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Hypertension

SNOMED: 59621000966 words•Updated 03/03/2026
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Exam Tips

  • Use NICE thresholds precisely: diagnose with ABPM/HBPM after clinic >=140/90 mmHg unless severe features mandate urgent action.
  • In OSCE stations, always mention both-arm BP at first assessment and pulse check for irregular rhythm before relying on automated devices.
  • Know staging: stage 1 (clinic 140/90-159/99 with out-of-office 135/85-149/94), stage 2 (clinic >=160/100 with out-of-office >=150/95), stage 3 severe (clinic >=180/120).
  • Accelerated hypertension is severe BP elevation plus retinal haemorrhage and/or papilloedema; this is same-day specialist referral.
  • For treatment viva questions, present the UK stepwise approach (A/C then A+C then A+C+D) and include monitoring for renal function and potassium after RAAS drugs.
  • Do not miss reversible causes in young patients, resistant hypertension, sudden deterioration, or hypokalaemia.

Definition

Hypertension is a chronic elevation of arterial blood pressure that is associated with progressively higher cardiovascular and renal risk across a continuum, rather than a single biological cut-off. In UK practice, it is usually suspected when clinic blood pressure is persistently >=140/90 mmHg and confirmed with out-of-office monitoring (ABPM or HBPM), then staged to guide treatment intensity and urgency.

Pathophysiology

Most cases are primary (essential) hypertension, caused by interacting genetic susceptibility and environmental factors that increase systemic vascular resistance and/or sodium-volume load. Key mechanisms include sympathetic overactivity, inappropriate renin-angiotensin-aldosterone system (RAAS) activation, endothelial dysfunction (reduced nitric oxide bioavailability), arterial stiffness, and renal pressure-natriuresis impairment, creating a self-perpetuating rise in blood pressure. Chronic exposure leads to target-organ remodeling: left ventricular hypertrophy, nephrosclerosis, cerebrovascular small-vessel disease, and retinal arteriolar damage (see schematic of target-organ damage pathways in standard cardiovascular pathology figures). Secondary hypertension is less common but clinically important because some causes are reversible (for example primary aldosteronism, renal artery stenosis, phaeochromocytoma, coarctation of the aorta).

Risk Factors

  • Increasing age
  • Family history/genetic predisposition
  • Black African or Black Caribbean ethnicity
  • Social deprivation
  • Chronic kidney disease
  • Diabetes mellitus
  • Obesity and central adiposity
  • High dietary salt intake
  • Excess alcohol use
  • Smoking
  • Physical inactivity
  • Psychological stress/anxiety
  • Drugs/substances: NSAIDs, corticosteroids, combined oral contraceptive, ciclosporin, erythropoietin, venlafaxine, sympathomimetics, stimulant ADHD medication, cocaine/amphetamines, liquorice-containing preparations

Clinical Features

Symptoms

  • Often asymptomatic and detected on screening
  • Headache (non-specific), dizziness, or visual disturbance in some patients
  • Symptoms suggesting end-organ injury in severe hypertension: chest pain, dyspnoea, confusion, focal neurology
  • Features suggesting secondary causes: episodic headache/sweats/palpitations (phaeochromocytoma), muscle weakness/polyuria (hyperaldosteronism), snoring/daytime somnolence (possible OSA), endocrine symptom clusters

Signs

  • Persistently elevated clinic BP (confirm with ABPM/HBPM)
  • Inter-arm difference >15 mmHg (repeat and use higher-reading arm thereafter)
  • Hypertensive retinopathy; retinal haemorrhage/papilloedema in accelerated hypertension (fundoscopy image reference: hypertensive retinopathy grading figures in ophthalmology texts)
  • Left ventricular heave/displaced apex or signs of heart failure in long-standing disease
  • Postural BP drop in older/frail patients or if symptomatic
  • Secondary-cause clues: abdominal bruit (renovascular disease), radio-femoral delay/weak femorals (coarctation), Cushingoid or thyroid/acromegalic stigmata

Investigations

Standardized clinic blood pressure (both arms, repeat readings):Clinic BP >=140/90 mmHg suggests hypertension; >=180/120 mmHg indicates severe hypertension requiring urgent risk assessment
Ambulatory blood pressure monitoring (ABPM):Diagnosis confirmed if daytime average >=135/85 mmHg (stage 1: 135/85-149/94; stage 2: >=150/95)
Home blood pressure monitoring (HBPM):Diagnosis confirmed if average (after discarding day 1) >=135/85 mmHg
Urinalysis and urine albumin: creatinine ratio:Proteinuria/albuminuria suggests kidney disease and higher cardiovascular risk
Urea, creatinine, eGFR, electrolytes:Baseline renal function; hypokalaemia with alkalosis suggests primary aldosteronism
HbA1c or fasting glucose and lipid profile:Detects comorbid diabetes/dyslipidaemia for global cardiovascular risk stratification
12-lead ECG:Left ventricular hypertrophy, prior ischaemia, arrhythmia
Fundoscopy:Arteriolar narrowing/AV nipping; retinal haemorrhage or papilloedema indicates accelerated hypertension and same-day specialist assessment
Targeted secondary-cause tests (when indicated):Examples: plasma aldosterone: renin ratio, plasma/urine metanephrines, thyroid function tests, renal ultrasound/renal artery imaging

Management

Lifestyle Modifications

  • Reduce salt intake (aim <6 g salt/day), adopt DASH-style diet, increase fruit/vegetables
  • Weight reduction for overweight/obesity
  • Regular aerobic and resistance exercise
  • Limit alcohol intake to UK recommended limits
  • Stop smoking and address overall cardiovascular risk
  • Reduce excess caffeine and manage stress/sleep

Pharmacological Treatment

First-line RAAS blockade (younger adults, diabetes, CKD, or albuminuria)

  • Ramipril 2.5 mg once daily initially, titrate to 10 mg once daily
  • Lisinopril 10 mg once daily initially, titrate up to 20-40 mg once daily
  • Losartan 50 mg once daily (if ACE inhibitor not tolerated), titrate to 100 mg once daily

Check creatinine/eGFR and potassium before and 1-2 weeks after initiation or dose increase. Contraindicated in pregnancy; avoid dual ACE inhibitor + ARB; caution in bilateral renal artery stenosis and hyperkalaemia.

First-line calcium-channel blocker (especially age >=55 or Black African/Caribbean ethnicity)

  • Amlodipine 5 mg once daily initially, increase to 10 mg once daily
  • Felodipine modified-release 5 mg once daily, increase as needed

Common adverse effects include ankle oedema, flushing, headache, gingival hyperplasia. Use non-dihydropyridines with caution alongside rate-limiting drugs.

Thiazide-like diuretic (if CCB unsuitable or as add-on)

  • Indapamide 2.5 mg once daily (or indapamide MR 1.5 mg once daily)
  • Chlortalidone 12.5-25 mg once daily

Monitor sodium, potassium, and renal function; may worsen gout and glucose tolerance.

Step-up combination therapy (typical UK sequence A + C + D)

  • ACE inhibitor or ARB + calcium-channel blocker
  • Then add thiazide-like diuretic if BP remains above target

Use single-pill combinations where possible to improve adherence; titrate at monthly intervals according to BP response and tolerability.

Resistant hypertension (specialist-guided add-on)

  • Spironolactone 25 mg once daily (if potassium <=4.5 mmol/L and suitable renal function)
  • If spironolactone unsuitable: alpha-blocker such as doxazosin MR 4 mg once daily or beta-blocker such as bisoprolol 2.5-5 mg once daily

Spironolactone risks hyperkalaemia, renal impairment, and gynaecomastia; avoid in pregnancy. Seek specialist advice and assess adherence/secondary causes.

Hypertensive emergency/accelerated hypertension

  • Urgent same-day specialist management; IV agents selected by local protocol (for example labetalol in monitored settings)

Do not rapidly lower BP in uncomplicated severe asymptomatic hypertension in primary care; emergency treatment is for acute target-organ damage.

Surgical / Interventional

  • Laparoscopic adrenalectomy for confirmed unilateral primary aldosteronism
  • Coarctation repair (endovascular or surgical) in suitable patients
  • Selected revascularization procedures for renovascular disease in specialist care

Complications

  • Coronary artery disease and myocardial infarction
  • Heart failure (including HFpEF and HFrEF)
  • Ischaemic and haemorrhagic stroke
  • Chronic kidney disease and albuminuric renal damage
  • Peripheral arterial disease
  • Hypertensive retinopathy
  • Vascular cognitive impairment and vascular dementia
  • Aortic aneurysm/dissection risk increase

Prognosis

Prognosis depends on blood pressure burden, overall cardiovascular risk, and target-organ involvement at diagnosis. Risk rises continuously with higher BP, but sustained BP reduction substantially lowers major events and mortality; even modest reductions produce clinically meaningful benefit. Control is often suboptimal in practice, so adherence, follow-up, and treatment intensification are critical.

Sources & References

💊BNF Drug References(50)

✅NICE Guidelines(1)

📖Textbook References(16)

  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 860)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 1039)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 860)[context]
  • David Randall PhD MRCP (Editor), John Booth PhD MRCP (Editor), K - Kumar and Clark's Clinical Medicine (2025, American Elsevier Publishing Co.) - libgen.li.pdf(pp. 538, 539)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 240)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 238)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 246)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 247)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 246)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 240)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 238)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 438)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 246)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 247)[context]
  • Guyton and Hall Textbook of Medical Physiology (John E. Hall, Michael E. Hall) (Z-Library).pdf(pp. 247)[context]
  • [Oxford Medical Handbooks] Ian Wilkinson, Tim Raine, Kate Wiles, Anna Goodhart, Catriona Ha - Oxford Handbook of Clinical Medicine (2017, Oxford University Press) - libgen.li.pdf(pp. 152, 153)[context]

Sources

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