This document defines and describes different types of aberrancy in ventricular conduction. It discusses mechanisms of aberrancy including premature arrival of supraventricular impulses and refractoriness of conducting tissue. Types of aberrancy include type A from fascicular refractoriness, type B from anomalous activation, and type C from paradoxical critical rate. Ashman phenomenon and acceleration/bradycardia-dependent aberrancy are also summarized.

1. TI ON
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2. IK
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3. DEFINITION
Alterations in QRS contour of supraventricular beats resulting from
impulse transmission during periods of physiologic refractoriness
and/or depressed conductivity
The supraventricular electrical impulse is conducted abnormally
through the ventricular conducting system

4. MECHANISMS OF ABERRANCY
Premature arrival of the supraventricular impulse before full recovery
Inadequate or unequal refractoriness of conducting tissue resulting 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

5. 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 contractile myocardial
Unsuccessful of restitutions of transmembrane electrolyte
concentration during relaxation and dilatation of the ventricles

6. TYPES OF ABERRATION
Type A: It is the common form and due to fascicular refractoriness.
The early impulse reach the RBB when still 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 critical rate

8. 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 followed by a relatively short cycle, the beat
with a short cycle often has RBBB morphology

9. ASHMAN PHENOMENON
Atrial fibrillation( AF)
Atrial tachycardia
Premature Atrial
Contractions

10. D/D-VPCS

11. 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 critical rate
The appearance and disappearance often depends on very small
changes in cycle length

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

14. BRADYCARDIA-DEPENDENT, PHASE 4 ABERRANCY
Occurrence of impaired intraventricular conduction after long pauses or
slowing of the heart to a critical rate
Due to a gradual loss transmembrane resting potential during a
prolonged diastole with excitation from a less negative take-off
potenial

16. PHASE 4 ABERRANCY
The presence of slow diastolic 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 diastolic potential)

17. 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 its influence on the subsequent
cardiac cycle

18. 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

19. 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 final or middle, while in hyperkalemia is always global or
diffuse

21. POSTEXTRASYSTOLIC ABERRATION
This variant is caused probably to slow diastolic depolarization, unequal
recovery of conducting or myocardial tissue, or increased diastolic
volume

22. ABERRANCY IN AVRT
When a bundle branch block pattern develops that is ipsilateral to the
accessory pathway that is participating in the tachycardia during
ORT
VA conduction time prolongs as a result of the additional time that is
required for conduction to travel from through the contralateral
ventricle and septum to reach the accessory pathway

23. 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)

24. ABERRANCY IN AVRT
Left bundle-branch block facilitates 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 unlikely