The supernormal period is a short window at the end of repolarization during which an impulse finds otherwise refractory tissue capable of conduction and/or excitability.¹,² Because it occurs during repolarization, it behaves similarly to other repolarization phenomena showing cycle length dependency (restitution).³,⁴ It is, therefore, not a static but rather a dynamic time window widening and shifting rightward with longer cycle lengths (analogous to the QT interval and QT dispersion). Its timing corresponds to the end or shortly after the T wave (the ECG marker of global ventricular myocardial repolarization), but it is repolarization of the tissue in question that determines the true supernormal period. Supernormality has been described in “all or none” (fast response) tissues with prolonged refractoriness (His-Purkinje, ventricular myocardium, accessory pathways [APs]) and not the AV node. Its most common manifestation is momentary resolution of BBB or AV block following a premature impulse (supernormal period of His-Purkinje conduction) (Figs. 22-1, 22-2, and 22-8).⁵,⁶,⁷,⁸,⁹ While episodes of supernormality during AV block result in “better than expected” conduction, sometimes “faster than expected” conduction occurs with paradoxical shortening of the PR interval (see Fig. 1-35). Spontaneous episodes of supernormality in APs are rare and require the unusual combination of AV block and a poorly conducting AP (Fig. 22-9; see also Fig. 9-20).³,⁴,¹⁰,¹¹,¹² Supernormality in the ventricle occurs when otherwise subthreshold pacing stimuli capture the ventricle only during a critical period at the end of ventricular repolarization (supernormal period of ventricular excitability) (Fig. 22-10).¹³ Supernormality might be due to a transient window of increased voltage in the transmembrane action potential at the end of repolarization.² However, the cellular basis of supernormality is unknown, and alternative mechanisms can also explain the phenomenon of unexpected conduction with prematurity.¹⁴,¹⁵

During premature beats, the gap phenomenon refers to temporary loss of conduction over a structure at intermediate coupling intervals when longer and shorter coupling intervals are








able to conduct (i.e., “gap” in conduction).¹⁶,¹⁷ A premature impulse reaching a site in its absolute refractory period will fail to conduct (phase 3 block). A more premature impulse, however, might encounter relative refractoriness in tissue proximal to this site resulting in conduction delay. Enough delay proximally allows the previously blocked site sufficient time to recover excitability and conduct distally (“proximal delay allowing distal conduction”). Gap phenomena have been described both antegradely (six types) and retrogradely (two types) along the conduction system, particularly in the setting of dual AV node physiology (the slow pathway [SP] providing delay proximal to the His-Purkinje system) (Figs. 22-3, 22-4, and 22-11, 22-12 and 22-13).¹⁸,¹⁹,²⁰,²¹