cardiac action potential
Summary
The cardiac action potential is the sequence of ion channel-mediated voltage changes that trigger cardiac myocyte contraction. Ventricular/atrial myocytes have a 5-phase action potential (0-4) driven by Na+, Ca2+, and K+ currents, while pacemaker cells (SA/AV node) have a distinct 3-phase potential with automatic depolarization. Understanding these phases is essential for explaining antiarrhythmic drug mechanisms and ECG correlations.
Detail
Ventricular myocyte action potential (5 phases):
Phase 4 (Resting membrane potential): ~-90mV, maintained by high K+ permeability (inward rectifier K+ channels, IK1).
Phase 0 (Rapid depolarization): Fast voltage-gated Na+ channels open (INa), causing rapid influx of Na+ and sharp upstroke. Threshold ~-70mV.
Phase 1 (Initial repolarization): Na+ channels inactivate; transient outward K+ current (Ito) causes brief repolarization, creating the notch.
Phase 2 (Plateau): L-type Ca2+ channels open, allowing sustained Ca2+ influx balanced by K+ efflux. This plateau corresponds to the ST segment on ECG and allows sustained contraction and prevents tetany. Ca2+ influx also triggers Ca2+-induced Ca2+ release (CICR) from sarcoplasmic reticulum (excitation-contraction coupling).
Phase 3 (Rapid repolarization): Ca2+ channels close; delayed rectifier K+ channels (IKr, IKs) open, causing rapid K+ efflux and return to resting potential.
Phase 4 (again): Return to resting state via Na+/K+ ATPase and Na+/Ca2+ exchanger restoring ionic gradients.
Pacemaker cells (SA/AV node) - 3 phases: Phase 4: Slow spontaneous depolarization due to "funny" Na+ channels (If) - unique automaticity. Phase 0: Depolarization via T-type and L-type Ca2+ channels (slower upstroke than myocytes, no fast Na+ channels). Phase 3: Repolarization via K+ efflux. No true resting potential - continuous depolarization drives automaticity.
Clinical significance: - Absolute refractory period (during phase 0-2) prevents tetanic contraction, protects against reentrant arrhythmias. - Antiarrhythmic drugs classified by phase/channel targeted (Vaughan-Williams classification): Class I (Na+ channel blockers - phase 0), Class II (beta-blockers - phase 4 pacemaker), Class III (K+ channel blockers - phase 3, prolongs QT), Class IV (Ca2+ channel blockers - phase 0 in nodal tissue, phase 2 in myocytes). - Long QT syndrome: prolonged phase 3 repolarization, risk of torsades de pointes. - Hyperkalemia: affects phase 4 resting potential, can cause arrhythmias. - Digoxin: inhibits Na+/K+ ATPase, increases intracellular Ca2+, enhances contractility but can cause arrhythmias.
Sources
- Guyton and Hall Textbook of Medical Physiology
- Costanzo Physiology
- First Aid for the USMLE Step 1
- Katzung's Basic and Clinical Pharmacology
Reviewed by AnkiBoss editorial — medical student review. Information here is for study reference only and is not medical advice. Spotted an error? Let us know.