Hypertension
Hypertension: Excerpt from Handbook of Diseases
An intermittent or a sustained elevation in diastolic or systolic blood pressure, hypertension occurs as two major types: essential (idiopathic) hypertension, the most common, and secondary hypertension, which results from kidney 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, heart disease, and renal failure. The prognosis is good if this disorder is detected early and if treatment begins before complications develop. Severely elevated blood pressure (hypertensive crisis) may be fatal.
Causes
Hypertension affects 15% to 20% of adults in the United States. If untreated, it carries a high mortality. Before age 55, a higher percentage of men than women have high blood pressure. This changes after age 55. (See Incidence of hypertension.)
Risk factors
Family history, race (most common in blacks), stress, obesity, a high intake of saturated fats or sodium, use of tobacco, sedentary lifestyle, and aging are risk factors for essential hypertension. Insulin resistance has also been implicated in some patients.
Clinical tip Systolic hypertension poses a risk that’s equal to or greater than diastolic elevations. It’s commonly seen in elderly people and presents a risk for stroke or myocardial infarction (MI).
Secondary hypertension may result from renovascular 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, and cyclosporine.
Blood pressure regulators
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 is unclear. Hypertension may also result from the failure of the following intrinsic regulatory mechanisms:
❑ Renal hypoperfusion causes the 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 the diameter of an artery 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. Highly 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: MI
❑ 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 that are greater than 120/80 mm Hg but less than 140/90 mm Hg indicate prehypertension; measurements that are greater than 140/90 mm Hg confirm hypertension. Moderate (stage 1) and severe (stage 2) stages are based on systolic and diastolic levels. Auscultation may reveal bruits over the abdominal aorta and the carotid, renal, and femoral arteries; ophthalmoscopy reveals arteriovenous nicking and, in hypertensive encephalopathy, papilledema.
The patient history and the following additional tests may show predisposing factors and help identify an underlying cause such as kidney disease:
❑ Urinalysis — The presence of protein, red blood cells, and white blood cells may indicate glomerulonephritis.
❑ Excretory urography — Renal atrophy indicates chronic kidney disease; one kidney that is more than ⅝"(1.5 cm) shorter than the other suggests unilateral kidney disease.
❑ Serum potassium — Levels less than 3.5 mEq/L may indicate adrenal dysfunction (primary hyperaldosteronism).
❑ Blood urea nitrogen (BUN) and serum creatinine levels — A BUN level that’s normal or elevated to more than 20 mg/dl and a serum creatinine level that’s normal or elevated to more than 1.5 mg/dl suggest kidney 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.
❑ Oral captopril challenge tests for renovascular hypertension. This functional diagnostic test depends on the abrupt inhibition of circulating angiotensin II by angiotensin-converting enzyme (ACE) inhibitors, removing the major support for perfusion through a stenotic kidney. The acutely ischemic kidney immediately releases more renin and undergoes a marked decrease in glomerular filtration rate and renal blood flow.
❑ Renal arteriography may show renal artery stenosis.
Treatment
Secondary hypertension treatment focuses on correcting the underlying cause and controlling hypertensive effects.
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 angioten-sin converting enzyme inhibitor (ACEI), angiotensin receptor blocker (ARB), beta-adrenergic blocker (BB), calcium channel blocker (CCB), or a combination.
❑ For stage 2 hypertension (SBP ≥ 60 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 ACEI, ARB, BB, or CCB).
❑ 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, BB, ACEI, ARB, or aldosterone antagonist
❑ Post myocardial infarction — BB, ACEI, or aldosterone antagonist
❑ High coronary disease risk — diuretic, BB, ACEI, or CCB
❑ Diabetes — diuretic, BB, ACEI, ARB, or CCB
❑ Chronic kidney disease — ACEI or ARB
❑ Recurrent stroke prevention — diuretic or ACEI.
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.
UNDER STUDY: Studies have shown that omega-3 fatty acids used in the treatment of hypertension significantly reduce total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels and lower systolic and diastolic blood pressure.
Clinical tip The treatment for renal artery stenosis includes the use of ACE inhibitors and renal artery stents.
Hypertensive emergencies
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 and severe pregnancy-induced hypertension, unstable angina, and acute MI.
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.
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 the patient to report adverse reactions to drugs.
❑ Advise the patient to avoid high-sodium antacids and over-the-counter cold and sinus medications, which contain harmful vasoconstrictors.
❑ Encourage the patient to change his dietary habits, if indicated. 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 the patient can’t afford the medication, refer him to an appropriate social service agency.
❑ Tell the patient and his family to keep a record of drugs used in the past, noting especially which ones were and weren’t effective. Suggest recording this information on a card so that the patient can show it to his physician.
❑ Tell the patient who has a renal artery stent to expect an increase in urine output the first few days after the procedure.
When routine blood pressure screening reveals elevated pressure:
❑ Make sure the cuff size is appropriate for the patient’s upper arm circumference.
❑ Measure 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 measurement.
❑ Advise the patient 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: Handbook of Diseases
- Author(s): Springhouse
- Year of Publication: 2003
- Copyright Details: Handbook of Diseases, Copyright © 2003 Lippincott Williams & Wilkins.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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More About This Book:
Title: Handbook of Diseases
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2003
ISBN: 1-58255-266-5
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