EP2: EP Diagnostics Part 2 and Ablation Flashcards
Surface ECG vs electrogram
-RV apex is as early as His due to how ventricles depolarise
What arrhythmias are shown?
a) AVNRT
b) AVRT
c) Atrial flutter
Rates of atrial rhythms
300/anticlockwise/macro re-entry - atrial flutter
Where is His electrogram recorded from?
-Catheter that lies across the posterior aspect of the tricuspid valve
What does this represent?
-V pacing with V to A conduction
-Going through AV node (earliest CS 9,10)
Why in retrograde conduction is A signal earliest in His channels?
-That is where the depolarisation has travelled through the AV node
-First part of the atria that is depolarised
-CS9-10 is also early because catheter is placed next to AV node
What does this represent?
-V pacing with V to A conduction
-Going through accessory pathway (earliest in CS 1,2)
What does no retrograde conduction look like?
-A signals are not related to V signals
-No VA conduction through AV node or accessory pathway
Could you have AVRT with no retrograde conduction?
-No because there is no retrograde conduction
-Accessory pathway can’t conduct retrograde (orthodromic)
-AV node can’t conduct retrograde (antidromic)
If someone has a concealed accessory pathway (no delta wave or short PR) what type of AVRT will one never see?
-Pathway can’t conduct antegradely because no delta wave, so no orthodromic
-Early V to A on left or right side
-Left or right atrium will be stimulated first
Does VA conduction matter if patient has atrial flutter/fibrillation?
Yes
-Accessory pathway can still conduct antegrade
-Doesn’t have decremental properties
-Can conduct into ventricle and degenerate into VF
Explain AVNRT
-Dual AV nodal pathways
-Fast conduction speed, long refractory
-Slow conduction speed, short refractory
Perpetual AVNRT explanation
AVNRT ablation
-EP study can reveal dual AV node physiology
-Normal AV node will show decremental properties
-In dual AV physiology, decrement is seen up to fast pathway blocking
-Then a jump is seen as conduction switches to slow pathway
Define AH jump
-With a 10ms decrease in the extrastimulus (A-A) coupling interval, there is a >50ms increase in the AH interval
Example of AH jump
-If we pace heart 10ms faster (480 after 500), increase in AH interval >50ms = AH jump
-Different from decrement which is slow lengthening of conduction time through AV node
What can happen after AH jump?
-Single atrial stimuli at faster rate
-Results in AH jump and tachycardia initiation
How to ablate AVNRT
-Mapping catheter advanced to Triangle of Koch
-RF energy applied to slow pathway, without involving AV node
-You might see junctional rhythm
-Do Jump testing
AVRT ablation (WPW)
-Overt accessory pathway causes short PR interval and delta wave
-Destroy abnormal pathway with radio-frequency (RF)
-By mapping around valve ring until earliest activation of ventricle is found (shortest AV signal)
-Ablating gives normal ECG and AH increase due to only AV nodal conduction
Ablation strategy for typical atrial flutter
-Radiofrequency catheter ablation of the Cavotricuspid isthmus
-Full thickness of CTI is ablated from tricuspid ring to IVC
-RF applied point to point (45-60s at each site) or continuously from TR to IVC
-Bidirectional CTI block checked by recording along the ablation line/differential pacing manoeuvres
Pathogenesis of AF
Initiating trigger: Rapidly firing ectopic foci from pulmonary vein
Substrate: Abnormal atrial tissue (mitral valve disease)
Pathogenesis of Atrial flutter
-Abnormal macro re-entry
-Counter clockwise
-Right atrium
Ablation strategy for atrial fibrillation
-Complete isolation of pulmonary veins by linear lesions around their antrum
-Using point to point RF ablation or single-shot ablation
-3D mapping system based on magnetic or impedance field
-Confirmation of electrical isolation by circular mapping catheter
How to see whether you’ve isolated pulmonary veins in PVI ablation?
-Pace and record
-If no signal received, you have isolated
