Hypertension Treatment & Management

Consider lifestyle modifications. As the cardiovascular disease risk factors are assessed in individuals with hypertension, pay attention to the lifestyles that favorably affect blood pressure (BP) level and reduce overall cardiovascular disease risk. A relatively small reduction in BP may affect the incidence of cardiovascular disease on a population basis. A decrease in BP of 2 mm Hg reduces the risk of stroke by 15% and the risk of coronary artery disease by 6% in a given population. In addition, a prospective study showed a reduction of 5 mm Hg in the nocturnal mean blood pressure and a possibly significant (17%) reduction in future adverse cardiovascular events if at least one antihypertensive medication is taken at bedtime.^[21]

The American Diabetes Association (ADA) 2011 standard of medical care states that in individuals with diabetes and mild hypertension, it may be reasonable to begin treatment with a trial of nonpharmacological therapy (diet, exercise, and other lifestyle modifications.) Mild hypertension as defined by the ADA guideline (systolic blood pressure 130-139 mmHg or diastolic blood pressure 80-89 mmHg) may be classified as prehypertension by other organizations.^[22]

Hypertension remains one of the most common causes of congestive heart failure (CHF). Antihypertensive therapy has been demonstrated to significantly reduce the risk of death from stroke and coronary heart disease. Two published meta-analyses have shown 14% and 26% reductions in cardiovascular mortality rates.

Other studies have demonstrated that a reduction in BP may result in improved renal function. Therefore, earlier detection of hypertensive nephrosclerosis using means to detect microalbuminuria and aggressive therapeutic interventions, particularly with ACE inhibitor drugs, may prevent progression to end-stage renal disease.^[3]

According to the ADA 2011 standards of medical care in diabetes, a majority of patients with diabetes mellitus have hypertension. In patients with type 1 diabetes, nephropathy is often the cause of hypertension, while, in type 2 diabetes, hypertension is one of a group of related cardiometabolic factors.^[22]

JNC VII

Key messages of the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VII) are as follows:^[1]

• Prehypertension (systolic 120-139, diastolic 80-89) requires health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and cardiovascular disease.
• In uncomplicated hypertension, a thiazide diuretic, either alone or combined with drugs from other classes, should be used for the drug treatment of most cases.
• In specific high-risk conditions, there are compelling indications for the use of other antihypertensive drug classes (eg, angiotensin-converting enzyme [ACE] inhibitors, angiotensin-receptor blockers [ARBs], beta blockers, calcium channel blockers).
• Two or more antihypertensive medications will be required to achieve goal BP (< 140/90 mm Hg or < 130/80 mm Hg) for patients with diabetes and chronic kidney disease.
• For patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using 2 agents, one of which usually will be a thiazide diuretic, should be considered.
• Regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan.

JNC VII recommendations to lower BP and decrease cardiovascular disease risk include the following:^[1]

• Lose weight if overweight. This can be accomplished with the DASH (Dietary Approaches to Stop Hypertension) diet, which is rich in fruits and vegetables and encourages the use of fat-free or low-fat milk and milk products.^{[23, 24]}
• Limit alcohol intake to no more than 1 oz (30 mL) of ethanol per day in men (ie, 24 oz [720 mL] of beer, 10 oz [300 mL] of wine, 2 oz [60 mL] of 100-proof whiskey) or 0.5 (15 mL) of ethanol per day for women and people of lighter weight.
• Increase aerobic activity (30-45 min most days of the week).
• Reduce sodium intake to no more than 100 mmol/d (2.4 g sodium or 6 g sodium chloride).
• Maintain adequate intake of dietary potassium (approximately 90 mmol/d).
• Maintain adequate intake of dietary calcium and magnesium for general health.
• Stop smoking and reduce intake of dietary saturated fat and cholesterol for overall cardiovascular health.

The 2010 American Heart Association-American Stroke Association (AHA-ASA) guidelines for the primary prevention of stroke makes the following recommendations:^[25]

• Hypertension: The AHA-ASA guidelines recommend regular blood pressure screening, lifestyle modification, and drug therapy. A lower risk of stroke and cardiovascular events are seen when systolic blood pressure levels are < 140 mm Hg and diastolic blood pressure < 90 mm Hg. In patients that have hypertension with diabetes or renal disease, the blood pressure goal is < 130/80 mm Hg.
• Diet and nutrition: A diet that is low in sodium and high in potassium is recommended to reduce blood pressure. Diets that promote the consumption of fruits, vegetables, and low-fat dairy products such as the DASH-style diet help lower blood pressure and may lower risk of stroke.
• Physical inactivity: Increasing physical activity is associated with a reduction in the risk of stroke. The goal is to engage in ≥30 minutes of moderate intensity activity on a daily basis.
• Obesity and body fat distribution: Weight reduction among overweight and obese persons, is recommended to reduce blood pressure and risk of stroke.

Dietary changes

A number of studies have documented an association between sodium chloride intake and BP. The effect of sodium chloride is particularly important in individuals who are middle-aged to elderly with a family history of hypertension. A moderate reduction in sodium chloride intake can lead to a small reduction in blood pressure. The American Heart Association recommends that the average daily consumption of sodium chloride not exceed 6 g; this may lower blood pressure by 2-8 mm Hg.

One randomized controlled trial published found that moderate dietary sodium reduction (approximately 2500 mg Na+/day or 6 g NaCl/day) added to angiotensin-converting enzyme inhibition compared with dual blockade (angiotensin-converting enzyme inhibitor and angiotensin receptor blocker) was more effective in reducing both proteinuria and blood pressure in nondiabetic patients with modest chronic kidney disease. Furthermore, a low sodium diet added to dual therapy yielded additional reductions in both blood pressure and proteinuria, emphasizing the beneficial effect of dietary salt reduction in the management of hypertensive patients with renal insufficiency.^[26]

The aforementioned DASH eating plan encompasses a diet rich in fruits, vegetables, and low-fat dairy products and may lower blood pressure by 8-14 mm Hg.^{[23, 24]}

The 2011 ADA standard of care supports the DASH diet, with the caution that high-quality studies of diet and exercise to lower blood pressure have not been performed on individuals with diabetes.^[22]

Dietary potassium, calcium, and magnesium consumption have an inverse association with blood pressures. Lower intake of these elements potentiates the affect of sodium on blood pressure. Oral potassium supplementation may lower both systolic and diastolic pressure. Calcium and magnesium supplementation have elicited small reductions in blood pressures.

In population studies, low levels of alcohol consumption have shown a favorable effect on blood pressure, with reductions of 2-4 mm Hg. However, the consumption of 3 or more drinks per day is associated with elevation of BP. Alcohol intake should be restricted to less than 1 oz of ethanol in men and 0.5 oz in women. The 2011 ADA standard supports limiting alcohol consumption in patients with diabetes and hypertension.^[22]

Weight loss and exercise

Up to 60% of all individuals with hypertension are more than 20% overweight. The centripetal fat distribution is associated with insulin resistance and hypertension. Even modest weight loss (5%) can lead to reduction in BP and improved insulin sensitivity. Weight reduction may lower blood pressure by 5-20 mm Hg per 10 kg of weight loss in a patient who weighs more than 10% of ideal body weight.

Regular aerobic physical activity can facilitate weight loss, decrease BP, and reduce the overall risk of cardiovascular disease. Blood pressure may be lowered by 4-9 mm Hg with moderately intense physical activity. These activities include brisk walking for 30 minutes a day, 5 days per week. More intense workouts for 20-30 minutes, 3-4 times a week may also lower BP and have additional health benefits.

Blumenthal et al found that in overweight or obese patients with high BP, adding exercise and weight loss to the DASH diet resulted in even larger reductions in BP and cardiovascular biomarkers of risk. Their randomized, controlled trial in 144 patients showed that after 4 months, clinic-measured blood pressure was reduced by 16.1/9.9 mm Hg in patients in the DASH-plus–weight management group, by 11.2/7.5 mm in patients managed with DASH alone, and by 3.4/3.8 mm in a control group eating a usual diet. Compared with DASH alone, DASH plus weight management also resulted in greater improvement in pulse wave velocity, baroreflex sensitivity, and left ventricular mass.^[27]

The 2011 ADA diabetes standard supports increasing physical activity.^[22]

According to the 2011 ADA standard, patients with diabetes and severe hypertension (systolic BP ≥ 140 or diastolic BP ≥ 90 mmHg) at diagnosis or afterwards should receive drug therapy along with lifestyle modifications.^[22]

Multiple clinical trials suggest that most antihypertensive drugs provide the same degree of cardiovascular protection for the same level of BP control. Well-designed prospective randomized trials, such as the Swedish Trial in Old Patients with Hypertension (STOP-2), the Nordic Diltiazem (NORDIL) trial, and the Intervention as a Goal in Hypertension Treatment (INSIGHT) trial, have shown a similar outcome with older drugs (eg, diuretics, beta-blockers) compared with the newer antihypertensive agents (eg, ACE inhibitors, calcium channel blockers).

Several situations demand the addition of a second drug because 2 drugs may be used at lower doses to avoid adverse effects, which may occur with higher doses of an individual agent. Diuretics generally potentiate the effects of other antihypertensive drugs by minimizing volume expansion. Specifically, the use of the diuretic thiazide in conjunction with a beta-blocker or an ACE inhibitor has an additive effect, controlling blood pressure in up to 85% of patients.

According to the 2011 ADA standard, two or more antihypertensive drugs at maximal doses should be used to achieve optimal blood pressure targets in patients with diabetes and hypertension. Either an ACE inhibitor or an ARB is usually required in patients with diabetes and hypertension. If the patient cannot tolerate one class of drugs, the other should be tried. If needed to achieve blood pressure goals, a thiazide diuretic is indicated for those patients with an estimated GFR (eGFR) ≥30 mL/min/1.73 m2 and a loop diuretic for those with an eGFR < 30 mL/min/1.73 m2. Regardless of which antihypertensive drugs are used, kidney function and serum potassium levels should be monitored.^[22]

A study by Leung et al found a 30% incidence of hyponatremia (Na < 130 mmol) in a long-term follow-up of patients who were exposed to thiazide diuretics for treatment of hypertension.^[28]

A study by Brown et al compared the combination of aliskiren and amlodipine with the use of monotherapy to control BP.^[29] The study found that combination therapy resulted in a greater reduction in mean systolic BP than monotherapy (6.5 mm Hg; 95% CI, 5.3-7.7).

Ruggenenti et al found that in patients with type 2 diabetes who have hypertension, combined manidipine and delapril therapy helped increase health for cardiovascular disease, retinopathy, and neuropathy and stabilized insulin sensitivity.^[30]

Patients with chronic kidney disease and hypertension were found in one study to have improved BP control and a reduced risk for cardiovascular events by taking at least one antihypertensive medication at bedtime.^[31]

Aortorenal bypass using a saphenous vein graft or a hypogastric artery is a revascularization technique for renovascular hypertension that has become much less common since the advent of renal artery angioplasty with stenting. Surgical resection is the treatment of choice for pheochromocytoma, because hypertension is cured by tumor resection. In patients with fibromuscular renal disease, angioplasty has a 60-80% success rate for improvement or cure of hypertension.

The primary goal of the emergency physician is to determine which patients with acute hypertension are exhibiting symptoms of end-organ damage and require immediate intravenous (IV) parenteral therapy. The fundamental principle in determining the necessary emergency department (ED) care of the hypertensive patient is the presence or absence of end-organ dysfunction.

Approximately 3-45% of adult ED patients have at least one increased BP during their stay in the ED. Many patients present to the ED with elevated BPs; however, only a small proportion of patients will require emergency treatment. In contrast, patients presenting with acutely elevated BPs (systolic BP >200 mm Hg or diastolic BP >120 mm Hg) without symptoms that are sustained throughout the ED stay and stay significantly elevated to this level on discharge should have initiation of medical therapy and close follow-up in the outpatient setting.^[32]

Usually, continuous IV infusions are the most appropriate initial therapy, especially in acutely ill infants with severe hypertension. The advantages of IV infusions are numerous, most importantly including the ability to quickly increase or decrease the rate of infusion to achieve the desired BP. As in patients of any age with malignant hypertension, take care to avoid too rapid a reduction in BP in order to avoid cerebral ischemia and hemorrhage; premature infants in particular are already at an increased risk because of the immaturity of their periventricular circulation. Because of the paucity of available data regarding the use of these agents in newborns, the choice of agent depends on the individual clinician’s experience.

In normal pregnancy, women’s MAP drops 10-15 mm Hg over the first half of pregnancy. Most women with mild chronic hypertension (ie, systolic BP 140-160 mm Hg, diastolic BP 90-100 mm Hg) have a similar decrease in BPs and may not require any medication during this period. Conversely, diastolic BP greater than 110 mm Hg has been associated with an increased risk of placental abruption and intrauterine growth restriction, and systolic BP greater than 160 mm Hg increases the risk of maternal intracerebral hemorrhage. Therefore, pregnant patients should be started on antihypertensive therapy if the systolic BP is greater than 160 mm Hg or the diastolic BP is greater than 100-105 mm Hg. The goal of pharmacologic treatment should be a diastolic BP of less than 100-105 mm Hg and a systolic BP less than 160 mm Hg.

Women with preexisting end-organ damage from chronic hypertension should have a lower threshold for starting antihypertensive medication (ie, >139/89) and a lower target BP (< 140/90).^[33]

Although the primary risk of chronic hypertension in pregnancy is development of superimposed preeclampsia, no evidence suggests that pharmacological treatment of mild hypertension reduces the incidence of preeclampsia in this population.^[34]

The systolic pressure continues to rise progressively throughout life, reaching the highest levels in later stages of life. Isolated systolic hypertension may be present in 10% of the population aged 70 years and in 24% of those aged 80 years. Furthermore, severe arteriosclerosis may lead to pseudohypertension. Isolated hypertension results in low cardiac output because of the decreased stroke volume and high peripheral resistance. This may reduce glomerular filtration further, which is why low activity of renal angiotensin aldosterone cascade is encountered in elderly individuals who are hypertensive.

Despite low PRA, blood pressure responds well to ACE inhibitor and ARB therapy. Low doses of diuretics may also be effective. Calcium antagonists are quite useful because of their strong antihypertensive effects.^[35] Often, combining 2 drugs at a lower dose may be preferable to using a single drug at a high dose that has the potential for adverse effects.

According to the 2011 American College of Cardiology Foundation (ACCF)/AHA Expert Consensus Document on Hypertension in the Elderly, there are insufficient data for strong evidence-based guidelines on managing hypertension in older patients. The ACCF/AHA document provides a consensus of expert opinion on clinical options; however, clinicians should take an individualized approach to the treatment of elderly patients.

The 2011 ACCF/AHA consensus document recommends starting the evaluation of the elderly patient with known or suspected hypertension with 3 measurements of blood pressure, to obtain an accurate BP value. If BP is elevated, the cause should be isolated. Any organ damage should be assessed. Other CVD risk factors or comorbid conditions should be identified, along with any potential barriers to treatment adherence.^[36]

The 2011 ACCF/AHA consensus advises against the routine use of laboratory testing in elderly patients. Instead, it recommends a more deliberative, focused approach. This would include a urinalysis for signs of renal damage (albuminuria/microalbuminuria); blood chemistries (especially potassium and creatinine with eGFR); total cholesterol, LDL, HDL, and triglycerides; fasting blood sugar (A1c if diabetes mellitus is suspected; and an ECG.^[36]

According to the ACCF/AHA consensus, lifestyle modifications may be all that is necessary to treat milder forms of hypertension in elderly patients. However, drug treatment for elderly patients with hypertension is generally recommended and should be started at the lowest dose possible, with gradual increases depending on response.^[36]

The Systolic Hypertension in the Elderly Program (SHEP) trial, a study by Kostis et al, found that chlorthalidone stepped-care therapy for 4.5 years was associated a longer life expectancy at 22 years of follow-up among patients with isolated systolic hypertension.^[37]

In the presence of hypertensive optic neuropathy, a rapid reduction of BP may pose a risk of worsening ischemic damage to the optic nerve. The optic nerve demonstrates autoregulation, so there is an adjustment in perfusion based on the elevated blood pressure. A precipitous reduction in BP will reduce perfusion to the optic nerve and central nervous system as a result of their autoregulatory changes, resulting in infarction of the optic nerve head and, potentially, acute ischemic neurologic lesions of the CNS.

The goals of therapy for renovascular hypertension (RVHT) are maintenance of normal BP and prevention of end-stage renal disease. The therapeutic options include medical therapy, percutaneous transluminal renal angioplasty (PTRA) and stenting, and surgical revascularization. These options must be individualized, because no randomized studies document the superiority of one option over the other. In a study focusing on patients with atherosclerotic renal artery stenosis, data suggested that revascularization therapy should be confined to patients who have renal ischemia with viable underlying renal function because they will experience the greatest clinical benefit.^[38] The indications for surgery or angioplasty include an inability to control BP while on a medical regimen, the need to preserve renal function, and intolerable effects of medical therapy.

With the advent of noninvasive techniques, aortal renal bypass using a saphenous vein or hypogastric artery is not commonly employed for revascularization. PTRA can be an effective treatment for hypertension and the preservation of renal function in a subset of patients that is difficult to identify.^[39] PTRA may be the initial choice in younger patients with fibromuscular lesions amenable to balloon angioplasty. Renal artery stenting of osteal lesions has been associated with improved long-term patency.

PTRA may also be used for arthrosclerotic renal artery stenosis; the outcome may be comparable to that of surgical revascularization. Medical therapy is required in the preoperative phase of interventional therapy. Medical therapy is also indicated for high-risk individuals and for older patients who have easily controlled hypertension. The specific population that will benefit from these techniques has yet to be clearly defined.

ACE inhibitors are quite effective in patients with unilateral renal artery stenosis; however, avoid ACE inhibitors in patients with bilateral renal artery stenosis or stenosis of a solitary kidney. A diuretic can be combined with an ACE inhibitor. Because of their glomerular vasodilatory effect, calcium antagonists are effective in renal artery stenosis and do not compromise renal function.^[40]

For most patients with RVHT, with the exception of persons with fibromuscular dysplasia, it is unclear whether revascularization will be beneficial. Fibromuscular dysplasia responds well to angioplasty. The causes of renovascular hypertension include atherosclerosis, fibromuscular dysplasia, coarctation of the aorta, embolic renal artery occlusion, aneurysm of the renal artery, and diffuse arteritis. Additionally, causes of diffuse bilateral renal ischemia, such as accelerated hypertension, vasculitis, hepatitis B, and IV drug abuse, may also lead to hypertension.

Some patients may have a persistent diastolic BP above 100 mm Hg despite the use of 3 or more different classes of antihypertensive medications.^[41] Although among more than one third of patients with resistant hypertension, ambulatory BP is normal; this stresses the importance of monitoring patients to achieve correct diagnosis and management.^[42] Patients who require 4 or more medications to control their BP should be considered resistant to treatment. A study has shown that the addition of low-dose spironolactone provides significant additive BP reduction in African-American and white patients who have resistant hypertension with or without primary hyperaldosteronism.

Catheter-based renal sympathetic denervation also lowers BP for an extended period of up to 2 years, according to a study of 153 patients with resistant hypertension in Australia, Europe, and the United States conducted by the American Heart Association.^[43] In addition, data suggest baroreceptor activation treatment (BAT) by an implantable stimulator can potentially safely reduce systolic blood pressure (SBP) over the long term in patients with resistant hypertension.^[44]

Inadequate treatment

Inadequate treatment was described as the most common cause of resistant hypertension in several published series. Patients may not be on an effective drug, or concomitant volume expansion may occur as a side effect of the drug.

Extracellular volume expansion

Extracellular volume expansion may contribute to the inability to lower systemic BP. The volume expansion may occur because of renal insufficiency, sodium retention due to treatment with vasodilators, high-salt diet, or insufficient dosing of diuretic. This situation can be treated with more aggressive diuretic therapy until clinical signs of extracellular volume depletion (eg, orthostatic hypotension) develop.

Noncompliance

Noncompliance with medical therapy or dietary modifications (eg, salt restriction) may play a role in causing resistant hypertension. Address noncompliance with extensive patient education, simplification of the drug regimen, use of fixed-dose combinations, and use of drugs with the fewest adverse effects.

Limited data suggests better compliance with ACE inhibitors and ARBs than some other antihypertensive medications.^[45]

Vasoactive substances

Resistant hypertension may be encountered in patients who are ingesting vasoactive substances despite taking antihypertensive drugs regularly. Use of salt and alcohol are the common examples; others include use of cocaine, amphetamines, anabolic steroids, oral contraceptives, cyclosporine, antidepressants, and nonsteroidal anti-inflammatory drugs.

Excluding secondary causes

Whenever confronted with resistant hypertension, try to exclude any secondary causes of hypertension. A reevaluation of the patient’s history, physical examination, and laboratory results may provide clues to secondary hypertension (eg, renal artery stenosis, primary hyperaldosteronism, obstructive sleep apnea). Primary hyperaldosteronism has a prevalence of 20% in this population. Obstructive sleep apnea is also associated with resistant hypertension, with 85% of patients with resistant hypertension having an elevated apnea/hypopnea index.^[46]

A study by Pedrosa et al also found that a good predictor for sleep apnea in patients older than 50 years with resistant hypertension is a large neck circumference and snoring.^[47]

Blood pressure rise secondary to anxiety may be observed in 20-30% of patients.^[48] This may be avoided by having patients rest prior to measurement, having a nurse check the blood pressure, or arranging to have the blood pressure monitored at home. Development of hypotensive symptoms on medications is an indication of so-called white-coat hypertension. White-coat hypertension can also be evaluated by the use of a 24-hour ambulatory monitor.

Pseudohypertension may be observed in elderly individuals who have thickened, calcified arteries. Much higher cuff pressure may be required to occlude a thickened brachial artery, and diastolic BP may also be overestimated. Consider pseudohypertension in situations in which no organ damage occurs despite marked hypertension, when patients develop hypotensive symptoms on medications, and when calcification of the brachial artery is observed on radiologic examination. Direct measurement of intra-arterial pressure may be required in this setting.

Following suspicion of pheochromocytoma, the presence of a tumor should be confirmed biochemically by measuring urine and plasma concentrations of catecholamine or their metabolites. In most situations, computed tomography (CT) or magnetic resonance imaging (MRI) may be used to localize the tumor in the abdomen. In the absence of abdominal imaging, nuclear scan with metaiodobenzylguanidine (MIBG) may further help with the localization.

Surgical resection is the treatment of choice because hypertension is cured by tumor resection. In the preoperative phase, combined alpha- and beta-adrenergic blockade is recommended for hypertension control. Alpha-adrenergic blockade is initiated with phenoxybenzamine or prazosin, and, following adequate alpha-adrenergic blockade, beta-adrenergic blockade is initiated. These patients are often volume contracted and require saline or sodium tablets. Catecholamines can be reduced further by metyrosine. For adrenal pheochromocytoma, laparoscopic adrenalectomy is becoming the procedure of choice in suitable patients. Follow-up 24-hour urinary excretion studies of catecholamines should be performed 2 weeks following surgery (and periodically thereafter) to detect recurrence, metastases, or development of second primary lesion.

The prevalence of primary hyperaldosteronism increases with the severity of hypertension, being 2% in stage 1 and 20% in resistant hypertension. Hypokalemia and metabolic alkalosis are important clues to the presence of primary hyperaldosteronism. However, these are relatively late manifestations, and in a large subset of patients, the serum potassium concentration and bicarbonate are within the reference range. Measurement of the plasma aldosterone/renin activity ratio is the best initial screening test for primary hyperaldosteronism. A ratio of over 20-30 suggests that primary hyperaldosteronism may be present. Some labs require a minimum plasma aldosterone level of 12 ng/dL.

The diagnosis of primary hyperaldosteronism can be confirmed by the determination of the aldosterone excretion rate in a 24-hour urine following IV or oral salt loading. If the urinary aldosterone excretion rate is greater than 12-14 μg/24 h, with urine sodium of at least than 200 mEq/24 h, this confirms the diagnosis of primary hyperaldosteronism.

The appropriate therapy depends on the cause of excessive aldosterone production. A CT scan may help localize an adrenal mass, indicating adrenal adenoma. If the results of the CT scan are inconclusive, adrenal venous sampling for aldosterone and cortisol levels should be performed. Medical therapy is indicated in patients with adrenal hyperplasia, patients with adenoma who are poor surgical risks, and patients with bilateral adenomas. These patients are best treated with sustained salt and water depletion. Hydrochlorothiazide or furosemide in combination with either spironolactone or amiloride corrects hypokalemia and normalizes the blood pressure. Some patients may require the addition of a vasodilator or a beta blocker for better control of hypertension.

Adrenal adenomas may be resected via a laparoscopic procedure. Surgical resection often leads to the control of blood pressure and the reversal of biochemical abnormalities. These patients may develop hypoaldosteronism during the postoperative follow-up period and require supplementation with fludrocortisone.

Consultations with a nutritionist and exercise specialist are often helpful in changing lifestyle and initiating weight loss. Consultations with an appropriate consultant are indicated for management of secondary hypertension attributable to a specific cause.

Various interventions can be implemented to improve BP control in patients with hypertension or to treat uncontrolled hypertension. These interventions include the following:

• Self-monitoring
• Educational interventions directed to the patient
• Educational interventions directed to the health professional
• Health professional (nurse or pharmacist)–led care
• Organizational interventions that aim to improve the delivery of care
• Appointment reminder systems

The Cochrane Collaboration has shown that these interventions are associated with large net BP reductions and that health professional (nurse or pharmacist)–led care may be a promising way of delivering care.^[49] A study by Pezzin et al found that extensive patient education, coupled with nurse-led monitoring and feedback, resulted in significant improvements in 3-month BP control and secondary BP outcomes in high-risk black patients with stage 2 hypertension.^[50] Cochrane recommendations include that family practices and community-based clinics should have an organized system of regular follow-up and review of their patients with hypertension. A randomized trial looking at home BP management found that systolic BP decreased among individuals with poor BP control at baseline using a combined treatment of nurse-administered behavioral management and nurse-administered and physician-administered medication management.^[51]

Antihypertensive drug therapy should be implemented by means of a vigorous stepped care approach when patients do not reach target BP levels.

A comprehensive strategy for reduction in mortality and morbidity from hypertension must include prevention strategies, earlier detection, and adequate treatment. Ideally, a population strategy should be used in order to lower BP in the community. More intensive efforts are required to lower blood pressure in high-risk population groups, which include individuals with a family history of hypertension, black ancestry, obesity,^[52] excessive sodium consumption, physical inactivity, and/or alcohol consumption. Even a small reduction in BP confers significant health benefits. A 2-mm Hg reduction in diastolic BP is estimated to decrease the risk of stroke by 15% and the risk of coronary heart disease by 6%.

Prevention of hypertension may be achieved by the following interventions:

• Weight control
• Increased physical activity
• Moderated sodium and alcohol intake
• Increased potassium intake
• A dietary pattern rich in fruits and vegetables and low-fat meat, fish, and dairy products (see Lifestyle Modifications)