Hypertension
Hypertension, an intermittent or sustained elevation in diastolic or systolic blood pressure, occurs as two major types: essential (idiopathic) hypertension, the most common, and secondary hypertension, which results from renal disease or another identifiable cause. Malignant hypertension is a severe, fulminant form of hypertension common to both types. Hypertension is a major cause of stroke, cardiac disease, and renal failure. The prognosis is good if this disorder is detected early and treatment begins before complications develop. Severely elevated blood pressure (hypertensive crisis) may be fatal. (See What happens in hypertensive crisis, page 1092 and 1093.)
Causes and incidence
Hypertension affects 25% of adults in the United States. If untreated, it carries a high mortality. Risk factors for hypertension include family history, race (most common in blacks), stress, obesity, a diet high in saturated fats or sodium, tobacco use, sedentary lifestyle, and aging.
Secondary hypertension may result from renal vascular disease; pheochromocytoma; primary hyperaldosteronism; Cushing’s syndrome; thyroid, pituitary, or parathyroid dysfunction; coarctation of the aorta; pregnancy; neurologic disorders; and use of hormonal contraceptives or other drugs, such as cocaine, epoetin alfa (erythropoietin), and cyclosporine.
Cardiac output and peripheral vascular resistance determine blood pressure. Increased blood volume, cardiac rate, and stroke volume as well as arteriolar vasoconstriction can raise blood pressure. The link to sustained hypertension, however, is unclear. Hypertension may also result from failure of intrinsic regulatory mechanisms:
❑ Renal hypoperfusion causes release of renin, which is converted by angiotensinogen, a liver enzyme, to angiotensin I. Angiotensin I is converted to angiotensin II, a powerful vasoconstrictor. The resulting vasoconstriction increases afterload. Angiotensin II stimulates adrenal secretion of aldosterone, which increases sodium reabsorption. Hypertonic-stimulated release of antidiuretic hormone from the pituitary gland follows, increasing water reabsorption, plasma volume, cardiac output, and blood pressure.
❑ Autoregulation changes an artery’s diameter to maintain perfusion despite fluctuations in systemic blood pressure. The intrinsic mechanisms responsible include stress relaxation (vessels gradually dilate when blood pressure rises to reduce peripheral resistance) and capillary fluid shift (plasma moves between vessels and extravascular spaces to maintain intravascular volume).
❑ When the blood pressure drops, baroreceptors in the aortic arch and carotid sinuses decrease their inhibition of the medulla’s vasomotor center, which increases sympathetic stimulation of the heart by norepinephrine. This, in turn, increases cardiac output by strengthening the contractile force, increasing the heart rate, and augmenting peripheral resistance by vasoconstriction. Stress can also stimulate the sympathetic nervous system to increase cardiac output and peripheral vascular resistance.
Signs and symptoms
Hypertension usually doesn’t produce clinical effects until vascular changes in the heart, brain, or kidneys occur. Severely elevated blood pressure damages the intima of small vessels, resulting in fibrin accumulation in the vessels, development of local edema and, possibly, intravascular clotting. Symptoms produced by this process depend on the location of the damaged vessels:
❑ brain — stroke
❑ retina — blindness
❑ heart — myocardial infarction
❑ kidneys — proteinuria, edema and, eventually, renal failure.
Hypertension increases the heart’s workload, causing left ventricular hypertrophy and, later, left- and right-sided heart failure and pulmonary edema.
Diagnosis
Serial blood pressure measurements are obtained and compared to previous readings and trends to reveal an increase in diastolic and systolic pressures. (See Classifying blood pressure readings, page 1094.)
Auscultation may reveal bruits over the abdominal aorta and the carotid, renal, and femoral arteries; ophthalmoscopy reveals arteriovenous nicking and, in hypertensive encephalopathy, papilledema. Patient history and the following additional tests may show predisposing factors and help identify an underlying cause such as renal disease:
❑ Urinalysis: Protein levels and red and white blood cell counts may indicate glomerulonephritis.
❑ Excretory urography: Renal atrophy indicates chronic renal disease; one kidney more than ⅝nbsp;(1.5 cm) shorter than the other suggests unilateral renal disease.
❑ Serum potassium: Levels less than 3.5 mEq/L may indicate adrenal dysfunction (primary hyperaldosteronism).
❑ Blood urea nitrogen (BUN) and serum creatinine: BUN level that’s normal or elevated to more than 20 mg/dl and serum creatinine level that’s normal or elevated to more than 1.5 mg/dl suggest renal disease.
Other tests help detect cardiovascular damage and other complications:
❑ Electrocardiography may show left ventricular hypertrophy or ischemia.
❑ Chest X-ray may show cardiomegaly.
❑ Echocardiography may show left ventricular hypertrophy.
Treatment
The National Institutes of Health recommend the following approach for treating primary hypertension:
❑ First, help the patient initiate necessary lifestyle modifications, including weight reduction, moderation of alcohol intake, regular physical exercise, reduction of sodium intake, and smoking cessation.
❑ If the patient fails to achieve the desired blood pressure or make significant progress, continue lifestyle modifications and begin drug therapy.
❑ For stage 1 hypertension (systolic [SBP] blood pressure 140 to 159 mm Hg, or diastolic blood pressure [DBP] 90 to 99 mm Hg) in the absence of compelling indications (heart failure, postmyocardial infarction, high coronary disease risk, diabetes, chronic kidney disease, or recurrent stroke prevention), give most patients thiazide-type diuretics. Consider using an angiotensin-converting enzyme (ACE) inhibitor, beta-adrenergic blocker, calcium channel blocker (CCB), angiotensin-receptor blocker (ARB), or a combination.
❑ For stage 2 hypertension (SBP ≥ 160 mm Hg, or DBP ≥ 100 mm Hg) in the absence of compelling indications, give most patients a two-drug combination (usually a thiazide-type diuretic and an ACE inhibitor, ARB, CCB, or beta-adrenergic blocker).
❑ If the patient has one or more compelling indications, base drug treatment on benefits from outcome studies or existing clinical guidelines. Treatment may include the following, depending on indication:
– Heart failure — diuretic, beta-adrenergic blocker, ACE inhibitor, ARB, or aldosterone antagonist
– High coronary disease risk — diuretic, beta-adrenergic blocker, ACE inhibitor, or CCB
– Diabetes — diuretic, beta-adrenergic blocker, ACE inhibitor, or CCB
– Chronic kidney disease — ACE inhibitor or ARB
– Postmyocardial failure — ACE inhibitor, beta-adrenergic blocker, or aldosterone antagonist
– Recurrent stroke prevention — diuretic or ACE inhibitor.
Give other antihypertensive drugs as needed.
❑ If the patient fails to achieve the desired blood pressure, continue lifestyle modifications and optimize drug dosages or add additional drugs until the goal blood pressure is achieved. Also, consider consultation with a hypertension specialist.
Treatment of secondary hypertension focuses on correcting the underlying cause and controlling hypertensive effects.
Typically, hypertensive emergencies require parenteral administration of a vasodilator or an adrenergic inhibitor or oral administration of a selected drug, such as nifedipine, captopril, clonidine, or labetalol, to rapidly reduce blood pressure. The initial goal is to reduce mean arterial blood pressure by no more than 25% (within minutes to hours) then to 160/110 within 2 hours while avoiding excessive falls in blood pressure that can precipitate renal, cerebral, or myocardial ischemia.
Examples of hypertensive emergencies include hypertensive encephalopathy, intracranial hemorrhage, acute left-sided heart failure with pulmonary edema, and dissecting aortic aneurysm. Hypertensive emergencies are also associated with eclampsia or severe gestational hypertension, unstable angina, and acute myocardial infarction.
Hypertension without accompanying symptoms or target-organ disease seldom requires emergency drug therapy.
Special considerations
❑ To encourage adherence to antihypertensive therapy, suggest that the patient establish a daily routine for taking his medication. Warn that uncontrolled hypertension may cause stroke and heart attack. Tell him to report adverse drug effects. Also, advise him to avoid high-sodium antacids and over-the-counter cold and sinus medications, which contain harmful vasoconstrictors.
❑ Encourage a change in dietary habits. Help the obese patient plan a weight-reduction diet; tell him to avoid high-sodium foods (pickles, potato chips, canned soups, and cold cuts) and table salt.
❑ Help the patient examine and modify his lifestyle (for example, by reducing stress and exercising regularly).
❑ If a patient is hospitalized with hypertension, find out if he was taking his prescribed medication. If he wasn’t, ask why. If he can’t afford the medication, refer him to appropriate social service agencies. Tell the patient and his family to keep a record of drugs used in the past, noting especially which ones were or weren’t effective. Suggest recording this information on a card so that the patient can show it to his physician.
❑ When routine blood pressure screening reveals elevated pressure, first make sure the cuff size is appropriate for the patient’s upper arm circumference. Take the pressure in both arms in lying, sitting, and standing positions. Ask the patient if he smoked, drank a beverage containing caffeine, or was emotionally upset before the test. Advise him to return for blood pressure testing at frequent and regular intervals.
❑ To help identify hypertension and prevent untreated hypertension, participate in public education programs dealing with hypertension and ways to reduce risk factors. Encourage public participation in blood pressure screening programs. Routinely screen all patients, especially those at risk (blacks and people with family histories of hypertension, stroke, or heart attack).
Pictures
Book Source Details
- Book Title: Professional Guide to Diseases (Eighth Edition)
- Author(s): Springhouse
- Year of Publication: 2005
- Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.
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Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2008 Williams & Wilkins.
More About Causes of High blood pressure
» Next page: Pulse pressure, widened (Professional Guide to Signs & Symptoms (Fifth Edition))
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