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Arterial Disease

Disease processes such as atherosclerosis can reduce the diameter of most medium and large arteries, causing an increase in arterial resistance and a subsequent decrease in blood flow. The signs and symptoms resulting from atherosclerotic disease depend on which arteries are stenotic (narrowed) and the severity of the reduction in blood flow. Regions commonly affected by atherosclerosis include the heart, brain, and legs.

Coronary artery disease is the most common serious manifestation of atherosclerosis. When the stenotic lesions are relatively mild, blood flow may be inadequate only when the myocardial demand is high, such as during exercise. If blood flow is inadequate to meet the metabolic needs of a particular tissue, the tissue is said to be ischemic. In the heart, short periods of ischemia may produce chest pain known as angina. As the disease progresses and the coronary stenosis becomes more severe, ischemia tends to occur at increasingly lower cardiac workloads, eventually resulting in angina at rest. In cases of severe stenosis and/or complete occlusion of the coronary arteries, blood flow may become inadequate to maintain myocardial viability, resulting in infarction (cell or tissue death). Millions of people in the United States are affected by coronary disease, with more than 1 million experiencing myocardial infarction each year and 700,000 ultimately dying from infarction, making this the leading cause of death in the nation.

Stenoses in the carotid or vertebral arteries can lead to ischemia and infarction—stroke or cerebrovascular accident—involving the brain. Strokes are the third leading cause of death in the United States and a leading cause of significant disability.

As with the heart, mild arterial disease involving the legs usually becomes symptomatic only when the demand for blood flow is high, such as during exercise involving the lower extremities. Muscle ischemia produces pain called claudication, which typically resolves rapidly when the patient rests. As the disease becomes more severe, symptoms may progress to include rest pain and, ultimately, limb infarction with gangrene.

In all of these cases, blood flow to the affected organ may be preserved by the development of collateral arteries, which can carry blood around the stenotic or occluded segments of arteries. When collateral flow is inadequate to meet needs, blood flow may be improved with angioplasty (using a balloon catheter, laser, etc.) or bypass surgery (using autologous vein or synthetic material to route blood around a blockage). More than 1 million revas-cularization procedures using these techniques are performed in the United States annually.

Returning to equation 3, despite the potential effect of blood viscosity on resistance, hematocrit normally does not change much and is usually not an important cause of changes in vascular resistance. Likewise, the length (L) of blood vessels does not change significantly (except with

Normal range: 38-54%

Normal range: 38-54%

la el cc

Normal range: 38-54%

Normal range: 38-54%

la el cc

0 20 40 60 80 100 Hematocrit (%)

Effect of hematocrit on blood viscosity.

"Above-normal hematocrits produce a sharp increase in viscosity. Because increased viscosity raises vascular resistance, hemoglobin and oxygen delivery may fall when the hematocrit rises above the normal range.

growth) and is, therefore, not important as a physiological determinant of vascular resistance. The remaining influence, vessel radius (r), is the major determinant of changes in SVR. Since resistance is inversely proportional to r4, small changes in the radius cause relatively large changes in vascular resistance. For example, the vascular resistance to skeletal muscle during exercise may decrease 25-fold. This fall in resistance results from a 2.2-fold increase in resistance vessel radius (i.e., 2.24 = ~25). Vessel radius is determined primarily by the contractile activity of smooth muscle in the vessel wall (see Chapter 16).

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