Cardiovascular
Hypertension
Focus | Summary |
Goal of Therapy | Reduce blood pressure and cardiovascular risk; prevent complications (e.g. MI, stroke, HF). Manage underlying conditions (lipids, rhythm, clot risk). |
Main Drug Classes (Hypertension & HF) | 1. ACE Inhibitors (-pril) 2. ARBs (-sartan) 3. Calcium Channel Blockers (-dipine) 4. Thiazide Diuretics (-thiazide) |
Mechanisms of Action | - ACEI: Inhibit conversion of angiotensin I → II → ↓ vasoconstriction & aldosterone. - ARBs: Block angiotensin II receptor (AT₁). - CCBs: Block calcium influx in vascular smooth muscle → vasodilation. - Thiazides: Inhibit Na⁺/Cl⁻ reabsorption in distal tubule → mild diuresis & ↓ BP. |
Key Indications | - HTN (first-line): ACEI/ARB, CCB, Thiazide. - HF: ACEI/ARB improve survival; diuretics relieve fluid overload. - Post-MI / Diabetes: ACEI/ARB for renal & cardiac protection. |
Contraindications / Cautions | - ACEI/ARB: Pregnancy, history of angioedema, renal artery stenosis - CCB: Heart block, caution in HF (non-DHP types like verapamil). - Thiazides: Gout (↑ uric acid), hyponatraemia, dehydration. |
Comparative Advantages | - ACEI/ARB: Renal & cardiac protection, ↓ mortality in HF. - CCB: Effective in elderly & African descent, minimal metabolic effects. - Thiazide: Cheap, long-acting, synergistic with ACEI/ARB. |
Common ADRs | - ACEI: Dry cough, hyperkalaemia, hypotension. - ARB: Hyperkalaemia (no cough). - CCB: Ankle oedema, flushing, headache .- Thiazide: ↓ K⁺, ↑ uric acid & glucose. |
Counselling Points | - Rise slowly from sitting (postural hypotension). - Report persistent cough (ACEI). - Avoid potassium supplements with ACEI/ARB. - Monitor electrolytes and renal function. |
High-Yield Suffixes | -pril = ACEI -sartan = ARB -dipine = CCB -thiazide = Thiazide diuretic |
Arrythmia
Focus | Summary |
Goal of Therapy | Control ventricular rate and prevent symptoms or complications (e.g. palpitations, heart failure) in atrial fibrillation. |
1st Line Drug Classes | 1. Beta Blockers (-olol) 2. Non-dihydropyridine CCBs (Verapamil, Diltiazem) |
Mechanism of Action | - Beta Blockers: Block β₁ receptors → ↓ heart rate & contractility. - Non-DHP CCBs: Block calcium influx in cardiac tissue → slow AV node conduction & ↓ HR. |
Indications / Use | - 1st line: Rate control in atrial fibrillation or flutter. - If LVEF ≤ 40% (heart failure): Use HF-specific beta blocker (e.g. bisoprolol, carvedilol).- Avoid verapamil/diltiazem if LVEF ≤ 40%. |
2nd Line Drugs | - Digoxin: Slows AV node conduction via vagal stimulation; for sedentary or heart failure patients when 1st line inadequate. - Amiodarone: Broad antiarrhythmic; used only if others fail due to long-term toxicity (thyroid, liver, lung). |
Contraindications / Cautions | - Beta Blockers: Asthma, severe bradycardia, heart block. - Non-DHP CCBs: Avoid in LV dysfunction or with β-blockers (↑ risk of heart block). - Digoxin: Monitor renal function & serum levels - Amiodarone: Long-term toxicity — avoid as 1st line. |
Comparative Advantages | - Beta Blockers: Improve survival post-MI, good for tachyarrhythmias. - CCBs: Useful if beta blockers contraindicated. - Digoxin: Effective in sedentary HF patients. - Amiodarone: Most potent rate + rhythm control (last resort). |
Common ADRs | - Beta Blockers: Bradycardia, fatigue, bronchospasm. - CCBs: Bradycardia, constipation (verapamil). - Digoxin: Nausea, visual halos, arrhythmia (toxicity). - Amiodarone: Photosensitivity, thyroid/liver/lung toxicity. |
High-Yield Suffixes | -olol = Beta blocker (no suffix) = Non-DHP CCBs (Verapamil, Diltiazem) (no suffix) = Digoxin / Amiodarone |