ABERRANT CONDUCTIO

N

DR BARIK

DEFINITION

Alterations in QRS contour of supraventricular beats result ing from impulse transmission during periods of physiologic refractoriness and/or depressed conductivity

The supraventricular electrical impulse is conducted abnormally through the ventricular conducting system

MECHANISMS OF ABERRANCY

Premature arrival of the supraventricular impulse before full recovery

Inadequate or unequal refractoriness of conducting t issue result ing in local delay or block of dromotropism

Prolongation of Action Potential (AP) secondary to lengthiness of the preceding cycle duration

A reduced take-off potential secondary to diastole depolarization

MECHANISMS OF ABERRANCY

Failure of the refractory period to shorten in response to acceleration of the heart rate

Concealed transseptal conduction with delay or block of bundle branch conduction

Diffuse depression of Intraventricular conduction including that of specialized as well as contracti le myocardial

Unsuccessful of restitutions of transmembrane electrolyte concentration during relaxation and dilatation of the ventricles

TYPES OF ABERRATION

Type A: It is the common form and due to fascicular refractoriness.

The early impulse reach the RBB when sti l l in refractory period and it has been unable to respond and conduct

Type B: It is due to anomalous supraventricular activation

Type C: It is due to paradoxical crit ical rate

ASHMAN PHENOMENON

Gouaux-Ashman phenomenon or Ashman phenomenon is an intraventricular conduction abnormality restricted to the His-Purkinje system, caused by a change in the HR

Modulated by metabolic and electrolyte abnormalities and the effects of drugs

Relatively long cycle was fol lowed by a relatively short cycle, the beat with a short cycle often has RBBB morphology

Atrial f ibril lation( AF)

Atrial tachycardia

Premature Atrial Contractions

ASHMAN PHENOMENON

D/D-VPCS

ACCELERATION-DEPENDENT ABERRANCY

TACHYCARDIA-DEPENDENT, IN PHASE 3 ABERRANCY, OR PHASE 3 ABERRATION

Resulting from the occurrence of impaired intraventricular conduction as the heart attains a specific crit ical rate

The appearance and disappearance often depends on very small changes in cycle length

Aberrancy often appears at relatively slow rates, frequently below 75 beats/min

BRADYCARDIA-DEPENDENT, PHASE 4 ABERRANCY

Occurrence of impaired intraventricular conduction after long pauses or slowing of the heart to a crit ical rate

Due to a gradual loss transmembrane resting potential during a prolonged diastole with excitation from a less negative take-off potenial

PHASE 4 ABERRANCY

The presence of slow diastol ic depolarization which need not be enhanced;

A shift in threshold potential toward zero.

A deterioration in membrane responsiveness so that significant conduction impairment develops at -75mV instead of -65mV;

Hypopolarization ( the lost of maximum diastol ic potential)

CONCEALED INTRAVENTRICULAR CONDUCTION

Concealed Intraventricular conduction is defined as the manifestations of concealed conduction into the bundle branch system

Conduction is inferred only because of i ts inf luence on the subsequent cardiac cycle

CONCEALED INTRAVENTRICULAR CONDUCTION

Trans-septal retrograde concealed intraventricular conduction

Perpetuation of functional BBB initiated by a premature supraventricular impulse

Alternation of aberrant ventricular conduction in supraventricular bigeminy

Normalization of intraventricular conduction with acceleration or rate in bradycardia-dependent BBB

ABERRANCY SECONDARY TO DRUGS AND METABOLIC OR ELECTROLYTE DISORDERS

Hyperkalemia

Diffuse QRS complexes widening, similar to left or RBBB, associated with anterior or posterior fascicular block is seen frequently

QRS complex widening is differentiated of genuine branch blocks, the delay is f inal or middle, while in hyperkalemia is always global or diffuse

POSTEXTRASYSTOLIC ABERRATION

This variant is caused probably to slow diastolic depolarization, unequal recovery of conducting or myocardial t issue, or increased diastolic volume

ABERRANCY IN AVRT

When a bundle branch block pattern develops that is ipsi lateral to the accessory pathway that is participating in the tachycardia during ORT

VA conduction t ime prolongs as a result of the additional t ime that is required for conduction to travel from through the contralateral ventricle and septum to reach the accessory pathway

ABERRANCY IN AVRT

Prolongation of the VA interval also results in prolongation of the tachycardia cycle length unless there is a compensatory shortening of the AV interval

Prolongation oftheVA interval during a bundle branch block is diagnostic of ORT, but occurs in only 7% of patients with PSVT

Development of left bundle branch aberration with tachycardia is strongly predictive of ORT (92% positive predictive value)

ABERRANCY IN AVRT

Left bundle-branch block facil i tates induction of ORT when a left-sided accessory pathway is present and most accessory pathways are located on the left side

Induction of AV nodal reentry requires significant AV nodal delay, which makes the H1-H2 interval longer and makes aberration unl ikely