Effective Refractory Period

During phases 0, 1, 2, and part of phase 3, the cell is refractory to the initiation of new action potentials. This is termed the effective refractory period (ERP). During the ERP, stimulation of the cell does not produce new, propagated action potentials. The reason for this is that the fast sodium channels are not fully reactivated and therefore cannot reopen to normal depolarizing stimuli.

The ERP acts as a protective mechanism in the heart by preventing multiple, compounded action potentials from occurring. If these were to occur, the heart would be unable to adequately fill with blood and eject blood. The length of the refractory period limits the frequency of action potentials (and therefore contractions) that can be generated by the heart.

Many antiarrhythmic drugs alter the ERP, thereby altering cellular excitability.  For example, drugs that block potassium channels (e.g., amiodarone, a Class III antiarrhythmic) retard phase 3 repolarization and increase the action potential duration, thereby increasing the ERP. Sodium-channel blockers (particularly Class IA) also increase the ERP by prolonging the inactivation state of fast-sodium channels.  Drugs that increase the ERP can be particularly effective in abolishing reentry currents that lead to tachyarrhythmias.

Revised 3/19/10