Hypertension

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Hypertension is usually asymptomatic, so diagnosis rests on reproducible measurement rather than symptoms. ABPM reduces misclassification from white-coat hypertension and exposes masked hypertension.

At diagnosis, estimate total cardiovascular risk and look for renal, retinal and cardiac target-organ damage. Secondary causes become more likely with young onset, abrupt or resistant hypertension, hypokalaemia, episodic adrenergic symptoms or a marked creatinine rise after renin-angiotensin blockade.

Lifestyle measures accompany, rather than delay, indicated drug treatment: reduce dietary salt, maintain healthy weight, exercise regularly, moderate alcohol and caffeine, stop smoking and address sleep apnoea when suspected.

Severe asymptomatic hypertension without acute target-organ damage is normally reduced with oral treatment over days to weeks. Rapid IV lowering can cause cerebral, coronary or renal hypoperfusion.

Key points

Measure BP with the person seated, relaxed, arm supported and an appropriately sized cuff; check the pulse first and use manual auscultation if it is irregular.
Measure both arms initially. If the difference remains greater than 15 mmHg after repeat measurement, use the arm with the higher reading thereafter.
Clinic BP 140/90 to 179/119 mmHg should usually be confirmed by ABPM; use HBPM if ABPM is unsuitable or not tolerated.
Diagnosis requires clinic BP at least 140/90 mmHg plus ABPM or HBPM average at least 135/85 mmHg.
Stage 1 is clinic 140/90 to 159/99 and home/daytime average 135/85 to 149/94; stage 2 is clinic at least 160/100 but below 180/120 and home/daytime average at least 150/95.
Offer antihypertensive treatment to adults with persistent stage 2 hypertension; discuss treatment for stage 1 under age 80 when target-organ damage, CVD, renal disease, diabetes or QRISK3 10-year risk at least 10% is present.
Usual clinic targets are below 140/90 if under 80 and below 150/90 if 80 or older; corresponding ABPM/HBPM targets are below 135/85 and below 145/85.
Resistant hypertension means uncontrolled BP despite tolerated optimal doses of an ACE inhibitor or ARB, a CCB and a thiazide-like diuretic; confirm with out-of-office BP and address adherence before step 4.
A postural fall of at least 20 mmHg systolic or 10 mmHg diastolic after standing for at least 1 minute is significant; review causes and base targets on standing BP if symptoms or a significant fall persist.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Primary hypertension

Most adult hypertension reflects interacting genetic susceptibility, ageing, excess dietary salt, adiposity, inactivity and alcohol. These influences alter renal sodium handling, vascular tone and arterial stiffness without one identifiable lesion.

Renal and renovascular disease

Chronic kidney parenchymal disease promotes sodium retention, while renal artery narrowing activates renin despite systemic pressure. Young onset, renal bruit or disproportionate renal impairment should increase suspicion.

Endocrine causes

Aldosterone excess, phaeochromocytoma and thyroid or cortisol disorders raise pressure through sodium retention, adrenergic drive or altered vascular resistance. Hypokalaemia or episodic symptoms provide useful clues.

Sleep, substances and medicines

Obstructive sleep apnoea, excess alcohol and medicines such as non-steroidal anti-inflammatory drugs, corticosteroids or sympathomimetics can sustain hypertension. Exposure review is particularly important when control suddenly worsens.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pressure regulation shifts
Altered renal sodium excretion, sympathetic activation and hormonal signalling increase circulating volume, cardiac output or systemic vascular resistance. Their relative contribution varies between individuals and over time.
2
Vascular remodelling
Persistent vasoconstriction and pressure stimulate arterial wall thickening and stiffness. Reduced vessel compliance further raises systolic pressure and helps perpetuate hypertension.
3
Endothelial and arterial injury
Mechanical stress impairs endothelial function and accelerates atherosclerosis. Small vessels develop narrowing and impaired autoregulation, while large arteries become vulnerable to plaque, aneurysm and dissection.
4
Cardiac adaptation
The left ventricle hypertrophies against increased afterload, initially preserving ejection. Stiffness raises filling pressure and may progress to dilatation, systolic failure, atrial enlargement and arrhythmia.
5
Target-organ damage
Chronic microvascular injury produces nephron loss, retinal damage and cerebral small-vessel disease. Abrupt severe pressure can overwhelm autoregulation and cause acute brain, heart, aortic or kidney injury.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Confirmable clinic hypertension

Clinic BP 140/90 to below 180/120 mmHg: repeat during the consultation, record the lower of the final two readings, then arrange ABPM or HBPM.

Severe hypertension without emergency featuresRed flag

BP 180/120 mmHg or higher but no retinal haemorrhage/papilloedema and no life-threatening symptoms: promptly test for target-organ damage. If none is found, confirm with ABPM/HBPM or repeat clinic BP and complete clinical review within 7 days.

Hypertensive emergencyRed flag

Severe BP elevation with acute encephalopathy, intracranial event, acute coronary syndrome, pulmonary oedema, aortic syndrome, acute kidney injury or malignant retinopathy. Absolute BP can be lower when the rise is abrupt.

Suspected phaeochromocytomaRed flag

Labile or postural hypertension with headache, palpitations, pallor, abdominal pain or diaphoresis requires same-day specialist assessment.

Possible secondary hypertension

Consider renal, renovascular, endocrine, drug-related and sleep-apnoea causes with onset under 40, resistant or accelerated disease, hypokalaemia, renal bruit, episodic symptoms or disproportionate target-organ damage; seek specialist evaluation when indicated.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Repeat standardised clinic BP in both armsFirst step
Why
Confirm the initial reading and identify an inter-arm difference.
Interpretation and limitations
If a repeat difference exceeds 15 mmHg, use the higher arm for subsequent measurements and consider vascular disease in context.
02
ABPMPreferred
Why
Preferred confirmation for clinic BP 140/90 to below 180/120 mmHg.
Interpretation and limitations
Use at least 2 readings per hour during usual waking hours and the mean of at least 14 waking readings. A daytime mean at least 135/85 confirms hypertension.
03
HBPM when ABPM is unsuitable
Why
Confirm diagnosis and monitor response.
Interpretation and limitations
Take 2 seated readings at least 1 minute apart, twice daily, for at least 4 and ideally 7 days; discard day 1 and average the rest. At least 135/85 confirms hypertension.
04
Urine albumin:creatinine ratio and dipstick haematuria
Why
Detect renal target-organ damage or renal disease.
Interpretation and limitations
Albuminuria or haematuria changes risk and may prompt CKD/renal-pathway assessment.
05
HbA1c, electrolytes, creatinine/eGFR, total and HDL cholesterol
Why
Identify diabetes, renal impairment, potassium disturbance and cardiovascular risk; establish treatment baselines.
Interpretation and limitations
Hypokalaemia may suggest aldosteronism; renal impairment affects drug choice and monitoring; calculate QRISK3 where appropriate.
06
Fundoscopy and 12-lead ECG
Why
Look for hypertensive retinopathy, papilloedema, LVH, ischaemia and arrhythmia.
Interpretation and limitations
Retinal haemorrhage or papilloedema with BP at least 180/120 requires same-day specialist assessment.
07
Lying and standing BP
Why
Assess dizziness/falls, type 2 diabetes, age 80 or older, and treatment-related hypotension.
Interpretation and limitations
A fall at least 20 systolic or 10 diastolic after standing at least 1 minute is significant; treat to standing BP when persistent.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

White-coat hypertension

Clinic pressure is repeatedly high while correctly performed ambulatory or home averages remain below the diagnostic range. Out-of-office confirmation prevents misclassification, although cardiovascular risk and future progression still merit review.

Masked hypertension

Clinic readings appear acceptable but home or ambulatory pressure is raised. Target-organ damage or inconsistent readings should prompt out-of-office assessment rather than reassurance from a single clinic value.

Measurement artefact

An undersized cuff, unsupported arm, recent activity or an automated reading during irregular rhythm can falsely elevate pressure. Repeating standardised manual measurement when indicated is discriminating.

Transient reactive elevation

Pain, anxiety, acute illness, urinary retention or recent stimulants may temporarily raise pressure. Resolution with the trigger and normal out-of-office readings distinguish this from sustained hypertension.

Apparent resistant hypertension

Missed doses, interfering medicines, measurement error, white-coat effect or suboptimal treatment can mimic true resistance. Confirming technique, adherence and out-of-office pressure helps identify pseudo-resistance; confirmed resistance also raises suspicion of secondary causes.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01NICE diagnosisConfirm and risk-stratifyFirst stepClinic BP 140/90 to below 180/120 mmHg without emergency features.

1Repeat clinic BP correctly, arrange ABPM or HBPM, and simultaneously investigate target-organ damage; do not wait for out-of-office confirmation before investigating.
2Document stage, standing BP where indicated, comorbidity, medicines/substances, family history, lifestyle and QRISK3.
3Offer lifestyle support to everyone; offer medication for persistent stage 2 and discuss it for stage 1 under 80 with target-organ damage, established CVD, renal disease, diabetes or QRISK3 at least 10%. Consider treatment in adults under 60 even when 10-year risk is below 10%, because lifetime risk may be underestimated.

02NICE stepwise treatmentPreferred long-term medicinesPreferredConfirmed hypertension requiring pharmacological treatment.

1Step 1: use an ACE inhibitor or ARB in type 2 diabetes at any age or in people under 55 who are not of Black African or African-Caribbean family origin. Use an ARB if ACE-inhibitor cough occurs; never combine an ACE inhibitor with an ARB.
2Step 1: use a CCB in people aged 55 or older without type 2 diabetes and in people of Black African or African-Caribbean family origin without type 2 diabetes at any age. If a CCB is not tolerated, for example because of oedema, use a thiazide-like diuretic.
3Step 2: add a CCB or thiazide-like diuretic to an ACE inhibitor/ARB; or add an ACE inhibitor/ARB or thiazide-like diuretic to a CCB.
4Step 3: combine an ACE inhibitor or ARB plus a CCB plus a thiazide-like diuretic at tolerated optimal doses.
5Review response, adherence, postural symptoms and biochemistry after each change, then titrate toward the age-specific clinic or out-of-office target.

03NICE resistant hypertensionStep 4 and specialist escalationEscalationBP remains uncontrolled on tolerated optimal ACE inhibitor/ARB plus CCB plus thiazide-like diuretic.

1Confirm elevated BP with ABPM/HBPM; assess postural hypotension and adherence.
2If serum potassium is 4.5 mmol/L or lower, consider low-dose spironolactone 25 mg once daily; use particular caution with reduced eGFR because hyperkalaemia risk rises. Some use for hypertension is off-label depending on product.
3If potassium is above 4.5 mmol/L, consider an alpha-blocker such as doxazosin or a beta-blocker selected for comorbidity and contraindications.
4Check sodium, potassium and renal function within 1 month of step-4 initiation and as required thereafter. If BP remains uncontrolled on four drugs at tolerated optimal doses, seek specialist advice.

04BIHS emergency pathwaySevere hypertension and acute target-organ injuryBP at least 180/120 mmHg with emergency features, or a clinical hypertensive emergency at a lower number.

1Arrange same-day emergency/specialist assessment, continuous monitoring and treatment of the specific organ syndrome. Do not give rapid IV therapy for severe asymptomatic hypertension.
2For hypertensive encephalopathy, a typical monitored target is no more than a 20–25% mean arterial pressure fall over the first several hours, then approximately 160/100–110 mmHg over the next 24 hours; stroke, pregnancy, acute coronary syndrome and aortic syndromes have condition-specific targets.
3AlternativeOne licensed monitored option is labetalol 50 mg IV over at least 1 minute, repeated at 5-minute intervals if required without exceeding 200 mg cumulatively. An alternative is nicardipine infusion at 3–5 mg/hour, increasing by 0.5–1 mg/hour every 15 minutes to a maximum 15 mg/hour; select the agent for the presenting syndrome and contraindications.
4Use an arterial line/critical-care environment for titratable IV therapy, reassess neurological, cardiac and renal perfusion, and avoid overshoot hypotension.

Key medicines and prescribing safety8 treatments · regimens, roles and cautions

NICE step-1 ACE inhibitor and component of steps 2–3.

Ramipril

Usually 2.5 mg orally once daily; start 1.25 mg once daily with marked renin-angiotensin activation or relevant diuretic use, then double at 2–4-week intervals to a maximum 10 mg/day according to response and tolerance.

Contraindicated in pregnancy, previous ACE-inhibitor angioedema and significant bilateral renal-artery stenosis; monitor creatinine/eGFR, potassium and BP. Pause/review in acute volume depletion and avoid ACE inhibitor plus ARB.

ARB alternative when an ACE inhibitor is not tolerated; NICE prefers an ARB over an ACE inhibitor for Black African or African-Caribbean adults when renin-angiotensin blockade is indicated.

Losartan

50 mg orally once daily; consider 25 mg once daily if intravascularly depleted, and increase to 100 mg once daily after response review, typically from about 1 month.

Contraindicated in pregnancy and severe hepatic impairment; monitor renal function and potassium and avoid dual ACE inhibitor/ARB treatment.

Preferred NICE step-1 CCB in older adults and Black African or African-Caribbean adults without type 2 diabetes; add-on at steps 2–3.

Amlodipine

5 mg orally once daily, increasing to 10 mg once daily if needed and tolerated.

Ankle oedema, flushing, headache and hypotension; use cautiously in severe aortic stenosis, cardiogenic shock and severe hepatic impairment.

Preferred thiazide-like diuretic when starting/changing diuretic therapy for hypertension.

Indapamide

2.5 mg orally each morning; increasing above 2.5 mg does not improve antihypertensive effect and increases adverse effects.

Monitor sodium, potassium, renal function, urate and glucose as clinically indicated; avoid in severe renal or hepatic failure and correct electrolyte depletion.

NICE option for confirmed resistant hypertension when potassium is 4.5 mmol/L or lower.

Spironolactone

Low-dose step 4 is typically 25 mg orally once daily.

Avoid in hyperkalaemia, anuria/acute renal insufficiency, Addison's disease and with another potassium-sparing diuretic or eplerenone. Monitor potassium/renal function closely; endocrine adverse effects and off-label status for some products require discussion.

Step-4 alternative when potassium is above 4.5 mmol/L or spironolactone is unsuitable.

Doxazosin

Start 1 mg orally once daily; after 1–2 weeks increase to 2 mg, then 4 mg if needed, titrating cautiously.

First-dose and postural hypotension, dizziness and falls; avoid as sole treatment where heart failure is present and reassess standing BP.

Licensed, monitored option for severe hypertension when rapid blood-pressure control is essential, selected after syndrome-specific assessment.

Labetalol IV

50 mg IV over at least 1 minute; if necessary, repeat 50 mg at 5-minute intervals to a maximum cumulative dose of 200 mg.

Avoid in severe bradycardia, sick-sinus or high-grade block, cardiogenic shock, uncontrolled heart failure, hypotension and asthma/wheezing. Keep the patient supine or left lateral, and monitor BP, pulse, perfusion and respiratory function throughout.

Licensed, titratable option for acute life-threatening hypertension, including hypertensive emergency, when continuous monitoring is available.

Nicardipine IV infusion

Start 3–5 mg/hour by continuous IV infusion; increase by 0.5–1 mg/hour every 15 minutes according to response, to a maximum 15 mg/hour. Reduce gradually when the target is reached.

Avoid in severe aortic stenosis, compensatory hypertension, unstable angina or within 8 days of myocardial infarction. Monitor BP and heart rate continuously; use cautiously in heart failure, renal or hepatic impairment, and watch for hypotension or reflex tachycardia.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Stroke and cognitive impairment

Large-artery atherosclerosis, small-vessel lipohyalinosis and vessel rupture increase ischaemic and haemorrhagic stroke risk. Cumulative cerebral small-vessel injury also contributes to vascular cognitive decline.

Coronary and aortic disease

Endothelial injury and increased myocardial demand accelerate coronary disease, while chronic wall stress promotes aortic aneurysm or dissection. Acute presentations may constitute a hypertensive emergency.

Heart failure and atrial fibrillation

Left-ventricular hypertrophy and fibrosis impair relaxation, eventually causing preserved- or reduced-ejection-fraction failure. Left-atrial enlargement encourages atrial fibrillation and its associated embolic risk.

Chronic kidney disease

Glomerular hypertension and small-vessel injury cause albuminuria and progressive nephron loss. Declining renal function then promotes sodium retention and can make blood pressure more difficult to control.

Hypertensive retinopathy

Retinal arteriolar damage produces narrowing, haemorrhages and exudates. In the setting of severe hypertension, retinal haemorrhage or papilloedema is evidence of acute target-organ injury requiring same-day specialist assessment.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

After starting or changing an ACE inhibitor/ARB for hypertension, check creatinine/eGFR, sodium and potassium in 1–2 weeks; check within 7 days in people at higher risk, and review BP within 1 month.
After adding step-4 diuretic therapy, check sodium, potassium and renal function within 1 month; check earlier when CKD, older age, diabetes, interacting medicines or intercurrent illness raise risk.
Use clinic targets below 140/90 if under 80 and below 150/90 if 80 or older; for ABPM/HBPM use below 135/85 and below 145/85 respectively.
Ask about dizziness, falls, oedema, cough, angioedema, adherence, NSAIDs, decongestants, stimulants, liquorice and salt substitutes.
For stable ACE inhibitor/ARB therapy, continue at least annual renal/electrolyte surveillance, more often when clinical status or interacting treatment changes.
In pregnancy or when planning pregnancy, stop ACE inhibitors/ARBs promptly and use the pregnancy hypertension pathway.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Out-of-office thresholds are lower

The diagnostic ABPM/HBPM threshold is 135/85, not 140/90, because home/daytime readings are usually lower than clinic readings.

Do not average an inter-arm difference away

A persistent difference greater than 15 mmHg means subsequent readings should come from the higher arm; otherwise hypertension may be undertreated.

Severe is not synonymous with emergency

A number at least 180/120 triggers urgent assessment, but IV treatment is reserved for acute target-organ injury. Conversely, acute organ injury after a rapid BP rise can be an emergency below that threshold.

Resistant hypertension must be proved

White-coat effect, missed doses, suboptimal doses, NSAIDs and secondary causes commonly mimic resistance; confirm out of office before adding step 4.

Standing BP can be the treatment BP

When postural hypotension is significant or symptomatic, using only seated targets risks falls and hypoperfusion.

11Common pitfallsFrequent interpretation and management errors.

01
Diagnosing hypertension from one hurried reading or from an automated device during an irregular rhythm.
02
Starting an ACE inhibitor and ARB together.
03
Giving rapid IV antihypertensives for an asymptomatic high reading without acute target-organ damage.
04
Adding spironolactone without confirming resistance or checking potassium and renal function.
05
Using a universal target without accounting for age, standing BP, frailty and treatment tolerability.
06
Missing pregnancy exposure to ACE inhibitors or ARBs.