Myocardial Action Potential & Clinical Correlations
This high-yield summary integrates the electrophysiological phases with critical clinical correlates relevant for NEET PG examinations.
1. Action Potential Phases & Drug Targets
| Phase | Primary Ion Flux | Clinical/Pharmacological Significance |
|---|---|---|
| Phase 0 | Na+ Influx | Target of Class I antiarrhythmics (e.g., Lidocaine, Flecainide). |
| Phase 2 | Ca2+ Influx | Target of CCBs (e.g., Verapamil); triggers contraction. |
| Phase 3 | K+ Efflux | Target of Class III antiarrhythmics (e.g., Amiodarone). |
| Phase 4 | K+ Conductance | Funny current ($I_f$) in nodes determines heart rate. |
2. High-Yield Clinical Corrections & Pearls
- Long QT Syndrome (LQTS):
- Often caused by mutations in K+ channels (delaying Phase 3 repolarization).
- Correction: Avoid medications that block K+ channels (e.g., macrolides, fluoroquinolones, Class III antiarrhythmics) to prevent Torsades de Pointes.
- Hyperkalemia:
- Increases resting membrane potential (Phase 4 becomes less negative), moving it closer to threshold.
- Clinical effect: Initially increases excitability, but eventually inactivates Na+ channels, slowing conduction (peaked T waves, wide QRS).
- Excitation-Contraction (E-C) Coupling:
- In myocytes, Ca2+ entry is essential.
- Clinical correction: Beta-blockers reduce cAMP, decreasing Ca2+ entry through L-type channels, thus reducing contractility (negative inotropy).
NEET PG Hint: Remember: The Effective Refractory Period (ERP) in cardiac muscle is prolonged by the plateau phase, which prevents tetanic contraction and allows for cardiac filling. Drugs that block K+ channels (Class III) specifically prolong the ERP, making them effective for rhythm control. For more high-yield cardiovascular protocols and free medical questions, visit mymedschool.org.