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Essential hypertensionHighlights

Summary

Overview

Basics

Definition

EpidemiologyAetiology

Pathophysiology

Prevention

Primary

Screening

Secondary

Diagnosis

History & examination

Tests

Differential

Step-by-step

CriteriaGuidelines

Case history

Treatment

Details

Step-by-step

Emerging

Guidelines

Evidence

Follow Up

Recommendations

Complications

PrognosisResources

References

Online resources

Patient leaflets

Credits

Email

Print

Feedback

Share

Add to Portfolio

Bookmark

Add notesHistory & exam

Key factors

presence of risk factors

BP >140/90 mmHg

retinopathy
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Other diagnostic factors

headache

visual changes

dyspnoea

chest pain

sensory or motor deficit

History & exam details

Diagnostic tests

1st tests to order

ECG

fasting metabolic panel with estimated GFR

fasting lipid panel

Hb urinalysis with microalbumin

Tests to consider

echocardiogram

carotid Dopplers

plasma renin activity (PRA)

plasma aldosterone

renal duplex ultrasound/MRA renal arteries

24-hour urine phaeochromocytoma screen

24-hour urine free cortisol

TSH

ambulatory BP monitor

Diagnostic tests details

Treatment details

Ongoing

no comorbidity (other than osteoporosis): non-pregnant stage 1 HTN (BP 140 to 159/90 to 99 mmHg)

o diuretic monotherapy + lifestyle modification

o ACE inhibitor/angiotensin-II receptor blocker monotherapy + lifestyle modification

o beta-blocker monotherapy + lifestyle modification

o dihydropyridine CCB monotherapy + lifestyle modification

stage 1 not at goal with monotherapy or stage 2 (BP 160/100 mmHg)
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o thiazide + ACE inhibitor/angiotensin-II receptor blocker + lifestyle modification

o ACE inhibitor/angiotensin-II receptor blocker + dihydropyridine CCB + lifestyle modification

o ACE inhibitor/angiotensin-II receptor blocker + beta-blocker + lifestyle modification

o thiazide + beta-blocker + lifestyle modification

o beta-blocker + dihydropyridine CCB + lifestyle modification

concomitant CAD without CHF: non-pregnant

stage 1 HTN (BP 140 to 159/90 to 99 mmHg)




o beta-blocker + dihydropyridine CCB + lifestyle modification

o beta-blocker + ACE inhibitor/angiotensin-II receptor blocker + lifestyle modification

o thiazide + beta-blocker + lifestyle modification

o ACE inhibitor/angiotensin-II receptor blocker + thiazide + lifestyle modification

concomitant CHF with ejection fraction less than 55%: non-pregnant

NYHA class I or II


o non-aldosterone-blocking diuretics

NYHA class III or IV

o ACE inhibitor/angiotensin-II receptor blocker + beta-blocker + aldosterone antagonist + lifestyle

modification

o non-aldosterone-blocking diuretics

o substitution or addition of isosorbide dinitrate/hydralazine

concomitant LVH without CAD: non-pregnant

angiotensin-II receptor blocker/ACE inhibitor monotherapy + lifestyle modification

concomitant diabetes or chronic renal disease without cardiovascular disease: non-pregnant

stage 1 HTN (BP 140 to 159/90 to 99 mmHg)

o ACE inhibitor/angiotensin-II receptor blocker monotherapy + lifestyle modification


o thiazide monotherapy + lifestyle modification



o ACE inhibitor/angiotensin-II receptor blocker + thiazide + lifestyle modification


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o ACE inhibitor/angiotensin-II receptor blocker + dihydropyridine CCB + lifestyle modification


concomitant atrial fibrillation without other comorbidity: non-pregnant

beta-blocker monotherapy + lifestyle modification

non-dihydropyridine CCB + lifestyle modification

concomitant benign prostatic hypertrophy without other comorbidity

alpha-blocker + lifestyle modification

concomitant Raynaud's disease, PVD, coronary, or spasm without other comorbidity: non-pregnant

dihydropyridine CCB + lifestyle modification

refractory/resistant to optimised triple therapy at any stage: non-pregnant without CHF

ACE inhibitor/angiotensin-II receptor blocker + thiazide + CCB + beta-blocker + lifestyle modification

hydralazine added to 3 agents

clonidine added to 3 agents

alpha-blocker added to 3 agents

minoxidil added to 3 agents

aliskiren added to 3 agents

pregnant

methyldopa + lifestyle modification

labetalol + lifestyle modification

Treatment details

Summary

Defined as BP greater than 140/90 mmHg.

Typically diagnosed by screening of an asymptomatic individual.

Treatment of uncontrolled HTN reduces the risks of mortality and of cardiac, vascular, renal, or

cerebrovascular complications.

Lifestyle changes are recommended for all patients: weight loss, exercise, decreased sodium intake,

and moderation of alcohol consumption.

Choice of drug therapy is often driven by considerations related to comorbid disease, but achievement of

BP goal supersedes choice of therapeutic agent(s).

Other related conditions

Assessment of hypertension

Overview of acute coronary syndrome

Overview of stroke
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Chronic congestive heart failure

Aortic dissection

Abdominal aortic aneurysm

Metabolic syndrome

Overview of diabetes

Obesity in adults

Chronic renal failure

Peripheral vascular disease

Assessment of dementia

Phaeochromocytoma

Primary aldosteronism

DefinitionEssential HTN is defined as BP greater than 140/90 mmHg.[1] [2] [3] Themain goal of treatment is to decrease the risk of mortality and ofcardiovascular and renal morbidity.[4] BP goal should be less than 130/80mmHg in patients with renal disease, and less than 140/90 mmHg in all otherpatients. Regarding patients with concomitant diabetes mellitus, there isgood-quality evidence that very intensive BP lowering (targeting a systolicpressure


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Mexican Americans.[12] The incidence increases with age in people of allancestries and both sexes. Prevalence is higher in men than in womenbefore 60 years of age, but equal after this age.[4] The lifetime risk is 90%for men and women who were normotensive at 55 years of age and surviveto 80 years.[13]

AetiologyA multifactorial and heterogeneous aetiology of essential HTN has beenproposed.[14]However, some initiating factors may be dampened as thehypertensive state progresses.[15]The following factors have been shown todisrupt the delicate balance of cardiac output and resistance, ultimatelyresulting in HTN:

Disturbance of auto-regulation (reflex and persistenly increasing vascular resistance to match an

increased cardiac output)[16]

Excess sodium intake through a variety of mechanisms[17] [18]

Renal sodium retention[19] [20] [21] [22]

Dysregulation of the renin-angiotensin-aldosterone axis, with elevated plasma renin activity (PRA)[23]

Increased sympathetic drive[24]

Increased peripheral resistance[25]

Endothelial dysfunction[26]

Cell membrane transporter perturbations[27]

Insulin resistance/hyperinsulinaemia.[28]

PathophysiologyBP, the product of cardiac output and peripheral vascular resistance, isaffected by preload, contractility, vessel hypertrophy, and peripheralconstriction. The pathology associated with, and the perpetuation of, thehypertensive state involves structural changes, remodelling, and hypertrophyin resistance arterioles.[15] These changes have also been associated withthe early and progressive development of small vessel atherosclerosis, whichis probably the cause of end-organ damage seen in advanced HTN. Thisoccurs through a complex series of interrelated processes includingthrombosis, endothelial injury and dysfunction, the inflammatory cascade,

oxidative stress, and autonomic dysregulation in the setting of geneticpredisposition.[29]Trials have demonstrated the importance of systolic BP in thepathophysiology of HTN and its associated complications, which differs fromolder conventional thinking.[30] The rise in systolic BP continues throughoutlife, in contrast to diastolic BP, which increases until approximately 50 years
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of age, tends to level off over the following decade, and may stabilise ordecline subsequently.

Primary preventionThe lifetime risk for development of HTN is high. Efforts should be made to

minimise risk factors, especially in patients with pre-HTN (defined as 120 to139/80 to 89 mmHg); these patients should be aggressively counselled toeffect lifestyle modifications so as to reduce their risk of developing HTN.Population-based approaches to prevent HTN have been proposed: the

American Public Health Association has advocated a 50% reduction in thesodium content of all foods.[41]Although sodium reduction has a modesteffect on BP lowering, the population effect on the huge number of at-riskpeople would potentially have significant consequences for cardiovascularmorbidity and mortality.

ScreeningThe vast majority of hypertensive patients will be detected during anasymptomatic screening during some contact with the medical system.Patients aged over 18 years who are asymptomatic (no evidence of end-organ damage and normal initial BP) should be screened every 2years.[1] [48]Asymptomatic patients with pre-HTN should be screenedannually for the development of HTN.[1]

These screening guidelines are often exceeded, as BP measurement isstandard for each encounter in many practice settings. Elevated readingsshould always be confirmed on a second visit prior to diagnosing HTN.

Secondary preventionAggressive lifestyle modifications should be initiated in patients with pre-HTN(BP 120 to 139/80 to 89 mmHg) to delay or prevent the onset of overt HTN.Furthermore, other cardiovascular risk parameters should be aggressivelymanaged. For example, LDL-cholesterol should be maintained at less than100 mg/dL (2.59 mmol/L) in people with type 2 diabetes. Accordingly,

patients with pre-HTN should be evaluated for occult cardiovascular risk byscreening for diabetes or dyslipidaemia with fasting blood sugar and lipidlevels.

History & examinationKey diagnostic factorshide allpresence of risk factors (common)
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Key risk factors include age >65 years, moderate/high alcohol intake, lack of exercise, FHx of HTN

or CAD, obesity, metabolic syndrome, diabetes mellitus, hyperuricaemia, black ancestry, and

obstructive sleep apnoea.BP >140/90 mmHg (common)

Anaeroid, mercury, or electronic cuff. Equipment needs calibration.

Diagnosis is made at lower cut-off of 130/80 mmHg for high-risk patients (diabetes or renal

disease).retinopathy (common)

Retinal vascular changes are seen commonly in longstanding HTN.

Other diagnostic factorshide allheadache (uncommon)

Rarely a presenting symptom, unless HTN is acute or in setting of hypertensive urgency.

visual changes (uncommon)

Decreased visual acuity or floaters, papilloedema (rare).

dyspnoea (uncommon)

Suggests possible CHF or CAD. Dyspnoea may be an anginal equivalent, particularly if a patient is

diabetic.chest pain (uncommon)

Suggests CAD.

sensory or motor deficit (uncommon)

Suggests cerebrovascular disease.

Risk factorshide all

Strong

obesity Data from the Nurses' Health Study showed that a gain of 5 kg above weight at 18 years of age

was associated with 60% higher risk of development of HTN in middle age.[31]A 4.5 mmHg

increase in BP has been associated with each 4.5 kg (10 lb) gain in weight.[32]

It has been postulated that the link between obesity and HTN is driven by increased circulating

volume, leading to increased cardiac output and persistently elevated peripheral vascular

resistance.[28]

Obesity is associated with the metabolic syndrome, insulin resistance, and type 2 diabetes.

Bariatric treatment of morbid obesity can reduce or eliminate risk factors for cardiovascular disease,with an effect on hypertension, diabetes, and dyslipidaemia.[33][34]

aerobic exercise less than 3 times/week

Patients with low level of fitness had a 52% greater relative risk of HTN at 12-year follow-up

compared with those with high levels of fitness.[35]moderate/high alcohol intake
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Chronic alcohol consumption of greater than 1.5 drinks per day has been shown to be associated

with an increased risk of developing HTN in young women.[37]The risk increases with more than 5

drinks per week in women and more than 7 drinks per week in men.

Acute alcohol consumption, in contrast, is associated with vasomotor relaxation.

metabolic syndrome

Abdominal obesity has been specifically associated with an increased risk of HTN, as compared

with generalised obesity.[38]

Insulin resistance and hyperinsulinaemia are thought to contribute to the development of HTN

through a variety of inflammatory mechanisms.[15]diabetes mellitus

Hyperglycaemia, hyperinsulinaemia, and insulin resistance lead to endothelial damage and

oxidative stress, and are independently associated with the development of HTN.[39]hyperuricaemia

A growing body of evidence has shown an association between elevated uric acid levels and HTN,

as well as cardiovascular events. The proposed causative mechanism involves renal afferent

thickening and constriction.[40]black ancestry

Highest incidence of HTN is seen in black non-Hispanic people, at all age levels.[4]

age >65 years

Incidence of HTN increases with age in people of all ancestries and both sexes.[4]

FHx HTN or CAD

sleep apnoea

Studies have shown around 50% of patients with sleep apnoea have essential HTN.[1]

Weak

sodium intake greater than 2.4 g/day

Individuals show a varied tolerance for sodium intake, and reduced sodium intake has modest

effect on BP lowering.[17] [18]low fruit and vegetable intake

Modest reduction in BP with 4 to 6 servings of fruits and vegetables coupled with lower sodium and

fat intake (Dietary Approaches to Stop Hypertension [DASH] diet).[36]dyslipidaemia

Risk of HTN is increased in setting of the metabolic syndrome.

Diagnostic tests1st tests to orderhide all

Test

ECG

Normal result does not rule out CAD.
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fasting metabolic panel with estimated GFR

Risk of HTN is increased if there are features of the metabolic syndrome.

Unprovoked hypokalaemia suggests hyperaldosteronism.

GFR is calculated according to the Modification of Diet in Renal Disease (MDRD) formula[44] [National

Foundaton: GFR calculator] (external link)

fasting lipid panel

Risk of HTN is increased in setting of the metabolic syndrome.

Hb

Anaemia accompanies chronic renal failure.

Polycythaemia may be seen with phaeochromocytoma.

urinalysis with microalbumin

Suggests end-organ damage.

Tests to considerhide all

Test

echocardiogram

Not routinely recommended, but suggested in patients with other cardiovascular risk factors. Quantifies

ventricular mass (LVM) and geometric LVH patterns, which have prognostic implications (i.e., increased

mortality and cardiovascular events in patients with increased LVM and abnormal geometric LVH).[45] [

carotid Dopplers

Not routinely recommended, but suggested in patients with other cardiovascular risk factors. Quantifies

and plaques, which have prognostic implications (i.e., increased cardiovascular events associated with h

values).[47]

plasma renin activity (PRA)

Indicated when unprovoked hypokalaemia present.

plasma aldosteroneIndicated when unprovoked hypokalaemia present.

renal duplex ultrasound/MRA renal arteries

Young patients (age


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Ultrasound provides haemodynamical information and magnetic resonance angiogram (MRA) provides a

information, in lieu of renal angiogram.

24-hour urine phaeochromocytoma screen

Indicated with symptoms/signs of catecholamine excess.

24-hour urine free cortisol

Indicated when stigmata of Cushing's disease present.

TSH

Indicated if signs/symptoms of hypo- or hyperthyroidism.

ambulatory BP monitor

Useful in patients with suspected white-coat HTN, apparent drug resistance, or episodic HTN.

Differential diagnosisCondition Differentiating signs/symptoms Differentiating tests

Drug-induced There may be signs of

acute intoxication,

withdrawal, or cravings

with

cocaine/sympathomimeti

cs use.

History of treatment with

or ingestion of non-

steroidal anti-

inflammatory drugs,OCPs,

sympathomimetics,

herbal medications (e.g.,

black cohosh, capsicum,

ma huang), or liquorice.

Drug toxicology screen may detect an illicit sub

Hypokalaemia if excessive liquorice.


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Chronic renal failure There may be pruritus,

halitosis, oedema, or

change in urine output.

High serum creatinine.

Chronic anaemia may be seen.

Renal ultrasound may identify sclerotic or polyc

Aortic coarctation Differential BP in upper

and lower extremities.

Absent femoral pulses.

CT, angiogram, or MRI confirms diagnosis.

Renal artery stenosis Typically younger

patients with difficult-to-

control HTN.

Renal artery bruits may

be present.

Renal duplex ultrasound or magnetic resonance

arteries confirms diagnosis.

Sleep apnoea,

obstructive Typically obese patients

with daytime

somnolence, snoring, or

choking during sleep.

Polysomnography shows nocturnal oxygen des

Hyperaldosteronism There may be weakness

or paraesthesiae.

Unprovoked hypokalaemia.

Plasma aldosterone high.

Plasma renin low.

Failure to suppress aldosterone with salt loadin

Hypothyroidism Dry skin, cold

intolerance, weight gain,sluggishness, and goitre.

TSH elevated in primary hypothyroidism.

Hyperthyroidism Heat intolerance, weight

loss, hyperphagia,

palpitations.

TSH suppressed and levels of free thyroid horm
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Hyperparathyroidism There are often no

differentiating

symptoms; however,

renal colic, abdominal

pain, or bone fracture

may occur.

Hypercalcaemia, with elevated or inappropriate

Cushing's syndrome Classic symptoms and

signs include weight

gain, moon face,

dorsicocervical fat pad,

abdominal striae, and

easy bruisability.

Abnormal dexamethasone suppression, 24-hou

night salivary cortisol.

Phaeochromocytoma Paroxysms of HTN,

flushing, and headache.

24-hour urine screen shows elevated vanillylma

and/or catecholamines.

Acromegaly Acral (hand/foot/jaw)

enlargement.

Elevated insulin-like growth factor-1 (IGF-1). Ele

level, not suppressed by glucose load.

Collagen vascular

disease Signs/symptoms of

systemic lupuserythematosus (SLE),

rheumatoid arthritis,

sclerodactly, or Hx

vasculitis.

Elevated ESR, abnormal complement levels, po

ribonucleoprotein (anti-RNP), anti-Smith antibo

Step-by-step diagnostic approachMost patients diagnosed with HTN are asymptomatic; therefore, screening isessential. Patients are usually evaluated through history, physicalexamination, and routine laboratory tests. The 3 objectives are to:

Assess risk factors

Reveal identifiable causes

Detect target-organ damage, including evidence of cardiovascular disease.
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Clinical evaluationHistory may elicit family history of HTN or CAD risk factors. It is important toassess overall cardiac risk burden.[2] The age of onset may be of valuewhen considering aetiology, as the proportion of secondary causesdiminishes with increasing age. Patients at increased risk for essential HTNinclude those over 65 years of age, or with diabetes, or of black ancestry.Excess alcohol intake or lack of exercise should be documented. A thoroughmedication history should be taken including screening for use of OCPs, non-steroidal anti-inflammatory drugs (NSAIDs), sympathomimetics, or herbalmedications. Most patients are asymptomatic, but clinical indications ofhyperthyroidism, hypothyroidism or catecholamine excess (e.g., tachycardia,weight loss, sweating, or palpitations), or end-organ damage (e.g., shortnessof breath, chest pain, or sensory/motor deficits) should be sought. Headacheor visual changes are unusual.

The physical examination should include:[1] BP: the patient should be seated quietly for at least 5 minutes, with feet on the floor and arm supported

at heart level. Caffeine, smoking, and exercise should be avoided for 30 minutes prior to examination. An

appropriately sized cuff should be used. The bladder should be 80% of the length of the upper arm, and the

width of the bladder should be at least 40% of the circumference of the upper arm. Two measurements should

be made and the average recorded.[1] Verification should be obtained in the contralateral arm. Pre-HTN is a

reading of 120 to 139/80 to 89 mmHg. HTN is above 140/90 mmHg in adults, or above 130/80 mmHg in patients

with renal disease

Examination of optic fundi

Calculation of BMI from height and weight

Auscultation for possible carotid, abdominal, or femoral bruits

Palpation of the thyroid gland

Examination of the heart and lungs

Examination of the abdomen for enlarged kidneys, masses, distended urinary bladder, or abnormal

aortic pulsation

Palpation of the lower extremities for oedema and pulses

Neurological assessment.

White-coat HTN is suspected when the patient has a higher BP reading whentaken in the office, compared with a reading taken by themselves at home.
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Ambulatory BP monitoring may be helpful in patients with suspected white-coat HTN, and also in cases of apparent drug resistance or episodic HTN.

Ambulatory monitoring may show disparity with office-based BP, butdiagnostic guidelines remain the same (2 BP readings on different daysgreater than stated goals for individual risk factors). Home BP monitoring is

useful for the initial diagnosis and the long-term follow-up of HTN.[42] HomeBP measurements are as good as ambulatory monitoring and superior tooffice measurements in regard to their association with pre-clinical organdamage assessed by echocardiographic left ventricular mass index.[43]

Physical examination may reveal end-organ damage associated withuntreated HTN: for example, retinopathy, vascular bruits, signs of CHF,evidence of aortic aneurysm (pulsatile mass/bruit), LVH (displaced point ofmaximal impact), or neurological deficit(s). Absence of femoral pulsessuggests coarctation of the aorta. An abdominal bruit may suggest aortic

aneurysm or renal artery stenosis. Occasionally, patients may have stigmataof endocrinopathy such as Cushing's disease (moon face, centripetal obesity,striae), acromegaly (acral enlargement), Graves' disease (goitre,exophthalmos, pretibial myxoedema), or hypothyroidism (dry skin, delayedreturn of deep tendon reflexes), indicating a secondary cause of HTN.

TestsRoutine metabolic panel and lipid levels are required. GFR is calculatedaccording to the Modification of Diet in Renal Disease (MDRD)

formula.[44] [National Kidney Foundaton: GFR calculator] (external link) Inparticular, features of the metabolic syndrome (hyperglycaemia,dyslipidaemia) or hyperuricaemia should be noted. Haemoglobin and routineurinalysis with microalbumin are also recommended for possible identificationof causes of HTN. An ECG should be obtained.More extensive testing for secondary causes of HTN is generally notindicated, unless BP is difficult to control or clinical or routine lab datasuggest identifiable secondary causes such as signs of unprovokedhypokalaemia or renal insufficiency.[1] Echocardiogram and carotid Dopplers

may have prognostic implications. They are not routinely recommended butare suggested in patients with other cardiovascular risk factors. There wasincreased risk of mortality and cardiovascular events in patients withincreased left ventricular mass and abnormal geometric left ventricularhypertrophy on echocardiogram.[45] [46] Increased cardiovascular eventswere associated with higher intima media thickness values on carotidDopplers.[47]
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If secondary HTN is suggested by history, or physical or routine laboratorytesting, further testing can be performed.[2]

Signs/symptoms of catecholamine excess require phaeochromocytoma screen.

Signs/symptoms of hyper- or hypothyroidism require TSH.

Unprovoked hypokalaemia prompts measurement of plasma renin activity (PRA)/aldosterone.

Renal artery imaging is done for young patients with difficult-to-control HTN or who have abdominal

bruits.[2]

Click to view diagnostic guideline references. Diagnostic criteriaThe seventh report of the Joint National Committee on the

Prevention, Detection, Evaluation and Treatment of

High Blood Pressure[1]The categories are based on the average of 2 or more seated BPmeasurements on 2 separate occasions.

-Normal: less than 120/80 mmHg

-Pre-HTN: 120 to 139/80 to 89 mmHg

-HTN: 140/90 mmHg or greater

Stage 1: 140 to 159/90 to 99 mmHg

Stage 2: 160/100 mmHg or greater

The main goal of treatment is to decrease the risk of mortality and of cardiovascular and renal

morbidity.[4] BP goal should be less than 130/80 mmHg in patients with renal disease, and less than 140/90

mmHg in all other patients. Regarding patients with concomitant diabetes mellitus, there is good-quality evidence

that very intensive BP lowering (targeting a systolic pressure


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Patient group

Treatment

line Treatmenthide all

no comorbidity (other than

osteoporosis): non-pregnant

stage 1 HTN (BP 140 to 159/90 to

99 mmHg)

1st diuretic monotherapy + lifestyle modification

May be most effective in older and black patients.

In several large clinical trials, no other agents have

proven superior to thiazide-type diuretics as

monotherapy for achieving goal reductions in

BP.[92]Indapamide is a non-thiazide (but thiazide-

like) diuretic.

Generally well tolerated. The lowest dose should be

titrated upwards until a therapeutic effect is

achieved or an adverse effect limits further titration.

If low to moderate dose is not effective to reach

goal, consider optimising dose or adding a second

drug. There is insufficient evidence about which

approach is superior.

Primary Options

hydrochlorothiazide : 12.5 to 50 mg orally once

daily

Secondary Options

chlorothiazide : 125-500 mg/day orally given in 1-2

divided doses

OR

chlortalidone : 12.5 to 50 mg orally once daily

Tertiary Options

indapamide: 1.25 to 5 mg orally once daily

2nd ACE inhibitor/angiotensin-II receptor blocker monotherapy

+ lifestyle modification

May be effective in younger, especially white

patients.


goal, dose may be optimised or second drug added.

There is insufficient evidence about which approach
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Patient group

Treatment




is superior.

Azilsartan is a new angiotensin-II receptor blocker

with a unique pharmacological profile, including

slowed rates of angiotensin-II type 1 receptor

dissociation and improved receptor specificity. It

has been shown to have greater efficacy than other

angiotensin-II receptor blockers, with similar safety

and tolerability.[93] [94] [95] [96] [97]

The lowest dose should be titrated upwards until atherapeutic effect is achieved or an adverse effect

limits further titration.

Primary Options

benazepril: 10-40 mg orally once daily

OR

captopril : 12.5 to 25 mg orally two to three times

daily initially, maximum 150 mg/day

ORenalapril : 5-40 mg orally once daily or in 2 divided

doses

OR

fosinopril : 10-40 mg orally once daily or in 2 divided

doses, maximum 80 mg/day

OR

lisinopril : 10-40 mg orally once daily, maximum 80

mg/day

OR

moexipril : 7.5 to 30 mg orally once daily

OR

perindopril : 4-8 mg orally once daily

OR

quinapril : 10-80 mg orally once daily or in 2 divided

doses
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Patient group

Treatment




OR

ramipril: 2.5 to 20 mg orally once daily

OR

trandolapril : 1-4 mg orally once daily, maximum 8

mg/day

Secondary Options

candesartan : 8-32 mg orally once daily or in 2

divided doses

OR

irbesartan : 150-300 mg orally once daily

OR

losartan: 25-100 mg orally given once daily or in 2

divided doses

OR

olmesartan : 20-40 mg orally once daily

OR

telmisartan: 20-80 mg orally once daily

OR

valsartan : 80-320 mg orally given once daily or in 2

divided doses

OR

azilsartan : 40-80 mg orally once daily

2nd beta-blocker monotherapy + lifestyle modification

White patients have shown greater BP lowering

when treated with beta-blockers compared with

black patients.[98]


goal, dose may be optimised or second drug added.


is superior.

Non-selective beta-blockers include carvedilol (also
http://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-57&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-57&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-58&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-59&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-60&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-61&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-61&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-62&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-63&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-63&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-64&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-413&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/26/resources/references.html#ref-98http://bestpractice.bmj.com/best-practice/monograph/26/resources/references.html#ref-98http://bestpractice.bmj.com/best-practice/monograph/26/resources/references.html#ref-98http://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-57&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-58&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-59&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-60&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-61&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-62&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-63&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-64&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-413&optionId=expsec-3&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/monograph/26/resources/references.html#ref-98


20/84

Patient group

Treatment




has alpha-blocking properties), labetalol,

penbutolol, pindolol, propranolol, and timolol.

Beta-1-selective blockers include acebutolol,

atenolol, betaxolol, bisoprolol, and metoprolol.

A review of the use of beta-blockers for HTN

highlights the demonstrated inferiority of atenolol

compared with other antihypertensives, an

inferiority not seen with other beta-blocking agents.

Atenolol is generally less cardioprotective and hasless BP-lowering effects compared with other

members of this class.[99] [100]

Abrupt cessation of therapy with certain beta-

blocking agents has led to exacerbations of angina

pectoris and, in some cases, MI. All beta-blockers

should be weaned over 1 to 2 weeks and patients

should be monitored for symptoms of angina.

The lowest dose should be titrated upwards until a

therapeutic effect is achieved or an adverse effectlimits further titration.

Primary Options

acebutolol : 200-800 mg orally once daily or in 2

divided doses, maximum 1200 mg/day

OR

betaxolol : 5-20 mg orally once daily

OR

bisoprolol : 2.5 to 10 mg orally once daily, maximum20 mg/day

OR

carvedilol: 6.25 mg orally (immediate-release)

twice daily initially, increase to 12.5 mg twice daily

after 1-2 weeks, maximum 50 mg/day given in 2

divided doses
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21/84

Patient group

Treatment




OR

labetalol : 100-400 mg orally twice daily, maximum

2400 mg/day given in 2-3 divided doses

OR

metoprolol : 50 mg orally (regular-release) twice

daily initially, increase at weekly intervals to

maximum 100-450 mg/day given in 2-3 divided

doses

OR

nebivolol: 5 mg orally once daily initially, increase

at 2-week intervals, maximum 40 mg/day

OR

propranolol : 40 mg orally (immediate-release) twice

daily initially, increasing to maximum 640 mg/day as

tolerated

Secondary Options

atenolol : 25-100 mg orally once daily

2nd dihydropyridine CCB monotherapy + lifestyle modification

May be effective in older or black patients.

Dihydropyridine calcium-channel blockers (CCBs)

are peripheral vasodilators.

If low-moderate dose is not effective to reach goal,

dose may be optimised or second drug added.


is superior. The lowest dose should be titrated upwards until a

therapeutic effect is achieved or an adverse effect


Primary Options

amlodipine : 2.5 to 10 mg orally once daily

OR
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22/84

Patient group

Treatment




felodipine : 2.5 to 10 mg orally once daily, maximum

20 mg/day

OR

isradipine : 2.5 to 10 mg/day orally given in 2

divided doses

OR

nicardipine : 20-40 mg orally (regular-release) three

times daily

OR

nifedipine : 30-60 mg orally (extended-release)

once daily

OR

nisoldipine : 20 mg orally once daily, maximum 60

mg/day

stage 1 not at goal with

monotherapy or stage 2 (BP

160/100 mmHg)

1st thiazide + ACE inhibitor/angiotensin-II receptor blocker +

lifestyle modification

Angiotensin-II receptor blockers may be used ifACE inhibitors are not tolerated.




Primary Options


daily

-- AND --benazepril: 10-40 mg orally once daily

or



or

enalapril : 5-40 mg orally once daily or in 2 divided
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23/84

Patient group

Treatment




doses

or

fosinopril : 10-40 mg orally once daily or in 2 divided

doses, maximum 80 mg/day

or


mg/day

or


or


or


doses

or


or


mg/day

Secondary Options


daily

-- AND --


divided doses

or


or

losartan: 25-100 mg orally once daily or in 2

divided doses

or

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24/84

Patient group

Treatment




or


or

valsartan : 80-320 mg orally given once daily or in 2

divided doses

2nd ACE inhibitor/angiotensin-II receptor blocker +

dihydropyridine CCB + lifestyle modification

Angiotensin-II receptor blockers may be used ifACE inhibitors are not tolerated.

Dihydropyridine calcium-channel blockers (CCBs)

are peripheral vasodilators.




Primary Options

benazepril: 10-40 mg orally once daily

or



or

enalapril : 5-40 mg orally given once daily or in 2

divided doses

or

fosinopril : 10-40 mg orally given once daily or in 2

divided doses, maximum 80 mg/day

or


mg/day

or


or
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25/84

Patient group

Treatment





or


doses

or


or


mg/day

-- AND --


or


20 mg/day

or


divided doses

or


times daily

or


once daily

or


mg/day

Secondary Options


divided doses

or


or
http://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-104&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-105&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-106&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-106&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-107&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-108&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-109&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-110&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-111&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-112&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-113&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-114&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-115&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-104&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-105&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-106&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-107&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-108&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-109&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-110&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-111&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-112&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-113&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-114&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-115&optionId=expsec-7&dd=MARTINDALE


26/84

Patient group

Treatment




losartan: 25-100 mg orally once daily or in 2

divided doses

or


or


or

valsartan : 80-320 mg orally once daily or in 2

divided doses

-- AND --


or


20 mg/day

or


divided doses

or


times daily

or


once daily

or


mg/day

2nd ACE inhibitor/angiotensin-II receptor blocker + beta-blocker

+ lifestyle modification

Angiotensin-II receptor blockers may be used if

ACE inhibitors are not tolerated.

Following abrupt cessation of therapy with certain

beta-blocking agents, exacerbations of angina
http://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-116&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-116&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=146449-117&optionId=expsec-7&dd=MARTINDALEhttp://bestpractice.bmj.com/best-practice/druglink.html?component-id=1464

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