Overview of hypertension in adults

Authors

Frank J Domino, MD

Norman M Kaplan, MD Section Editor

George L Bakris, MD Deputy Editor

John P Forman, MD, MSc

Last literature review version 19.1: January 2011 | This topic last

updated: February 14, 2011 (More)

INTRODUCTION — The treatment of hypertension is the most common

reason for office visits of non-pregnant adults to physicians in the United

States and for use of prescription drugs [1]. Analysis of NHANES data from

1999-2000 and United States Census bureau information results in an

approximately 29 to 31 percent incidence of hypertension in the 18 year

and older population of the United States [2,3]. This translates into 58 to 65

million hypertensives in the adult population in the United States, which is

substantially higher than the 43.2 million estimate derived from the 1988-

1991 NHANES-III survey [3,4].

The number of patients with hypertension is likely to grow as the population

ages, since either isolated systolic hypertension or combined systolic and

diastolic hypertension occurs in over one-half of persons older than 65

years (figure 1) [5]. The rising incidence of obesity will also increase the

number of hypertensive individuals [5]. (See "Treatment of hypertension in

the elderly, particularly isolated systolic hypertension".)

Despite the prevalence of hypertension and its associated complications,

control of the disease is far from adequate [6-8]. Data from NHANES show

that only 34 percent of persons with hypertension have their blood pressure

under control, defined as a level below 140/90 mmHg (table 1) [7]. Slightly

higher rates of control were reported in a regional population study

(approximately 45 and 55 percent of men and women, respectively, have

controlled hypertension) [8].

There are numerous potential reasons for low rates of blood pressure

control, including poor access to health care and medications, and lack of

adherence with long-term therapy for a condition that is usually

asymptomatic [9]. The latter may be particularly true when the therapy

may interfere with the patient's quality of life and when its immediate

benefits may not be obvious to the patient. Thus, hypertension will likely

remain the most common risk factor for heart attack and stroke [10].

The definition, complications, diagnosis, evaluation, and management of

hypertension are reviewed here. Detailed discussions of all of these issues

are found separately. (See appropriate topic reviews.)

DEFINITIONS

Hypertension — Major societies have published definitions of hypertension,

as will be described below. Hypertension was defined as a blood pressure

≥140/≥90 mmHg. However, subsequent trials have identified groups of

patients at higher risk in whom goal blood pressures below this value may

be associated with improved outcomes. (See 'Goal blood pressure' below.)

The following definitions were suggested in 2003 by the seventh report of

the Joint National Committee (JNC 7) based upon the average of two or

more properly measured readings at each of two or more visits after an

initial screen [7]:

Normal blood pressure: systolic <120 mmHg and diastolic <80

mmHgPrehypertension: systolic 120-139 mmHg or diastolic 80-89

mmHgHypertension:

Stage 1: systolic 140-159 mmHg or diastolic 90-99 mmHg

Stage 2: systolic ≥160 or diastolic ≥100 mmHg

Isolated systolic hypertension is considered to be present when the blood

pressure is ≥140/<90 mmHg and isolated diastolic hypertension is

considered to be present when the blood pressure is <140/≥90 mmHg.

These definitions apply to adults on no antihypertensive medications and

who are not acutely ill. If there is a disparity in category between the

systolic and diastolic pressures, the higher value determines the severity of

the hypertension. The systolic pressure is the greater predictor of risk in

patients over the age of 50 to 60 [11].

Similar but not identical definitions were suggested in the European

Societies of Hypertension and Cardiology guidelines for the management of

arterial hypertension that were published in 2007 [12]:

Optimal blood pressure: systolic <120 mmHg and diastolic <80

mmHgNormal: systolic 120-129 mmHg and/or diastolic 80-84 mmHgHigh

normal: systolic 130-139 mmHg and/or diastolic 85-89 mmHgHypertension:

Grade 1: systolic 140-159 mmHg and/or diastolic 90-99 mmHg

Grade 2: systolic 160-179 mmHg and/or diastolic 100-109 mmHg

Grade 3: systolic ≥180 mmHg and/or diastolic ≥110 mmHg

Isolated systolic hypertension: systolic ≥140 mmHg and diastolic <90

mmHg

The prevalence of the different types of hypertension (systolic and diastolic,

isolated systolic, and isolated diastolic) was evaluated in a study of 26,587

subjects ≥35 years of age in five cities in China [13]. Systolic and diastolic

hypertension were present in 18.4 percent, isolated systolic hypertension in

7.1 percent, and isolated diastolic hypertension in 6.7 percent [13].

Malignant hypertension — Malignant hypertension refers to marked

hypertension with retinal hemorrhages, exudates, or papilledema [14].

These findings may be associated with hypertensive encephalopathy. (See

"Hypertensive emergencies: Malignant hypertension and hypertensive

encephalopathy in adults".)

Malignant hypertension is usually associated with diastolic pressures above

120 mmHg. However, it can occur at diastolic pressures as low as 100

mmHg in previously normotensive patients with acute hypertension due to

preeclampsia or acute glomerulonephritis.

Hypertensive urgency — Severe hypertension (as defined by a diastolic

blood pressure above 120 mmHg) in asymptomatic patients is referred to as

hypertensive urgency. There is no proven benefit from rapid reduction in BP

in asymptomatic patients who have no evidence of acute end-organ damage

and are at little short-term risk [15-17]. (See "Management of severe

asymptomatic hypertension (hypertensive urgencies)".)

ESSENTIAL (PRIMARY) HYPERTENSION

Pathogenesis — The pathogenesis of essential hypertension is poorly

understood. A variety of factors have been implicated, including:

Increased sympathetic neural activity, with enhanced beta-adrenergic

responsiveness. (See "Prehypertension and borderline

hypertension".)Increased angiotensin II activity and mineralocorticoid

excess. (See "Low-renin essential (primary) hypertension".)Hypertension is

about twice as common in subjects who have one or two hypertensive

parents and multiple epidemiologic studies suggest that genetic factors

account for approximately 30 percent of the variation in blood pressure in

various populations [18]. (See "Genetic factors in the pathogenesis of

essential hypertension".)Reduced adult nephron mass may predispose to

hypertension, which may be related to genetic factors, intrauterine

developmental disturbance (eg, hypoxia, drugs, nutritional deficiency), and

post-natal environment (eg, malnutrition, infections). (See "Possible role of

low birth weight in the pathogenesis of essential hypertension".)

Risk factors — The etiology of essential (idiopathic or primary) hypertension

and secondary hypertension (due to a known cause) differ. A variety of risk

factors have been associated with essential hypertension:

Hypertension tends to be both more common and more severe in blacks.

(See "Hypertensive complications in blacks".)Hypertension in maternal,

paternal or both parents is independently associated with the development

of hypertension over the course of adult life [19].Evidence for a relationship

between salt intake and essential hypertension continues to mount. It is

likely that increased salt intake is a necessary but not sufficient cause for

hypertension. (See "Salt intake, salt restriction, and essential

hypertension".)Multiple studies show a clear association between excess

alcohol intake and the development of hypertension. (See "Cardiovascular

benefits and risks of moderate alcohol consumption", section on

'Hypertension'.)Obesity is associated with an increased prevalence and

incidence of hypertension [20-22], and weight gain appears to be a main

determinant of the rise in blood pressure (BP) that is commonly seen with

aging [23]. (See "Obesity and weight reduction in hypertension".)Physical

inactivity is associated with an increased risk of developing hypertension

[24-26], and exercise is an effective means of lowering blood pressure.

(See "Exercise in the treatment of hypertension", section on 'Efficacy'.)

Dyslipidemia may also be associated with the development of hypertension,

and is independent of obesity [21,27].Data are conflicting as to whether a

high intake of fructose from sugar-sweetened beverages is [28] or is not

[29] associated with an increased risk of developing hypertension.

Hypertension may be more common among those with certain personality

traits, such as hostile attitudes and time urgency/impatience [30].

SECONDARY HYPERTENSION — A number of identifiable disorders may be

associated with secondary hypertension, and the pathogenesis of

hypertension is related to the underlying condition. (See "Who should be

screened for renovascular or other causes of secondary hypertension?".)

Primary renal disease — Hypertension is a frequent finding in both acute

and chronic renal disease, particularly with glomerular or vascular disorders.

(See "Hypertension in kidney disease".)Oral agents — Oral contraceptives

often raise the blood pressure within the normal range but can induce overt

hypertension. (See "Effect of oral contraceptives and postmenopausal

hormone therapy on blood pressure".)Drug-induced — Chronic nonsteroidal

antiinflammatory agents and many antidepressants can induce

hypertension. Chronic alcohol intake and alcohol abuse can also raise blood

pressure. (See "NSAIDs and acetaminophen: Effects on blood pressure and

hypertension" and "Cardiovascular benefits and risks of moderate alcohol

consumption", section on 'Hypertension'.)Pheochromocytoma — About one-

half of patients with pheochromocytoma have paroxysmal hypertension,

most of the rest have what appears to be essential hypertension. (See

"Clinical presentation and diagnosis of pheochromocytoma" and "Treatment

of pheochromocytoma in adults".)Primary aldosteronism — The presence of

primary mineralocorticoid excess, primarily aldosterone, should be

suspected in any patient with the triad of hypertension, unexplained

hypokalemia, and metabolic alkalosis. However, some patients have a

normal plasma potassium concentration. (See "Approach to the patient with

hypertension and hypokalemia".)Renovascular disease — Renovascular

disease is an important correctable cause of secondary hypertension. The

frequency with which it occurs is variable. (See "Screening for renovascular

hypertension".)Cushing's syndrome — Moderate diastolic hypertension is a

major cause of morbidity and death in patients with Cushing's syndrome.

(See "Epidemiology and clinical manifestations of Cushing's

syndrome".)Other endocrine disorders — Hypertension may be induced by

hypothyroidism, hyperthyroidism, and hyperparathyroidism. (See

"Cardiovascular effects of hypothyroidism" and "Cardiovascular effects of

hyperthyroidism".)Sleep apnea syndrome — Disordered breathing during

sleep appears to be an independent risk factor for awake systemic

hypertension. (See "Cardiovascular effects of obstructive sleep

apnea".)Coarctation of the aorta — Coarctation of the aorta is one of the

major causes of hypertension in young children [31]. (See "Clinical

manifestations and diagnosis of coarctation of the aorta".)

COMPLICATIONS — Hypertension is associated with a number of serious

adverse effects. The likelihood of developing these complications varies with

the blood pressure. The increase in risk begins as the blood pressure rises

above 110/75 mmHg in all age groups (figure 2A-B) [32-34]. However, this

relationship does not prove causality, which can only be demonstrated by

randomized trials showing benefit from blood pressure reduction.

The increase in cardiovascular risk associated with hypertension is

importantly affected by the presence or absence of other risk factors (figure

3) [35]. (See "Cardiovascular risks of hypertension".)

Hypertension is quantitatively the major risk factor for premature

cardiovascular disease, being more common than cigarette smoking,

dyslipidemia, and diabetes, the other major risk factors [36]. In older

patients, systolic pressure and perhaps pulse pressure are more powerful

determinants of risk than diastolic pressure [11,37].Hypertension increases

the risk of heart failure at all ages with the hazard increasing with the

degree of blood pressure elevation [38]. (See "Epidemiology and causes of

heart failure".)Left ventricular hypertrophy is a common problem in patients

with hypertension [39], and is associated with an enhanced incidence of

heart failure, ventricular arrhythmias, death following myocardial infarction,

and sudden cardiac death (figure 4) [40]. (See "Clinical implications and

treatment of left ventricular hypertrophy in hypertension".)Hypertension is

the most common and most important risk factor for stroke, the incidence

of which can be markedly reduced by effective antihypertensive therapy

[41]. (See "Clinical diagnosis of stroke subtypes", section on 'Ecology and

risk factors'.)Hypertension is the most important risk factor for the

development of intracerebral hemorrhage [42]. (See "Spontaneous

intracerebral hemorrhage: Pathogenesis, clinical features, and

diagnosis".)Hypertension is a risk factor for chronic kidney disease and end-

stage renal disease (figure 5) [43,44]. It can both directly cause kidney

disease, called hypertensive nephrosclerosis, and accelerate the progression

of a variety of underlying renal diseases. (See "Clinical features and

treatment of hypertensive nephrosclerosis" and "Antihypertensive therapy

and progression of nondiabetic chronic kidney disease".)Marked elevations

in blood pressure can cause an acute, life-threatening emergency (table 2)

[45]. (See "Hypertensive emergencies: Malignant hypertension and

hypertensive encephalopathy in adults".)

DIAGNOSIS

Screening — The optimal interval for screening for hypertension is not

known. The 2007 United States Preventive Services Task Force (USPSTF)

guidelines on screening for high blood pressure recommend screening every

two years for persons with systolic and diastolic pressures below 120 mmHg

and 80 mmHg, respectively (normal BP in JNC 7), and yearly for persons

with a systolic pressure of 120 to 139 mmHg or a diastolic pressure of 80 to

89 mmHg (prehypertension in JNC 7) [46]. (See "Overview of preventive

medicine in adults".)

The risk of developing hypertension in patients who do not have

hypertension is not uniform, being higher in prehypertension than with

normal blood pressure and in those with other risk factors for hypertension.

These issues are discussed separately. (See "Prehypertension and

borderline hypertension".)

Measurement — Proper measurement and interpretation of the blood

pressure is essential in the diagnosis and management of hypertension.

Figure 6 outlines the recommendations that have been made to achieve

maximum accuracy in this process (table 3) [47]. The preferred technique is

discussed in detail separately. (See "Technique of blood pressure

measurement in the diagnosis of hypertension".)

A recent study found no clinical difference in blood pressure readings from a

bare arm compared to those measured over a sleeved arm [48].

In the absence of end-organ damage, the diagnosis of mild hypertension

should not be made until the blood pressure has been measured on at least

three to six visits, spaced over a period of weeks to months. Sequential

studies have shown that the blood pressure drops by an average of 10 to 15

mmHg between visits one and three in patients who appear to have mild

hypertension on a first visit to a new doctor, with a stable value not being

achieved until more than six visits in some cases [49,50]. Thus, many

patients considered to be hypertensive at the initial visit are in fact

normotensive.

White coat hypertension and ambulatory monitoring — Approximately 20 to

25 percent of patients with mild office hypertension (diastolic pressure 90 to

104 mmHg) have what is called "white-coat" or isolated office hypertension

in that their blood pressure is repeatedly normal when measured at home,

at work, or by ambulatory blood pressure monitoring [51]. This problem is

more common in the elderly, but is infrequent (less than 5 percent) in

patients with office diastolic pressures ≥105 mmHg. One way to minimize

the white coat effect is to have the blood pressure in the office taken by a

nurse or technician, rather than the physician (figure 6) [52].

Ambulatory blood pressure monitoring (ABPM), which typically involves

automated inflation of the BP cuff and recording of the blood pressure at

preset intervals (usually every 15 to 20 minutes during the day and every

30 to 60 minutes during sleep), can be used to confirm or exclude the

presence of white coat hypertension in patients with persistent office

hypertension but normal blood pressure readings in the ambulatory setting

[53].

A more detailed discussion of white coat hypertension and ambulatory blood

pressure monitoring is provided separately. (See "Ambulatory blood

pressure monitoring and white coat hypertension in adults".)

Masked hypertension — 24-hour monitoring of larger populations has

revealed a significant number of patients with elevated out-of-office

readings despite normal office readings (eg, masked hypertension) [54].

Cardiovascular risk appears to be elevated in such patients to a similar

extent as patients with sustained hypertension [55].

This is consistent with the risk of hypertensive cardiovascular complications

(including the development and regression of left ventricular hypertrophy)

being more closely correlated with 24-hour or daytime ambulatory

monitoring than with the office pressure. (See "Ambulatory blood pressure

monitoring and white coat hypertension in adults".)

Indications for ABPM — In addition to patients with suspected white coat

hypertension, ambulatory monitoring should be considered in the following

circumstances:

Suspected episodic hypertension (eg, pheochromocytoma)Hypertension

resistant to increasing medicationHypotensive symptoms while taking

antihypertensive medicationsAutonomic dysfunction

(See "Ambulatory blood pressure monitoring and white coat hypertension in

adults", section on 'Indications for ABPM'.)

EVALUATION — Once it has been determined that the patient has persistent

hypertension, an evaluation should be performed to ascertain the following

information:

To determine the extent of target organ damage.To assess the patient's

overall cardiovascular risk status. (See "Overview of the risk factors for

cardiovascular disease".)To rule out identifiable and often curable causes of

hypertension.

Most patients with presumed essential hypertension undergo a relatively

limited work-up because extensive laboratory testing is of limited utility.

However, it is important to be aware of the clinical clues suggesting the

possible presence of one of the causes of secondary hypertension (table 4),

which is an indication for a more extensive evaluation. Many of these

disorders can be cured, leading to partial or complete normalization of the

blood pressure; but it is not cost-effective to perform a complete evaluation

in every hypertensive patient. These issues are discussed in detail

elsewhere. (See "Initial evaluation of the hypertensive adult" and "Who

should be screened for renovascular or other causes of secondary

hypertension?".)

History — The history should search for those facts that help determine the

presence of precipitating or aggravating factors (including prescription

medications, non-prescription nonsteroidal antiinflammatory agents, and

alcohol consumption), the natural course of the blood pressure, the extent

of target organ damage, and the presence of other risk factors for

cardiovascular disease (table 5).

Physical examination — The main goals on the physical examination are to

evaluate for signs of end-organ damage (such as retinopathy) and for

evidence of a cause of secondary hypertension (table 6).

Laboratory testing — The only testing that should be routinely performed

includes [7,12]:

Hematocrit, urinalysis, routine blood chemistries (glucose, creatinine,

electrolytes), and estimated glomerular filtration rateFasting (9 to 12 hours)

lipid profile (total and HDL-cholesterol, triglycerides)Electrocardiogram

Additional tests — Additional tests may be indicated in certain settings:

Testing for microalbuminuria is at present primarily limited to patients with

diabetes to screen for early nephropathy, although it is increasingly

recognized to be an independent risk factor for cardiovascular disease [56].

A discussion of screening for microalbuminuria among nondiabetics with

hypertension is presented separately. (See "Microalbuminuria and

cardiovascular disease" and "Epidemiology of chronic kidney

disease".)Limited echocardiography is a more sensitive method to detect

left ventricular hypertrophy than the ECG and is considerably less expensive

than a complete echocardiographic examination. The main indication for

echocardiography is to detect possible end-organ damage in a patient with

borderline blood pressure values, thereby identifying some patients who

would not be treated based upon clinical criteria alone [57]. (See "Clinical

implications and treatment of left ventricular hypertrophy in hypertension",

section on 'Indications for echocardiography in hypertensive patients'.)

Testing for renovascular hypertension — Renovascular hypertension is likely

the most common correctable cause of secondary hypertension. The

incidence of this condition varies with the clinical setting. It probably occurs

in less than 1 percent of patients with mild hypertension [58]. In

comparison, between 10 and 45 percent of white patients with severe or

malignant hypertension have renal artery stenosis [59]. (See "Who should

be screened for renovascular or other causes of secondary hypertension?".)

Radiographic testing for renovascular disease is indicated only in patients in

whom the history is suggestive and in whom a corrective procedure will be

recommended if significant renal artery stenosis is detected.

The following are settings in which renovascular hypertension or another

cause of secondary hypertension should be suspected:

Severe or refractory hypertension, including retinal hemorrhages or

papilledema; bilateral renovascular disease may be present in those

patients who also have a plasma creatinine above 1.5 mg/dL (132

µmol/L).An acute rise in blood pressure over a previously stable baseline —

this includes renovascular disease superimposed upon underlying and often

well-controlled essential hypertension.Proven age of onset before puberty or

above age 50.An acute elevation in the plasma creatinine concentration that

is either unexplained or occurs after the institution of therapy with an

angiotensin converting enzyme inhibitor or angiotensin II receptor blocker

(in the absence of an excessive reduction in blood pressure). (See "Renal

effects of ACE inhibitors in hypertension".)Moderate to severe hypertension

in a patient with diffuse atherosclerosis or an incidentally discovered

asymmetry in renal disease. A unilateral small kidney (≤9 cm) has a 75

percent correlation with the presence of large vessel occlusive disease.A

systolic-diastolic abdominal bruit that lateralizes to one side. This finding

has a sensitivity of approximately 40 percent (and is therefore absent in

many patients) but has a specificity as high as 99 percent [60]. Systolic

bruits alone are more sensitive but less specific. The patient should be

supine, moderate pressure should be placed on the diaphragm of the

stethoscope, and auscultation should be performed in the epigastrium and

all four abdominal quadrants.Negative family history for

hypertension.Moderate to severe hypertension in patients with recurrent

episodes of acute (flash) pulmonary edema or otherwise unexplained

congestive heart failure.

The recommended tests will vary based upon renal function and the clinical

suspicion of renovascular disease. (See "Screening for renovascular

hypertension".)

Testing for other causes of identifiable hypertension — Other causes of

identifiable hypertension also must be excluded in the appropriate settings.

The presence of primary renal disease is suggested by an elevated plasma

creatinine concentration, a calculated GFR below 60 mL/min per 1.73 m2,

or proteinuria. (See "Hypertension in kidney disease".)Pheochromocytoma

should be suspected if there are paroxysmal elevations in blood pressure

(which may be superimposed upon stable chronic hypertension), particularly

if associated with the triad of headache (usually pounding), palpitations,

and sweating. (See "Clinical presentation and diagnosis of

pheochromocytoma".)Measurement of plasma renin activity and aldosterone

concentration is usually performed only in patients with possible low-renin

forms of hypertension, such as primary hyperaldosteronism. Otherwise

unexplained hypokalemia is the primary clinical clue to the latter disorder in

which the plasma aldosterone to plasma renin activity ratio should be

obtained as a screening test. (See "Approach to the patient with

hypertension and hypokalemia".)Cushing's syndrome (including that due to

corticosteroid administration) is usually suggested by the classic physical

findings of cushingoid facies, central obesity, ecchymoses, and muscle

weakness. (See "Epidemiology and clinical manifestations of Cushing's

syndrome".)The sleep apnea syndrome should be suspected in obese

individuals who snore loudly while asleep, awake with headache, and fall

asleep inappropriately during the day. (See "Cardiovascular effects of

obstructive sleep apnea".)Coarctation of the aorta is characterized by

decreased or lagging peripheral pulses and a vascular bruit over the back.

(See "Clinical manifestations and diagnosis of coarctation of the

aorta".)Hypertension may be induced by both hypothyroidism, suspected

because of suggestive symptoms or an elevated plasma thyroid stimulating

hormone level, and primary hyperparathyroidism, suspected because of

otherwise unexplained hypercalcemia. (See "Cardiovascular effects of

hypothyroidism" and "Cardiovascular effects of hyperthyroidism".)

TREATMENT

Benefits of blood pressure control — In clinical trials, antihypertensive

therapy compared to placebo has been associated with significant 20 to 25

percent reduction in the incidence of major cardiovascular events (eg,

stroke, heart failure, and myocardial infarction) [61].

However, percent reduction does not tell the absolute benefit which is

dependent upon the incidence of cardiovascular complications. In the

aggregate, antihypertensive therapy for four to five years prevented a

coronary event in 0.7 percent of patients and a cerebrovascular event in 1.3

percent for a total benefit of approximately 2 percent; this included a

reduction in cardiovascular mortality of 0.8 percent (figure 7) [62]. Thus,

100 patients must be treated for four to five years to prevent a complication

in two. It is presumed that these statistics underestimate the true benefit of

treating mild hypertension, since the trials were of too short duration (five

to seven years) to determine efficacy in a longer term disease. (See

"Hypertension: Who should be treated?".)

Equal if not greater benefits have been shown with the treatment of elderly

hypertensive patients (over age 65), most of whom have isolated systolic

hypertension. Because the elderly start at such higher overall cardiovascular

risk, short term reductions in their hypertension provide apparently greater

benefits than that observed in younger patients. (See "Treatment of

hypertension in the elderly, particularly isolated systolic hypertension".)

Who should be treated? — Using the above definitions from JNC 7, the

following general approach can be used to determine which patients with

hypertension require antihypertensive therapy [7,63,64]. This approach

largely includes the recommendations of JNC 7 for risk stratification and

treatment and assumes accurate measurement of the blood pressure (table

7) [7]. A review of the potential errors involved with the procedure is

available elsewhere. (See "Technique of blood pressure measurement in the

diagnosis of hypertension".)

All patients should undergo appropriate nonpharmacologic (lifestyle)

modification (table 8). (See 'Nonpharmacologic therapy' below.)

The following decisions about antihypertensive medications are generally

not made until there has been an adequate trial of nonpharmacologic

therapy.

In the absence of end-organ damage, a patient should not be labeled as

having hypertension unless the blood pressure is persistently elevated after

three to six visits over a several month period. In one study, for example,

there was a mean 15/7 reduction in blood pressure in untreated patients

between the first and third visits to a new physician [49]. This difference

has prognostic importance. The Medical Research Council Mild Hypertension

Trial found a close correlation between cardiovascular risk and the systolic

pressure measured three months after entry into the trial [65]. In contrast,

a transient increase in systolic pressure at entry due to a white coat

response was not associated with increased risk. During the initial

evaluation period before a therapeutic decision is made, patients should

also be encouraged to measure their blood pressure at home or

work.Antihypertensive medications should generally be begun if the systolic

pressure is persistently ≥140 mmHg and/or the diastolic pressure is

persistently ≥90 mmHg in the office and at home despite attempted

nonpharmacologic therapy [7,66,67]. Starting with two drugs may be

considered in patients with a baseline blood pressure above 160/100

mmHg. This strategy may increase the likelihood that target blood

pressures are achieved in a reasonable time period, but should be used

cautiously in patients at increased risk for orthostatic hypotension (such as

diabetics and the elderly). (See "Choice of therapy in essential

hypertension: Recommendations".)

There is some evidence supporting a lower goal blood pressure in patients

with atherosclerotic cardiovascular disease and patients with chronic kidney

disease complicated by proteinuria. The supportive data are presented

separately. (See "What is goal blood pressure in the treatment of

hypertension?" and "Blood pressure management in patients with

atherosclerotic cardiovascular disease", section on 'Goal blood pressure' and

"Antihypertensive therapy and progression of nondiabetic chronic kidney

disease", section on 'Goal blood pressure'.)Patients with office hypertension,

normal values at home, and no evidence of end-organ damage should

undergo ambulatory blood pressure monitoring to see if they are truly

hypertensive. (See "Ambulatory blood pressure monitoring and white coat

hypertension in adults".)In a number of conditions (eg, atrial fibrillation,

heart failure, post-myocardial infarction), certain antihypertensive drugs are

given to improve survival or the underlying disease and other drugs are

contraindicated, independent of the blood pressure (table 9). (See

"Indications and contraindications to the use of specific antihypertensive

drugs".)

Nonpharmacologic therapy — Treatment of hypertension generally begins

with nonpharmacologic therapy (also called lifestyle modification), including

moderate dietary salt restriction, weight reduction in obese patients,

avoidance of excess alcohol intake, and regular aerobic exercise (table 8)

[7,31,68].

Dietary salt restriction — A low salt diet will usually lower high blood

pressure and may prevent the onset of hypertension. In well-controlled

randomized trials, the overall impact of moderate sodium reduction is a fall

in blood pressure in hypertensive and normotensive individuals of 4.8/2.5

and 1.9/1.1 mmHg, respectively (figure 8) [69,70]. The recommendation is

to reduce dietary intake from the usual 150 to 200 meq/day down to 100

meq/day (approximately 2.3 g of sodium or 6 g of salt [one gram of sodium

equals 44 meq; one gram of sodium chloride contains 17 meq of sodium])

[7]. (See "Salt intake, salt restriction, and essential hypertension".)Weight

loss — Weight loss in obese individuals can lead to a significant fall in blood

pressure. The decline in blood pressure induced by weight loss can occur in

the absence of dietary sodium restriction [71], but even modest sodium

restriction (a decline in intake of 20 to 40 meq/day) may produce an

additive antihypertensive effect [72]. The weight loss-induced decline in BP

generally ranges from 0.5 to 2 mmHg for every 1 kg of weight lost (figure

9) [73]. (See "Diet in the treatment and prevention of hypertension" and

"Obesity and weight reduction in hypertension".)DASH diet — The DASH

diet consists of increased intake of fruits and vegetables and low-fat dairy

products and can be combined with salt restriction. (See "Diet in the

treatment and prevention of hypertension", section on 'DASH trial' and "Diet

in the treatment and prevention of hypertension", section on 'Low sodium

DASH'.)Exercise — Long-term aerobic exercise regimens have in most

studies had a beneficial effect on the systemic blood pressure. (See

"Exercise in the treatment of hypertension".)Limited alcohol intake —

Women who consume two or more alcoholic beverages per day and men

who have three or more drinks per day have a significantly increased

incidence of hypertension compared to nondrinkers [24,74]; this effect is

dose-related and is most prominent when intake exceeds five drinks per day

[75]. On the other hand, decreasing alcohol intake in individuals who drink

excessively significantly lowers blood pressure [76], and moderate alcohol

use appears to reduce the risk of cardiovascular disease. (See

"Cardiovascular benefits and risks of moderate alcohol consumption".)

The aggregate effect of moderate alcohol intake in patients with underlying

hypertension is uncertain. An alcohol intake of one to two drinks per day

appears to reduce cardiovascular risk, as it does in normotensive subjects

[77]. (See "Cardiovascular benefits and risks of moderate alcohol

consumption", section on 'Hypertension'.)Comprehensive intervention —

The benefits of comprehensive lifestyle modification with all five of the

above modalities were examined in the PREMIER trial [78,79]. At 18

months, there was a lower prevalence of hypertension (22 versus 32

percent), and less use of antihypertensive medications (10 to 14 versus 19

percent), although the difference was not statistically significant. Similarly,

among baseline hypertensive patients in the two intervention groups, there

was a trend for a lower prevalence of hypertension (40 versus 63 percent),

and less use of antihypertensive medications (20 versus 40 percent). (See

"Diet in the treatment and prevention of hypertension", section on

'PREMIER trial'.)Patient education — Patient education is an important

nonpharmacologic intervention, and has been demonstrated to result in

improved blood pressure control [80]. In addition to education of patients

by their clinicians, blood pressure control may be improved when patients

with hypertension hear the personal stories of their peers with

hypertension. This novel approach was examined in 299 black patients with

hypertension from a single inner-city clinic who were randomly assigned to

watch one of two types of DVDs [81]. The intervention group received DVDs

depicting peers from the clinic population who told their personal stories of

dealing with and managing their blood pressure; the control group received

DVDs containing a series of nonspecific health tips. After six months, those

who watched the DVDs containing patient stories had a significantly greater

6.4 mmHg reduction in systolic blood pressure. Other — Other

nonpharmacologic therapies that may be beneficial include adequate

potassium intake and cessation of smoking:

Adequate potassium intake may contribute to the control of hypertension

[82]. However, this must be implemented with caution in patients at risk for

hyperkalemia, such as those with chronic kidney disease or

hypoaldosteronism. (See "Potassium and hypertension".)Although smoking

itself does not appear to cause persistent hypertension, it markedly

increases the cardiovascular risk in hypertensive patients. (See "Smoking

and hypertension".)

Drug treatment

General efficacy — The 2007 American Heart Association statement on the

treatment of blood pressure in ischemic heart disease, the 2007 European

Society of Hypertension/European Society of Cardiology guidelines on the

management of hypertension, and meta-analyses from 2008 and 2009

concluded that the amount of blood pressure reduction is the major

determinant of reduction in cardiovascular risk in patients with

hypertension, not the choice of antihypertensive drug [61,66,67,83]. Some

patients have an indication for a specific drug or drugs that is unrelated to

essential hypertension, which will influence the choice of therapy (table 9).

(See "Indications and contraindications to the use of specific

antihypertensive drugs".)

Initial monotherapy in uncomplicated hypertension — In the absence of a

specific indication, there are three main classes of drugs that are used for

initial monotherapy: thiazide diuretics, long-acting calcium channel blockers

(most often a dihydropyridine), and ACE inhibitors or angiotensin II

receptor blockers. It is the attained blood pressure, not the specific drug(s)

used, that is the primary determinant of outcome. Beta blockers are not

commonly used for initial monotherapy in the absence of a specific

indication, since they may have an adverse effect on some cardiovascular

outcomes, particularly in older patients. (See "Choice of therapy in essential

hypertension: Recommendations".)

Combination therapy — Single agent therapy does not control the blood

pressure in some patients at diagnosis (particularly those more than 20/10

mmHg above goal) and, over time, in an increasing proportion of patients

who were initially controlled with monotherapy (eg, approximately 40

percent at five years in the ALLHAT trial compared to approximately 30

percent at one year) [84]. (See "Choice of therapy in essential

hypertension: Recommendations", section on 'Combination therapy'.)

Goal blood pressure — The goal blood pressures presented below refer to

the levels at which more intensive antihypertensive therapy to produce a

further reduction in BP is not recommended. These goals are in keeping

with the JNC 7 and assume that the patient is at average risk (eg,

uncomplicated hypertension) [7].

The goal of antihypertensive therapy in patients with uncomplicated

combined systolic and diastolic hypertension is a blood pressure of below

140/90 mmHg; treatment goals are determined by the higher BP category.

Similar goals have been recommended for nondiabetic patients with

coronary heart disease. (See "What is goal blood pressure in the treatment

of hypertension?" and "Secondary prevention of cardiovascular disease:

Risk factor reduction", section on 'Goal blood pressure'.)

A number of clinical trials suggest possible benefit from a lower blood

pressure goal in two settings: atherosclerotic cardiovascular disease and

proteinuric chronic kidney disease. These issues are discussed elsewhere.

(See "Blood pressure management in patients with atherosclerotic

cardiovascular disease", section on 'Goal blood pressure' and

"Antihypertensive therapy and progression of nondiabetic chronic kidney

disease", section on 'Goal blood pressure'.)

For the rapidly growing population of hypertensive individuals over age 65

with isolated systolic hypertension (eg, a diastolic blood pressure below 90

mmHg), caution is needed not to reduce the diastolic blood pressure to less

65 mmHg to attain a goal systolic pressure less than 140 mmHg, since such

low diastolic pressures have been associated with an increased risk of

stroke [64,85]. Thus, the level of systolic blood pressure that is reached

with two or three antihypertensive agents (even if greater than 140 mmHg)

may be a more reasonable interim goal in such individuals [31]. (See

"Treatment of hypertension in the elderly, particularly isolated systolic

hypertension" and "Secondary prevention of stroke: Risk factor reduction".)

These recommendations assume that the blood pressure is being gradually

reduced, since acutely lowering blood pressure in patients with severe

underlying hypertension can clearly lead to deleterious cerebrovascular and

coronary events. (See "Management of severe asymptomatic hypertension

(hypertensive urgencies)".)

Resistant hypertension — Some patients have hypertension that is

seemingly resistant to conventional medical therapy. Resistance is usually

defined as a diastolic blood pressure (BP) above 95 to 100 mmHg despite

intake of three or more antihypertensive medications.

One or more of the following problems usually contributes to the inability to

adequately lower the blood pressure in this setting [7,86]:

Suboptimal therapyExtracellular volume expansionPoor compliance with

medical or dietary therapySecondary hypertensionOffice or "white coat"

hypertensionPseudohypertensionIngestion of substances that can elevate

the blood pressure

(See "Definition, risk factors, and evaluation of resistant hypertension" and

"Treatment of resistant hypertension".)

Discontinuing therapy — Some patients with mild hypertension are well

controlled, often on a single medication. After a period of years, the

question arises as to whether antihypertensive therapy can be gradually

diminished or even discontinued.

Several studies that have evaluated the effect of discontinuation of

treatment have shown that between 5 and 55 percent of patients remain

normotensive for at least one to two years [87]; a larger fraction of patients

do well with a decrease in the number and/or dosage of medications taken

[88,89].

Gradual discontinuation of therapy is most likely to be effective in patients

with mild initial hypertension who are well controlled on a single drug and

who can often be maintained on nonpharmacologic therapy such as weight

loss and sodium restriction [87]. More gradual tapering of drug dosage is

indicated in well-controlled patients taking multiple drugs [90]. (See "Can

therapy be discontinued in well-controlled hypertension?".)

Abrupt cessation of therapy with a short-acting beta-blocker (such as

propranolol) or the short-acting alpha-2-agonist clonidine can lead to a

potentially fatal withdrawal syndrome. Gradual discontinuation of these

agents over a period of weeks (including switching to longer-acting drugs of

the same class such as atenolol or methyldopa) should prevent this

problem. (See "Withdrawal syndromes with antihypertensive therapy".)

INFORMATION FOR PATIENTS — Educational materials on this topic are

available for patients. (See "Patient information: High blood pressure in

adults" and "Patient information: High blood pressure treatment in

adults" and "Patient information: High blood pressure, diet, and weight".)

We encourage you to print or e-mail these topic reviews, or to refer patients

to our public web site, www.uptodate.com/patients, which includes these

and other topics.

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