## Class IA Antiarrhythmics: Mechanism and Characteristics **Key Point:** Class IA antiarrhythmics are characterized by dual blockade of fast sodium channels AND potassium channels, resulting in both decreased conduction velocity AND prolonged repolarization. ### Mechanism of Action **High-Yield:** Class IA drugs produce: 1. **Sodium channel blockade** → slowed Phase 0 depolarization → decreased conduction velocity 2. **Potassium channel blockade** → prolonged Phase 3 repolarization → increased action potential duration (APD) 3. Combined effect: **moderate slowing of conduction with significant QT prolongation** ### Class IA Agents | Drug | Sodium Block | Potassium Block | Membrane Stabilization | QT Prolongation | | --- | --- | --- | --- | --- | | **Quinidine** | ✓ Strong | ✓ Strong | ✓ Marked | ✓ Significant | | **Procainamide** | ✓ Strong | ✓ Moderate | ✓ Marked | ✓ Moderate | | **Disopyramide** | ✓ Strong | ✓ Strong | ✓ Marked | ✓ Significant | **Clinical Pearl:** Quinidine is the prototypical Class IA agent — it has the strongest potassium channel blocking effect among Class IA drugs, explaining its pronounced QT prolongation and torsades de pointes risk. ### Why Other Classes Differ - **Class IB** (lidocaine, mexiletine): Na^+^ block + **shorten** APD (K^+^ channel opening) - **Class IC** (flecainide, propafenone): Marked Na^+^ block, minimal K^+^ block, minimal APD change - **Class II** (beta-blockers): AV nodal conduction slowing only - **Class III** (amiodarone, sotalol): K^+^ channel block (APD prolongation) without Na^+^ block - **Class IV** (verapamil, diltiazem): Ca^2+^ channel block, AV nodal effects **Mnemonic:** IA = **I**ntermediate (between IB and IC) — both Na and K block, moderate conduction slowing, significant repolarization prolongation. [cite:Harrison 21e Ch 297] 
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