Hypertension, Blood Pressure and Prevention — UKMLA-oriented extension, mapped to the GMC content map applying from September 2026. Emergencies are recognition-and-escalation teaching: follow local protocols and current specialist guidance.
7.01 Hypertension: Why It Matters
Hypertension is a major modifiable driver of stroke, myocardial infarction, heart failure, chronic kidney disease, atrial fibrillation and aortic disease. Sustained pressure damages the arterial endothelium, accelerates atherosclerosis and produces concentric LV hypertrophy; over time myocardial stiffness, fibrosis and diastolic dysfunction may develop. Most patients have no symptoms, so diagnosis depends on reliable measurements rather than headache or flushing.
UKMLA pearl: Treat cardiovascular risk as a whole: smoking, lipids, diabetes, renal disease and deprivation may modify the benefit of blood-pressure treatment.
7.02 Accurate Blood Pressure Measurement
- Clinic: Rest, correct cuff size, arm supported at heart level, feet on floor; measure both arms initially. Repeat inter-arm differences exceeding 15 mmHg and subsequently use the higher-reading arm if persistent.
- Confirm: If clinic BP is 140/90 to below 180/120 mmHg, offer daytime ambulatory monitoring (ABPM); use home monitoring (HBPM) when ABPM is not tolerated.
- HBPM: Two readings at least 1 minute apart, morning and evening, for 4–7 days; discard day 1 and average the remainder.
- Special circumstances: Irregular rhythms, anxiety, inappropriate cuff size and calcified arteries may distort results; measure standing BP when postural hypotension is suspected.
7.03 Stages of Hypertension and Thresholds
| Category | Clinic pressure | Daytime ABPM / HBPM |
|---|---|---|
| Diagnostic threshold | ≥140/90 mmHg | ≥135/85 mmHg |
| Stage 1 | 140/90–159/99 | 135/85–149/94 |
| Stage 2 | ≥160/100 but <180/120 | ≥150/95 |
| Severe hypertension | ≥180 systolic or ≥120 diastolic | Do not delay urgent assessment for ABPM if there are red flags |
The categories above reflect NICE NG136 rather than a universal international definition. Ask about end-organ symptoms, then assess urine albumin:creatinine ratio, urine haematuria, creatinine/eGFR, electrolytes, HbA1c, lipids, fundi and 12-lead ECG. The diagnosis requires persistent elevation; single anxious clinic readings can reflect a white-coat effect.
7.04 Assessing Target-Organ Damage and Cardiovascular Risk
- Cardiac: ECG evidence of LVH, coronary disease, AF or heart failure; echocardiography if clinically indicated.
- Renal: Raised urine ACR, reduced eGFR and persistent haematuria; review kidney function before and after renin–angiotensin system blockade.
- Brain and retina: Prior stroke/TIA, visual symptoms, retinal haemorrhage or papilloedema.
- Primary prevention: Use an appropriate validated risk calculator such as QRISK3 alongside judgement about underestimation in inflammatory disease, CKD and some demographic groups.
Target-organ damage may justify treatment at lower blood pressures and prompts a search for secondary causes. Risk estimation is not the same as diagnosing coronary artery disease.
7.05 When to Start Antihypertensive Medication
- Stage 2: Offer drug treatment alongside lifestyle measures, regardless of estimated short-term cardiovascular risk.
- Stage 1, under 80: Discuss medication if target-organ damage, established cardiovascular disease, renal disease, diabetes, or estimated 10-year CVD risk at least 10%; individualise decisions.
- Age 80 and over: Consider treatment in sustained stage 1 hypertension, using clinical judgement about frailty, falls, orthostasis and competing risks.
- Lifestyle: Lower salt intake, maintain physical activity and healthy weight, reduce alcohol excess, stop smoking and review medicines raising BP (NSAIDs, steroids, stimulants).
A treatment decision is a conversation about absolute benefit, adverse effects, medicine burden and what matters to the patient.
7.06 Stepwise Drug Treatment for Hypertension
- Step 1 (A): ACE inhibitor or ARB for most adults under 55 and adults with type 2 diabetes regardless of age, taking account of NICE recommendations and contraindications. Step 1 (C): Calcium-channel blocker at 55 or older without type 2 diabetes, or in adults of Black African or African–Caribbean family origin without type 2 diabetes.
- Step 2: Combine A + C; if C is not tolerated, use a thiazide-like diuretic (D).
- Step 3: A + C + D at optimal tolerated doses. Common options are ramipril, amlodipine and indapamide; monitor renal function, sodium and potassium.
- Resistant hypertension: Confirm adherence and out-of-office readings; consider low-dose spironolactone if potassium ≤4.5 mmol/L or an alpha-/beta-blocker if higher, with specialist advice where appropriate.
Drug safety: ACE inhibitors/ARBs are teratogenic, potassium can rise, and dual ACE inhibitor plus ARB is not recommended. Monitor U&Es after initiation or titration.
7.07 Blood Pressure Targets and Follow-up
| Population | Clinic target | ABPM/HBPM target |
|---|---|---|
| Adults under 80 with uncomplicated hypertension | <140/90 | <135/85 |
| Adults aged 80 or over | <150/90 | <145/85 |
Different targets apply to some CKD and diabetes subgroups, especially heavy proteinuria; follow the condition-specific NICE guideline. Check standing BP and symptoms in older adults, people with diabetes or those experiencing dizziness. Reassess adherence, drug effects, renal function and patient priorities at reviews rather than treating a numerical target in isolation.
7.08 Secondary Hypertension and Resistant Hypertension
Consider an underlying cause in young patients, abrupt onset, severe or resistant hypertension, hypokalaemia, episodic symptoms or a marked creatinine rise after ACE inhibitor therapy. Causes include renal parenchymal disease, renovascular disease, primary aldosteronism, obstructive sleep apnoea, phaeochromocytoma, thyroid disorders, Cushing syndrome and drug/substance effects. Hypokalaemia with resistant hypertension suggests aldosterone excess; episodic headache, sweating and palpitations suggest catecholamine excess, although most hypertension is not caused by a phaeochromocytoma.
Distinguish true resistance from white-coat effect, non-adherence, incorrect cuff technique and excessive salt intake. Targeted investigations and specialist referral are preferable to indiscriminate endocrine testing.
7.09 Severe Hypertension: Emergency or Not?
Severe BP elevation alone is not synonymous with a hypertensive emergency. Emergency means severe pressure with acute target-organ injury: encephalopathy, stroke syndromes, acute coronary syndrome, pulmonary oedema, aortic dissection, acute kidney injury or retinal haemorrhage/papilloedema. At clinic BP ≥180/120 mmHg with such features, or suspected phaeochromocytoma, NICE advises same-day specialist assessment; investigate severity, symptoms, neurological state, ECG, urine and renal function.
Clinical reasoning: Rapid indiscriminate BP reduction in an asymptomatic patient may impair cerebral or renal perfusion. Aortic dissection is an exception requiring immediate specialist-directed impulse/BP control.
7.10 Postural Hypotension and Falls
Postural (orthostatic) hypotension is a sustained fall in systolic BP of at least 20 mmHg or diastolic BP at least 10 mmHg on standing, conventionally assessed within three minutes. Check supine/seated and standing pressures, symptoms, hydration, medications, autonomic neuropathy, blood loss and cardiac disease. In older adults, consequences include falls, syncope, fear of mobilisation and loss of independence. Management prioritises reversible factors, fluid and salt advice when appropriate, careful medication review, slow positional changes and compression/other measures; specialist treatment is needed for severe neurogenic cases.
Exam distinction: Orthostatic hypotension is a clinical physiological phenomenon, not synonymous with vasovagal syncope.
7.11 Primary Prevention, Lipids and Statins
Cardiovascular prevention is based on absolute risk, not on cholesterol or BP in isolation. For primary prevention, assess smoking, BP, lipids, diabetes, renal disease and family history; offer lifestyle support and discuss statin therapy according to NICE lipid guidance and QRISK3 where appropriate. Established coronary, cerebral or peripheral atherosclerotic disease usually calls for intensive secondary prevention, including a high-intensity statin unless contraindicated. Consider familial hypercholesterolaemia in unusually high LDL cholesterol or premature coronary disease in relatives.
Explain that statins reduce hepatic cholesterol synthesis and up-regulate LDL receptors; adverse muscle symptoms require clinical assessment rather than automatic permanent cessation.