repolarization
Summary
Repolarization is the phase of the cardiac (or neuronal) action potential during which the membrane potential returns to its resting negative value after depolarization, primarily via efflux of potassium ions. In the heart, ventricular repolarization corresponds to the T wave on ECG. Abnormalities in repolarization underlie many arrhythmias, including long QT syndrome and Torsades de Pointes.
Detail
In cardiac myocytes, the action potential has 5 phases (0-4). Phase 0 is rapid depolarization due to fast Na+ influx. Phases 1-3 constitute repolarization: Phase 1 is early rapid repolarization from transient K+ outflow (Ito) and Na+ channel inactivation; Phase 2 is the plateau, where Ca2+ influx through L-type calcium channels balances K+ efflux, maintaining prolonged depolarization critical for excitation-contraction coupling and preventing tetany; Phase 3 is rapid repolarization due to increased K+ efflux (via IKr and IKs, the rapid and slow delayed rectifier channels) as Ca2+ channels close, returning membrane potential to resting level (~-90 mV). Phase 4 is the resting membrane potential, maintained by the Na+/K+ ATPase and background K+ currents (IK1) in ventricular cells, or spontaneous depolarization in pacemaker cells (funny current, If). On the surface ECG, ventricular repolarization is represented by the T wave, while atrial repolarization is typically hidden within the QRS complex. The QT interval reflects the total duration of ventricular depolarization and repolarization. Repolarization is highly sensitive to electrolyte disturbances and drugs: hypokalemia prolongs repolarization (widened T waves, U waves, risk of Torsades de Pointes), hyperkalemia shortens repolarization but peaks T waves, and drugs blocking IKr (Class III antiarrhythmics like sotalol, amiodarone, and many non-cardiac drugs such as certain antibiotics and antipsychotics) can prolong the QT interval, increasing arrhythmia risk. Congenital long QT syndromes (e.g., LQT1-KCNQ1, LQT2-KCNH1/HERG, LQT3-SCN5A) result from mutations in ion channels controlling repolarization currents, predisposing to sudden cardiac death via polymorphic ventricular tachycardia (Torsades de Pointes). In neurons, repolarization follows depolarization due to voltage-gated K+ channel opening and Na+ channel inactivation, restoring resting membrane potential and enabling the refractory period, which ensures unidirectional propagation of the action potential.
Sources
- Guyton and Hall Textbook of Medical Physiology
- First Aid for the USMLE Step 1
- Costanzo Physiology
- Braunwald's Heart Disease
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