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🩺 HKMLE Master Notes: Hypertension & Systemic Disorders Affecting the Heart

Sources: Harrison's 22E (2025) · Robbins & Cotran Pathologic Basis of Disease · Goldman-Cecil Medicine · 2025 AHA/ACC Guideline (PMID 40811516) (Davidson's is not in the library; equivalent or superior content sourced from the above)

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RAAS Diagram (Robbins, Fig. 11.4)

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PART 1 — ESSENTIAL (PRIMARY) HYPERTENSION

1.1 Definition & Classification (2025 AHA/ACC)

ESH 2023 vs AHA 2025: ESH keeps threshold at ≥140/90. AHA defines HTN from ≥130/80. In HK exams, know both thresholds — "grade 1 HTN" in ESH = Stage 1 in AHA.

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1.2 Epidemiology

• ~1.3 billion people worldwide have hypertension
• Prevalence rises steeply with age; >70% of adults ≥70 years
• Using AHA ≥130/80 criteria → ~half of general population are hypertensive
• Hong Kong prevalence ~27% of adults (standard 140/90 threshold)

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1.3 Pathophysiology of Essential Hypertension

• Sodium retention (impaired pressure natriuresis → ↑ fluid vol → ↑ CO → ↑ SVR)
• Neurogenic activation (↑ SNS tone → vasoconstriction, ↑ renin)
• Angiotensin II excess (RAAS overactivation)
• Renin–aldosterone axis dysfunction
• Endothelial dysfunction (↓ NO, ↑ endothelin)
• Structural vascular remodeling (↑ wall:lumen ratio)

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1.4 Vascular Pathology in Hypertension (Robbins)

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1.5 Target Organ Damage (TOD)

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1.6 Management — Lifestyle (Non-Pharmacological)

• Alcohol ≤2 drinks/day
• Weight loss (1 kg → −1 mmHg SBP)
• Exercise ≥150 min/week aerobic
• DASH diet
• Sodium <2300 mg/day (optimal <1500 mg/day)
• K⁺ adequate intake (3500–5000 mg/day)

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1.7 Pharmacological Treatment

Prefer chlorthalidone or indapamide over hydrochlorothiazide (HCTZ) — longer-acting, more effective SBP reduction (Harrison's 22E)

1. Single agent if Stage 1 + low risk, or lifestyle alone
2. Dual therapy (A+C preferred) for most Stage 2 or high-risk Stage 1
3. Triple therapy (A+C+D) for uncontrolled
4. • MRA (spironolactone) for resistant HTN

• ACEi + ARB combination (↑ AKI, hyperK)
• ACEi/ARB in pregnancy
• β-blocker in asthma/reactive airways
• CCB (non-DHP) in HFrEF

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1.8 Resistant Hypertension

• Pseudoresistance excluded (poor measurement, white coat)
• Adherence confirmed
• Secondary causes excluded
• Tiazide-like diuretic substituted (switch HCTZ → chlorthalidone)
• Add spironolactone (MRA) as 4th agent

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PART 2 — SECONDARY HYPERTENSION

2.1 When to Suspect Secondary HTN

• Resistant hypertension (≥3 drugs still uncontrolled)
• Abrupt worsening of previously controlled BP
• Worsening disproportionate TOD for the BP level
• Lab abnormalities: unprovoked hypokalemia, proteinuria, LVH
• Young patient (<30 years) with severe HTN

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2.2 Causes of Secondary Hypertension

• Thyroid disease (hypo → diastolic HTN; hyper → systolic HTN)
• Coarctation of the aorta (young, radio-femoral delay, rib notching)
• Monogenic HTN syndromes (Liddle syndrome, Gordon syndrome, 11β-hydroxylase def, 17α-hydroxylase def)
• Drug-induced (NSAIDs, OCP, sympathomimetics, liquorice, calcineurin inhibitors, erythropoietin)

Paroxysmal HTN · Palpitations · Perspiration · Pallor · Pain (headache)

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2.3 Monogenic Hypertension — Quick Table

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2.4 Renovascular HTN — Pathophysiology

1. Renal artery stenosis → ↓ glomerular flow → ↓ afferent arteriole pressure → ↑ renin secretion
2. Renin → Ang I → Ang II → vasoconstriction + ↑ aldosterone → Na⁺/H₂O retention → ↑ BP

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PART 3 — SYSTEMIC DISORDERS AFFECTING THE HEART

3.1 Hypertensive Heart Disease (HHD) — Robbins Pathology

1. LVH (usually concentric) in the absence of other cardiovascular pathology
2. Clinical history or pathologic evidence of HTN in other organs

• Heart weight may exceed 500 g (normal ≤400 g)
• LV wall thickness may exceed 2.0 cm (normal ≤1.2 cm)
• Initially without ventricular dilatation → concentric hypertrophy
• Over time: ↑ interstitial fibrosis → stiffness → diastolic dysfunction → LA enlargement

• Earliest: ↑ transverse diameter of myocytes (may be subtle)
• Advanced: cellular + nuclear enlargement, perivascular + interstitial fibrosis

"Even mild hypertension (≥140/90) — if sufficiently prolonged — induces LVH"

1. Normal longevity (well-controlled)
2. IHD (atherosclerosis + ↑ O₂ demand from hypertrophic muscle)
3. Renal damage / cerebrovascular stroke
4. Progressive HF (HFpEF) or Sudden Cardiac Death
5. AF (from LA enlargement)

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3.2 Cor Pulmonale (Pulmonary Hypertensive Heart Disease)

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3.3 Other Systemic Disorders — Heart Involvement

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3.4 Key ECG/Investigation Clues for HK Exams

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PART 4 — CHEAT SHEET / QUICK RECALL

BP Classification Mnemonic: "Normal Elevated 1-2 Crisis" = 120/80 → 130/80 → 140/90 → 180/120

Secondary HTN Causes — "CHOPS-R":

Resistant HTN Workup — "PASTA":

Drug mnemonics:

• "ACE first in DM/CKD" — ACEi/ARB protect kidneys
• "CCB for elderly/Black" — amlodipine
• "No ACE in pregnancy" — use methyldopa/labetalol
• "Chlorthalidone > HCTZ" — longer acting, more effective
• "Spiro for resistant" — 4th drug = MRA

HHD Diagnosis Criteria (Robbins):

1. Concentric LVH (no other CV pathology) + 2. Clinical/pathological evidence of HTN

Systemic disease → specific cardiac lesion:

• SLE → Libman-Sacks (mitral, undersurface)
• Carcinoid → Right-sided valvular disease (TR + PS)
• Amyloid → Restrictive CMP + low-voltage ECG
• Sarcoid → Heart block + VT
• Haemochromatosis → DCM
• Marfan → Aortic root ± MVP

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PART 5 — RECENT GUIDELINE UPDATES (High-Yield HK)

⚠️ HKMLE High-Yield: The exams may test both AHA (≥130/80) and ESH (≥140/90) thresholds. Know that the 2025 AHA/ACC keeps BP target at <130/80 for high-risk patients. Renal denervation is now a guideline-endorsed option for truly resistant HTN (FDA 2023).

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PART 6 — HKMLE PEARL BOXES

Pearl 1: Unprovoked hypokalemia in a hypertensive patient → primary hyperaldosteronism until proven otherwise. Screen with ARR.

Pearl 2: Creatinine rise >30% after starting ACEi/ARB → suspect bilateral renal artery stenosis or severe unilateral RAS. Stop ACEi/ARB.

Pearl 3: Hypertension + flash pulmonary oedema + abdominal bruit = renovascular HTN (atherosclerotic RAS).

Pearl 4: OSA is the most common secondary cause of hypertension. Always consider in obese, resistant HTN patients.

Pearl 5: In Cushing's syndrome, hypertension is due to mineralocorticoid excess from cortisol + DOC (not just cortisol).

Pearl 6: "Onion-skin" lesion on renal biopsy = malignant hypertension (hyperplastic arteriolosclerosis).

Pearl 7: LV wall >2 cm + LV mass >500 g → severe systemic HHD (Robbins criteria).

Pearl 8: Carcinoid tumor of the gut → 5-HT inactivated in lung → right-sided valve disease. Carcinoid in lung → left-sided disease.

Pearl 9: Libman-Sacks endocarditis in SLE is non-infective, sterile, affects mitral valve (usually undersurface/posterior leaflet), and is associated with antiphospholipid syndrome.

Pearl 10: Hypertensive heart disease = concentric LVH → diastolic dysfunction → HFpEF (preserved EF). Do NOT confuse with DCM (eccentric, reduced EF).

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