I have all the data I need to construct a comprehensive, high-yield HKMLE cardiovascular pharmacology guide. Let me now compose the full notes.
High-Yield HKMLE: Cardiovascular Pharmacology Notes
HKMLE Paper Mapping (standard HKMLE/MCHK structure):
- Paper I - Medicine (60 MCQs): Hypertension, Heart Failure, ACS, Arrhythmias, Lipids, Anticoagulation
- Paper II - Surgery/Emergency (45 MCQs): Perioperative cardiac drugs, Shock, Acute MI management
- Paper III - Paediatrics/OG (30 MCQs): Cardiac drugs in pregnancy, Neonatal cardiac conditions
Most cardiovascular pharmacology questions appear in Paper I Medicine.
1. ACE INHIBITORS (-prils)
Mnemonic: "PRILS PRODUCE POTASSIUM, PROVOKE COUGH"
| Feature | Detail |
|---|
| Mechanism | Block ACE → ↓ angiotensin II → vasodilation + ↓ aldosterone; also prevent bradykinin breakdown (→ cough) |
| Key Indications | Hypertension, Heart Failure (HFrEF), Post-MI, Diabetic nephropathy, Proteinuria |
| Major Side Effects | Dry cough (most common), Hyperkalaemia, Angioedema (rare but dangerous), First-dose hypotension, Teratogenicity |
| Contraindications | Pregnancy (teratogen), Bilateral renal artery stenosis, Hyperkalaemia, Prior angioedema |
| HKMLE Tip | Cough → switch to ARB. Angioedema is ACE inhibitor only (ARBs rarely cause it). Renal artery stenosis causes acute kidney injury. |
Key drugs: Enalapril, Ramipril, Lisinopril, Captopril (also used in hypertensive crisis)
2. ANGIOTENSIN RECEPTOR BLOCKERS (ARBs, -sartans)
Mnemonic: "SARTANS SPARE THE COUGH"
| Feature | Detail |
|---|
| Mechanism | Block AT1 receptor → same hemodynamic effect as ACEi, but NO bradykinin effect |
| Key Indications | ACEi-intolerant patients (esp. cough), Hypertension, HFrEF, Diabetic nephropathy |
| Major Side Effects | Hyperkalaemia, Hypotension, Renal impairment - but NO cough, NO angioedema |
| Contraindications | Pregnancy, Bilateral renal artery stenosis, Hyperkalaemia |
| HKMLE Tip | Do NOT combine ACEi + ARB (↑ renal failure risk, no mortality benefit). |
Key drugs: Losartan, Valsartan, Candesartan, Irbesartan
3. BETA-BLOCKERS (-olols)
Mnemonic: "BASH" = Bradycardia, Asthma (contraindicated), Sexual dysfunction, HF (use cautiously)
| Feature | Detail |
|---|
| Mechanism | β1-blockade → ↓ HR, ↓ contractility, ↓ renin; β2-blockade (non-selective) → bronchoconstriction |
| Key Indications | HFrEF (reduce mortality), Post-MI, Angina, Hypertension, AF rate control, SVT, Hyperthyroidism |
| Major Side Effects | Bradycardia, Heart block, Hypotension, Bronchoconstriction (non-selective), Fatigue, Masking hypoglycaemia in diabetics, Erectile dysfunction |
| Contraindications | Asthma/COPD (relative), Cardiogenic shock, Severe bradycardia, 2nd/3rd degree heart block, Decompensated HF (initiate only when stable) |
| HKMLE Tip | Cardioselective (β1 only): metoprolol, atenolol, bisoprolol - safer in COPD. Non-selective: propranolol (also used in portal HTN, migraine prophylaxis, essential tremor). |
Key drugs for HKMLE: Bisoprolol/Carvedilol (HF), Metoprolol (ACS/AF), Esmolol (IV, acute SVT), Propranolol (portal HTN, thyroid storm)
4. CALCIUM CHANNEL BLOCKERS (CCBs)
Mnemonic: Two types: "DHP = Dilate Peripheral vessels" vs "Non-DHP = Node-slowing"
| Class | Drugs | Main Action | Key Use |
|---|
| Dihydropyridines (DHP) | Amlodipine, Nifedipine, Felodipine | Peripheral vasodilation (vascular selectivity) | Hypertension, Angina |
| Non-DHP | Verapamil, Diltiazem | AV node slowing + vasodilation | AF rate control, SVT, Angina |
| Feature | DHP | Non-DHP |
|---|
| Side Effects | Peripheral oedema, Flushing, Reflex tachycardia | Bradycardia, Constipation (verapamil!), Heart block |
| Contraindications | Unstable angina (short-acting nifedipine) | Avoid with β-blockers (complete heart block risk), HFrEF |
HKMLE Pearl: Verapamil + β-blocker = complete heart block. Amlodipine is safest CCB in HFrEF (for HTN).
5. DIURETICS
5a. Loop Diuretics
Mnemonic: "FUROSEMIDE FLUSHES EVERYTHING" (K, Na, Mg, Ca)
| Feature | Detail |
|---|
| Mechanism | Block Na-K-2Cl cotransporter in thick ascending limb of Loop of Henle |
| Key Indications | Acute pulmonary oedema, Decompensated HF, Oedema (cirrhosis, nephrotic syndrome), Hypercalcaemia |
| Major Side Effects | Hypokalaemia, Hyponatraemia, Hypomagnesaemia, Metabolic alkalosis, Ototoxicity (high doses), Hyperuricaemia (gout) |
| Contraindications | Anuria, Allergy to sulfonamides (relative) |
Key drugs: Furosemide (most common), Bumetanide
5b. Thiazide Diuretics
Mnemonic: "THIAZIDES TAKE AWAY K, Mg, Na - but KEEP calcium"
| Feature | Detail |
|---|
| Mechanism | Block Na-Cl cotransporter in distal convoluted tubule |
| Key Indications | Hypertension (first-line), Mild HF, Nephrolithiasis (Ca stones - reduces urinary Ca!), Nephrogenic DI |
| Major Side Effects | Hypokalaemia, Hyperuricaemia (gout), Hyperglycaemia, Hyperlipidaemia, Hypercalcaemia (unlike loop), Sexual dysfunction |
| Contraindications | Gout (relative), Severe renal impairment (eGFR <30), Hyponatraemia |
Key drugs: Hydrochlorothiazide, Indapamide, Chlorthalidone
5c. Potassium-Sparing Diuretics
| Drug | Mechanism | Key Use | Side Effect |
|---|
| Spironolactone | Aldosterone antagonist | HFrEF (reduces mortality), Secondary hyperaldosteronism, Ascites | Gynaecomastia, Hyperkalaemia |
| Eplerenone | Aldosterone antagonist (selective) | Post-MI HF (fewer androgen effects) | Hyperkalaemia |
| Amiloride | ENaC blocker | K-sparing adjunct | Hyperkalaemia |
HKMLE Pearl: Spironolactone KILLS in HF (mortality benefit - RALES trial). Gynaecomastia = switch to eplerenone.
6. NITRATES
Mnemonic: "NITRATES = NO→ cGMP → relax smooth muscle"
| Feature | Detail |
|---|
| Mechanism | Release NO → ↑ cGMP → venodilation (↓ preload) and at high doses arterial dilation (↓ afterload) |
| Key Indications | Angina (acute and prophylaxis), Acute HF (↓ preload), Hypertensive emergency with pulmonary oedema |
| Major Side Effects | Headache (most common), Hypotension, Reflex tachycardia, Tolerance (with continuous use) |
| Contraindications | Concurrent PDE-5 inhibitors (sildenafil) - severe hypotension, Hypertrophic obstructive cardiomyopathy (HOCM), Severe aortic stenosis, Right ventricular infarction |
HKMLE Pearl: GTN + Sildenafil = potentially fatal hypotension. Nitrate tolerance - avoid with 8-12 hour nitrate-free period.
7. ANTIARRHYTHMIC DRUGS (Vaughan-Williams Classification)
Mnemonic: "1 Na, 2 Beta, 3 K (prolong), 4 Ca"
Quick Reference Table
| Class | Mechanism | Key Drugs | Key Indications | Major Side Effects |
|---|
| IA | Na+ block (slows phase 0, prolongs repolarisation) | Quinidine, Procainamide, Disopyramide | AF, VT | QT prolongation, Torsades de pointes, Quinidine → cinchonism, Procainamide → drug-induced lupus |
| IB | Na+ block (shortens phase 3, ischaemic tissue only) | Lidocaine, Mexiletine | Ventricular arrhythmias (post-MI) | CNS: nystagmus, seizures, confusion |
| IC | Na+ block (markedly slows phase 0) | Flecainide, Propafenone | AF/flutter (no structural heart disease), SVT | Proarrhythmic, contraindicated in structural heart disease |
| II | β-blockade (slows phase 4) | Metoprolol, Esmolol, Atenolol | AF rate control, SVT, post-MI VT prevention | Bradycardia, Bronchospasm, Heart block |
| III | K+ block (prolongs phase 3, ↑ refractory period) | Amiodarone, Sotalol, Dronedarone | AF/flutter, VT/VF | See amiodarone table below |
| IV | Ca2+ block (AV node) | Verapamil, Diltiazem | SVT, AF rate control | Bradycardia, Heart block, Constipation |
| Others | - | Adenosine, Digoxin, Magnesium | See below | - |
AMIODARONE (Most Tested Antiarrhythmic!)
Mnemonic: "AMIODARONE Affects ALL Organs" (multi-class: I/II/III/IV properties)
| Feature | Detail |
|---|
| Mechanism | Primarily K+ channel blocker (Class III); also blocks Na+, Ca2+ channels, and β-receptors |
| Key Indications | AF (rhythm control), Refractory VT/VF, WPW syndrome with AF |
| Major Side Effects (high-yield!) | Pulmonary toxicity (most serious, check CXR + PFTs), Thyroid dysfunction (both hypo- and hyperthyroidism - contains iodine), Corneal microdeposits (blurred vision), Photosensitivity (slate-grey skin), Hepatotoxicity, Peripheral neuropathy |
| Monitoring | TFT, LFT, CXR, PFTs every 6-12 months |
| Contraindications | Pregnancy, Bradycardia/AV block, Thyroid disease (relative) |
| Drug Interactions | Potentiates warfarin (↑ INR), Digoxin toxicity |
ADENOSINE
| Feature | Detail |
|---|
| Mechanism | Activates A1 receptors → hyperpolarises AV node → transiently blocks AV conduction |
| Key Indications | First-line for acute SVT termination, Diagnostic tool to unmask atrial flutter |
| Side Effects | Chest tightness, Flushing, Transient bronchospasm, Brief asystole (seconds) |
| Contraindications | Asthma (use verapamil instead), WPW + AF (risk of VF), 2nd/3rd degree AV block |
| HKMLE Tip | Half-life ~10 seconds. Give as rapid IV bolus in large vein. Caffeine/theophylline antagonise it (block A1 receptors). |
DIGOXIN
| Feature | Detail |
|---|
| Mechanism | Inhibits Na+/K+ ATPase → ↑ intracellular Ca2+ (positive inotropy); also ↑ vagal tone → slows AV node |
| Key Indications | AF rate control (especially HF + AF), Symptomatic HFrEF (added to ACEi + β-blocker) |
| Major Side Effects | Digoxin toxicity: nausea/vomiting, yellow-green vision, arrhythmias (any arrhythmia!), bradycardia, heart block |
| Toxicity precipitants | Hypokalaemia (most important!), Hypomagnesaemia, Renal failure, Hypothyroidism, Amiodarone (↑ digoxin levels) |
| Contraindications | Hypertrophic obstructive cardiomyopathy (HOCM), WPW + AF, AV block |
HKMLE Pearl: Any arrhythmia in a patient on digoxin = consider digoxin toxicity. Hypokalaemia (from diuretics) precipitates toxicity. Treatment = correct K+, digoxin-specific antibody fragments (Digifab) for severe cases.
8. STATINS (HMG-CoA Reductase Inhibitors)
Mnemonic: "-statin" drugs = "STAT lower cholesterol"
| Feature | Detail |
|---|
| Mechanism | Block HMG-CoA reductase → ↓ hepatic cholesterol synthesis → ↑ LDL receptors → ↓ LDL |
| Key Indications | Primary/secondary prevention of CVD, Hypercholesterolaemia, Post-MI (regardless of baseline LDL) |
| Major Side Effects | Myopathy/Myalgia (check CK), Rhabdomyolysis (rare but serious), Hepatotoxicity (raised ALT), GI upset |
| Contraindications | Pregnancy, Active liver disease, Concurrent use of drugs ↑ statin levels (e.g. gemfibrozil with simvastatin → rhabdomyolysis) |
| HKMLE Tip | Rosuvastatin/Atorvastatin = highest potency. Simvastatin + gemfibrozil = avoid (rhabdomyolysis). Check LFTs and CK. |
9. ANTIPLATELET DRUGS
| Drug | Mechanism | Indication | Key Side Effects |
|---|
| Aspirin | Irreversibly blocks COX-1 → ↓ TXA2 → ↓ platelet aggregation | ACS, Post-MI, Stroke prevention, PCI | GI bleeding, Peptic ulcer, Aspirin-exacerbated asthma (Samter's triad) |
| Clopidogrel | Irreversibly blocks P2Y12 ADP receptor | ACS, PCI (dual antiplatelet with aspirin = DAPT), Peripheral arterial disease | Bleeding, TTP (rare) |
| Ticagrelor | Reversibly blocks P2Y12 | ACS (preferred over clopidogrel in NSTEMI/STEMI) | Dyspnoea (unique!), Bleeding, Bradycardia |
| Prasugrel | Irreversibly blocks P2Y12 | ACS undergoing PCI | Higher bleeding risk; avoid in stroke/TIA, age >75, weight <60 kg |
HKMLE Pearl: Dual antiplatelet therapy (DAPT) = aspirin + P2Y12 inhibitor for 12 months post-ACS/PCI. Ticagrelor causes dyspnoea without bronchospasm (do not confuse with asthma).
10. ANTICOAGULANTS
| Drug | Mechanism | Key Indication | Reversal Agent |
|---|
| Warfarin | Vitamin K antagonist (inhibits II, VII, IX, X, Protein C/S) | AF (stroke prevention), DVT/PE, Mechanical heart valves | Vitamin K (slow), FFP/PCC (urgent) |
| Heparin (UFH) | Activates antithrombin III → inactivates IIa (thrombin) + Xa | Acute DVT/PE, ACS bridging, Pregnancy (safe) | Protamine sulfate |
| LMWH (enoxaparin) | Activates antithrombin III → mainly anti-Xa | DVT prophylaxis/treatment, ACS, Pregnancy | Protamine (partial) |
| DOACs | Rivaroxaban/Apixaban = anti-Xa; Dabigatran = anti-IIa (thrombin) | AF (non-valvular), DVT/PE | Idarucizumab (dabigatran); Andexanet alfa (Xa inhibitors) |
HKMLE Pearls:
- Warfarin interactions: Warfarin potentiated by amiodarone, metronidazole, fluconazole. Reduced by rifampicin, carbamazepine.
- Heparin-induced thrombocytopaenia (HIT): Stop heparin, switch to argatroban/lepirudin/fondaparinux. Never give platelets (paradoxically thrombogenic).
- DOACs not used with mechanical heart valves (warfarin required).
11. ACUTE CORONARY SYNDROME (ACS) - Drug Management Summary
Mnemonic: "MONA BASH" (acute) + "ABCDE" (post-MI)
Acute management MONA:
- M - Morphine (pain relief; note: may ↑ mortality in NSTEMI - use cautiously)
- O - Oxygen (only if SpO2 <94%)
- N - Nitrates (sublingual GTN - pain relief, preload reduction)
- A - Aspirin 300mg loading dose
Post-MI secondary prevention ABCDE:
- A - Aspirin + P2Y12 inhibitor (DAPT)
- B - Beta-blocker
- C - Cholesterol (statin)
- D - DAPT continued + ACEI/ARB
- E - Exercise/Eplerenone (if HF post-MI)
12. HEART FAILURE - Drug Summary Table
| Drug Class | Mortality Benefit? | Key Indication |
|---|
| ACEi/ARB | YES (reduce mortality) | All HFrEF (EF <40%) |
| Beta-blocker (bisoprolol, carvedilol, metoprolol) | YES | HFrEF (start when stable) |
| Spironolactone/Eplerenone | YES | HFrEF + symptomatic despite ACEi + BB |
| Sacubitril/Valsartan (ARNI) | YES | Replace ACEi in HFrEF if still symptomatic |
| Furosemide | Symptom relief only | Fluid overload/decompensation |
| Digoxin | Symptom benefit only | AF + HF, refractory HFrEF |
| SGLT2 inhibitors (dapagliflozin) | YES (new evidence) | HFrEF and HFpEF |
| Ivabradine | Reduces hospitalisation | HFrEF + HR >70, sinus rhythm, on max BB dose |
HKMLE Pearl: "Triple therapy" in HF = ACEi + BB + Aldosterone antagonist. Now SGLT2 inhibitors form "fantastic four." Furosemide controls symptoms but does NOT reduce mortality.
13. VASODILATORS / OTHERS
| Drug | Mechanism | Key Use | Side Effect |
|---|
| Hydralazine | Direct arteriolar vasodilator | HF in pregnancy (safe), Hypertensive crisis in pregnancy (eclampsia) | Drug-induced lupus (like procainamide), Reflex tachycardia, Headache |
| Sodium nitroprusside | Releases NO → ↓ preload + afterload | Hypertensive emergency (IV only), Aortic dissection | Cyanide toxicity (thiocyanate) in prolonged use |
| Ivabradine | Blocks funny current (If) in SA node → ↓ HR only (no inotropy change) | HFrEF (HR >70 on max BB), Stable angina | Bradycardia, Phosphenes (visual flashes) |
HKMLE Paper Distribution Summary
| Topic | Most Likely Paper | MCQ Type |
|---|
| Antihypertensive drug selection | Paper I Medicine | Single best answer (patient scenario) |
| Antiarrhythmic drugs + Vaughan-Williams | Paper I Medicine | Drug identification by mechanism/side effect |
| Heart failure drug management | Paper I Medicine | Management sequence question |
| Digoxin toxicity | Paper I Medicine | Toxicity/ECG scenario |
| Anticoagulant reversal (HIT, warfarin overdose) | Paper I Medicine | Emergency management |
| Statins + rhabdomyolysis | Paper I Medicine | Drug interaction scenario |
| ACS management (STEMI/NSTEMI) | Paper I/Paper II | Protocol/drug sequence |
| Pregnancy - safe/unsafe cardiac drugs | Paper III OG | Contraindication scenario |
| Perioperative beta-blocker/anticoagulation | Paper II Surgery | Perioperative management |
QUICK MNEMONICS CHEAT SHEET
| Topic | Mnemonic |
|---|
| ACEi side effects | CAPTOPRIL = Cough, Angioedema, Potassium ↑, Teratogenic, low bP, Renal failure, Increased renin, Liver problems |
| Drugs causing drug-induced lupus | SHIPS = Sulfonamides, Hydralazine, Isoniazid, Procainamide, Statins (rare) |
| Amiodarone toxicities | THYROID LUNGS LIVER EYES SKIN (TFT, PFTs, LFTs, corneal deposits, photodermatitis) |
| Digoxin toxicity precipitants | DIAL = Diuretics (hypokalaemia), Impaired renal function, Amiodarone, Low Mg |
| Post-MI drugs | ABCDE as above |
| Contraindications to beta-blockers | ABCDE = Asthma, Bradycardia, Cardiogenic shock, Diabetes (relative), Elavated K (hyperK is the effect, not CI) |
Sources: Lippincott Illustrated Reviews Pharmacology; Goodman & Gilman's Pharmacological Basis of Therapeutics; Braunwald's Heart Disease; Harrison's Principles of Internal Medicine 22E (2025).