overview of hypertension in adults
TRANSCRIPT
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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