SGD REVIEW

IN THE CLINIC In certain types of arterial disease, particularly hypertension, the subendothelial layers of vessels tend to degenerate locally, and small regions of the endothelium may lose their normal support. The viscous drag on the arterial wall may cause a tear between a normally supported and an unsupported region of the endothelial lining. Blood may then flow from the vessel lumen through the rift in the lining and dissect between the various layers of the artery. Such a lesion is called a dissecting aneurysm. It occurs most often in the proximal portions of the aorta and is extremely serious. One reason for its predilection for this site is the high velocity of blood flow, with associated large shear rate (du/dy) values at the endothelial wall. Shear stress at the vessel wall also influences many other vascular functions, such as the permeability of the vessel walls to large molecules, the synthetic activity of endothelial cells, the integrity of the formed elements in blood, and blood coagulation. An increase in shear stress on the endothelial wall is also an effective stimulus for the release of nitrous oxide (NO) from vascular endothelial cells; NO is a potent vasodilator (see Microcirculation and Lymphatics). IN THE CLINIC In chronic hypertension, a condition characterized by a persistent elevation in TPR, the arterial pressure-volume curve resembles that shown in Figure 1719, B. Because arteries become substantially less compliant when arterial pressure rises, an increase in TPR will elevate systolic pressure more than it will elevate diastolic pressure. Diastolic pressure is elevated in such individuals, but ordinarily not more than 10 to 40 mm Hg above the average normal level of 80 mm Hg. Not uncommonly, however, systolic pressure is elevated by 50 to 100 mm Hg above the average normal level of 120 mm Hg. The combination of increased resistance and diminished arterial compliance is represented in Figure 17-20. IN THE CLINIC Some of the drugs used to treat chronic hypertension interfere with the reflex adaptation to standing. Similarly, astronauts exposed to weightlessness lose their adaptations after a few days in space, and they experience pronounced difficulties when they first return to earth. When such astronauts and other individuals with impaired reflex adaptations stand, their blood pressure may drop substantially. This response is called orthostatic hypotension, which may cause lightheadedness or fainting. IN THE CLINIC The superficial veins in the neck are ordinarily partially

collapsed when a normal individual is sitting or standing. Venous return from the head is conducted largely through the deeper cervical veins, which are protected from collapse because they are tethered to surrounding structures. When central venous pressure is abnormally elevated, the superficial neck veins are distended, and they do not collapse even when the subject sits or stands. Such cervical venous distention is an important clinical sign of congestive heart failure. IN THE CLINIC The auxiliary pumping mechanism generated by skeletal muscle contractions is much less effective in people with varicose veins in their legs. The valves in these defective veins do not function properly, and therefore when the leg muscles contract, the blood in the leg veins is forced in the retrograde as well as the antegrade direction. Thus, when an individual with varicose veins stands or walks, venous pressure in the ankles and feet is excessively high. The consequent high capillary pressure leads to the accumulation of edema fluid in the ankles and feet.