## Antiarrhythmic Classification by Mechanism **Key Point:** Class I antiarrhythmics are sodium channel blockers that decrease the rate of depolarization during Phase 0 of the cardiac action potential, thereby slowing conduction velocity throughout the heart. ### Class I Mechanism Class I drugs inhibit the fast inward sodium current (I~Na~), which is responsible for the rapid depolarization phase in atrial and ventricular myocardium and the His-Purkinje system. This action: - Slows conduction velocity - Increases the refractory period - Decreases automaticity - Widens the QRS complex on ECG ### Class I Subclassification | Subclass | Example | Additional Effect | QRS Width | |----------|---------|-------------------|----------| | Ia | Quinidine, Procainamide | Na^+^ block + K^+^ block | Marked ↑ | | Ib | Lidocaine, Mexiletine | Na^+^ block + shortens APD | Minimal ↑ | | Ic | Flecainide, Propafenone | Marked Na^+^ block | Marked ↑ | **High-Yield:** Class I drugs are the most commonly used antiarrhythmics and are subdivided based on their effects on action potential duration (APD) and refractory period. **Clinical Pearl:** Class Ia drugs (quinidine, procainamide, disopyramide) also block potassium channels, prolonging the action potential duration and QT interval. Class Ib drugs (lidocaine) shorten APD, while Class Ic drugs (flecainide, propafenone) have minimal effect on APD but cause marked QRS widening. ### Contrast with Other Classes - **Class II:** Beta-blockers; slow AV nodal conduction via beta-1 blockade - **Class III:** Potassium channel blockers; prolong action potential duration and refractory period - **Class IV:** Calcium channel blockers; slow AV nodal conduction via L-type calcium channel blockade 
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