Porth's Essentials of Pathophysiology, 4e

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Disorders of Blood Flow and Blood Pressure

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trials, antihypertensive therapy has been associated with reductions in stroke incidence averaging 30% to 40%; myocardial infarction, 20% to 25%; and heart failure, more than 50%. 29 Hypertension increases the workload of the left ven- tricle by increasing the pressure against which the heart must pump as it ejects blood into the systemic circula- tion. 30 As the workload of the heart increases, the left ventricular wall hypertrophies to compensate for the increased pressure work. Despite its adaptive advan- tage, left ventricular hypertrophy is a major risk factor for coronary heart disease, cardiac arrhythmias, sud- den death, and congestive heart failure. Hypertensive left ventricular hypertrophy regresses with therapy. Regression is most closely related to systolic pressure reduction and does not appear to reflect the particular type of medication used. Chronic hypertension can lead to nephrosclerosis, a common cause of chronic kidney disease (see Chapter 25). Hypertensive kidney disease is more common in blacks than whites. Hypertension also plays an impor- tant role in accelerating the course of other types of kid- ney disease, particularly diabetic nephropathy. Because of the risk for diabetic nephropathy, the American Diabetes Association recommends that persons with diabetes maintain their blood pressure at levels less than 130/80 mm Hg 31 (see Chapter 33). Dementia and cognitive impairment occur more com- monly in persons with hypertension. 29 Hypertension, particularly systolic hypertension, is a major risk factor for ischemic stroke and intracerebral hemorrhage 30 (see Chapter 37). Narrowing and sclerosis of small penetrat- ing arteries in the subcortical regions of the brain are common findings on autopsy in persons with chronic hypertension. 29 These changes are thought to contribute to hypoperfusion, loss of autoregulation of blood flow, and impairment of the blood–brain barrier, ultimately leading to subcortical white matter demyelination. Magnetic resonance imaging studies have revealed more extensive white matter lesions and brain atrophy in hypertensive versus normotensive persons. Effective antihypertensive therapy strongly reduces the risk of development of significant white matter changes; how- ever, existing white matter changes, once established, do not appear to be reversible. 29 Diagnosis andTreatment Unlike disorders of other body systems that are diag- nosed by methods such as radiography and tissue examination, hypertension and other blood pressure disorders are determined by repeated blood pressure measurements. Laboratory tests, x-ray films, and other diagnostic tests usually are done to exclude secondary hypertension and determine the presence or extent of target-organ damage. The increased availability of hypertensive screening clinics provides one of the best means for early detec- tion. Because blood pressure in many individuals is highly variable, unless the pressure is extremely elevated or associated with symptoms it should be measured

on different occasions over a period of several months before a diagnosis of hypertension is made. Ambulatory and self/home measurement of blood pressure may provide valuable information outside the clinician’s office regarding a person’s blood pressure and response to treatment. Self/home measurement can help detect “white coat hypertension,” a condition in which the blood pressure is consistently elevated in the health care provider’s office but normal at other times; it can also be used to assess the response to treatment measure, motivate adherence to treatment regimes, and eventu- ally reduce health care costs. 29,30 The main objective for treatment of hypertension is to achieve and maintain arterial blood pressure below 140/90 mm Hg, with the goal of preventing morbidity and mortality. In persons with hypertension and diabe- tes or renal disease, the goal is blood pressure below 130/80 mm Hg. Treatment methods include lifestyle modification and, when necessary, pharmacologic agents to achieve and maintain blood pressure within an optimal range. 29 Lifestyle Modification. Lifestyle modification has been shown to reduce blood pressure, enhance the effects of antihypertensive drug therapy, and prevent cardiovas- cular risk. Major lifestyle modifications shown to lower blood pressure include weight reduction in persons who are overweight or obese, regular physical activity, reduc- tion of dietary sodium intake, and limitation of alcohol intake to no more than two drinks per day for most men and one drink for women and persons of lighter weight. 48 Pharmacologic Treatment. The decision to initiate pharmacologic treatment is based on the severity of the hypertension, the presence of target-organ disease, and the existence of other conditions and risk factors. 29,48 Drug selection is based on the stage of hypertension. Among the drugs used in the treatment of hyperten- sion are diuretics, β -adrenergic receptor inhibitors, ACE inhibitors or angiotensin II receptor blockers, calcium channel blockers, central α 2 -adrenergic agonists, α 1 - adrenergic receptor blockers, and vasodilators. The physiologic mechanisms whereby the different antihypertension drugs produce a reduction in blood pressure differ among agents. Diuretics lower blood pressure initially by decreasing vascular volume (by sup- pressing renal reabsorption of sodium and increasing sodium and water excretion) and cardiac output. With continued therapy, a reduction in peripheral resistance becomes a major mechanism of blood pressure reduc- tion. The β -adrenergic receptor inhibitors are effective in treating hypertension because they decrease heart rate, cardiac output, and renin release by the kidney. The ACE inhibitors act by inhibiting the conversion of angiotensin I to angiotensin II, thus decreasing angiotensin II levels and reducing its effect on vasoconstriction, aldosterone levels, intrarenal blood flow, and glomerular filtration rate. The calcium channel blockers decrease periph- eral vascular resistance by inhibiting the movement of calcium into arterial smooth muscle cells. The centrally