The prevalence of high blood pressure, or hypertension, is on the rise in the U.S.¹ In 1999 to 2000, an estimated 28.7% of the population, more than 58 million Americans, had hypertension.¹ This represents an increase of 3.7% since 1988 to 1991.¹ In 2003, hypertension was listed as a primary or contributing cause of death in about 277,000 Americans.²

Practitioners have updated guidelines to aid them in the management of hypertension.³ Contained in the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7), the new guidelines provide information about risk assessment, classification, and treatment.³

Risk assessment

Of the estimated 58 million Americans with hypertension in 1999 to 2000, only about one-third had met established blood pressure (BP) goals.¹ Another 30% were not even aware they had the disease.¹ The prevalence of hypertension was highest in non-Hispanic blacks, tended to be higher in women, and increased with advanced age.¹ Recent data suggest that even people free of hypertension at age 55 still have a 90% lifetime risk of developing it.³

Hypertension is one of the leading risk factors for cardiovascular disease.⁴ The higher the BP, the greater the risk of MI, heart failure, stroke, and kidney disease.³ The risk of CVD beginning at a BP of 115/75 mmHg doubles with each 20 mmHg incremental increase in systolic BP (SBP) or 10 mmHg incremental increase in diastolic BP (DBP).³ In younger people elevated DBP is associated with more CVD risk than increased SBP.³ However, starting at age 50, SBP becomes the more important risk factor.^3,5

Hypertension classification

BP classification is based on the average of two or more properly measured, seated BP measurements made on each of two or more office visits.³ See table for a summary of the JNC 7 BP classification.³ This classification differs from JNC 6 in two ways. First, a new “prehypertension” category has been added.³ These patients are at increased risk for clinical hypertension. Although they don’t require drug therapy, they should practice lifestyle modification.³ Lifestyle changes can potentially lower BP and reduce the risk of progression to hypertension. Also in JNC 7, stages 2 and 3 hypertension have been combined into a single stage 2 category to simplify treatment.³

Treatment — rationale and goals

One of the best ways to lower the complications associated with hypertension is to reduce BP. In clinical trials, antihypertensive therapy has been associated with a 35% to 40% reduction in stroke, a 20% to 25% reduction in MI, and a more than 50% reduction in heart failure.¹³

The ultimate goal of antihypertensive therapy is to reduce cardiovascular and renal morbidity and mortality.³ In most people, the BP goal is less than 140/90 mmHg.³ However, in people with diabetes or renal disease, the goal is less than 130/80 mmHg.³ This is because people with hypertension and diabetes or renal disease are at higher risk for developing CVD and kidney failure.^3,5 Traditionally, hypertension management has emphasized the treatment of elevated DBP.⁵ However, because most people with hypertension (especially older people) will meet the diastolic goal once the systolic goal is met, therapy should be targeted at meeting SBP goals.^3,5

Lifestyle modifications: Even in people with normal BP, a healthy lifestyle is encouraged to prevent high BP.³ In those with prehypertension and hypertension, lifestyle intervention is essential and should be used even when drug therapy is required. Lifestyle modifications reduce BP, enhance antihypertensive drug efficacy, and reduce CVD risk.³ The JNC 7 recommends five methods of lifestyle modification to manage hypertension:

• Weight reduction. In patients who are overweight or obese, a 10-kg weight loss may decrease SBP by 5 to 20 mmHg.³
• Dietary approaches to stop hypertension (DASH) diet. The DASH eating plan is rich in fruits, vegetables, and low-fat dairy products with a reduced content of saturated and total fat. This diet may reduce SBP by 8 to 14 mmHg.³
• Dietary sodium reduction. Reducing dietary sodium intake to no more than 100 mmol per day (2.4 grams of sodium or 6 grams of sodium chloride) may decrease SBP by 2 to 8 mmHg.³
• Physical activity. Regular aerobic exercise (at least 30 minutes daily, most days of the week) may reduce SBP by 4 to 9 mmHg.³
• Moderate consumption of alcohol. Limiting alcohol to two drinks daily in men and one drink daily in women and lighter-weight individuals may reduce SBP by 2 to 4 mmHg.³

Drug therapy: The complications of hypertension are reduced by several classes of drugs including thiazide-type diuretics, angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), beta-blockers (BBs), and calcium-channel blockers (CCBs).³ Based on clinical outcome data, the JNC 7 recommends thiazide diuretics as initial therapy in most patients with hypertension, either alone or combined with an ACEI, ARB, BB, or CCB.³ (For a list of high-risk conditions that are compelling indictors for these other agents, see the sidebar below.)

Most people with hypertension will require two or more drugs to meet BP goals.^3,5 In patients who fail to achieve BP goals with adequate doses of one drug, a second agent from another class should be added.³ When BP is greater than 20 mmHg above the SBP goal or 10 mmHg above the DBP goal, consideration should be given to initiating therapy with two drugs, one of which usually should be a thiazide-type diuretic.^3,5 Initial combination therapy should be used cautiously in people at high risk for orthostatic hypotension (e.g., people with diabetes, elderly).³

The following represents a review of antihypertensive therapy by drug class. Information about individual agents and dosing is available as part of the JNC 7 report at www.nhlbi.nih.gov/guidelines/hypertension/index.htm.

Diuretics: Thiazide diuretics, such as hydrochlorothiazide, are usually less expensive than other antihypertensive agents and are the recommended initial therapy in most patients with hypertension.^3,6 Thiazides have favorable effects in hypertensive patients at high risk for coronary disease and in those with diabetes or heart failure.³ They also decrease the incidence of first-time and recurrent strokes.³ Thiazides have decreased efficacy in patients with advanced renal disease.⁴ In these patients and those with symptomatic heart failure, loop diuretics (e.g., furosemide [Lasix]) are preferred.^3,4

Thiazide diuretics may cause electrolyte disturbances including hypokalemia, hypomagnesemia, hyponatremia, and hypercalcemia.^4,7,8 Electrolyte effects are similar with loop diuretics except that hypocalcemia may occur.^4,7 In patients receiving thiazide or loop diuretics, a potassium supplement may be given to prevent hypokalemia, or they may be used in combination with a potassium-sparing diuretic (e.g., hydrochlorothiazide with triamterene [Maxzide]). Thiazide and loop diuretics may cause elevations in lipids and serum glucose.^4,7 These effects are usually transient and are lessened by using lower diuretic doses.⁴ Thiazide and loop diuretics may increase uric acid levels and should be used cautiously in people with gout.^3,4,7,8 Serum electrolytes, uric acid levels, renal function, and glucose should be monitored periodically.⁷ Thiazide and loop diuretics are generally contraindicated in patients allergic to sulfonamide-derived drugs (e.g., sulfonylureas such as glipizide [Glucotrol]) because of a potential for cross-hypersensitivity.⁷

Angiotensin-converting enzyme inhibitors: The ACEIs are beneficial in treating hypertension in patients with acute coronary syndromes (unstable angina or MI), heart failure, diabetes, and chronic kidney disease.^3,4,8 Recurrent stroke rates may be lowered by combining an ACEI and thiazide diuretic.³ ACEIs also reduce albuminuria in patients with diabetes and slow the progression of diabetic and nondiabetic renal disease.^3,4

The most common side effect of ACEIs is a persistent cough.^4,7,8 These drugs may also cause hyperkalemia and renal insufficiency, so serum potassium levels and renal function should be monitored.⁷ They should be used cautiously in patients receiving drugs known to increase potassium (e.g., potassium supplements, potassium-sparing diuretics). The ACEIs are contraindicated in patients with previous ACEI-induced angioedema or with bilateral renal artery stenosis and in pregnancy.^3,4,7,8

Angiotensin receptor blockers: The ARBs are useful BP-lowering agents in patients with heart failure, diabetes, and chronic kidney disease.^3,8 The ARB valsartan (Diovan) was found to be as effective as captopril (Capoten), an ACEI, in preventing death in patients at high risk for cardiovascular events after MI.⁹ Like ACEIs, the ARBs have been shown to decrease albuminuria and slow the progression of diabetic and nondiabetic kidney disease.³ Occasionally, ARBs may be used in combination with ACEIs, especially for the treatment of kidney disease.¹⁰ ACEIs and ARBs may also prevent or delay the onset of new type 2 diabetes. This has been demonstrated in the results of several large clinical trials.¹³

The ARBs often are used as an alternative to ACEIs because cough is much less common.^3,4,8 Like ACEIs, the ARBs also may cause hyperkalemia and renal dysfunction.^4,7 Potassium levels and renal function should be monitored.⁷ They should be used cautiously in patients receiving drugs known to increase potassium levels and in patients with a history of ACEI-induced angioedema.⁴ The ARBs are contraindicated in pregnancy and in bilateral renal artery stenosis.^3,7,8

Beta-blockers: Beta-blockers reduce cardiovascular mortality in hypertensive patients with ischemic heart disease, diabetes, and heart failure.³ In patients with ischemic heart disease (including stable and unstable angina and acute MI), antihypertensive therapy should be initiated with a beta-blocker unless contraindicated.^3,4,8 Beta-blockers also are useful for treating supraventricular tachyarrhythmias, migraine headache, and thyrotoxicosis (short-term).⁴

Many of the side effects of beta-blockers are an extension of their pharmacological effects. Blocking beta-1 receptors in the heart is associated with bradycardia, so heart rate should be monitored regularly.^4,7 Beta-blockers may cause atrioventricular conduction abnormalities and are contraindicated in second- and third-degree heart block.^3,4,7 Heart failure may develop when beta-blockers are used at high initial doses in patients with preexisting left ventricular dysfunction.⁴ When using beta-blockers in patients with stable heart failure, they should be initiated at a low dose and slowly titrated upward.⁴

Blocking beta-2 receptors in the lungs may lead to bronchospasm in patients with bronchospastic diseases such as asthma.⁴ In general, beta-blockers should be avoided in patients with bronchospastic diseases.^3,7 Beta-1 selective or cardioselective agents (e.g., metoprolol [Toprol]) can be used cautiously in low doses in patients who cannot tolerate or do not respond to other antihypertensive therapies.⁷

Beta-blockers also may increase serum glucose and lipid levels.^4,8 These effects are usually transient and of little clinical significance.⁴ Beta-blockers, especially nonselective agents, may blunt hypoglycemic awareness in diabetics.^3,4,7 Cardioselective agents are preferred in diabetics.⁴

Calcium channel blockers: Long-acting CCBs are beneficial in hypertensive patients with stable angina as an alternative to beta-blockers.^3,4 They have also been shown to decrease CVD risk in patients with diabetes.³ There are two types of CCBs: dihydropyridines (e.g., amlodipine [Norvasc]) and nondihydropyridines (verapamil [Calan] and diltiazem [Cardizem]).^4,7 Short-acting CCBs should not be used for the treatment of hypertension.^3,8 In particular, the short-acting dihydropyridines (e.g., nonsustained-release nifedipine [Procardia]) have been associated with increased cardiovascular risk.^3,4 Both dihydropyridine and nondihydropyridine CCBs are similar in antihypertensive efficacy, but their pharmacodynamic effects and potential side effects differ.

The dihydropyridines cause peripheral vasodilation, which may in turn cause an increase in heart rate, flushing, dizziness, and peripheral edema.^4,7 The nondihydropyridines, verapamil in particular, have cardiac depressive effects and decrease heart rate and slow atrioventricular conduction.⁴ These properties make the nondihydropyridines useful for treating supraventricular arrhythmias.^3,4 However, because of these same properties, the nondihydropyridines should not be used in second- or third-degree heart block and severe heart failure.^7,8 Caution is warranted when administering beta-blockers and nondihydropyridine CCBs together (especially intravenous formulations) because of a potential for added cardiac depressive effects.⁷ Long-acting dihydropyridine CCBs are preferred when combination therapy with beta-blockers is necessary.³ Consuming grapefruit or grapefruit juice with many of the CCBs may result in elevated serum concentrations with subsequent toxicity and should be avoided.¹¹

Alternative antihypertensive agents: Aldosterone blockade has been shown to be cardioprotective.¹² Spironolactone (Aldactone), a potassium-sparing diuretic and first generation aldosterone blocker, reduces mortality in heart failure.^4,12 A newer agent, eplerenone (Inspra), is a derivative of spironolactone but has more specific affinity for aldosterone receptors.¹³ It is the first agent approved in a new class of antihypertensive agents called selective aldosterone receptor antagonists.⁵ Eplerenone is approved for treating hypertension and congestive heart failure after acute MI.¹² The most common side effect of eplerenone is hyperkalemia.⁵ It is contraindicated in patients with a serum potassium greater than 5.5 meq/L and those with renal dysfunction.^5,12 Caution is warranted when combining aldosterone antagonists with ACEIs and ARBs.^3,5,12

The alpha 1-blockers (e.g., doxazosin [Cardura]) appear to confer less cardiac benefit than other antihypertensive agents.⁴ In the Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial, the doxazosin treatment arm was stopped prematurely because of a higher rate of cardiovascular events compared to diuretic-treated patients.^4-6 However, these agents are useful in treating prostate enlargement. They now are generally reserved for the treatment of hypertension in men with benign prostatic hypertrophy, usually in addition to other standard antihypertensive therapy.^4,5

Other classes of agents available for the treatment of hypertension include central alpha2-agonists (e.g., clonidine [Catapres]) and vasodilators (e.g., hydralazine [Apresoline]). These drugs tend to have more side effects than other agents and are generally reserved for patients whose blood pressure is more difficult to control.⁴

Special populations

In older people, drug therapy is started at lower doses and titrated slowly to avoid orthostatic hypotension.^3,4 In African Americans, BP response during monotherapy is usually better with diuretics or CCBs than with ACEIs, ARBs, or beta-blockers,^3,4,8 but combination regimens that include a diuretic are equally effective in African Americans and Caucasians.^3,4 In pregnancy, methyldopa (Aldomet) is usually the drug of choice.^3,4 Alternative agents include beta-blockers, CCBs, and vasodilators.³ ACEIs and ARBs are contraindicated in pregnancy because of possible serious neonatal problems.^4,7

Nursing implications

The final message of the JNC 7 guidelines is the importance of motivation. Hypertension will be controlled only if patients are motivated to adhere to their treatment plan.³ As frontline care providers, nurses are in an ideal position to motivate patients to modify their lifestyles and adhere to antihypertensive drug therapy. With effective communication, nurses can help patients understand hypertension, complications of the disease, goals of therapy, and medication use.