## Distinguishing Class IA from Class IB Antiarrhythmics ### Mechanism of Action Both Class IA and Class IB antiarrhythmics are sodium channel blockers, but they differ fundamentally in their effects on **action potential duration (APD)** and **refractoriness**. **Key Point:** Class IA agents **prolong** action potential duration and refractoriness, while Class IB agents **shorten** action potential duration despite blocking sodium channels. ### Electrophysiologic Effects | Feature | Class IA | Class IB | |---------|----------|----------| | **Sodium channel blockade** | Yes (moderate) | Yes (mild) | | **Action potential duration** | Prolonged | Shortened | | **Refractory period** | Prolonged | Shortened | | **QT interval** | Prolonged | Normal or shortened | | **Conduction velocity** | Decreased | Decreased (less than IA) | ### Clinical Examples **Class IA agents:** Quinidine, Procainamide, Disopyramide - Prolong APD via additional potassium channel blockade - Risk of torsades de pointes (QT prolongation) **Class IB agents:** Lidocaine, Mexiletine - Shorten APD via enhanced potassium channel activity - Safer profile; less proarrhythmic **High-Yield:** The **APD effect** is the cardinal discriminator. Class IA = **Prolongs** APD (think "IA = Increases APD"); Class IB = **Reduces** APD. **Clinical Pearl:** Class IB agents are preferred in acute MI because they reduce the risk of reentrant arrhythmias without the proarrhythmic risk of QT prolongation seen with Class IA agents.
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