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Electrophysiology AVNRT
This document provides an overview of AV nodal reentrant tachycardia (AVNRT) including its mechanisms, diagnosis using electrophysiology study techniques, and treatment with catheter ablation. It discusses the criteria for diagnosing dual AV nodal physiology, how AVNRT is initiated via programmed stimulation, its characteristic surface ECG patterns, and how the arrhythmia responds to different tests such as atrial and ventricular stimulation. The document emphasizes that AVNRT is the most common type of supraventricular tachycardia and is due to reentry involving slow and fast pathways in the AV node.
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Electrophysiology AVNRT
- 1.
- 2. WE’VE TALKED ABOUT… EQUIPMENT RELEVANTANATOMY CATHETERS and PLACEMENT BASIC INTERVALS TESTS OF SN FUNCTION EXTRASTIMULUS TESTING REFRACTORY PERIODS INCREMENTAL PACING MINIMUM PROTOCOL FOR DIAGNOSTIC EPS
- 3. AND NOW… TACHYARRHYTHMIA MECH REENTRYMECH SVT AVNRT
- 4.
- 5. • Basic mechanismsof tachyarrhythmias – Enhanced impulse formation – Abnormal conduction
- 6. • Enhanced impulseformation – Abnormal automaticity (Phase 4) • Least affected by Extrastimulus testing • Overdrive pacing – either overdrive suppression or No effect
- 7. • Enhanced impulseformation – Triggered activity (Phase 3) • Least common mech of SVT – eg. Digitalis induced • Initiated by overdrive pacing without conduction delay or block • Overdrive pacing – Acceleration
- 8. • Abnormal conduction– impulse propagation – Reentry • Pathway - Anatomic, Functional, Both
- 9.
- 10. 3 conditions forreentry • Atleast 2 functional (or anatomic) distinct pathways • Joining proximally and distally • Forming a closed circuit of conduction
- 11. 3 conditions forreentry • Unidirectional block in 1 of the pathways
- 12. 3 conditions forreentry • Slow conduction down the unblocked pathway – allowing the previously blocked pathway time to recover excitability
- 13. 3 characteristics ofreentry • Initiated by timed extrastimulus – more effectively than rapid pacing • Programmed stimulation can also terminate Tachy
- 14. 3 characteristics ofreentry • No direct relation of pacing cycle length to the tachy cycle length
- 15. 3 characteristics ofreentry • Extrastimulus can reset or entrain the Tachy in presence of fusion Reentry is the MC mech of SVTs
- 16.
- 17.
- 18. 1 • Mode ofinitiation Relation of – Basic drive cycle length – ES coupling interval – Onset of tachy – Tachy cycle length • Differentiates triggered activity from reentry
- 19. 2 • Atrial activationsequence • P-QRS relation
- 20. 3 • Effect ofBBB during Tachy – Spontaneous or induced BBB – On cycle length – V-A conduction time
- 21. 4 • Requirement ofatria, HB, Ventricle – in initation and maintenance of tachy – Effect of AV dissociation on tachy
- 22. 5 • Effect ofatrial or ventricular stimulation during tachy • Differentiates AT, AVNRT, CBT • EXCITABLE GAP
- 23. 6 • Effect ofdrugs or physiological maneuvers during Tachy
- 24.
- 25. • MC SVT •>50% SVTs • Concept by Mines in 1913 • Moe demonstrated on rabbit AVN! – Dual AVN pathways
- 26. Typical or CommonAVNRT
- 27. Typical or CommonAVNRT Alpha Beta
- 28. Atypical or uncommonAVNRT
- 29. Evidence of dualAVN pathways • 2 PR or AH intervals during NSR or at similar paced cycle length • Double response to an APC or VPC • Ability to preempt Atrial echo by VPC during Slow pathway conduction during SVT
- 30. Definition of DualAVN pathway
- 31.
- 32. Definition of ‘JUMP’ •> 50 ms increment in A-H interval with a small (~10 ms) decrease in coupling interval of Atrial extrastimulus
- 33. Definition of ‘JUMP’ •> 50 ms increment in A-H interval with a small (~10 ms) decrease in coupling interval of Atrial extrastimulus • Usually 70-100 ms jump • Maybe upto 500ms or more!
- 35. Apart from thetypical JUMP by AES Other markers of dual AVN pathways – Jump during NSR/Drive pacing – Beat to beat change of > 50 ms in AH during pacing – Pacing induced increase in AH > PCL!
- 37. Apart from thetypical JUMP by AES Other markers of dual AVN pathways – Jump during NSR/Drive pacing – Beat to beat change of > 50 ms in AH during pacing – Pacing induced increase in AH > PCL! – Double response to an APC or VPC
- 39. Apart from thetypical JUMP by AES Other markers of dual AVN pathways – Jump during NSR/Drive pacing – Beat to beat change of > 50 ms in AH during pacing – Pacing induced increase in AH > PCL! – Double response to an APC or VPC – May even lead to 1:2 Nonreentrant Tachy!
- 41. • AV nodalconduction delay (A-H) is of prime importance in AVNRT – Not coupling interval of AES ‘CRITICAL AV DELAY’ or ‘CRITICAL AH INTERVAL’
- 42. AES from CSvs HRA • Site of stimulation can affect ability to induce Dual pathway conduction and AVNRT • Critical AV nodal delay (A-H)required to initiate reentry – is shorter in CS stimulation vs HRA
- 43. AES from CSvs HRA • Dual pathway conduction and AVNRT • EASIER to induce from HRA
- 44. AES from CSvs HRA • Dual pathway conduction and AVNRT • EASIER to induce from HRA • Implication – Pace from CS if no induction from HRA – Post RFA check induction from both HRA and CS
- 45. Induction If single AESdoesn’t increase AH sufficiently – Double APC – Atrial pacing – Shorter drive cycle length – Isoproterenol, Atropine – CS stimulation
- 46. Induction 85% Typical AVNRT Dualpathway seen in response to single HRA AES
- 47. Induction 85% Typical AVNRT Dualpathway seen in response to single HRA AES Using all above methods Dual Pathway seen in 95% patients
- 48. Induction 5-10% show MULTIPLEpathways Multiple jumps of >50 ms with shorter coupling intervals AVNRT of different rates
- 49. Induction Upto 25% Non-AVNRTpopulation also – Dual pathway seen by these protocols But Only ‘JUMP’ seen
- 50. Induction Upto 25% Non-AVNRTpopulation also – Dual pathway seen by these protocols But Only ‘JUMP’ seen No Echo No Reentry over fast pathway No AVNRT
- 51. Induction Upto 25% Non-AVNRTpopulation also – Dual pathway seen by these protocols But Only ‘JUMP’ seen No Echo No Reentry over fast pathway No AVNRT Therefore, LIMITATION IS RETROGRADE CONDUCTION OVER FAST PATHWAY
- 52. Induction by VES Ventricularstimulation inducing AVNRT 10-40% Typical AVNRT patients Ventr PACING more effective than VES Only 10% induction by single VES Due to H-P refractoriness
- 53. Induction by VES TypicalAVNRT patients – retrograde conduction over FP very good Ventr PACING more effective than VES Only 10% induction by single VES Due to H-P refractoriness
- 54. Induction by VPacing – Mechanism • Retrograde over fast, concealed over slow – Dual pathway not seen – No critical VA delay BEFORE AVNRT – VA increases only when AVNRT induced
- 55. Induction by VPacing – Mechanism • FP retrograde refractory period > Slow pathway – Dual AV pathway seen – Atypical AVNRT induced
- 58. DETERMINANTS OF INDUCTIONOF AVNRT
- 59. DETERMINANTS OF INDUCTIONOF AVNRT • Rapid retograde conduction in FP – Typical AVNRT patients – 1:1 VA conduction at <400ms PCL
- 60. DETERMINANTS OF INDUCTIONOF AVNRT • Rapid retograde conduction in FP – Typical AVNRT patients – 1:1 VA conduction at <400ms PCL • Critical “A-H” – due to SP
- 61. DETERMINANTS OF INDUCTIONOF AVNRT • Rapid retograde conduction in FP – Typical AVNRT patients – 1:1 VA conduction at <400ms PCL • Critical “A-H” – due to SP • Ability to sustain repetitive antegrade conduction in SP – Typical AVNRT - 1:1 AV conduction at <350ms PCL
- 62. DETERMINANTS OF INDUCTIONOF AVNRT Low inducibility No VA conduction VA conduction worse than AV – VA WCL at PCL > 500 ms
- 63. DETERMINANTS OF INDUCTIONOF AVNRT Shorter the AH at NSR/Pacing Shorter the critical AH increment needed to induce AVNRT Better the VA conduction So called LGL syndome!
- 64. AVNRT: SURFACE ECGAND EPS
- 65. AVNRT HBE • 70%- atrial activation before or at onset of QRS • 25% - buried within QRS
- 66.
- 67. AVNRT Surface ECG •40% - No P waves seen
- 68. AVNRT Surface ECG •40% - No P waves seen • 55% - Terminal QRS distorted by P Pseudo R in V1 Pseudo S in Inferior leads Nonsp. Terminal QRS notching
- 69. AVNRT Surface ECG •40% - No P waves seen • 55% - Terminal QRS distorted by P Pseudo R in V1 Pseudo S in Inferior leads Nonsp. Terminal QRS notching • 1-2% - Very early P – Pseudo Q in Inferior leads Rare but specific
- 70. AVNRT Surface ECG •Basic – Atrial activation arising in MIDLINE – Requires atleast 50 ms to complete atrial depolarization Therefore these typical ECGs Make Bypass tracts less likely Atrial activation is from midline (likely from AVN)
- 71. Atypical AVNRT SurfaceECG • <5% AVNRTs • R-P / P-R is >1 • Difference from bypass tract needed • More Common in Post ablation pts.
- 72. EFFECT OF BBBON AVNRT
- 73. Effect of BBBon AVNRT • No effect on A-A of AVNRT • No effect on H-H of AVNRT
- 74. Effect of BBBon AVNRT • No effect on A-A of AVNRT • No effect on H-H of AVNRT • H-V may prolong during BBB – increase V-V by equal amount – but no effect on AVNRT
- 75. Effect of BBBon AVNRT • No effect on A-A of AVNRT • No effect on H-H of AVNRT • H-V may prolong during BBB – increase V-V by equal amount – but no effect on AVNRT • VES during AVNRT – can produce BBB (usually LBBB) – but no effect on AVNRT
- 77. Atria not needed •Retrograde VA blocks • 2:1 block • AV dissociation • No atrial activation at all
- 82. Response to APCduring SVT
- 85.
- 86.
- 87.
- 88. 1 • Mode ofinitiation Relation of – Basic drive cycle length – ES coupling interval – Onset of tachy – Tachy cycle length • Differentiates triggered activity from reentry
- 89. 2 • Atrial activationsequence • P-QRS relation
- 90. 3 • Effect ofBBB during Tachy – Spontaneous or induced BBB – On cycle length – V-A conduction time
- 91. 4 • Requirement ofatria, HB, Ventricle – in initation and maintenance of tachy – Effect of AV dissociation on tachy
- 92. 5 • Effect ofatrial or ventricular stimulation during tachy • Differentiates AT, AVNRT, CBT • EXCITABLE GAP
- 93. 6 • Effect ofdrugs or physiological maneuvers during Tachy
- 94.
- 95. ….NEXT presentations • AVRT •Ventricular Pre-excitation • Atrial Tachycardia • Ventricular arrhythmias • Catheter ablation