β-blockers

Beta-adrenergic blockers (β-blockers) are antagonists of β1 (cardiac) and β2 (smooth muscle, bronchial) adrenergic receptors. Classes: (1) Non-selective (propranolol, nadolol) block β1 and β2; (2) β1-selective (atenolol, metoprolol, bisoprolol)—block β1 at lower doses but lose selectivity at high doses; (3) Combined α/β blockers (carvedilol, labetalol) block both α1 and β receptors; (4) Intrinsic sympathomimetic activity (ISA: pindolol, acebutolol)—partial agonists with less bradycardia. Mechanisms: β1 blockade decreases heart rate (negative chronotropy), contractility (negative inotropy), and AV nodal conduction (negative dromotropy); β2 blockade causes bronchoconstriction and vasoconstriction. Effects: reduced myocardial oxygen demand, slower AV nodal conduction (useful for SVT/AF rate control), reduced blood pressure. Indications: (1) Hypertension (first-line); (2) Coronary artery disease/angina (reduce ischemia, decrease mortality post-MI); (3) Arrhythmias (SVT, AF rate control, VT in ischemic disease); (4) Heart failure (reduced EF—evidence of mortality benefit with carvedilol, metoprolol succinate, bisoprolol; NOT used in acute decompensation); (5) Hyperthyroidism (symptom control); (6) Migraine/tremor prophylaxis. Contraindications: decompensated heart failure, bradycardia, heart block, asthma/COPD (especially non-selective agents—relative), peripheral arterial disease. Adverse effects: fatigue, sexual dysfunction, bradycardia, heart block, bronchoconstriction, hyperglycemia masking hypoglycemia symptoms (important in diabetics). Abrupt discontinuation causes rebound hypertension/tachycardia (beta-blocker withdrawal syndrome). Carvedilol and labetalol have alpha-blocking effects (additional vasodilation). On boards: β-blockers are proven to reduce mortality post-MI and in systolic heart failure; always initiate (not discontinue) in appropriate conditions.