Repolarization can finish before excitability returns. The interval between APD₉₀ and ERP is post-repolarization refractoriness (PRR).Refractoriness is set by voltage, not by a fixed fraction of the action potential. ERP runs from phase 0 through mid-to-late phase 3 and ends at roughly −55 mV, the point at which enough Nav1.5 has recovered to support a propagating response — normally just before 90% repolarization, so the ratio sits a little under 1.0. Give a slowly-dissociating blocker and the two quantities come apart: the membrane is back at rest and the channels are still occupied.
| ERP / APD₉₀ | State | Electrophysiological meaning |
|---|---|---|
| 0.85 – 0.98 | Normal baseline | Nav1.5 recovers in a strictly voltage-dependent way as repolarization finishes. Excitability returns at about −55 mV, leaving a very narrow window before the membrane reaches resting potential. |
| < 0.80 | Increased vulnerability | ERP has shortened out of proportion to APD. A larger excitable gap opens, and premature stimuli can conduct slowly through incompletely repolarized tissue — the condition that facilitates reentry. |
| > 1.00 | Post-repolarization refractoriness | Refractoriness now extends past complete repolarization into phase 4. The membrane is back at −85 to −90 mV and the tissue is still inexcitable, because channels remain drug-bound. |
| Observation | Follows from |
|---|---|
| Class Ib shortens APD in normal ventricle yet prolongs ERP in ischemic tissue | Inactivated-state binding + depolarized RMP holding more channels inactivated |
| Class Ic widens QRS at rest, not just during tachycardia | τ > 10 s exceeds the diastolic interval at any physiological rate, so block never fully washes out |
| Class Ib has almost no ECG signature in healthy myocardium | τ < 1 s permits near-complete recovery during a normal diastolic interval |
| Reentry can terminate without any change in APD | PRR raises ERP independently of repolarization — the wavefront meets refractory tissue |