Give me high-yield HKMLE notes on [cardiovascular] with mnemonics, in an easy-to-read format. Include only what is necessary for HKMLE. Do not add extra details unless they are clinically important for the exam. For each drug or drug class, tell me: 1. Mechanism (simple) 2. Key indications (HKMLE-relevant) 3. Major side effects (exam-tested) 4. Contraindications (if any) 5. Where this topic appears in HKMLE (e.g., Paper I Medicine 60 MCQs, Paper II Surgery 45 MCQs, etc.) Use tables where helpful. Keep it short. No long paragraphs.

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HKMLE exam cardiovascular pharmacology high yield topics Paper I Paper II

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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"
FeatureDetail
MechanismBlock ACE → ↓ angiotensin II → vasodilation + ↓ aldosterone; also prevent bradykinin breakdown (→ cough)
Key IndicationsHypertension, Heart Failure (HFrEF), Post-MI, Diabetic nephropathy, Proteinuria
Major Side EffectsDry cough (most common), Hyperkalaemia, Angioedema (rare but dangerous), First-dose hypotension, Teratogenicity
ContraindicationsPregnancy (teratogen), Bilateral renal artery stenosis, Hyperkalaemia, Prior angioedema
HKMLE TipCough → 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"
FeatureDetail
MechanismBlock AT1 receptor → same hemodynamic effect as ACEi, but NO bradykinin effect
Key IndicationsACEi-intolerant patients (esp. cough), Hypertension, HFrEF, Diabetic nephropathy
Major Side EffectsHyperkalaemia, Hypotension, Renal impairment - but NO cough, NO angioedema
ContraindicationsPregnancy, Bilateral renal artery stenosis, Hyperkalaemia
HKMLE TipDo 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)
FeatureDetail
Mechanismβ1-blockade → ↓ HR, ↓ contractility, ↓ renin; β2-blockade (non-selective) → bronchoconstriction
Key IndicationsHFrEF (reduce mortality), Post-MI, Angina, Hypertension, AF rate control, SVT, Hyperthyroidism
Major Side EffectsBradycardia, Heart block, Hypotension, Bronchoconstriction (non-selective), Fatigue, Masking hypoglycaemia in diabetics, Erectile dysfunction
ContraindicationsAsthma/COPD (relative), Cardiogenic shock, Severe bradycardia, 2nd/3rd degree heart block, Decompensated HF (initiate only when stable)
HKMLE TipCardioselective (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"
ClassDrugsMain ActionKey Use
Dihydropyridines (DHP)Amlodipine, Nifedipine, FelodipinePeripheral vasodilation (vascular selectivity)Hypertension, Angina
Non-DHPVerapamil, DiltiazemAV node slowing + vasodilationAF rate control, SVT, Angina
FeatureDHPNon-DHP
Side EffectsPeripheral oedema, Flushing, Reflex tachycardiaBradycardia, Constipation (verapamil!), Heart block
ContraindicationsUnstable 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)
FeatureDetail
MechanismBlock Na-K-2Cl cotransporter in thick ascending limb of Loop of Henle
Key IndicationsAcute pulmonary oedema, Decompensated HF, Oedema (cirrhosis, nephrotic syndrome), Hypercalcaemia
Major Side EffectsHypokalaemia, Hyponatraemia, Hypomagnesaemia, Metabolic alkalosis, Ototoxicity (high doses), Hyperuricaemia (gout)
ContraindicationsAnuria, Allergy to sulfonamides (relative)
Key drugs: Furosemide (most common), Bumetanide

5b. Thiazide Diuretics

Mnemonic: "THIAZIDES TAKE AWAY K, Mg, Na - but KEEP calcium"
FeatureDetail
MechanismBlock Na-Cl cotransporter in distal convoluted tubule
Key IndicationsHypertension (first-line), Mild HF, Nephrolithiasis (Ca stones - reduces urinary Ca!), Nephrogenic DI
Major Side EffectsHypokalaemia, Hyperuricaemia (gout), Hyperglycaemia, Hyperlipidaemia, Hypercalcaemia (unlike loop), Sexual dysfunction
ContraindicationsGout (relative), Severe renal impairment (eGFR <30), Hyponatraemia
Key drugs: Hydrochlorothiazide, Indapamide, Chlorthalidone

5c. Potassium-Sparing Diuretics

DrugMechanismKey UseSide Effect
SpironolactoneAldosterone antagonistHFrEF (reduces mortality), Secondary hyperaldosteronism, AscitesGynaecomastia, Hyperkalaemia
EplerenoneAldosterone antagonist (selective)Post-MI HF (fewer androgen effects)Hyperkalaemia
AmilorideENaC blockerK-sparing adjunctHyperkalaemia
HKMLE Pearl: Spironolactone KILLS in HF (mortality benefit - RALES trial). Gynaecomastia = switch to eplerenone.

6. NITRATES

Mnemonic: "NITRATES = NO→ cGMP → relax smooth muscle"
FeatureDetail
MechanismRelease NO → ↑ cGMP → venodilation (↓ preload) and at high doses arterial dilation (↓ afterload)
Key IndicationsAngina (acute and prophylaxis), Acute HF (↓ preload), Hypertensive emergency with pulmonary oedema
Major Side EffectsHeadache (most common), Hypotension, Reflex tachycardia, Tolerance (with continuous use)
ContraindicationsConcurrent 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

ClassMechanismKey DrugsKey IndicationsMajor Side Effects
IANa+ block (slows phase 0, prolongs repolarisation)Quinidine, Procainamide, DisopyramideAF, VTQT prolongation, Torsades de pointes, Quinidine → cinchonism, Procainamide → drug-induced lupus
IBNa+ block (shortens phase 3, ischaemic tissue only)Lidocaine, MexiletineVentricular arrhythmias (post-MI)CNS: nystagmus, seizures, confusion
ICNa+ block (markedly slows phase 0)Flecainide, PropafenoneAF/flutter (no structural heart disease), SVTProarrhythmic, contraindicated in structural heart disease
IIβ-blockade (slows phase 4)Metoprolol, Esmolol, AtenololAF rate control, SVT, post-MI VT preventionBradycardia, Bronchospasm, Heart block
IIIK+ block (prolongs phase 3, ↑ refractory period)Amiodarone, Sotalol, DronedaroneAF/flutter, VT/VFSee amiodarone table below
IVCa2+ block (AV node)Verapamil, DiltiazemSVT, AF rate controlBradycardia, Heart block, Constipation
Others-Adenosine, Digoxin, MagnesiumSee below-

AMIODARONE (Most Tested Antiarrhythmic!)

Mnemonic: "AMIODARONE Affects ALL Organs" (multi-class: I/II/III/IV properties)
FeatureDetail
MechanismPrimarily K+ channel blocker (Class III); also blocks Na+, Ca2+ channels, and β-receptors
Key IndicationsAF (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
MonitoringTFT, LFT, CXR, PFTs every 6-12 months
ContraindicationsPregnancy, Bradycardia/AV block, Thyroid disease (relative)
Drug InteractionsPotentiates warfarin (↑ INR), Digoxin toxicity

ADENOSINE

FeatureDetail
MechanismActivates A1 receptors → hyperpolarises AV node → transiently blocks AV conduction
Key IndicationsFirst-line for acute SVT termination, Diagnostic tool to unmask atrial flutter
Side EffectsChest tightness, Flushing, Transient bronchospasm, Brief asystole (seconds)
ContraindicationsAsthma (use verapamil instead), WPW + AF (risk of VF), 2nd/3rd degree AV block
HKMLE TipHalf-life ~10 seconds. Give as rapid IV bolus in large vein. Caffeine/theophylline antagonise it (block A1 receptors).

DIGOXIN

FeatureDetail
MechanismInhibits Na+/K+ ATPase → ↑ intracellular Ca2+ (positive inotropy); also ↑ vagal tone → slows AV node
Key IndicationsAF rate control (especially HF + AF), Symptomatic HFrEF (added to ACEi + β-blocker)
Major Side EffectsDigoxin toxicity: nausea/vomiting, yellow-green vision, arrhythmias (any arrhythmia!), bradycardia, heart block
Toxicity precipitantsHypokalaemia (most important!), Hypomagnesaemia, Renal failure, Hypothyroidism, Amiodarone (↑ digoxin levels)
ContraindicationsHypertrophic 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"
FeatureDetail
MechanismBlock HMG-CoA reductase → ↓ hepatic cholesterol synthesis → ↑ LDL receptors → ↓ LDL
Key IndicationsPrimary/secondary prevention of CVD, Hypercholesterolaemia, Post-MI (regardless of baseline LDL)
Major Side EffectsMyopathy/Myalgia (check CK), Rhabdomyolysis (rare but serious), Hepatotoxicity (raised ALT), GI upset
ContraindicationsPregnancy, Active liver disease, Concurrent use of drugs ↑ statin levels (e.g. gemfibrozil with simvastatin → rhabdomyolysis)
HKMLE TipRosuvastatin/Atorvastatin = highest potency. Simvastatin + gemfibrozil = avoid (rhabdomyolysis). Check LFTs and CK.

9. ANTIPLATELET DRUGS

DrugMechanismIndicationKey Side Effects
AspirinIrreversibly blocks COX-1 → ↓ TXA2 → ↓ platelet aggregationACS, Post-MI, Stroke prevention, PCIGI bleeding, Peptic ulcer, Aspirin-exacerbated asthma (Samter's triad)
ClopidogrelIrreversibly blocks P2Y12 ADP receptorACS, PCI (dual antiplatelet with aspirin = DAPT), Peripheral arterial diseaseBleeding, TTP (rare)
TicagrelorReversibly blocks P2Y12ACS (preferred over clopidogrel in NSTEMI/STEMI)Dyspnoea (unique!), Bleeding, Bradycardia
PrasugrelIrreversibly blocks P2Y12ACS undergoing PCIHigher 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

DrugMechanismKey IndicationReversal Agent
WarfarinVitamin K antagonist (inhibits II, VII, IX, X, Protein C/S)AF (stroke prevention), DVT/PE, Mechanical heart valvesVitamin K (slow), FFP/PCC (urgent)
Heparin (UFH)Activates antithrombin III → inactivates IIa (thrombin) + XaAcute DVT/PE, ACS bridging, Pregnancy (safe)Protamine sulfate
LMWH (enoxaparin)Activates antithrombin III → mainly anti-XaDVT prophylaxis/treatment, ACS, PregnancyProtamine (partial)
DOACsRivaroxaban/Apixaban = anti-Xa; Dabigatran = anti-IIa (thrombin)AF (non-valvular), DVT/PEIdarucizumab (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 ClassMortality Benefit?Key Indication
ACEi/ARBYES (reduce mortality)All HFrEF (EF <40%)
Beta-blocker (bisoprolol, carvedilol, metoprolol)YESHFrEF (start when stable)
Spironolactone/EplerenoneYESHFrEF + symptomatic despite ACEi + BB
Sacubitril/Valsartan (ARNI)YESReplace ACEi in HFrEF if still symptomatic
FurosemideSymptom relief onlyFluid overload/decompensation
DigoxinSymptom benefit onlyAF + HF, refractory HFrEF
SGLT2 inhibitors (dapagliflozin)YES (new evidence)HFrEF and HFpEF
IvabradineReduces hospitalisationHFrEF + 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

DrugMechanismKey UseSide Effect
HydralazineDirect arteriolar vasodilatorHF in pregnancy (safe), Hypertensive crisis in pregnancy (eclampsia)Drug-induced lupus (like procainamide), Reflex tachycardia, Headache
Sodium nitroprussideReleases NO → ↓ preload + afterloadHypertensive emergency (IV only), Aortic dissectionCyanide toxicity (thiocyanate) in prolonged use
IvabradineBlocks funny current (If) in SA node → ↓ HR only (no inotropy change)HFrEF (HR >70 on max BB), Stable anginaBradycardia, Phosphenes (visual flashes)

HKMLE Paper Distribution Summary

TopicMost Likely PaperMCQ Type
Antihypertensive drug selectionPaper I MedicineSingle best answer (patient scenario)
Antiarrhythmic drugs + Vaughan-WilliamsPaper I MedicineDrug identification by mechanism/side effect
Heart failure drug managementPaper I MedicineManagement sequence question
Digoxin toxicityPaper I MedicineToxicity/ECG scenario
Anticoagulant reversal (HIT, warfarin overdose)Paper I MedicineEmergency management
Statins + rhabdomyolysisPaper I MedicineDrug interaction scenario
ACS management (STEMI/NSTEMI)Paper I/Paper IIProtocol/drug sequence
Pregnancy - safe/unsafe cardiac drugsPaper III OGContraindication scenario
Perioperative beta-blocker/anticoagulationPaper II SurgeryPerioperative management

QUICK MNEMONICS CHEAT SHEET

TopicMnemonic
ACEi side effectsCAPTOPRIL = Cough, Angioedema, Potassium ↑, Teratogenic, low bP, Renal failure, Increased renin, Liver problems
Drugs causing drug-induced lupusSHIPS = Sulfonamides, Hydralazine, Isoniazid, Procainamide, Statins (rare)
Amiodarone toxicitiesTHYROID LUNGS LIVER EYES SKIN (TFT, PFTs, LFTs, corneal deposits, photodermatitis)
Digoxin toxicity precipitantsDIAL = Diuretics (hypokalaemia), Impaired renal function, Amiodarone, Low Mg
Post-MI drugsABCDE as above
Contraindications to beta-blockersABCDE = 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).
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