TextbookCardiologyHypertension

Hypertension

Sustained elevation of systemic arterial blood pressure (clinic BP ≥140/90 mmHg or ABPM/HBPM ≥135/85 mmHg). Affects ~30% of UK adults and is the leading modifiable risk factor for cardiovascular disease.

Key Facts

NICE CG136 defines hypertension as clinic BP ≥140/90 mmHg AND ABPM/HBPM daytime average ≥135/85 mmHg Stage 1: clinic BP 140/90–159/99 mmHg, ABPM 135/85–149/94 mmHg Stage 2: clinic BP 160/100–179/119 mmHg, ABPM 150/95 mmHg or higher Stage 3 (severe): clinic systolic BP ≥180 mmHg or diastolic BP ≥120 mmHg First-line treatment: ACEi/ARB if <55 years or diabetic; CCB if ≥55 years or Black African/Caribbean QRISK3 should be used for cardiovascular risk assessment in all hypertensive patients Target BP: clinic <140/90 mmHg (or <150/90 mmHg if ≥80 years); ABPM <135/85 mmHg Secondary causes account for ~5-10% of cases: renal artery stenosis, phaeochromocytoma, Conn syndrome, Cushing syndrome

Overview

Key Facts

Hypertension is the most common modifiable cardiovascular risk factor, affecting approximately 30% of adults in the UK. It is defined by NICE (CG136/NG136) as a sustained clinic blood pressure ≥140/90 mmHg confirmed by ambulatory (ABPM) or home blood pressure monitoring (HBPM) with a daytime average ≥135/85 mmHg.

Epidemiology

  • Prevalence: ~30% of UK adults (~14.4 million people)
  • Only ~60% of hypertensives are diagnosed; of those, ~40% achieve target BP
  • More common in men <65 years; women overtake after menopause
  • Higher prevalence in Black African/Caribbean populations
  • Accounts for ~50% of coronary heart disease and ~60% of strokes

Aetiology

Primary (essential) hypertension (~90-95%):

  • Multifactorial: genetic predisposition, obesity, high salt intake, excessive alcohol, physical inactivity, stress

Secondary hypertension (~5-10%):

  • Renal: chronic kidney disease, renal artery stenosis, polycystic kidney disease
  • Endocrine: primary hyperaldosteronism (Conn syndrome), phaeochromocytoma, Cushing syndrome, acromegaly, hyperthyroidism
  • Vascular: coarctation of the aorta
  • Drug-induced: NSAIDs, oral contraceptives, corticosteroids, ciclosporin
  • Obstructive sleep apnoea

Pathophysiology

Hypertension results from increased peripheral vascular resistance and/or increased cardiac output. Key mechanisms include:

  • Activation of the renin-angiotensin-aldosterone system (RAAS)
  • Sympathetic nervous system overactivity
  • Endothelial dysfunction with reduced nitric oxide bioavailability
  • Sodium retention and volume expansion
  • Arterial stiffness and vascular remodelling
  • Target organ damage affects heart (LVH, heart failure), brain (stroke), kidneys (nephrosclerosis), and eyes (hypertensive retinopathy)

Clinical Presentation

Typical Presentation

Hypertension is usually asymptomatic and detected incidentally during routine health checks. Symptoms typically only occur with severe hypertension or end-organ damage.

Symptoms of Severe Hypertension

  • Headache (typically occipital, morning)
  • Visual disturbance
  • Epistaxis
  • Dizziness

End-Organ Damage Presentations

  • Cardiac: exertional dyspnoea, chest pain, palpitations (LVH, heart failure, IHD)
  • Cerebrovascular: TIA, stroke, vascular dementia
  • Renal: proteinuria, haematuria, declining eGFR
  • Retinal: blurred vision, visual field defects
  • Peripheral vascular: intermittent claudication

Red Flags

  • Systolic BP ≥180 mmHg or diastolic BP ≥120 mmHg (severe/stage 3)
  • Signs of papilloedema or retinal haemorrhage (malignant hypertension)
  • Flash pulmonary oedema
  • Acute kidney injury
  • Hypertensive encephalopathy: headache, confusion, seizures
  • New-onset proteinuria or haematuria
  • Young patient (<40 years) with hypertension — suspect secondary cause

Differential Diagnosis

DiagnosisKey FeaturesInvestigation
White coat hypertensionElevated clinic BP, normal ABPM/HBPMABPM/HBPM
Masked hypertensionNormal clinic BP, elevated ABPM/HBPMABPM/HBPM
Renal artery stenosisAbdominal bruit, flash pulmonary oedema, resistant hypertensionMR angiography, Doppler USS
Primary hyperaldosteronismHypokalaemia, resistant hypertensionAldosterone:renin ratio
PhaeochromocytomaParoxysmal headache, sweating, palpitations, pallor24h urinary metanephrines
Cushing syndromeCentral obesity, striae, moon face, buffalo humpOvernight dexamethasone suppression test
Coarctation of aortaRadio-femoral delay, upper limb hypertension, rib notching on CXREchocardiography, CT/MR angiography
Obstructive sleep apnoeaSnoring, daytime somnolence, obesityEpworth Sleepiness Scale, polysomnography

Diagnosis / Investigation

Bedside

  • Blood pressure: clinic BP (both arms initially), ABPM (gold standard for diagnosis per NICE), or HBPM
  • Urinalysis: proteinuria, haematuria (end-organ damage)
  • ECG: left ventricular hypertrophy (Sokolow-Lyon criteria), rhythm abnormalities
  • Fundoscopy: hypertensive retinopathy grading (Keith-Wagener-Barker)

Bloods

  • U&Es: renal function, hypokalaemia (suggests hyperaldosteronism)
  • eGFR: chronic kidney disease assessment
  • HbA1c/fasting glucose: diabetes screening
  • Lipid profile: cardiovascular risk assessment
  • FBC: baseline
  • TFTs: if secondary cause suspected
  • Aldosterone:renin ratio: if resistant hypertension or hypokalaemia
  • 24h urinary metanephrines/catecholamines: if phaeochromocytoma suspected

Imaging

  • Echocardiography: LVH assessment, cardiac function
  • Renal ultrasound: renal size asymmetry, polycystic kidneys
  • Renal artery Doppler/MR angiography: renal artery stenosis

Special Tests

  • QRISK3: 10-year cardiovascular risk assessment
  • Overnight dexamethasone suppression test: Cushing syndrome screen
  • ACR (albumin:creatinine ratio): quantify proteinuria

Management

Non-pharmacological

  • Lifestyle modifications (all patients):
    • Reduce dietary salt to <6g/day
    • DASH diet (rich in fruits, vegetables, low-fat dairy)
    • Regular aerobic exercise (≥150 min/week moderate intensity)
    • Weight loss if BMI >25 kg/m²
    • Limit alcohol intake (≤14 units/week)
    • Smoking cessation
    • Reduce caffeine intake

Pharmacological

NICE CG136 stepwise approach:

Step 1:

  • Age <55 or diabetic (any age): ACE inhibitor (e.g., ramipril 1.25–10mg OD) or ARB (e.g., candesartan 8–32mg OD)
  • Age ≥55 or Black African/Caribbean origin: Calcium channel blocker (e.g., amlodipine 5–10mg OD)

Step 2:

  • ACEi/ARB + CCB combination

Step 3:

  • ACEi/ARB + CCB + thiazide-like diuretic (e.g., indapamide 2.5mg OD)

Step 4 (resistant hypertension):

  • Consider adding spironolactone 25–50mg OD if K⁺ ≤4.5 mmol/L
  • If K⁺ >4.5 mmol/L: alpha-blocker (doxazosin 4–8mg OD) or beta-blocker (bisoprolol 5–10mg OD)
  • Seek specialist advice — investigate for secondary causes

Landmark trials:

  • SPRINT: intensive BP control (SBP <120) reduced CV events by 25%
  • ALLHAT: thiazide-type diuretic (chlorthalidone) as effective as ACEi/CCB
  • ASCOT-BPLA: amlodipine ± perindopril superior to atenolol ± bendroflumethiazide

Surgical/Interventional

  • Renal denervation: investigational, not currently recommended by NICE
  • Surgical correction of secondary causes (e.g., adrenalectomy for Conn syndrome)

Referral Criteria

  • Stage 3 hypertension with signs of end-organ damage — same-day specialist assessment
  • Suspected secondary hypertension
  • Resistant hypertension (uncontrolled on 3 drugs)
  • Age <40 years with stage 1 hypertension
  • Pregnancy-related hypertension

Prognosis

  • Uncontrolled hypertension increases stroke risk by 3-4 fold and MI risk by 2-3 fold
  • Each 10 mmHg reduction in SBP reduces stroke risk by ~40% and IHD by ~20%
  • 5-year cardiovascular event rate: ~15-20% for stage 2 hypertension with high QRISK3
  • Well-controlled hypertension has near-normal life expectancy
  • Malignant hypertension: untreated 1-year mortality ~90%; with treatment ~5-year survival >70%
  • End-organ damage (LVH, CKD, retinopathy) worsens prognosis significantly

Other Relevant Information

Hypertensive Retinopathy Grading (Keith-Wagener-Barker)

GradeFeatures
IArteriolar narrowing/silver wiring
IIAV nipping
IIIFlame haemorrhages, cotton wool spots, hard exudates
IVPapilloedema

BP Staging Summary

StageClinic BPABPM/HBPM
Stage 1140/90–159/99135/85–149/94
Stage 2≥160/100≥150/95
Stage 3≥180/120N/A

NICE Treatment Pathway Summary

Step<55 or Diabetic≥55 or Black
1ACEi/ARBCCB
2ACEi/ARB + CCBACEi/ARB + CCB
3ACEi/ARB + CCB + Thiazide-likeACEi/ARB + CCB + Thiazide-like
4+ Spironolactone (if K⁺ ≤4.5)+ Spironolactone (if K⁺ ≤4.5)
Hypertension Revision Notes | MedPrep