## Phase 0: Rapid Depolarization **Key Point:** Phase 0 of the ventricular action potential is characterized by rapid depolarization, which is driven by the influx of Na⁺ ions through voltage-gated sodium channels (Nav channels). ### Mechanism 1. When the membrane potential reaches threshold (~−60 mV), voltage-gated Na⁺ channels open 2. Na⁺ rushes into the cell down its electrochemical gradient 3. This produces the steep upstroke with a slope of ~500–1000 V/s 4. Sodium channels rapidly inactivate once the membrane potential becomes positive ### Comparison of Ion Channels in Cardiac Action Potential | Phase | Primary Ion Channel | Ion | Effect | |-------|-------------------|-----|--------| | 0 (Depolarization) | Voltage-gated Na⁺ channels | Na⁺ influx | Rapid upstroke | | 1 (Early repolarization) | Transient outward K⁺ channels | K⁺ efflux | Notch formation | | 2 (Plateau) | L-type Ca²⁺ channels | Ca²⁺ influx | Sustained depolarization | | 3 (Repolarization) | Delayed rectifier K⁺ channels | K⁺ efflux | Return to resting potential | | 4 (Resting) | Inward rectifier K⁺ channels | K⁺ efflux | Maintains resting potential | **High-Yield:** The rapid Na⁺ influx is essential for fast conduction velocity in ventricular and atrial muscle, and in the His-Purkinje system. This is why sodium channel blockers (Class I antiarrhythmics) slow conduction. **Clinical Pearl:** Drugs that block sodium channels (quinidine, procainamide, flecainide) flatten the Phase 0 slope and slow conduction velocity, which can be seen as widening of the QRS complex on ECG.
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