The prevalence of high blood pressure, or hypertension, in the United States has increased from approximately 50 million from 1988 through 1994 to 65 million in the period from 1999 to 2004.¹ In 2005, an estimated 33.6% of the population, more than 73 million Americans, had hypertension.² From 1995 to 2005, the death rate from high blood pressure increased 25% and the actual number of deaths increased 56%. In 2005, high blood pressure killed approximately 58,000 people.²

The current guideline to aid in the management of hypertension is the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC 7). The guideline provides information about risk assessment, classification and treatment.³

Risk Assessment

Of the estimated 73 million Americans with hypertension in 2005, about 45% had met established blood pressure goals.² One in five were not even aware they had the disease.² The prevalence of hypertension was highest in non-Hispanic blacks, tended to be higher in women, and increased with advanced age.4 Recent data suggest that even people free of hypertension at age 55 still have a 90% lifetime risk of developing high blood pressure.³
 
Hypertension is a major risk factor for cardiovascular disease and renal disease, and early data indicates that untreated high blood pressure shortens life expectancy by approximately five years.⁵ The higher the blood pressure, the greater the risk of MI, heart failure, stroke and kidney disease.³ The risk of cardiovascular disease beginning at a BP of 115/75 mmHg doubles with each 20 mmHg incremental increase in systolic BP or 10 mmHg incremental increase in diastolic BP.³ In younger people, elevated diastolic BP is associated with more cardiovascular disease risk than increased systolic BP.³ However, starting at age 50, systolic BP becomes the more important risk factor.^3,5

Hypertension Classification

Blood pressure 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 “Blood Pressure Classification in Adults” 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.^1,3
 
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 cardiovascular disease and kidney failure.^3,6 Traditionally, hypertension management has emphasized the treatment of elevated diastolic BP.⁶ 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 systolic BP goals.^3,6
 
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 cardiovascular disease 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 systolic BP by 5 mmHg to 20 mmHg.³
 
Dietary approaches to stop hypertension 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 systolic BP by 8 mmHg to 14 mmHg.³
 
Dietary sodium reduction: Reducing dietary sodium intake to no more than 100 mmol per day (2.4 g of sodium or 6 g of sodium chloride) may decrease systolic BP by 2 mmHg to 8 mmHg.³
 
Physical activity: Regular aerobic exercise (at least 30 minutes daily, most days of the week) may reduce systolic BP by 4 mmHg 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 people may reduce systolic BP by 2 mmHg 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 indicators for these other agents, see the sidebar.)

Most people with hypertension require two or more drugs to meet BP goals.3,6 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 systolic BP goal or 10 mmHg above the diastolic BP goal, consideration should be given to initiating therapy with two drugs, one of which usually should be a thiazide-type diuretic.^3,6 Initial combination therapy should be used cautiously in people at high risk for orthostatic hypotension (e.g., people with diabetes, elderly).^3,7
 
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.^3,8 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. In these patients and those with symptomatic heart failure, loop diuretics (e.g., furosemide [Lasix]) are preferred.³
 
Thiazide diuretics may cause electrolyte disturbances including hypokalemia,hypomagnesemia, hyponatremia and hypercalcemia.^9,10 Electrolyte effects are similar with loop diuretics except hypocalcemia may occur.⁹ 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.⁹ These effects are usually transient and are lessened by using lower diuretic doses. Thiazide and loop diuretics may increase uric acid levels and should be used cautiously in people with gout.^3,9,10 Serum electrolytes, uric acid levels, renal function and glucose should be monitored periodically.⁹ 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.⁹

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.^3,10 Recurrent stroke rates may be lowered by combining an ACEI and a thiazide diuretic.³ ACEIs also reduce albuminuria in patients with diabetes and slow the progression of diabetic and nondiabetic renal disease.³
 
The most common side effect of ACEIs is a persistent cough.^9,10 These drugs may also cause hyperkalemia and renal insufficiency, so serum potassium levels and renal function should be monitored.⁹ 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.^3,9,10
 
Angiotensin receptor blockers: The ARBs are useful BP-lowering agents in patients with heart failure, diabetes and chronic kidney disease.^3,10 A meta-analysis of six studies involving nearly 50,000 patients revealed that the ARBs are equally efficient as the ACEIs in reducing the risk for myocardial infarction, stroke and death.¹¹ 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.¹² 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.^3,10 Like ACEIs, the ARBs also may cause hyperkalemia and renal dysfunction.⁹ Potassium levels and renal function should be monitored.9 They should be used cautiously in patients receiving drugs known to increase potassium levels and in patients with a history of ACEI-induced angioedema.³ The ARBs are contraindicated in pregnancy and in bilateral renal artery stenosis.^3,9,10
 
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.^3,10
 
Many of the adverse 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.⁹ Beta-blockers may cause atrioventricular conduction abnormalities and are contraindicated in second- and third-degree heart block.^3,9 Heart failure may develop when beta-blockers are used at high initial doses in patients with preexisting left ventricular dysfunction.⁹ When using beta-blockers in patients with stable heart failure, they should be initiated at a low dose and slowly titrated upward.⁹

Blocking beta-2 receptors in the lungs may lead to bronchospasm in patients with bronchospastic diseases, such as asthma. In general, beta-blockers should be avoided in patients with bronchospastic diseases.⁹ 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.⁹

Beta-blockers also may increase serum glucose and lipid levels.¹⁰ These effects are usually transient and of little clinical significance. Beta-blockers, especially nonselective agents, may blunt hypoglycemic awareness in diabetics.3,9 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 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]).⁹ Short-acting CCBs should not be used for the treatment of hypertension.^3,9 In particular, the short-acting dihydropyridines (e.g., nonsustained-release nifedipine [Procardia]) have been associated with increased cardiovascular risk.³ 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.9 The nondihydropyridines, verapamil in particular, have cardiac depressive effects and decrease heart rate and slow atrioventricular conduction.⁹ These properties make the nondihydropyridines useful for treating supraventricular arrhythmias.³ However, because of these same properties, the nondihydropyridines should not be used in second- or third-degree heart block and severe heart failure.^9,10 Caution is warranted when administering beta-blockers and nondihydropyridine CCBs together (especially intravenous formulations) because of a potential for added cardiac depressive effects.⁹ 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.¹⁴

Alternative antihypertensive agents: Aldosterone blockade has been shown to be cardioprotective.¹⁵ Spironolactone (Aldactone), a potassium-sparing diuretic and first-generation aldosterone blocker, reduces mortality in heart failure.¹⁵ A newer agent, eplerenone (Inspra), is a derivative of spironolactone but has more specific affinity for aldosterone receptors.¹⁵ It is the first agent approved in a new class of antihypertensive agents called selective aldosterone receptor antagonists.⁶ Eplerenone is approved for treating hypertension and congestive heart failure after acute MI.¹⁵ The most common side effect of eplerenone is hyperkalemia.⁶ It is contraindicated in patients with a serum potassium greater than 5.5 meq/L and those with renal dysfunction.^6,15 Caution is warranted when combining aldosterone antagonists with ACEIs and ARBs.^3,6,15

Regarding alpha 1-blockers (e.g., doxazosin [Cardura]), 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.^6,8 However, these agents are useful in treating prostate enlargement. They now generally are reserved for the treatment of hypertension in men with benign prostatic hypertrophy usually in addition to other standard antihypertensive therapy.⁶

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.³

New therapies for high blood pressure currently under study include darusentan (endothelin receptor type A antagonist) for resistant hypertension, a vaccine to block the activity of angiotensin II, cannabinoid-1 receptor antagonists and alagebrium (interferes with cross-linkages of collagen and elastin to reduce arterial and myocardial stiffness).^16-19

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,^3,10 but combination regimens that include a diuretic are equally effective in African Americans and Caucasians.³ 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.⁹ For people with diabetes mellitus, ACEIs and ARBs are usually the drugs of choice.³

Clinical 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, physical therapists are in an ideal position to motivate patients to modify their lifestyles and adhere to antihypertensive drug therapy. With effective communication, physical therapists can help patients understand hypertension, complications of the disease, goals of therapy, and medication use.

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