Ch13: Hypertension（高血压）

Preparatory Mindset

Hypertension is the most common chronic disease in internal medicine and the leading modifiable risk factor for stroke, MI, heart failure and renal failure — "the silent killer" that the exam always includes. The skills: (1) diagnose — sustained office BP ≥140/90 mmHg (HK/ESC), with out-of-office confirmation (home/ambulatory) for diagnosis, and identify secondary causes (renovascular, primary aldosteronism, phaeochromocytoma, Cushing, OSA, renal disease, coarctation, drugs); (2) stratify risk and set targets (HK: <130/80 in most, older adults less strict); (3) treat — lifestyle first, then the drug ladder (ACEi/ARB, CCB, thiazide diuretic, β-blocker), combination therapy, and hypertensive emergency management (target-organ damage — IV labetalol/nitroprusside with controlled BP reduction). The HKHA Hypertensive Crisis (C 23–24) section is LMCHK-critical — the emergency vs urgency distinction and the IV drug protocols are frequently examined.

Core Concepts

Definition & classification

• Hypertension = sustained elevation of arterial blood pressure; defined as office BP ≥140/90 mmHg (ESC/HK) — confirmed by repeated measurements ± home/ambulatory monitoring (white-coat and masked hypertension require out-of-office BP).
• Classification by level (office): normal <120/80; high-normal 120–129/80–84; grade 1 HT 140–159/90–99; grade 2 HT 160–179/100–109; grade 3 HT ≥180/110.
• Systolic vs diastolic: isolated systolic hypertension (common in elderly — wide pulse pressure), isolated diastolic (younger).
• "Recent Hype in Hypertension" (teacher lecture) — the modern debate: lower targets (<130/80), out-of-office BP, cardiovascular risk-based treatment, treatment-resistant hypertension.

Epidemiology & importance

• Extremely common: ~1 in 3 adults globally; increases steeply with age (>65 y: >50%); more than half of those with HT are untreated/uncontrolled ("the silent killer").
• Hypertension drives the cardiovascular continuum: endothelial dysfunction → atherosclerosis → MI/stroke/heart failure/ESRD (see CHD chapter). Each 20/10 mmHg above 115/75 roughly doubles cardiovascular risk.
• Risk factors: age, family history, obesity, high salt intake, alcohol, smoking, physical inactivity, stress, OSA.

Etiology — essential vs secondary

• Essential (primary) HT ~90–95%: no single identifiable cause — polygenic + environmental (salt, obesity, ageing).
• Secondary HT ~5–10% (look for these clues): renal parenchymal disease (most common secondary), renovascular HT (renal artery stenosis — fibromuscular dysplasia in young women, atherosclerosis in elderly; flash pulmonary oedema), primary aldosteronism (Conn — HT + hypokalaemia + metabolic alkalosis), phaeochromocytoma (paroxysmal HT, headache, palpitations, sweating), Cushing syndrome, thyroid disease, OSA (non-dipping nocturnal HT), coarctation of aorta (young, arm-leg BP gradient), drugs (NSAIDs, OCP, steroids, liquorice, sympathomimetics).
• Red flags for secondary: onset <30 or >55, resistant HT (≥3 drugs incl. diuretic), abrupt onset, hypokalaemia, abdominal bruit, target-organ damage disproportionate to duration.

Complications (target-organ damage)

• Brain: stroke (ischaemic/haemorrhagic), hypertensive encephalopathy, dementia.
• Heart: LVH, heart failure (HFpEF/HFrEF), coronary artery disease/MI, atrial fibrillation.
• Kidney: nephrosclerosis, chronic kidney disease, ESRD (hypertension + diabetes multiply risk).
• Eyes: hypertensive retinopathy (Keith-Wagener grades I–IV; grade III = flame haemorrhages + cotton-wool spots, IV = papilloedema), malignant hypertension.
• Vessels: aortic dissection, peripheral arterial disease, aneurysm.

Diagnosis & evaluation

• Confirm with repeated office readings (≥2 visits) + home BP monitoring/24-h ambulatory BP (daytime average ≥135/85 ≈ office 140/90).
• History: family history, salt/alcohol, smoking, drugs (NSAIDs, OCP, steroids), snoring (OSA), paroxysmal symptoms (phaeochromocytoma).
• Examination: both arms (coarctation/ dissection), BP in legs, BMI, fundoscopy, abdominal bruit, radiofemoral delay, Cushingoid features.
• Investigations: FBC, U&E (K⁺, Na⁺, Cr), glucose/HbA1c, lipids, uric acid, urine (proteinuria, albumin:Cr ratio), ECG (LVH), echo (LVH), USG kidneys/Doppler if renovascular suspected; aldosterone:renin ratio (primary aldosteronism), metanephrines (phaeochromocytoma), overnight oximetry/polysomnography (OSA); CXR.

Treatment — lifestyle

• All patients: weight loss, salt restriction (<5–6 g/day), DASH diet (fruit/vegetables), alcohol moderation, smoking cessation, aerobic exercise (30 min/day most days), stress management, sleep (OSA treatment — CPAP).

Treatment — pharmacological

- ACEi / ARB — first-line especially with diabetes, proteinuria, heart failure, post-MI (reno-protective); contraindicated in pregnancy; monitor K⁺/Cr. - Calcium-channel blocker (CCB) — dihydropyridine (amlodipine) — good in elderly, isolated systolic HT, black patients; ankle oedema. - Thiazide/thiazide-like diuretic (indapamide, chlorthalidone) — elderly, salt-sensitive; monitor K⁺, urate (gout), glucose, Na⁺. - β-blocker — not first-line for uncomplicated HT (ESC 2018), but indicated with CAD, post-MI, heart failure, tachyarrhythmia. - MRA (spironolactone) — resistant HT; monitor K⁺.

• First-line classes (in combination, usually starting 2 drugs if BP >20/10 above target):
• Combination logic: ACEi/ARB + CCB or thiazide preferred; avoid ACEi + ARB (no added benefit, more adverse events); fixed-dose combinations improve adherence.
• Targets: HK/ESC: <130/80 mmHg for most; elderly (≥65 y): <140/90 (and systolic 130–140 if tolerated); diabetes/CKD: <130/80 (with ACEi/ARB proteinuric).
• Resistant HT (BP uncontrolled on 3 drugs incl. diuretic): exclude secondary causes + non-adherence + white-coat; add spironolactone.
• Pregnancy: methyldopa, labetalol, nifedipine; avoid ACEi/ARB (fetotoxic).

Hypertensive emergencies & urgencies (HKHA)

- Admit ICU/CCU with continuous BP monitoring. - With compelling condition (aortic dissection, severe pre-eclampsia/eclampsia, phaeochromocytoma crisis): reduce SBP <140 mmHg within the first hour; <120 mmHg in aortic dissection. - Without compelling condition: reduce SBP by no more than 25% within the first hour, then to 160/100 mmHg within 2–6 h if stable, then cautiously to normal over 24–48 h (avoid precipitous drops — cerebral/renal ischaemia).

- Labetalol: 20 mg IV bolus, then 20–80 mg q10 min (max 300 mg total), then 0.5–2 mg/min infusion (titrate to 10 mg/min) — good in most emergencies; avoid in acute LV failure (β-blockade). - Sodium nitroprusside: start 0.25–0.5 μg/kg/min, ↑ by 0.5 μg/kg/min q5 min (max 10); limit <3 μg/kg/min if eGFR <30; protect from light; avoid in pregnancy; avoid >48 h (thiocyanide toxicity); especially good for acute LV failure. - Hydralazine 10–20 mg slow IV (repeat q4–6 h) — pregnancy/pre-eclampsia; avoid in AMI and dissection; not first-line (unpredictable effect). - Phentolamine 5–10 mg IV — catecholamine crisis (phaeochromocytoma, clonidine withdrawal, sympathomimetic excess). - Nitroglycerin — acute coronary syndromes/APO.

• Hypertensive emergency: severe BP elevation (>180/120 mmHg) WITH evidence of new or worsening target-organ damage — hypertensive encephalopathy, acute MI, acute LV failure/pulmonary oedema, unstable angina, dissecting aortic aneurysm, acute renal failure, eclampsia (acute ICH and acute ischaemic stroke handled separately).
• IV medications:
• Condition-specific choices: APO — nitroprusside/GTN + loop diuretic (avoid diazoxide/hydralazine; avoid labetalol/β-blocker in LV dysfunction); angina/AMI — GTN, nitroprusside, labetalol, CCB; sympathetic excess (phaeochromocytoma, clonidine withdrawal, cocaine/MAOI) — phentolamine/labetalol/nitroprusside; β-blocker alone contraindicated (unopposed α-vasoconstriction); aortic dissection — nitroprusside + labetalol, SBP 100–120, HR 60–70; pregnancy — hydralazine/nicardipine/labetalol (no nitroprusside, no ACEi).
• Hypertensive urgency: severe BP elevation in stable patients without acute target-organ damage — often medication non-compliance; treat by reinstituting/intensifying oral antihypertensives (no IV, no ICU).
• Always look for the cause of the crisis (e.g., renal artery stenosis, phaeochromocytoma, drug withdrawal).

High-Yield Points

• HT = office BP ≥140/90 (ESC/HK); confirm with home/ABPM; target <130/80 for most (HK/ESC).
• Secondary causes: renal disease (most common), renovascular, primary aldosteronism (HT + hypokalaemia), phaeochromocytoma (paroxysmal + triad), Cushing, OSA, coarctation, drugs (NSAIDs/OCP/steroids).
• First-line: ACEi/ARB, CCB, thiazide diuretic; β-blocker for CAD/HF/tachyarrhythmia; MRA for resistant HT.
• Avoid ACEi+ARB combination; ACEi/ARB contraindicated in pregnancy (also avoid in bilateral RAS).
• Emergency = >180/120 + target-organ damage → ICU + IV (labetalol/nitroprusside); urgency = stable → oral meds.
• Emergency BP targets: compelling condition → <140 in 1 h (dissection <120); else ↓≤25% in 1 h → 160/100 in 2–6 h → normal in 24–48 h.
• Nitroprusside: not in pregnancy, ≤48 h, light-protected; hydralazine: pregnancy, avoid in AMI/dissection.
• Sympathetic excess: phentolamine/labetalol — never β-blocker alone.

Topic Summary

Hypertension — the most common chronic disease — is diagnosed by sustained office BP ≥140/90 mmHg with out-of-office confirmation, and almost always essential in origin, but secondary causes (renal disease, primary aldosteronism, phaeochromocytoma, renovascular, OSA) must be sought, especially in young, resistant or abrupt-onset disease. Management is lifestyle-first plus a first-line drug ladder (ACEi/ARB, CCB, thiazide) targeting <130/80 mmHg, with combination therapy and MRA for resistant cases. The exam-critical division is emergency vs urgency: hypertensive emergency (>180/120 with target-organ damage) requires ICU care and IV therapy (labetalol, nitroprusside, phentolamine) with controlled BP reduction, while urgency is managed by reinstituting oral drugs — the HKHA Hypertensive Crisis protocol being an LMCHK priority.