The Ashman phenomenon refers to aberration occurring when a short cycle follows a long one (long-short cycle sequence) (see Fig. 10-1).^11,¹³ Aberrancy is caused by the physiological changes of the conduction system refractory periods associated with the R-R interval. Normally, the refractory period of the HPS lengthens as the heart rate slows and shortens as the heart rate increases, even when heart rate changes are abrupt. Thus, aberrant conduction can result when a short cycle follows a long R-R interval. In this scenario, the QRS complex that ends the long pause is conducted normally but creates a prolonged ERP of the bundle branches. If the next QRS complex occurs after a short coupling interval, it may be conducted aberrantly because one of the bundles is still refractory as a result of a lengthening of the refractory period (phase 3 block; Fig. 10-2).^6,⁷

FIGURE 10-2 Atrial tachycardia (AT) with variable atrioventricular (AV) conduction and intermittent aberrancy. Left, AT with 2:1 AV conduction and normal QRS morphology is observed. Once 1:1 AV conduction occurs (QRS 3), left bundle branch block (LBBB) aberration develops (caused by long-short cycle sequence, phase 3 block). LBBB aberration is also observed during QRS 4, likely secondary to concealed transseptal conduction causing perpetuation of aberration. After a pause, both bundle branches recover from refractoriness producing a normal QRS 5. Ashman phenomenon (long-short cycle sequence) explains phase 3 block during QRS 6, but this time it manifests as a right bundle branch block (RBBB) pattern. This is because activation during QRS 4 propagated down the right bundle branch (RB) and across the septum, thus activating the left bundle branch (LB) retrogradely after some delay (concealed transseptal conduction), so that the LB-LB interval (between QRS 4 and QRS 5) resulted in a shorter effective refractory period (ERP) of the LB following QRS 5. Conversely, the RB-RB interval (between QRS 4 and QRS 5) was longer and, consequently, the ERP of the RB was still prolonged following QRS 5, thereby setting the stage for a long-short cycle sequence of the RB but not the LB. Therefore, RBBB (rather than LBBB) aberration develops. RBBB aberration during QRS complexes 7 and 8 is secondary to either concealed transseptal conduction or rate-dependent aberration. However, because LBBB (rather than RBBB) was observed during QRS 4 (although QRS 4 occurred following a similar cycle length to that of QRS 8), concealed transseptal conduction is more likely to be the mechanism of aberration. After a pause, both bundle branches recover from refractoriness to produce a normal QRS 9. Long-short cycle sequence explains phase 3 block during QRS 10, but this time it manifests as LBBB. This is because activation during QRS 8 propagated down the LB and across the septum, thus activating the RB after some delay (concealed transseptal conduction). The result is that the RB-RB interval (following QRS 8) and ERP of the RB became shorter, whereas the LB-LB interval (following QRS 8) was longer. Consequently, the ERP of the LB was still prolonged following QRS 9, thereby setting the stage for a long-short cycle sequence and LBBB aberration. LBBB aberration during QRS 11 is caused by concealed transseptal conduction. The Ashman phenomenon (long-short cycle sequence) underlies RBBB aberration during QRS 14. HRA = high right atrium.

RBBB aberration is more common than LBBB in this setting because the RB has a longer ERP than the LB. The Ashman phenomenon can occur during second-degree AV block (see Fig. 9-9), but it is most common during atrial fibrillation (AF), whereby the irregularity of the ventricular response results in frequently occurring long-short cycle sequences.

The aberrancy can be present for one beat and have a morphology resembling a premature ventricular complex (PVC), or it can involve several sequential complexes, a finding suggesting ventricular tachycardia (VT). In the setting of aberrancy during AF, the long-short cycle sequence characteristic of the Ashman phenomenon may not be helpful in differentiating aberration from ventricular ectopy. Although a long cycle (pause) sets the stage for the Ashman phenomenon, it also tends to precipitate ventricular ectopy. Furthermore, concealed conduction occurs frequently during AF, and, therefore, it is never possible to know from the surface ECG exactly when a bundle branch is activated. Thus, if an aberrant beat does end a long-short cycle sequence during AF, it can be because of refractoriness of a bundle branch secondary to concealed conduction into it, rather than because of changes in the length of the ventricular cycle.⁸^–¹⁰ ¹²

Nevertheless, there are several features of ventricular ectopy that can help distinguish a PVC from an aberrantly conducted or Ashman beat during AF. PVCs are usually followed by a longer R-R cycle, indicating the occurrence of a compensatory pause, the result of retrograde conduction into the AVN and anterograde block of the impulse originating in the atrium. A ventricular origin is also likely when there is a fixed coupling cycle between the normal and aberrant QRS complexes. The presence of long and identical R-R cycles after the aberrated beats and the absence of a long-short cycle sequence associated with the wide or aberrant QRS complex also suggest ventricular ectopy. Additionally, the absence of aberrancy, despite the presence of R-R cycle length (CL) combinations that are longer and shorter than those associated with the wide QRS complex, suggests ventricular ectopy. QRS morphology inconsistent with LBBB or RBBB aberrancy argues against aberration (Fig. 10-3).^6,⁸^–¹⁰ ^,12

FIGURE 10-3 Premature ventricular complexes during atrial fibrillation. Several features suggest that the wide QRS complexes are caused by ventricular ectopy rather than aberration. QRS morphology is inconsistent with LBBB or RBBB aberrancy. Additionally, there is a fixed coupling cycle between the normal and aberrant QRS complex. The absence of a long-short cycle sequence associated with the wide QRS complex and the absence of aberrancy despite the presence of R-R cycle length combinations that are longer and shorter than those associated with the wide QRS complex also suggest ventricular ectopy.

Aberration caused by the Ashman phenomenon can persist for several cycles. The persistence of aberration can reflect a time-dependent adjustment of refractoriness of the bundle branch to the abrupt change in CL, or it can be the result of concealed transseptal activation (see later).

Aberration Caused by Heart Rate Acceleration

As the heart rate accelerates, the HPS refractory period shortens; normal conduction tends to be preserved because of this response. However, refractoriness of the HPS eventually reaches a critical value beyond which an increase in heart rate no longer abbreviates it; at this point, AV block may occur. Conversely, the refractory period lengthens as the heart rate slows. Acceleration-dependent BBB is a result of failure of the action potential of the bundle branches to shorten, or, paradoxically, the action potential lengthens in response to acceleration of the heart rate (Fig. 10-4).^3,¹¹ As noted, the ERP of the RB normally shortens at faster heart rates to a greater degree than that of the LB; this finding explains the more frequent RBBB aberration at longer CLs and LBBB aberration at shorter CLs.^4,^8,¹⁰

FIGURE 10-4 Supraventricular tachycardia (SVT) with tachycardia-dependent (phase 3) right bundle branch block. Delivery of a late ventricular extrastimulus (arrow) during the SVT preexcites the right bundle branch (and either peels back or shortens its refractoriness) and restores normal conduction.

This form of aberration is a marker of some type of cardiac abnormality when it appears at relatively slow heart rates (less than 70 beats/min), displays LBBB (Fig. 10-5), appears after several cycles of accelerated but regular rate, or appears with gradual rather than abrupt acceleration of the heart rate and at CL shortening by less than 5 milliseconds. Because of the small changes in the duration of the CL that may initiate aberration (critical cycle), recognition of acceleration-dependent aberration may require a long record to document the gradual, and at times minimal, shortening of the R-R interval.⁸^–¹⁰

FIGURE 10-5 Acceleration-dependent aberration. The lead II continuous rhythm strip demonstrates sinus rhythm with rate-related left bundle branch block (LBBB). Note that small changes in rate can result in acceleration-dependent aberration. LBBB develops at a sinus rate faster than 70 beats/min, and normal QRS complexes are observed at slower sinus rates. The LBBB and the slow rate at which aberration develops strongly suggest an abnormality in the left bundle branch (LB), rather than physiological aberration, often associated with underlying structural heart disease such as cardiomyopathy. Interestingly, the onset and offset of the LBBB demonstrate hysteresis in that the cycle length (CL) required to initiate the LBBB is shorter than the CL required to maintain it, probably because of retrograde concealed penetration of the LB.

With increasing heart rate or persistence of fast heart rate, acceleration-dependent aberration can occasionally disappear. The normalization of a previously aberrant QRS complex can be explained by a greater shortening of the ERP of the bundle branches than that of the AVN or by a time-dependent gradual shortening of the refractory period of the affected bundle branch (a phenomenon occasionally referred to as restitution).⁶

During slowing of the heart rate, intraventricular conduction often fails to normalize at the critical CL, and aberration persists at cycles longer than the critical cycle that initiated the aberration. Once acceleration-dependent BBB is established, the actual cycle for the blocked bundle does not begin until approximately halfway through the QRS complex because of concealed transseptal conduction (see later); thus, it is necessary for the heart rate to slow down more than would be expected to reestablish normal conduction.⁸^–¹⁰

Phase 4 Block

Phase 4 block occurs when conduction of an impulse is blocked in tissues well after their normal refractory periods have ended.^3,¹¹ Phase 4 block is governed by the same physiological principles as those for phase 3 block. Membrane responsiveness is determined by the relationship of the membrane potential at excitation with the maximum height of phase 0. The availability of the Na⁺ channels is reduced at less negative membrane potentials, and activation at a reduced membrane potential is likely to cause aberration or block.⁶

The cause of membrane depolarization (i.e., reduction of membrane potential) in the setting of phase 4 block, however, is different from that in phase 3 block. Enhanced phase 4 depolarization within the bundle branches can be caused by enhanced automaticity or partial depolarization of injured myocardial tissue, or both. In this setting, the maximum diastolic potential immediately follows repolarization, from which point the membrane potential is steadily reduced (by the pacemaker current). This reduction, in turn, results in inactivation of some Na⁺ channels. Thus, an action potential initiated early in the cycle (immediately after repolarization) would have a steeper and higher phase 0 and consequently better conduction than would an action potential initiated later in the cycle when the membrane potential at the time of the stimulus is reduced, with resulting reductions in the velocity and height of phase 0 and slower conduction.^8,^10,¹²

Phase 4 aberration is one explanation for the development of aberration at the end of a long cycle. As a result of a gradual spontaneous depolarization made possible by a prolonged cycle, the cell is activated from a less negative potential, and the result is impaired conduction. This type of aberration is sometimes referred to as bradycardia-dependent BBB (Fig. 10-6).⁶ Importantly, the membrane potential has to depolarize significantly before conduction becomes impaired. Mild depolarization can actually improve conduction because the voltage is closer to threshold.

FIGURE 10-6 Bradycardia-dependent left bundle branch block (LBBB). Normal intraventricular conduction is observed during sinus rhythm. Premature atrial complexes (hidden within the T waves) are not conducted to the ventricles, resulting in pauses. The sinus complex following the pause is conducted with LBBB pattern (arrows) presumably secondary to phase 4 block. See text for discussion.

Phase 4 aberration would be expected in the setting of bradycardia or enhanced normal automaticity. However, despite the fact that bradycardia is common and cells with phase 4 depolarization are abundant, phase 4 block is not commonly seen; most reported cases are associated with structural heart disease. One explanation for this phenomenon is that in normal fibers, conduction is well maintained at membrane potentials more negative than −70 to −75 mV. Significant conduction disturbances are first manifested when the membrane potential is less negative than −70 mV at the time of stimulation; local block appears at −65 to −60 mV. Because the threshold potential for normal His-Purkinje fibers is −70 mV, spontaneous firing occurs before the membrane can actually be reduced to the potential necessary for conduction impairment or block. Phase 4 block is therefore pathological when it does occur, and it requires one or more of the following: (1) the presence of slow diastolic depolarization, which needs to be enhanced; (2) a decrease in excitability (a shift in threshold potential toward zero) so that, in the presence of significant bradycardia, sufficient time elapses before the impulse arrives, thus enabling the bundle branch fibers to reach a potential at which conduction is impaired; and (3) a deterioration in membrane responsiveness so that significant conduction impairment develops at −75 mV instead of −65 mV; this occurrence would also negate the necessity for such a long cycle before conduction fails.^8,^10,¹²

Bradycardia-dependent or phase 4 block almost always manifests an LBBB pattern, likely because the left ventricular (LV) conduction system is more susceptible to ischemic damage and has a higher rate of spontaneous phase 4 depolarization than the right ventricle (RV).¹²

Both tachycardia-dependent and bradycardia-dependent BBB can be seen in the same patient with an intermediate range of CLs associated with normal conduction. The prognosis of rate-dependent BBB largely depends on the presence and severity of the underlying heart disease. Its clinical implications are not clear, and it usually occurs in diseased tissue and in the setting of myocardial infarction (MI), especially inferior wall MI.⁶

Aberration Caused by Concealed Transseptal Conduction

Concealed transseptal conduction is the underlying mechanism of aberration occurring in several situations, including perpetuation of aberrant conduction during tachyarrhythmias, unexpected persistence of acceleration-dependent aberration, and alternation of aberration during atrial bigeminal rhythm.⁸^–¹⁰ ^,12 ^,14 ^,15

Perpetuation of Aberrant Conduction during Tachyarrhythmias

During a supraventricular tachycardia (SVT) with normal ventricular activation, a PVC originating from the RV can retrogradely activate the RB early, whereas retrograde activation of the LB occurs later, following transseptal conduction of the PVC. Consequently, although the RB ERP expires in time for the next SVT impulse, the LB remains refractory because its actual cycle began later than the RB. Therefore, the next SVT impulse traveling down the His bundle (HB) encounters an excitable RB and a refractory LB; thus, it propagates to the RV over the RB (with an LBBB pattern, phase 3 aberration). Conduction subsequently propagates from the RV across the septum to the LV. By this time, the distal LB has recovered, allowing for retrograde penetration of the LB by the SVT impulse propagating transseptally, thereby rendering the LB refractory to each subsequent SVT impulse (Fig. 10-7). This process is repeated, and the LBBB pattern continues until another well-timed PVC preexcites the LB (and either peels back or shortens its refractoriness), so that the next impulse from above finds the LB fully recovered (see Fig. 10-4).^4,^14,¹⁵

FIGURE 10-7 Perpetuation of aberrant conduction during supraventricular tachycardia (SVT) secondary to concealed transseptal conduction. At left, SVT is associated with normal ventricular activation and narrow QRS complexes. Critically timed ventricular extrastimulus delivered from the right ventricle (arrow) precipitates left bundle branch block aberrancy during the SVT. See text for discussion.

Unexpected Persistence of Acceleration-Dependent Aberration

Acceleration-dependent BBB develops at a critical rate faster than the rate at which it disappears (Fig. 10-8). This paradox is most commonly ascribed to concealed conduction from the contralateral conducting bundle branch across the septum with delayed activation of the blocked bundle. Such concealed transseptal activation results in a bundle branch–to–bundle branch (RB-RB or LB-LB) interval shorter than the manifest R-R cycle. The reason is that the actual cycle for the blocked bundle does not begin until approximately halfway through the QRS complex, because it takes 60 to 100 milliseconds for the impulse to propagate down the RB and transseptally reach the blocked LB. Consequently, for normal conduction to resume, the cycle (R-R interval) during deceleration must be longer than the critical cycle during acceleration by at least 60 to 100 milliseconds.⁸^–¹⁰ ^,12 ^,14 ^,15