GC058 High Blood Pressure
High blood pressure (hypertension) is a chronic cardiovascular condition defined by persistently elevated systemic arterial pressure, typically ≥140/90 mmHg, that increases the risk of end-organ damage to the heart, brain, kidneys, and vasculature.
High Blood Pressure: Hypertension
This set of notes synthesises the core GC 058 (High Blood Pressure) lecture by Professor Hung-Fat Tse with supporting material from GC 066 (Fluctuating BP), GC 224 (Hypertension and Pregnancy), GC 084 (Heart Failure), GC 034 (CKD), the Block A Clinical Pharmacology of anti-HT medications deck, and relevant past papers. The big idea is straightforward: hypertension is the number one modifiable risk factor for cardiovascular death worldwide, and your job as a clinician is to measure it correctly, confirm it, look for secondary causes and target organ damage, stratify risk, then treat to target — for life.
How this fits in exams: The 4th Summative frequently tests BP classification thresholds, white-coat vs masked HTN, secondary HTN clues (phaeochromocytoma, Conn's, renal artery stenosis, coarctation), compelling indications for specific drug classes, contraindications, hypertensive emergencies, and BP in pregnancy. Expect MCQ stems on drug choice given a clinical scenario, SAQs asking you to list investigations for newly diagnosed HTN, and mini-cases combining HTN with CKD or DM.
HT is the presence of abnormally high BP ( > 140/90 mmHg). It is a progressive "cardiovascular syndrome" associated with target organ damage, often present before high BP values are observed. [1]
Why does this definition matter?
Blood pressure is a continuous variable — the 140/90 threshold is where clinical trials consistently show treatment benefit outweighs harm. But damage starts earlier, which is why newer guidelines (ACC/AHA 2017) define Stage 1 at 130/80. For HKUMed exams, use the GC lecture definition of ≥ 140/90 unless specified otherwise. [1][2]
| Category | Office SBP (mmHg) | Office DBP (mmHg) |
|---|---|---|
| Optimal | < 120 | < 80 |
| Normal | 120–129 | 80–84 |
| High-normal | 130–139 | 85–89 |
| Grade 1 HTN | 140–159 | 90–99 |
| Grade 2 HTN | 160–179 | 100–109 |
| Grade 3 HTN | ≥ 180 | ≥ 110 |
| Isolated Systolic HTN | ≥ 140 | < 90 |
Elevated diastolic BP as well as systolic BP are equally important: risk of 20 mmHg systolic BP = 10 mmHg diastolic BP. [1]
This means that every 20/10 mmHg increment above 115/75 doubles cardiovascular mortality risk (Lewington et al. Lancet 2002). [1]
Raised systolic BP without significantly raised diastolic BP is termed "Isolated Systolic Hypertension (ISH)" — common in elderly. [1]
Why ISH in the elderly? With ageing, large elastic arteries (aorta) stiffen due to loss of elastin and increased collagen crosslinking. Stiff arteries cannot buffer systolic ejection → SBP rises. Meanwhile, reduced elastic recoil lowers DBP. The result is widened pulse pressure and ISH. This also explains why elderly patients are prone to postural hypotension (loss of baroreceptor sensitivity + stiff vessels). [1][3]
Exam Trap
Don't confuse ISH with "benign" hypertension. ISH carries significant stroke and HF risk and must be treated. Thiazide diuretics and dihydropyridine CCBs are first-line for ISH in the elderly.
Hypertension affects approximately 1 billion people worldwide. It is the #1 risk factor for death globally (WHO 2011). [1]
- Hong Kong prevalence: ~20% of adults [1]
- Global trends: Of those with HTN, only a minority are diagnosed, treated, AND controlled. The "rule of halves" historically applied (half undiagnosed, half of diagnosed untreated, half of treated uncontrolled), though rates have improved.
- Uncontrolled HTN leads to stroke (×2–3), CHD (×3), CKD (×5–6), and heart failure (×3). [1]
Diabetes and Hypertension: Bad Companions — Stroke ↑2×, CHD ↑3×, LVH ↑2×, CHF ↑3×, CKD ↑5–6×. [1]
3. Pathophysiology — Why Does Essential HTN Occur?
What causes "Essential" HT? Environmental + Genetic factors. [1]
All hypertension ultimately results from increased cardiac output (CO), increased total peripheral resistance (TPR), or both. [4]
In young hypertensives: The initial phase is often a high-CO state driven by sympathetic overactivity, RAAS activation, and increased renal sodium reabsorption. Over time, structural vascular remodelling (arteriolar hypertrophy, endothelial dysfunction) shifts the physiology to a high-TPR state.
In elderly hypertensives: Arterial stiffness dominates → ISH as described above. Renal disease and aldosterone excess also contribute. [1]
- RAAS (Renin-Angiotensin-Aldosterone System): Angiotensin II is a potent arteriolar vasoconstrictor and stimulates aldosterone → Na+/water retention → ↑ blood volume → ↑ BP. This is why ACEI/ARBs are so effective.
- Sympathetic nervous system: ↑ catecholamines → ↑ HR, ↑ contractility, ↑ vasoconstriction.
- Renal sodium handling: Guyton's pressure-natriuresis curve is shifted rightward in essential HTN — the kidneys need a higher perfusion pressure to excrete the same amount of sodium.
- Endothelial dysfunction: ↓ nitric oxide, ↑ endothelin-1 → vasoconstriction.
- Arterial stiffness: Particularly in ageing.
- Excess dietary sodium (DASH diet evidence)
- Obesity → insulin resistance → sympathetic activation + sodium retention
- Alcohol excess
- Physical inactivity
- Stress
- Positive family history (essential HTN is polygenic)
- Specific monogenic forms exist but are rare (e.g., Liddle syndrome, GRA)
4. Measuring Blood Pressure Correctly
Hypertension is not a disease of the left arm! [1]
This is a reminder to measure BP in both arms, consider postural BP, and think about out-of-office BP to get a true picture.
- Patient seated for ≥ 5 minutes, back supported, legs uncrossed, arm at heart level
- Appropriate cuff size (bladder covers ≥ 80% of arm circumference)
- No caffeine, exercise, or smoking for 30 minutes prior
- Take ≥ 2 readings, 1–2 minutes apart; use the average
- Measure in BOTH arms initially — if persistent difference > 15–20 mmHg, use the higher arm (and investigate for subclavian stenosis or coarctation)
- Check standing BP (at 1 and 3 minutes) in elderly, diabetics, those on antihypertensives — to detect orthostatic hypotension
| Setting | SBP/DBP Threshold for HTN |
|---|---|
| Office | ≥ 140/90 |
| Home BP (HBPM) | ≥ 135/85 |
| 24-hr ABPM – Daytime | ≥ 135/85 |
| 24-hr ABPM – Night-time | ≥ 120/70 |
| 24-hr ABPM – Overall | ≥ 130/80 |
Normal values are different for office and home BP (10 mmHg lower). [1]
High Yield
The difference between office and home/ABPM thresholds is a favourite MCQ topic. Remember: home/ABPM thresholds are approximately 5 mmHg lower for SBP and DBP compared to office readings.
Self-measurement of BP at home is of clinical value and its prognostic significance is now demonstrated. [1]
Advantages:
- More readings → better representation of true BP
- Detects white-coat effect
- Improves patient adherence
- Assesses therapeutic coverage (trough drug effect)
Should be discouraged when: it causes patient anxiety or leads to self-modification of treatment. [1]
Indications for ABPM: considerable variability of office BP, marked discrepancy between office vs. home BP, resistant HTN, suspected hypotensive episodes (especially elderly and DM), suspected pre-eclampsia in pregnancy. [1]
ABPM provides night-time readings — this is a unique advantage over HBPM. Night-time BP (the "dipping" pattern) has strong prognostic value. Non-dippers (< 10% nocturnal fall) and reverse dippers have worse cardiovascular outcomes. [5]
5. White-Coat HTN & Masked HTN
Definition: Office BP is persistently elevated whereas BP outside clinic is normal, usually diagnosed by ambulatory or home BP monitoring. Prevalence: 15–30% of general population, commonly in elderly and pregnant women. [1]
Risk: Less than sustained HTN, probably small risk greater than normal people, may be a precursor to sustained HTN. Should reassure patient that the risk is low or absent. Need close follow-up and monitoring again. [1]
Why does it happen? An exaggerated alerting/anxiety response to the clinical environment activating the sympathetic nervous system → transient BP elevation.
Clinical implications:
- Must consider in ALL newly diagnosed HTN patients before starting treatment
- Do NOT start medications based on office readings alone without confirming with HBPM/ABPM
- These patients need regular follow-up as they may develop sustained HTN over time
The opposite: Normal office BP but elevated out-of-office BP. This is more dangerous than white-coat HTN because it goes undetected and carries cardiovascular risk similar to sustained HTN.
CV events per 1000 patient-years: Normal ~5, White coat ~7, Masked ~30, Uncontrolled ~35. [1]
Clinical Pearl
Masked HTN has a worse prognosis than white-coat HTN and approaches the risk of sustained uncontrolled HTN. Suspect it in patients with target organ damage (LVH, proteinuria) despite "normal" office BP.
6. Clinical Evaluation of Newly Diagnosed HTN
Aims of clinical evaluation: (1) Confirm chronic elevation of BP and determine level, (2) Uncover correctable secondary forms, (3) Establish pretreatment baseline, (4) Assess factors that may influence therapy, (5) Determine if target organ damage is present, (6) Determine if other CVD risk factors are present. [1]
6.1 History
Duration and previous BP levels, family history of HT, age, other risk factors (smoking, DM, dyslipidaemia, family history of premature CVD), patient's lifestyle (diet, physical activity, family status, work, educational level). [1]
Most patients are asymptomatic ("silent killer"). Elevated BP itself may cause: headaches, dizziness, palpitations, easy fatigability, and impotence. [1]
Brain and eyes: headache, vertigo, impaired vision, TIA, sensory/motor deficit. Heart: palpitation, chest pain, SOB, swollen ankles. Kidney: thirst, polyuria, nocturia, haematuria. Peripheral arteries: cold extremities, intermittent claudication. [1]
Family history of renal disease (polycystic kidney), renal disease/UTI/haematuria/analgesic abuse (parenchymal renal disease), drug/substance intake, snoring/daytime somnolence/obesity (OSA), episodes of sweating/headache/anxiety/palpitation (phaeochromocytoma), muscle weakness/tetany (aldosteronism), kidney stones/depression/lethargy (hyperparathyroidism), fatigue/weight gain/hair loss (hypothyroidism), heat intolerance/weight loss/tremor (hyperthyroidism). [1]
6.2 Physical Examination
General appearance. BP and pulses in both upper extremities (supine and standing). Height and weight = BMI, waist circumference. Fundi examination. Palpation and auscultation of all peripheral arteries. CVS examination. [1]
Cushing features, neurofibromatosis skin stigmata (phaeochromocytoma), palpable enlarged kidneys (polycystic kidney), abdominal bruits (renovascular HTN), precordial/chest murmurs (coarctation), diminished/delayed femoral pulses with reduced femoral BP (coarctation). [1]
Brain: carotid bruits, motor/sensory defects. Retina: fundoscopic abnormalities. Heart: displaced apex, abnormal rhythms, S3 gallop, pulmonary rales, peripheral oedema. Peripheral arteries: absent/reduced/asymmetric pulses, cold extremities, ischaemic skin lesions. [1]
| Grade | Finding | Significance |
|---|---|---|
| I | Arteriolar narrowing (silver wiring) | Mild, chronic |
| II | AV nipping | Moderate, chronic |
| III | Flame haemorrhages + cotton wool spots + hard exudates | Severe; indicates accelerated HTN |
| IV | Papilloedema | Malignant HTN — medical emergency |
Basic tests for initial evaluation: [1]
| Test | Why |
|---|---|
| Urine analysis (dipstick + microscopy) | R/O renal disease, proteinuria (TOD), haematuria |
| Serum creatinine, urea | Baseline kidney function, R/O kidney failure |
| Serum K⁺ and Ca²⁺ | Hypokalaemia → hyperaldosteronism; Hypercalcaemia → hyperparathyroidism |
| Serum glucose | R/O diabetes |
| Lipid profile (TC, HDL, LDL, TG) | Associated CVD risk factors |
| Serum uric acid | Baseline (thiazides ↑ uric acid), gout risk |
| ECG | LVH, ischaemia, arrhythmia, heart block |
| TSH | R/O thyroid disorders |
| CXR | Cardiomegaly, heart failure, coarctation (rib notching) |
Identifying Target Organ Damage
Heart: ECG/Echo/CXR for LVH and diastolic dysfunction. Kidney: serum creatinine and dipstick for proteinuria. Large arteries: ultrasound for atherosclerotic plaque. Eyes: fundoscopy for retinal artery changes. [1]
CVD Risk Factors: Hypertension, cigarette smoking, obesity (BMI > 30), physical inactivity, dyslipidaemia, DM, microalbuminuria or eGFR < 60, age ( > 55 men, > 65 women), family history of premature CVD (men < 55, women < 65). [1]
Metabolic syndrome components marked with asterisk: HTN, obesity, dyslipidaemia, DM. [1]
The concept of total cardiovascular risk is critical — you don't just treat BP in isolation; you must address all modifiable risk factors simultaneously (smoking cessation, statin therapy, glycaemic control, antiplatelet therapy where indicated).
9. Secondary Hypertension
Essential HTN accounts for 92–94% in the general population but only 65–85% in specialist clinics. [1]
Indications to search: Age of onset < 30 or > 55, severe HTN (180/110), abrupt onset or rapid worsening, resistance to previously effective therapy. Specific: palpable kidney/renal bruit/abnormal urinalysis, symptoms of phaeochromocytoma, unexplained hypokalaemia (primary aldosteronism), signs of Cushing syndrome, delayed/absent femoral pulses (coarctation). [1]
A — Accuracy of diagnosis, Apnea (OSA). B — Bruit (renal artery stenosis), Bad kidney (renal failure, polycystic kidney). C — Catecholamine (phaeochromocytoma), Cushing, Coarctation. D — Diet (salt/alcohol/obesity), Drugs (NSAIDs, COX-2 inhibitors, estrogens/OCP, immunosuppressants, EPO, sympathomimetics, steroids). E — Erythropoietin, Endocrine (hyperaldosteronism, thyroid disease, hyperparathyroidism). [1]
High Yield Drug-Induced HTN
Commonly tested drugs causing HTN: NSAIDs (inhibit renal prostaglandins → Na retention), combined OCP (estrogen-related), corticosteroids, cyclosporine/tacrolimus, sympathomimetics, erythropoietin. Always ask about drug history in a hypertensive patient.
| Cause | Key Clinical Feature | Screening Test | Confirmatory |
|---|---|---|---|
| Renovascular (RAS) | Abdominal bruit, flash pulmonary oedema, ↑Cr with ACEI/ARB | Renal duplex USS | MRA/CTA, renal angiography |
| Primary aldosteronism (Conn's) | Unexplained hypokalaemia, resistant HTN | Aldosterone:renin ratio (ARR) | Salt loading test, adrenal CT, adrenal vein sampling |
| Phaeochromocytoma | Paroxysmal headache, sweating, palpitation, pallor | 24-hr urine metanephrines, plasma free metanephrines | CT/MRI adrenals, MIBG scan |
| Cushing syndrome | Moon face, truncal obesity, striae, buffalo hump, proximal weakness | Overnight dexamethasone suppression test, 24-hr urine cortisol | Low-dose then high-dose DST, pituitary MRI |
| Coarctation of aorta | Radio-femoral delay, BP difference between arms and legs, rib notching on CXR | Echo, CT aorta | Cardiac catheterisation |
| OSA | Snoring, daytime somnolence, obesity, large neck | Epworth Sleepiness Scale | Polysomnography |
| Thyroid disease | Hypo: fatigue, weight gain, diastolic HTN. Hyper: weight loss, tremor, systolic HTN | TSH | Free T3/T4 |
| Renal parenchymal | Abnormal urinalysis, elevated creatinine, history of renal disease | Serum Cr, urine protein/sediment, USS kidneys | Renal biopsy if indicated |
Renovascular HTN: Indications for renal artery revascularisation — flash pulmonary oedema, ACS with severe HTN, resistant HTN, ischaemic nephropathy with CKD. [1]
OSA treatment: Weight reduction, CPAP, mandibular advancement splints. [1]
Risk factors for adverse prognosis: black race, youth, male sex, persistent DBP > 115, smoking, DM, hypercholesterolaemia, obesity, excess alcohol. Evidence of end organ damage: cardiac enlargement, ECG ischaemia/LV strain, MI, CHF, retinal exudates/haemorrhages, papilloedema, impaired renal function, CVA. [1]
Risk stratification combines:
- BP grade
- Number of CVD risk factors
- Presence of target organ damage (subclinical)
- Established CVD or CKD
This determines when to start drugs (immediately for Grade 3 or with TOD/CVD) vs. lifestyle first (Grade 1 without TOD and low overall risk).
Goal: To achieve the maximum reduction in total risk of CVD — need for treatment of other risk factors + BP control. Target: below 140/85–80 mmHg in young/middle-aged or diabetic patients; below 150–140/90 mmHg in elderly. Successful management = good communication and relationship as treatment is for life. [1]
ESC 2018 / ISH 2020 BP Targets (Exam Framing)
| Population | Office BP Target |
|---|---|
| Age < 65, including DM and CKD | < 130/80 mmHg (but not < 120/70) |
| Age ≥ 65 | SBP 130–139 mmHg (tolerated); DBP < 80 |
| Frail elderly | Individualise; < 150/90 acceptable |
| CKD (KDIGO 2021) | < 120/80 [6] |
Treatment goal from lecture roadmap: < 150/90 or < 140/80 for young ( < 65), DM and renal diseases. [1]
Exam Framing vs Current Practice
The GC lecture uses < 140/80 for DM/CKD as the goal on the treatment roadmap. KDIGO 2021 is more aggressive at < 120/80 for CKD. In the exam, use whichever threshold the question context provides; if none, default to the lecture slide values.
Lifestyle measures can serve as initial therapy before medication, an adjunct to medication, and can facilitate medication step-down or even withdrawal. [1]
| Intervention | Mean SBP Reduction |
|---|---|
| Weight reduction (if BMI > 25; 10 kg loss) | 5–20 mmHg |
| Halving salt intake (10 → 5 g/day) | 2–8 mmHg |
| Regular exercise (brisk walking 30 min/day) | 4–9 mmHg |
| DASH diet (fruits, vegetables, low-fat dairy, low total fat) | 8–14 mmHg |
| Moderation of alcohol ( < 2 drinks/day) | 2–4 mmHg |
DASH diet alone can reduce SBP by 8–14 mmHg — nearly equivalent to a single drug! [1]
Other lifestyle measures from ISH 2020: increase potassium intake, stress reduction, smoking cessation (primarily for CVD risk reduction, less direct BP effect). [1]
13. Pharmacological Treatment
First-line: ACEI/ARB (A), Beta-blocker (B) — now less favoured as initial monotherapy, CCB (C), Diuretic — thiazide/thiazide-like (D). [1]
| Drug Class | Mechanism | Key Indications | Key Contraindications | Key Side Effects |
|---|---|---|---|---|
| ACEI (e.g., ramipril, perindopril) | Blocks ACE → ↓ Ang II → vasodilation + ↓ aldosterone | HF, post-MI, DM nephropathy, proteinuria, CKD | Pregnancy, bilateral RAS, hyperkalaemia, angioedema hx | Dry cough (10–15%), hyperkalaemia, angioedema, AKI |
| ARB (e.g., losartan, valsartan) | Blocks AT1 receptor | Same as ACEI; ACEI-intolerant (cough) | Pregnancy, bilateral RAS, hyperkalaemia | Hyperkalaemia, AKI (bilateral RAS); NO dry cough |
| CCB – DHP (e.g., amlodipine, nifedipine) | Blocks L-type Ca²⁺ channels → arteriolar vasodilation | ISH in elderly, angina | — | Peripheral oedema, headache, flushing, reflex tachycardia, worsening GERD |
| CCB – Non-DHP (e.g., verapamil, diltiazem) | Blocks cardiac L-type Ca²⁺ channels → ↓ HR, ↓ contractility | Angina, SVT, rate control in AF | HF (↓ inotropy), severe bradycardia, used with BB (risk of complete heart block) | Constipation (verapamil), bradycardia, heart block |
| Thiazide/Thiazide-like (e.g., HCTZ, indapamide, chlorthalidone) | Inhibits NaCl co-transporter in DCT → ↑ Na excretion → ↓ blood volume | ISH in elderly, osteoporosis (↓ Ca excretion), Black patients | Gout (↑ uric acid), severe hypokalaemia | Hypokalaemia, hyponatraemia, hyperuricaemia, hyperglycaemia, hypercalcaemia |
| Beta-blocker (e.g., bisoprolol, atenolol, metoprolol) | Blocks β1 → ↓ HR, ↓ contractility, ↓ renin | Post-MI, HF (specific agents), angina, rate control, young HTN with anxiety/tachycardia | Asthma (non-selective), severe bradycardia, decompensated HF | Exercise intolerance, fatigue, erectile dysfunction, masking hypoglycaemia, bronchospasm |
Do NOT Combine ACEI + ARB for HTN
Do not combine ACEI and ARB for HTN — increased risk of hyperkalaemia, AKI, and no additional cardiovascular benefit (ONTARGET trial). The lecture explicitly states this. [1]
First-line combinations: CCB + ACEI/ARB OR ACEI/ARB + Diuretic. Triple: CCB + ACEI/ARB + Diuretic. Rationale: synergistic effects, act on different mechanisms, counteracting adverse effects. [1]
Why combine early? Most hypertensive patients (especially Grade 2+) will need ≥ 2 drugs. Using low doses of two complementary agents gives better BP reduction with fewer side effects than maximising one drug. Single-pill combinations (SPC/fixed-dose combinations) improve adherence. [1]
| Clinical Scenario | Preferred Drug(s) | Why |
|---|---|---|
| Post-MI | BB, ACEI/ARB | ↓ mortality, ↓ remodelling |
| Heart failure (HFrEF) | ACEI/ARB, BB (bisoprolol/carvedilol/metoprolol succinate), MRA, diuretic | Neurohormonal blockade ↓ mortality |
| DM with proteinuria/CKD | ACEI/ARB | Renoprotective; ↓ intraglomerular pressure by dilating efferent arteriole |
| Stable angina | BB, CCB | ↓ myocardial O₂ demand |
| AF rate control | BB, non-DHP CCB (diltiazem/verapamil) | ↓ AV node conduction |
| Aortic aneurysm | BB | ↓ dP/dt (rate of rise of aortic pressure) |
| BPH + HTN | Alpha-blocker (doxazosin) | Dual benefit: ↓ BP + ↓ urinary symptoms [6] |
| Osteoporosis | Thiazide | ↓ urinary Ca excretion |
| Pregnancy | Labetalol, nifedipine, methyldopa | Safe in pregnancy (ACEI/ARB absolutely contraindicated) |
Key monitoring parameters for each drug class: [1]
| Drug Class | Monitor | Key Adverse Effects |
|---|---|---|
| Diuretic | BP, Cr, K⁺, Mg²⁺, Na⁺, uric acid | Electrolyte depletion, gout, orthostatic hypotension |
| Aldosterone antagonist | BP, Cr, K⁺ | Hyperkalaemia (especially in CKD), gynaecomastia (spironolactone) |
| ACEI | BP, Cr, K⁺ | Dry cough, hyperkalaemia, AKI (bilateral RAS), angioedema |
| ARB | BP, Cr, K⁺ | Hyperkalaemia, AKI (bilateral RAS) |
| DHP CCB | BP, HR | Peripheral oedema, headache, flushing, reflex tachycardia |
| Non-DHP CCB | BP, HR | Heart block, constipation |
| Beta-blocker | BP, HR | Exercise intolerance, erectile dysfunction, masking hypoglycaemia |
Why does ACEI cause cough but ARB does not?
ACEI blocks the degradation of bradykinin (ACE normally breaks down bradykinin). Accumulated bradykinin in the lungs stimulates C-fibres → dry cough. ARBs block AT1 receptors without affecting bradykinin metabolism → no cough. This is why ARBs are the go-to alternative for ACEI-intolerant patients.
Resistant HTN: BP above goal despite ≥ 3 drugs at optimal doses including a diuretic. [1]
Step-by-Step Approach
Step 1: Exclude pseudoresistance — check adherence, timing of drug, confirm with home/ambulatory BP. Step 2: Look for contributing factors — high salt diet, obesity, interfering agents (NSAIDs, OCP). Step 3: Second look for secondary HTN. Step 4: Medical Rx — increase doses, add aldosterone blocker (spironolactone), use loop diuretic in renal disease, add potent vasodilator. Step 5: Referral. [1]
Common causes of pseudoresistance:
- Poor adherence (most common!)
- White-coat effect
- Incorrect BP measurement (wrong cuff size)
- Drug interactions (NSAIDs negating antihypertensive effect)
Spironolactone is the best-studied add-on for true resistant HTN (PATHWAY-2 trial). [1]
15. Hypertensive Emergencies & Urgencies
Malignant Hypertension: < 1% of HTN population, 25–50% 5-year mortality. Marked BP elevation DBP > 140 mmHg. Papilloedema + retinal haemorrhages + exudates. May present with HT encephalopathy, cardiac decompensation, acute renal failure. [1]
| Hypertensive Emergency (Rx within 1 hr) | Hypertensive Urgency (Rx within 24 hrs) |
|---|---|
| Malignant HTN | HTN with grade III/IV retinal changes |
| HT encephalopathy | Severe perioperative HTN |
| Acute HF | |
| Unstable angina/MI | |
| Dissecting aortic aneurysm | |
| Cerebral haemorrhage | |
| Acute renal failure | |
| Severe pre-eclampsia/eclampsia | |
| Adrenergic crisis (phaeo) |
Indication for IV treatment: HT encephalopathy (including malignant HTN, eclampsia), acute LV failure due to HTN, dissecting aneurysm. [1]
CAUTION: Emergency reduction of BP in accelerated HTN associated with acute stroke is CONTRAINDICATED because of loss of cerebral autoregulation → risk of cerebral infarction. [1]
Why? In chronic HTN, the autoregulation curve shifts rightward. The brain has adapted to higher perfusion pressures. If you abruptly drop BP, cerebral blood flow falls below the ischaemic threshold → watershed infarction. [7]
General rule: Reduce MAP by no more than 20–25% in the first hour, then gradually to 160/100 over the next 2–6 hours.
| Emergency | First-Line | Alternative |
|---|---|---|
| HT encephalopathy | Labetalol, Nicardipine | Nitroprusside |
| Acute aortic dissection | Nitroprusside + IV metoprolol (or labetalol alone) | Target SBP < 110 mmHg |
| Acute pulmonary oedema | Nitroprusside + loop diuretic | GTN |
| ACS | GTN (nitroglycerin) | Labetalol |
| Acute ischaemic stroke (BP > 220/120) | Labetalol, Nicardipine | MAP ↓ 15% in 1 hr |
| Cerebral haemorrhage (SBP > 180) | Labetalol, Nicardipine | Target SBP < 180 |
| Pre-eclampsia/Eclampsia | Labetalol + MgSO₄ | Nicardipine |
| Phaeochromocytoma crisis | Phentolamine (α-blocker) | Nitroprusside |
Aortic Dissection — Why BB First?
In aortic dissection, the priority is to reduce aortic wall shear stress. This requires lowering both BP AND dP/dt (rate of rise of aortic pressure). BB reduces HR and contractility → ↓ dP/dt. Always give BB BEFORE vasodilators like nitroprusside, because vasodilators alone can cause reflex tachycardia → ↑ shear stress → worsening dissection.
16. HTN in Special Populations
| Disorder | Definition | Key Features |
|---|---|---|
| Chronic HTN | HTN present before pregnancy or diagnosed before 20 weeks | Pre-existing; proteinuria absent initially |
| Gestational HTN | New HTN after 20 weeks WITHOUT proteinuria | Resolves within 12 weeks postpartum |
| Pre-eclampsia | New HTN after 20 weeks WITH proteinuria (≥ 300 mg/24h or PCR ≥ 30) or end-organ dysfunction | Can progress to eclampsia (seizures) |
| Superimposed pre-eclampsia | Pre-eclampsia features developing in a woman with chronic HTN |
Drugs safe in pregnancy: Labetalol, nifedipine (modified-release), methyldopa. [8]
Drugs CONTRAINDICATED in pregnancy: ACEI, ARBs (teratogenic — renal agenesis, oligohydramnios), atenolol (IUGR), diuretics (volume depletion). [8]
From 2020 MCQ Q10: A 40-year-old woman at 13 weeks gestation with BP 150/98, no proteinuria → Chronic hypertension (HTN present before 20 weeks). [9]
From 2023 MCQ Q13: A 20-year-old at 34 weeks with new BP 150/100 and proteinuria 3+ → Pre-eclampsia. [10]
From 2021 SAQ Q1: Pre-eclampsia with seizure → Eclampsia; treatment = IV MgSO₄. Antihypertensives in pregnancy: labetalol, nifedipine (and methyldopa). [11]
Target BP in CKD: < 120/80 (KDIGO 2021). [6]
- ACEI/ARB are preferred if albuminuria is present (renoprotective — dilate efferent arteriole → ↓ intraglomerular pressure → ↓ proteinuria progression)
- Monitor K⁺ and Cr after starting/uptitrating ACEI/ARB — accept up to 30% rise in Cr, but if > 30% or K⁺ > 5.5, consider bilateral RAS or hold drug
- Avoid combining ACEI + ARB
- Thiazides lose efficacy when eGFR < 30 → switch to loop diuretics
- Newer agents: SGLT2 inhibitors and finerenone (non-steroidal MRA) have renal and CV benefit in CKD + DM [6]
Coexistence of DM and HTN dramatically amplifies CVD risk (see "Bad Companions" slide). ACEI/ARBs are preferred first-line for their renoprotective effect. Address all risk factors: glycaemic control, lipids, antiplatelet therapy, smoking cessation. [1]
NNT for severe diastolic HTN (115–129): 3. NNT for mild-moderate diastolic HTN (90–109): 141. NNT for uncomplicated HTN age 36–64 to prevent stroke: 850. [1]
What this tells us: The sicker the patient, the greater the absolute benefit of treatment. Treating severe HTN is a no-brainer (NNT = 3!). In mild HTN without risk factors in young patients, lifestyle measures alone may suffice initially.
The ISH 2020 summary slides emphasise: [1]
- Confirm diagnosis with out-of-office BP
- Assess total CVD risk (RF + TOD + established CVD)
- Screen for secondary causes if indicated
- Start lifestyle measures in ALL
- Pharmacotherapy based on risk stratification and compelling indications
- Use combination therapy early (SPC preferred)
- Treat to target
- Lifelong follow-up and adherence monitoring
19. Likely Exam Questions
-
A 55-year-old man has attacks of headache, palpitations, and diaphoresis with very high BP during attacks. Most likely diagnosis? → Phaeochromocytoma (classic triad). [9]
-
Advantage of ABPM over HBPM? → Provides night-time readings. [5]
-
A 40-year-old at 13 weeks gestation with BP 150/98, no proteinuria. Diagnosis? → Chronic hypertension (before 20 weeks). [9]
-
Which drug is contraindicated in bilateral renal artery stenosis? → ACEI/ARB (loss of efferent arteriolar tone → ↓ GFR → AKI). [1]
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ACEI side effect that does NOT occur with ARBs? → Dry cough (bradykinin accumulation). [1]
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List 4 investigations for a newly diagnosed hypertensive patient and explain why. (See Section 7)
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List 5 features suggesting secondary HTN. (See Section 9)
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Name 3 antihypertensives safe in pregnancy. → Labetalol, nifedipine, methyldopa. [8][11]
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In hypertensive emergency with acute aortic dissection, what is the target SBP and first-line drug? → SBP < 110 mmHg; IV labetalol (or IV BB + nitroprusside). [1]
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What is the definition of resistant hypertension and what is the recommended add-on drug? → BP above goal despite ≥ 3 optimal-dose drugs including a diuretic; add spironolactone. [1]
- A 53-year-old woman on amlodipine for 10 years presents with ankle oedema, Cr 400, proteinuria 2+, BP 146/88. What investigations? → USS kidneys (size, obstruction, RAS), urine PCR/ACR, FBC (anaemia of CKD), calcium/phosphate/PTH (CKD-MBD), serum globulins (myeloma screen), HbA1c. [12]
| Trap | Correct Approach |
|---|---|
| Treating "white-coat HTN" with drugs | Confirm with HBPM/ABPM first; reassure and monitor |
| Combining ACEI + ARB for better BP control | NEVER for HTN (↑ AKI, ↑ hyperkalaemia, no benefit) |
| Dropping BP rapidly in acute stroke | CONTRAINDICATED (loss of autoregulation → infarction) |
| Using atenolol in pregnancy | Atenolol causes IUGR; use labetalol instead |
| Using ACEI/ARB in pregnancy | Absolutely contraindicated (teratogenic) |
| Forgetting to check for postural hypotension | Always in elderly, DM, those on α-blockers |
| Attributing ankle oedema on amlodipine to HF | DHP CCB oedema is due to arteriolar vasodilatation → capillary leak, NOT fluid overload |
| Starting thiazide in CKD with eGFR < 30 | Thiazides ineffective; switch to loop diuretic |
| Phaeochromocytoma — giving BB first without α-blockade | Must give α-blocker first (phenoxybenzamine/phentolamine), then BB; BB alone → unopposed α → hypertensive crisis |
High Yield Summary
Hypertension is defined as office BP ≥ 140/90 mmHg (HBPM ≥ 135/85). CV mortality doubles with each 20/10 mmHg rise above 115/75. Always confirm with out-of-office BP to exclude white-coat HTN. Evaluate every new hypertensive for: (1) secondary causes (ABCDE mnemonic), (2) target organ damage (heart, kidney, brain, eyes, arteries), (3) total CVD risk. Lifestyle measures (DASH diet, salt restriction, exercise, weight loss) are foundational. First-line drugs: ACEI/ARB, CCB, thiazide — choose based on compelling indications. Preferred combinations: ACEI/ARB + CCB or ACEI/ARB + diuretic. Never combine ACEI + ARB. For resistant HTN, add spironolactone. In hypertensive emergency, reduce MAP by 20–25% in the first hour (except in aortic dissection: target SBP < 110). In pregnancy, use labetalol/nifedipine/methyldopa; ACEI/ARBs are contraindicated. Treatment is for life — communication and adherence are key.
Active Recall - High Blood Pressure
[1] Lecture slides: GC 058. High Blood Pressure.pdf (all pages) [2] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.320 — HTN classification) [3] Senior notes: Block A - High blood pressure_ hypertension.pdf (p.1 — ISH, definitions) [4] Senior notes: Block A - Clinical Pharmacology of anti-HT and anti-HF medications.pdf (p.1 — BP = CO × TPR formula) [5] Past papers: 2022 Fourth Summative MCQ.pdf (Q33 — ABPM advantage: night-time readings) [6] Senior notes: Block A - Chronic Kidney Disease and its Complications.pdf (p.18 — CKD BP target, drug considerations) [7] Senior notes: Ryan Ho Neurology.pdf (p.154 — cerebral autoregulation curve and HTN) [8] Lecture slides: GC 224. Hypertension and Pregnancy.pdf; GC 115. I am pregnant medical problems complicating pregnancy.pdf [9] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q10 — chronic HTN in pregnancy; Q42 — phaeochromocytoma) [10] Past papers: 2023 Fourth Summative MCQ.pdf (Q13 — pre-eclampsia) [11] Past papers: 2021 Fourth Summative SAQ.pdf (Q1 — pre-eclampsia, eclampsia, antihypertensives in pregnancy) [12] Past papers: 2019 Fourth Summative SAQ.pdf (Q3 — HTN + CKD investigations)
GC057 Glomerular And Tubulo-interstitial Diseases And Acute Kidney Injury
Glomerular and tubulo-interstitial diseases encompass inflammatory, immune-mediated, or toxic disorders affecting the glomeruli or renal interstitium and tubules, which, along with acute kidney injury, result in a rapid or progressive decline in kidney filtration, concentration, and excretory functions.
GC059 High Fever Low BP
A clinical scenario of high fever accompanied by low blood pressure, typically indicative of sepsis or septic shock resulting from a systemic inflammatory response to infection.