## Ionic Basis of Cardiac Action Potential Phases ### Phase-by-Phase Breakdown | Phase | Duration | Primary Ion Current | Mechanism | |-------|----------|-------------------|----------| | Phase 0 | ~1–2 ms | Inward Na+ (INa) | Voltage-gated Na+ channels open; rapid depolarization | | Phase 1 | ~10–20 ms | Outward K+ (Ito) + Inward Ca2+ (ICa) balance | Transient outward K+ current (Ito) dominates | | Phase 2 | ~200–300 ms | Inward Ca2+ (ICa-L) vs outward K+ (IK) | Plateau maintained by balance | | Phase 3 | ~150 ms | Outward K+ (IK, IK1) | K+ efflux; Ca2+ channel inactivation | | Phase 4 | Variable | Inward-rectifier K+ (IK1) | Resting potential maintained | ### Key Point: **Phase 1 early repolarization is NOT mediated solely by IK1.** Phase 1 is primarily driven by the **transient outward K+ current (Ito)**, which is a voltage-gated potassium channel that activates quickly and inactivates quickly. IK1 (inward-rectifier K+) is responsible for maintaining the resting membrane potential in Phase 4, not Phase 1 repolarization. ### High-Yield: The **transient outward current (Ito)** is the hallmark of Phase 1. This current is prominent in atrial and ventricular myocytes and is responsible for the characteristic "notch" or "dome" appearance of the ventricular action potential. IK1 becomes active only after significant repolarization has occurred. ### Clinical Pearl: Blocking Ito (e.g., with certain antiarrhythmics or in genetic channelopathies like Brugada syndrome) can abolish Phase 1 and flatten the action potential dome, increasing the risk of re-entrant arrhythmias. ### Mnemonic: **IKON** — **I**nward-rectifier K+ is for **K**eeping resting potential; **I**to is for **T**ransient **O**utward early repolarization. [cite:Guyton & Hall Textbook of Medical Physiology Ch 10]
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