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BIOC33H3 (127)
Lecture

Hypertension

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Department
Biological Sciences
Course
BIOC33H3
Professor
Stephen Reid
Semester
Fall

Description
Chapter 33: Hypertension  Hypertension, or high blood pressure (BP), is defined as a persistent systolic blood pressure (SBP) greater than or equal to 140 mm Hg, diastolic blood pressure (DBP) greater than or equal to 90 mm Hg, or current use of antihypertensive medication. There is a direct relationship between hypertension and cardiovascular disease (CVD).  Contributing factors to the development of hypertension include cardiovascular risk factors combined with socioeconomic conditions and ethnic differences.  Hypertension is generally an asymptomatic condition. Individuals who remain undiagnosed and untreated for hypertension present the greatest challenge and opportunity for health care providers. REGULATION OF BLOOD PRESSURE  BP is the force exerted by the blood against the walls of the blood vessel. It must be adequate to maintain tissue perfusion during activity and rest.  Regulation of BP involves nervous, cardiovascular, endothelial, renal, and endocrine functions. o Sympathetic nervous system (SNS) activation increases heart rate (HR) and cardiac contractility, produces widespread vasoconstriction in the peripheral arterioles, and promotes the release of renin from the kidneys. o Baroreceptors, located in the carotid artery and the arch of the aorta, sense changes in BP. When BP is increased, these receptors send inhibitory impulses to the sympathetic vasomotor center in the brainstem resulting in decreased HR, decreased force of contraction, and vasodilation in peripheral arterioles. o A decrease in BP leads to activation of the SNS resulting in constriction of the peripheral arterioles, increased HR, and increased contractility of the heart. o In the presence of long-standing hypertension, the baroreceptors become adjusted to elevated levels of BP and recognize this level as “normal.” o Norepinephrine (NE), released from SNS nerve endings, activates receptors located in the sinoatrial node, myocardium, and vascular smooth muscle. o Vascular endothelium produces vasoactive substances and growth factors.  Nitric oxide, an endothelium-derived relaxing factor (EDRF), helps maintain low arterial tone at rest, inhibits growth of the smooth muscle layer, and inhibits platelet aggregation.  Endothelin (ET), produced by the endothelial cells, is an extremely potent vasoconstrictor. o Kidneys contribute to BP regulation by controlling sodium excretion and extracellular fluid (ECF) volume.  Sodium retention results in water retention, which causes an increased ECF volume. This increases the venous return to the heart, increasing the stroke volume, which elevates the BP through an increase in CO. o Endocrine system:  The adrenal medulla releases epinephrine in response to SNS stimulation. Epinephrine activates 2-adrenergic receptors causing vasodilation. In peripheral arterioles with only1 -adrenergic receptors (skin and kidneys), epinephrine causes vasoconstriction.  The adrenal cortex is stimulated by A-II to release aldosterone. Aldosterone stimulates the kidneys to retain sodium and water. This increases BP by increasing CO.  ADH is released from the posterior pituitary gland in response to an increased blood sodium and osmolarity level. ADH increases the ECF volume by promoting the reabsorption of water in the distal and collecting tubules of the kidneys resulting in an increase in blood volume and BP. CLASSIFICATION OF HYPERTENSION  Hypertension is classified as follows: o Prehypertension: BP 120 to 139 / 80 to 89 mm Hg o Hypertension, Stage 1: BP 140 to 159 / 90 to 99 mm Hg o Hypertension, Stage 2: systolic BP greater than or equal to 160 or diastolic BP greater than or equal to 100 mm Hg.  Subtypes of hypertension: o Isolated systolic hypertension (ISH): average SBP greater than or equal to 140 mm Hg coupled with an average DBP less than 90 mm Hg. ISH is more common in older adults. Control of ISH decreases the incidence of stroke, heart failure, cardiovascular mortality, and total mortality. o Pseudohypertension (false hypertension) occurs with advanced arteriosclerosis. Pseudohypertension is suspected if arteries feel rigid or when few retinal or cardiac signs are found relative to the pressures obtained by cuff. ETIOLOGY OF HYPERTENSION  Primary (essential or idiopathic) hypertension: elevated BP without an identified cause; accounts for 90% to 95% of all cases of hypertension.  Secondary hypertension: elevated BP with a specific cause; accounts for 5% to 10% of hypertension in adults. PATHOPHYSIOLOGY OF PRIMARY HYPERTENSION  The hemodynamic hallmark of hypertension is persistently increased SVR.  Water and sodium retention: o A high-sodium intake may activate a number of pressor mechanisms and cause water retention.  Altered renin-angiotensin mechanism: o High plasma renin activity (PRA) results in the increased conversion of angiotensinogen to angiotensin I causing arteriolar constriction, vascular hypertrophy, and aldosterone secretion.  Stress and increased SNS activity: o Arterial pressure is influenced by factors such as anger, fear, and pain. o Physiologic responses to stress, which are normally protective, may persist to a pathologic degree, resulting in prolonged increase in SNS activity. o Increased SNS stimulation produces increased vasoconstriction, increased HR, and increased renin release.  Insulin resistance and hyperinsulinemia: o Abnormalities of glucose, insulin, and lipoprotein metabolism are common in primary hypertension. o High insulin concentration in the blood stimulates SNS activity and impairs nitric oxide–mediated vasodilation. o Additional pressor effects of insulin include vascular hypertrophy and increased renal sodium reabsorption.  Endothelial cell dysfunction: o Some hypertensive people have a reduced vasodilator response to nitric oxide. o Endothelin produces pronounced and prolonged vasoconstriction. CLINICAL MANIFESTATIONS OF HYPERTENSION  Often called the “silent killer” because it is frequently asymptomatic until it becomes severe and target organ disease occurs.  Target organ diseases occur in the heart (hypertensive heart disease), brain (cerebrovascular disease), peripheral vasculature (peripheral vascular disease), kidney (nephrosclerosis), and eyes (retinal damage).  Hypertension is a major risk factor for coronary artery disease (CAD).  Sustained high BP increases the cardiac workload and produces left ventricular hypertrophy (LVH). Progressive LVH, especially in association with CAD, is associated with the development of heart failure.  Hypertension is a major risk factor for cerebral atherosclerosis and stroke.  Hypertension speeds up the process of atherosclerosis in the peripheral blood vessels, leading to the development of peripheral vascular disease, aortic aneurysm, and aortic dissection.  Intermittent claudication (ischemic muscle pain precipitated by activity and relieved with rest) is a classic symptom of peripheral vascular disease involving the arteries.  Hypertension is one of the leading causes of end-stage renal disease, especially among African Americans. The earliest manifestation of renal dysfunction is usually nocturia.  The retina provides important information about the severity and duration of hypertension. Damage to retinal vessels provides an indication of concurrent vessel damage in the heart, brain, and kidney. Manifestations of severe retinal damage include blurring of vision, retinal hemorrhage, and loss of vision. DIAGNOSTIC STUDIES  Basic laboratory studies are performed to (1) identify or rule out causes of secondary hypertension, (2) evaluate target organ disease, (3) determine overall cardiovascular risk, or (4) establish baseline levels before initiating therapy.  Routine urinalysis, BUN, serum creatinine, and creatinine clearance levels are used to screen for renal involvement and to provide baseline information about kidney function.  Measurement of serum electrolytes, especially potassium levels, is done to detect hyperaldosteronism, a cause of secondary hypertension.  Blood glucose levels assist in the diagnosis of diabetes mellitus.  Lipid profile provides information about additional risk factors that predispose to atherosclerosis and cardiovascular disease.  Uric acid levels are determined to establish a baseline, because the levels often rise with diuretic therapy.  ECG and echocardiography provide information about the cardiac status.  Ambulatory blood pressure monitoring (ABPM) is a noninvasive, fully automated system that measures BP at preset intervals over a 24-hour period. o Some patients with hypertension do not show a normal, nocturnal dip in BP and are referred to as “nondippers.” o The absence of diurnal variability has been associated with more target organ damage and an increased risk for cardiovascular events. The presence or absence of diurnal variability can be determined by ABPM. NURSING AND COLLABORATIVE MANAGEMENT  Treatment goals are to lower BP to less than 140 mm Hg systolic and less than 90 mm Hg diastolic for most persons with hypertension (less than 130 mm Hg systolic and less than 80 mm Hg diastolic for those with diabetes mellitus and chronic kidney disease).  Lifestyle modifications are indicated for all patients with prehypertension and hypertension and include the following: o Weight reduction. A weight loss of 10 kg (22 lb) may decrease SBP by approximately 5 to 20 mm Hg. o Dietary Approaches to Stop Hypertension (DASH) eating plan. Involves eating several servings of fish each week, eating plenty of fruits and vegetables, increasing fiber intake, and drinking a lot of water. The DASH diet significantly lowers BP. o Restriction of dietary sodium to less than 6 g of salt (NaCl) or less than 2.4 g of sodium per day. o This involves avoiding foods known to be high in sodium (e.g., canned soups) and not adding salt in the preparation of foods or at meals. o There is evidence that greater levels of dietary potassium, calcium, vitamin D, and omega-3 fatty acids are associated with lower BP in those with hypertension. o Restriction of alcohol to no more than two drinks per day for men and no more than one drink per day for women o Regular aerobic physical activity (e.g., brisk walking) at least 30 minutes a day most days of the week. Moderately in
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