Aberrant conduction

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ABERRANT CONDUCTION

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Aberrant conduction

  1. 1. TI ON C N DU CO NT RA ERAB
  2. 2. IK BARDR
  3. 3. DEFINITIONAlterations in QRS contour of supraventricular beats resulting from impulse transmission during periods of physiologic refractoriness and/or depressed conductivityThe supraventricular electrical impulse is conducted abnormally through the ventricular conducting system
  4. 4. MECHANISMS OF ABERRANCYPremature arrival of the supraventricular impulse before full recoveryInadequate or unequal refractoriness of conducting tissue resulting in local delay or block of dromotropismProlongation of Action Potential (AP) secondary to lengthiness of the preceding cycle durationA reduced take-off potential secondary to diastole depolarization
  5. 5. MECHANISMS OF ABERRANCYFailure of the refractory period to shorten in response to acceleration of the heart rateConcealed transseptal conduction with delay or block of bundle branch conductionDiffuse depression of Intraventricular conduction including that of specialized as well as contractile myocardialUnsuccessful of restitutions of transmembrane electrolyte concentration during relaxation and dilatation of the ventricles
  6. 6. TYPES OF ABERRATIONType 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 conductType B: It is due to anomalous supraventricular activationType C: It is due to paradoxical critical rate
  7. 7. ASHMAN PHENOMENONGouaux-Ashman phenomenon or Ashman phenomenon is an intraventricular conduction abnormality restricted to the His- Purkinje system, caused by a change in the HRModulated by metabolic and electrolyte abnormalities and the effects of drugsRelatively long cycle was followed by a relatively short cycle, the beat with a short cycle often has RBBB morphology
  8. 8. ASHMAN PHENOMENON Atrial fibrillation( AF)Atrial tachycardia Premature Atrial Contractions
  9. 9. D/D-VPCS
  10. 10. ACCELERATION-DEPENDENT ABERRANCYTACHYCARDIA-DEPENDENT, IN PHASE 3 ABERRANCY, OR PHASE 3 ABERRATIONResulting from the occurrence of impaired intraventricular conduction as the heart attains a specific critical rateThe appearance and disappearance often depends on very small changes in cycle length
  11. 11. Aberrancy often appears at relatively slow rates, frequently below 75 beats/min
  12. 12. 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
  13. 13. PHASE 4 ABERRANCYThe 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)
  14. 14. 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
  15. 15. CONCEALED INTRAVENTRICULAR CONDUCTIONTrans-septal retrograde concealed intraventricular conductionPerpetuation of functional BBB initiated by a premature supraventricular impulseAlternation of aberrant ventricular conduction in supraventricular bigeminyNormalization of intraventricular conduction with acceleration or rate in bradycardia-dependent BBB
  16. 16. 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
  17. 17. POSTEXTRASYSTOLIC ABERRATION This variant is caused probably to slow diastolic depolarization, unequal recovery of conducting or myocardial tissue, or increased diastolic volume
  18. 18. ABERRANCY IN AVRTWhen a bundle branch block pattern develops that is ipsilateral to the accessory pathway that is participating in the tachycardia during ORTVA 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
  19. 19. ABERRANCY IN AVRTProlongation of the VA interval also results in prolongation of the tachycardia cycle length unless there is a compensatory shortening of the AV intervalProlongation oftheVA interval during a bundle branch block is diagnostic of ORT, but occurs in only 7% of patients with PSVTDevelopment of left bundle branch aberration with tachycardia is strongly predictive of ORT (92% positive predictive value)
  20. 20. ABERRANCY IN AVRTLeft bundle-branch block facilitates induction of ORT when a left-sided accessory pathway is present and most accessory pathways are located on the left sideInduction of AV nodal reentry requires significant AV nodal delay, which makes the H1-H2 interval longer and makes aberration unlikely

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