Hypertension

Persistent elevation of BP in the systemic arterial circulation to a level higher than expected for the age, sex, and race of the individual

Aetiology

Primary hypertension

• Primary hypertension is hypertension with no singular identifiable cause - accounts for up to 90% of patients

• Risk factors:
• ↑ age (main driver)
• Smoking
• Genetics/family history
• Obesity, OSA
• ↑ alcohol intake
• ↑ salt intake

Secondary hypertension

• Secondary hypertension is caused by an identifiable singular cause, removal or reversal of which leads to normalization of BP

• Causes include:
• Renal disease (most commonly)
• Endocrine - adrenal gland hyperfunction/tumours, aldosteronism, Cushing’s, pheochromocytoma
• Coarction of the aorta
• Drugs e.g. corticosteroids
• Pregnancy associated hypertension - pre-eclampsia, eclampsia

Pathophysiology

Subtypes of hypertension

• Stable elevation of BP over many years

• Asymptomatic, incidental finding often in health checks

• Consequences - LV hypertrophy, congestive cardiac failure, ↑ atheroma, thickening of tunica media, ↑ aneurysm rupture, renal disease

• Acute, severe elevation of BP - diastolic pressure >130-140 mmHg

• Can develop from benign primary or secondary hypertension, or arise de novo

• Needs urgent treatment to prevent death - cerebral oedema, acute renal and heart failure, haemorrhage

• Hypertension that only exists when BP is measured during medical consultations

• Discrepancy of more than 20/10 mmHg between clinic and average daytime ABPM

Classification of hypertension

• Clinic BP is 140/90 mmHg or higher and

• ABPM or HBPM daytime average is 135/85 mmHg or higher

• Clinic BP is 160/100 mmHg or higher and

• ABPM or HBPM daytime average is 150/95 mmHg

• Clinic systolic BP is 180 mmHg or higher or

• Clinic diastolic BP is 110 mmHg or higher

Clinical presentation

Symptoms

• Usually asymptomatic - incidental finding

• Malignant hypertension will present acutely; symptoms include headache, blurred vision, N+V, chest pain and altered mental status

Signs

• Pulses bruits

• Examine fundi (hypertensive retinopathy)

Investigations

Blood pressure monitoring

• ABPM if clinic BP >140/90 mmHg

• HBPM if ABPM declined/not tolerated

Management

Monitoring - to assess for end organ damage

• Urine - haematuria, Alb:Cr ratio

• Bloods - FBC, U+Es, eGFR, glucose, fasting lipids, electrolytes

• Fundoscopy - hypertensive retinopathy

• 12 lead ECG - LVH, old infarct

• Calculate 10-year CV risk e.g. ASSIGN, QRISK3

Lifestyle interventions

• Stage 1 hypertension is usually managed through lifestyle interventions alone - exercise, smoking cessation, dietary modification (limit alcohol, salt intake and caffeine)
• Some exceptions include if there is target organ damage, CVD or 10-year CVD risk >10%

Medical management

• ACE-inhibitor (e.g. ramipril) if <= 55 years old
• If unable to tolerate ACE-inhibitor then switch to ARB (e.g. candesartan)

• DHP-Calcium Channel Blocker (e.g. nefedipine) if >55 years old OR African or Caribbean ethnicity

• Combine CCB and ACE-i/ARB

• Add thiazide-like diuretic (e.g. indapamide)

• If blood potassium <4.5mmol/L then add spironolactone

• If >4.5mmol/L increase thiazide-like diuretic dose

• Other options at this point if the potassium is >4.5mmol/L include:
• Alpha blocker (e.g. doxacosin)
• Beta blocker (e.g. atenolol)
• Referral to cardiology for further advice

• Statins for primary prevention if 10-year CV risk is >20%

BP targets

• <80 years: clinic BP <140/90 mmHg (or <135/85 AMPM/HBPM)

• 80 years: clinic BP <150/90 mmHg (or <145/85 AMPM/HBPM)

• Diabetics: clinic BP <130/80 mmHg

• White coat effect: ABPM/HBPM <135/85 if under 80 or <145/85 if over 80