, hyperaldosteronism, and some glucocorticoid steroid treatments.
Restoring homeostasis in these patients depends upon reversing the condition that triggered the hypervolemia. Viscosity is the thickness of fluids that affects their ability to flow. Clean water, for example, is less viscous than mud. The viscosity of blood is directly proportional to resistance and inversely proportional to flow; therefore, any condition that causes viscosity to increase will also increase resistance and decrease flow.
For example, imagine sipping milk, then a milkshake, through the same size straw. You experience more resistance and therefore less flow from the milkshake. Conversely, any condition that causes viscosity to decrease such as when the milkshake melts will decrease resistance and increase flow. Normally the viscosity of blood does not change over short periods of time. The two primary determinants of blood viscosity are the formed elements and plasma proteins.
Since the vast majority of formed elements are erythrocytes, any condition affecting erythropoiesis, such as polycythemia or anemia, can alter viscosity.
Since most plasma proteins are produced by the liver, any condition affecting liver function can also change the viscosity slightly and therefore decrease blood flow. Liver abnormalities include hepatitis, cirrhosis, alcohol damage, and drug toxicities.
While leukocytes and platelets are normally a small component of the formed elements, there are some rare conditions in which severe overproduction can impact viscosity as well.
The length of a vessel is directly proportional to its resistance: the longer the vessel, the greater the resistance and the lower the flow. As with blood volume, this makes intuitive sense, since the increased surface area of the vessel will impede the flow of blood. Likewise, if the vessel is shortened, the resistance will decrease and flow will increase. The length of our blood vessels increases throughout childhood as we grow, of course, but is unchanging in adults under normal physiological circumstances.
Further, the distribution of vessels is not the same in all tissues. Adipose tissue does not have an extensive vascular supply. One pound of adipose tissue contains approximately miles of vessels, whereas skeletal muscle contains more than twice that. Overall, vessels decrease in length only during loss of mass or amputation. An individual weighing pounds has approximately 60, miles of vessels in the body.
Gaining about 10 pounds adds from to miles of vessels, depending upon the nature of the gained tissue. One of the great benefits of weight reduction is the reduced stress to the heart, which does not have to overcome the resistance of as many miles of vessels.
In contrast to length, the diameter of blood vessels changes throughout the body, according to the type of vessel, as we discussed earlier. The diameter of any given vessel may also change frequently throughout the day in response to neural and chemical signals that trigger vasodilation and vasoconstriction. The vascular tone of the vessel is the contractile state of the smooth muscle and the primary determinant of diameter, and thus of resistance and flow.
The effect of vessel diameter on resistance is inverse: Given the same volume of blood, an increased diameter means there is less blood contacting the vessel wall, thus lower friction and lower resistance, subsequently increasing flow. A decreased diameter means more of the blood contacts the vessel wall, and resistance increases, subsequently decreasing flow.
The influence of lumen diameter on resistance is dramatic: A slight increase or decrease in diameter causes a huge decrease or increase in resistance. This means, for example, that if an artery or arteriole constricts to one-half of its original radius, the resistance to flow will increase 16 times. Recall that we classified arterioles as resistance vessels, because given their small lumen, they dramatically slow the flow of blood from arteries.
In fact, arterioles are the site of greatest resistance in the entire vascular network. This may seem surprising, given that capillaries have a smaller size. How can this phenomenon be explained? Figure 4 compares vessel diameter, total cross-sectional area, average blood pressure, and blood velocity through the systemic vessels.
Although the diameter of an individual capillary is significantly smaller than the diameter of an arteriole, there are vastly more capillaries in the body than there are other types of blood vessels. Part c shows that blood pressure drops unevenly as blood travels from arteries to arterioles, capillaries, venules, and veins, and encounters greater resistance.
However, the site of the most precipitous drop, and the site of greatest resistance, is the arterioles. This explains why vasodilation and vasoconstriction of arterioles play more significant roles in regulating blood pressure than do the vasodilation and vasoconstriction of other vessels.
Figure 4. The relationships among blood vessels that can be compared include a vessel diameter, b total cross-sectional area, c average blood pressure, and d velocity of blood flow. Part d shows that the velocity speed of blood flow decreases dramatically as the blood moves from arteries to arterioles to capillaries. This slow flow rate allows more time for exchange processes to occur. As blood flows through the veins, the rate of velocity increases, as blood is returned to the heart.
Compliance allows an artery to expand when blood is pumped through it from the heart, and then to recoil after the surge has passed. This helps promote blood flow. In arteriosclerosis, compliance is reduced, and pressure and resistance within the vessel increase. This is a leading cause of hypertension and coronary heart disease, as it causes the heart to work harder to generate a pressure great enough to overcome the resistance.
Arteriosclerosis begins with injury to the endothelium of an artery, which may be caused by irritation from high blood glucose, infection, tobacco use, excessive blood lipids, and other factors.
Artery walls that are constantly stressed by blood flowing at high pressure are also more likely to be injured—which means that hypertension can promote arteriosclerosis, as well as result from it. Recall that tissue injury causes inflammation. As inflammation spreads into the artery wall, it weakens and scars it, leaving it stiff sclerotic. As a result, compliance is reduced. Moreover, circulating triglycerides and cholesterol can seep between the damaged lining cells and become trapped within the artery wall, where they are frequently joined by leukocytes, calcium, and cellular debris.
Eventually, this buildup, called plaque, can narrow arteries enough to impair blood flow. Figure 5. Sometimes a plaque can rupture, causing microscopic tears in the artery wall that allow blood to leak into the tissue on the other side. When this happens, platelets rush to the site to clot the blood. This clot can further obstruct the artery and—if it occurs in a coronary or cerebral artery—cause a sudden heart attack or stroke.
Alternatively, plaque can break off and travel through the bloodstream as an embolus until it blocks a more distant, smaller artery. Ischemia in turn leads to hypoxia—decreased supply of oxygen to the tissues. Hypoxia involving cardiac muscle or brain tissue can lead to cell death and severe impairment of brain or heart function. A major risk factor for both arteriosclerosis and atherosclerosis is advanced age, as the conditions tend to progress over time.
However, obesity, poor nutrition, lack of physical activity, and tobacco use all are major risk factors. Treatment includes lifestyle changes, such as weight loss, smoking cessation, regular exercise, and adoption of a diet low in sodium and saturated fats.
Medications to reduce cholesterol and blood pressure may be prescribed. For blocked coronary arteries, surgery is warranted. In angioplasty, a catheter is inserted into the vessel at the point of narrowing, and a second catheter with a balloon-like tip is inflated to widen the opening. To prevent subsequent collapse of the vessel, a small mesh tube called a stent is often inserted. In an endarterectomy, plaque is surgically removed from the walls of a vessel.
The pressure is greatest when blood is pumped out of the heart into the arteries. When the heart relaxes between beats blood is not moving out of the heart , the pressure falls in the arteries. The top number, or systolic pressure , refers to the pressure inside the artery when the heart contracts and pumps blood through the body.
The bottom number, or diastolic pressure , refers to the pressure inside the artery when the heart is at rest and is filling with blood. Both the systolic and diastolic pressures are recorded as "mm Hg" millimeters of mercury. This recording represents how high the mercury column in the blood pressure cuff is raised by the pressure of the blood. Blood pressure is measured with a blood pressure cuff and stethoscope by a nurse or other healthcare provider.
You can also take your own blood pressure with an electronic blood pressure monitor. These are available at most pharmacies. Use these numbers as a guide only. As described below, the major distributing arteries that arise from the aorta branch into successively smaller arterial vessels until they become capillaries. These smallest vessels join together to form veins, which then continue to join together with other veins until they enter either the superior or inferior vena cava that bring the blood back into the right atrium of the heart.
The relative sizes and functions of different blood vessels are summarized in the following table:. The aorta , besides being the main vessel to distribute blood to the arterial system, dampens the pulsatile pressure that results from the intermittent outflow from the left ventricle. The actual dampening is a function of the aortic compliance. Large arteries branching off the aorta e. These large arteries, although capable of constricting and dilating, serve virtually no role in the regulation of pressure and blood flow under normal physiological conditions.
Once the distributing artery reaches the organ to which it supplies blood, it branches into smaller arteries that distribute blood flow within the organ. These vessels continue to branch and become arterioles.
Together, the small arteries and arterioles represent the primary vessels that are involved in the regulation of arterial blood pressure as well as blood flow within the organ.
These vessels are highly innervated by autonomic nerves particularly sympathetic adrenergic , and respond to changes in nerve activity and circulating hormones by constricting or dilating. Therefore, these vessels are referred to as resistance vessels. As arterioles become smaller in diameter, they lose their smooth muscle.
Vessels that have no smooth muscle, but are composed of endothelial cells and a basement membrane, are termed capillaries , and represent the smallest vessels within the microcirculation. Capillaries are the primary exchange vessels within the body.
Across the capillary endothelium, oxygen, carbon dioxide, water, electrolytes, proteins, metabolic substrates and by-products e. When capillaries join together, they form postcapillary venules , which also serve as exchange vessels, particularly for large macromolecules as well as fluid.
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