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.
Abnormalities of glucose, insulin, and lipoprotein metabolism are common in primary hypertension.
Additional pressor effects of insulin include vascular hypertrophy and increased renal sodium reabsorption.
Endothelial cell dysfunction:
Some hypertensive people have a reduced vasodilator response to nitric oxide. 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 produces pronounced and prolonged vasoconstriction.
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 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.
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.
ECG and echocardiography provide information about the cardiac status.
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:
Weight reduction. A weight loss of 10 kg (22 lb) may decrease SBP by approximately 5 to 20 mm Hg.
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.
Restriction of dietary sodium to less than 6 g of salt (NaCl) or less than 2.4 g of sodium per day.
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.
Regular aerobic physical activity (e.g., brisk walking) at least 30 minutes a day most days of the week. Moderately intense activity such as brisk walking, jogging, and swimming can lower BP, promote relaxation, and decrease or control body weight.
It is strongly recommended that tobacco use be avoided.
Stress can raise BP on a short-term basis and has been implicated in the development of hypertension. Relaxation therapy, guided imagery, and biofeedback may be useful in helping patients manage stress, thus decreasing BP.
Drug therapy is not recommended for those persons with prehypertension unless it is required by another condition, such as diabetes mellitus or chronic kidney disease.
The overall goals for the patient with hypertension include (1) achievement and maintenance of the goal BP; (2) acceptance and implementation of the therapeutic plan; (3) minimal or no unpleasant side effects of therapy; and (4) ability to manage and cope with illness.
Drugs currently available for treating hypertension work by (1) decreasing the volume of circulating blood, and/or (2) reducing SVR.
Diuretics promote sodium and water excretion, reduce plasma volume, decrease sodium in the arteriolar walls, and reduce the vascular response to catecholamines.
Adrenergic-inhibiting agents act by diminishing the SNS effects that increase BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit norepinephrine release or to block the adrenergic receptors on blood vessels.
Direct vasodilators decrease the BP by relaxing vascular smooth muscle and reducing SVR.
Calcium channel blockers increase sodium excretion and cause arteriolar vasodilation by preventing the movement of extracellular calcium into cells.
Angiotensin-converting enzyme (ACE) inhibitors prevent the conversion of angiotensin I to angiotensin II and reduce angiotensin II (A-II)–mediated vasoconstriction and sodium and water retention.
A-II receptor blockers (ARBs) prevent angiotensin II from binding to its receptors in the walls of the blood vessels.
Thiazide-type diuretics are used as initial therapy for most patients with hypertension, either alone or in combination with one of the other classes.
When BP is more than 20/10 mm Hg above SBP and DBP goals, a second drug should be considered. Most patients who are hypertensive will require two or more antihypertensive medications to achieve their BP goals.
Side effects and adverse effects of antihypertensive drugs may be so severe or undesirable that the patient does not comply with therapy.
Hyperuricemia, hyperglycemia, and hypokalemia are common side effects with both thiazide and loop diuretics.
ACE inhibitors lead to high levels of bradykinin, which can cause coughing. An individual who develops a cough with the use of ACE inhibitors may be switched to an ARB.
Hyperkalemia can be a serious side effect of the potassium-sparing diuretics and ACE inhibitors.
Sexual dysfunction may occur with some of the diuretics.
Orthostatic hypotension and sexual dysfunction are two undesirable effects of adrenergic-inhibiting agents.
Tachycardia and orthostatic hypotension are potential adverse effects of both vasodilators and angiotensin inhibitors.
Patient and family teaching related to drug therapy is needed to identify and minimize side effects and to cope with therapeutic effects. Side effects may be an initial response to a drug and may decrease with continued use of the drug.
Hypertensive crisis is a severe and abrupt elevation in BP, arbitrarily defined as a DBP more than 140 mm Hg.
Hypertensive crisis occurs most often in patients with a history of hypertension who have failed to comply with their prescribed medications or who have been undermedicated.
Hypertensive crisis related to cocaine or crack use is becoming a more frequent problem. Other drugs such as amphetamines, phencyclidine (PCP), and lysergic acid diethylamide (LSD) may also precipitate hypertensive crisis that may be complicated by drug-induced seizures, stroke, MI, or encephalopathy.
Hypertensive emergency develops over hours to days and is defined as BP that is severely elevated (more than 180/120 mm Hg) with evidence of acute target organ damage.
Hypertensive emergencies can precipitate encephalopathy, intracranial or subarachnoid hemorrhage, acute left ventricular failure with pulmonary edema, MI, renal failure, dissecting aortic aneurysm, and retinopathy.
Hypertensive emergencies require hospitalization, intravenous (IV) administration of antihypertensive drugs, and intensive care monitoring.
The primary nursing responsibilities for long-term management of hypertension are to assist the patient in reducing BP and complying with the treatment plan. Nursing actions include patient and family teaching, detection and reporting of adverse treatment effects, compliance assessment and enhancement, and evaluation of therapeutic effectiveness.
Patient and family teaching includes the following: (1) nutritional therapy, (2) drug therapy, (3) physical activity, (4) home monitoring of BP (if appropriate), and (5) tobacco cessation (if applicable).