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Electrophysiology AVNRT

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Electrophysiology study of AVNRT arrhythmia in heart

Published in: Health & Medicine

Electrophysiology AVNRT

  1. 1. EP STUDY REENTRY AVNRT
  2. 2. WE’VE TALKED ABOUT… EQUIPMENT RELEVANT ANATOMY CATHETERS and PLACEMENT BASIC INTERVALS TESTS OF SN FUNCTION EXTRASTIMULUS TESTING REFRACTORY PERIODS INCREMENTAL PACING MINIMUM PROTOCOL FOR DIAGNOSTIC EPS
  3. 3. AND NOW… TACHYARRHYTHMIA MECH REENTRY MECH SVT AVNRT
  4. 4. TACHYARRHYTHMIAS
  5. 5. • Basic mechanisms of tachyarrhythmias – Enhanced impulse formation – Abnormal conduction
  6. 6. • Enhanced impulse formation – Abnormal automaticity (Phase 4) • Least affected by Extrastimulus testing • Overdrive pacing – either overdrive suppression or No effect
  7. 7. • Enhanced impulse formation – 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. 8. • Abnormal conduction – impulse propagation – Reentry • Pathway - Anatomic, Functional, Both
  9. 9. REENTRY
  10. 10. 3 conditions for reentry • Atleast 2 functional (or anatomic) distinct pathways • Joining proximally and distally • Forming a closed circuit of conduction
  11. 11. 3 conditions for reentry • Unidirectional block in 1 of the pathways
  12. 12. 3 conditions for reentry • Slow conduction down the unblocked pathway – allowing the previously blocked pathway time to recover excitability
  13. 13. 3 characteristics of reentry • Initiated by timed extrastimulus – more effectively than rapid pacing • Programmed stimulation can also terminate Tachy
  14. 14. 3 characteristics of reentry • No direct relation of pacing cycle length to the tachy cycle length
  15. 15. 3 characteristics of reentry • Extrastimulus can reset or entrain the Tachy in presence of fusion Reentry is the MC mech of SVTs
  16. 16. EP EVALUATION OF SVT
  17. 17. 6 TENETS
  18. 18. 1 • Mode of initiation Relation of – Basic drive cycle length – ES coupling interval – Onset of tachy – Tachy cycle length • Differentiates triggered activity from reentry
  19. 19. 2 • Atrial activation sequence • P-QRS relation
  20. 20. 3 • Effect of BBB during Tachy – Spontaneous or induced BBB – On cycle length – V-A conduction time
  21. 21. 4 • Requirement of atria, HB, Ventricle – in initation and maintenance of tachy – Effect of AV dissociation on tachy
  22. 22. 5 • Effect of atrial or ventricular stimulation during tachy • Differentiates AT, AVNRT, CBT • EXCITABLE GAP
  23. 23. 6 • Effect of drugs or physiological maneuvers during Tachy
  24. 24. AVNRT
  25. 25. • MC SVT • >50% SVTs • Concept by Mines in 1913 • Moe demonstrated on rabbit AVN! – Dual AVN pathways
  26. 26. Typical or Common AVNRT
  27. 27. Typical or Common AVNRT Alpha Beta
  28. 28. Atypical or uncommon AVNRT
  29. 29. Evidence of dual AVN 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. 30. Definition of Dual AVN pathway
  31. 31. Definition of ‘JUMP’
  32. 32. Definition of ‘JUMP’ • > 50 ms increment in A-H interval with a small (~10 ms) decrease in coupling interval of Atrial extrastimulus
  33. 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!
  34. 34. Apart from the typical 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!
  35. 35. Apart from the typical 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
  36. 36. Apart from the typical 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!
  37. 37. • AV nodal conduction delay (A-H) is of prime importance in AVNRT – Not coupling interval of AES ‘CRITICAL AV DELAY’ or ‘CRITICAL AH INTERVAL’
  38. 38. AES from CS vs 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
  39. 39. AES from CS vs HRA • Dual pathway conduction and AVNRT • EASIER to induce from HRA
  40. 40. AES from CS vs 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
  41. 41. Induction If single AES doesn’t increase AH sufficiently – Double APC – Atrial pacing – Shorter drive cycle length – Isoproterenol, Atropine – CS stimulation
  42. 42. Induction 85% Typical AVNRT Dual pathway seen in response to single HRA AES
  43. 43. Induction 85% Typical AVNRT Dual pathway seen in response to single HRA AES Using all above methods Dual Pathway seen in 95% patients
  44. 44. Induction 5-10% show MULTIPLE pathways Multiple jumps of >50 ms with shorter coupling intervals AVNRT of different rates
  45. 45. Induction Upto 25% Non-AVNRT population also – Dual pathway seen by these protocols But Only ‘JUMP’ seen
  46. 46. Induction Upto 25% Non-AVNRT population also – Dual pathway seen by these protocols But Only ‘JUMP’ seen No Echo No Reentry over fast pathway No AVNRT
  47. 47. Induction Upto 25% Non-AVNRT population 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
  48. 48. Induction by VES Ventricular stimulation inducing AVNRT 10-40% Typical AVNRT patients Ventr PACING more effective than VES Only 10% induction by single VES Due to H-P refractoriness
  49. 49. Induction by VES Typical AVNRT patients – retrograde conduction over FP very good Ventr PACING more effective than VES Only 10% induction by single VES Due to H-P refractoriness
  50. 50. Induction by V Pacing – Mechanism • Retrograde over fast, concealed over slow – Dual pathway not seen – No critical VA delay BEFORE AVNRT – VA increases only when AVNRT induced
  51. 51. Induction by V Pacing – Mechanism • FP retrograde refractory period > Slow pathway – Dual AV pathway seen – Atypical AVNRT induced
  52. 52. DETERMINANTS OF INDUCTION OF AVNRT
  53. 53. DETERMINANTS OF INDUCTION OF AVNRT • Rapid retograde conduction in FP – Typical AVNRT patients – 1:1 VA conduction at <400ms PCL
  54. 54. DETERMINANTS OF INDUCTION OF AVNRT • Rapid retograde conduction in FP – Typical AVNRT patients – 1:1 VA conduction at <400ms PCL • Critical “A-H” – due to SP
  55. 55. DETERMINANTS OF INDUCTION OF 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
  56. 56. DETERMINANTS OF INDUCTION OF AVNRT Low inducibility No VA conduction VA conduction worse than AV – VA WCL at PCL > 500 ms
  57. 57. DETERMINANTS OF INDUCTION OF AVNRT Shorter the AH at NSR/Pacing Shorter the critical AH increment needed to induce AVNRT Better the VA conduction So called LGL syndome!
  58. 58. AVNRT: SURFACE ECG AND EPS
  59. 59. AVNRT HBE • 70% - atrial activation before or at onset of QRS • 25% - buried within QRS
  60. 60. AVNRT Surface ECG
  61. 61. AVNRT Surface ECG • 40% - No P waves seen
  62. 62. 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
  63. 63. 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
  64. 64. 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)
  65. 65. Atypical AVNRT Surface ECG • <5% AVNRTs • R-P / P-R is >1 • Difference from bypass tract needed • More Common in Post ablation pts.
  66. 66. EFFECT OF BBB ON AVNRT
  67. 67. Effect of BBB on AVNRT • No effect on A-A of AVNRT • No effect on H-H of AVNRT
  68. 68. Effect of BBB on 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
  69. 69. Effect of BBB on 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
  70. 70. Atria not needed • Retrograde VA blocks • 2:1 block • AV dissociation • No atrial activation at all
  71. 71. Response to APC during SVT
  72. 72. Excitable GAP
  73. 73. Pharmacology/Maneuvers • Propranolol • Isoproterenol/Atropine • Vagal maneuvers
  74. 74. 6 TENETS
  75. 75. 1 • Mode of initiation Relation of – Basic drive cycle length – ES coupling interval – Onset of tachy – Tachy cycle length • Differentiates triggered activity from reentry
  76. 76. 2 • Atrial activation sequence • P-QRS relation
  77. 77. 3 • Effect of BBB during Tachy – Spontaneous or induced BBB – On cycle length – V-A conduction time
  78. 78. 4 • Requirement of atria, HB, Ventricle – in initation and maintenance of tachy – Effect of AV dissociation on tachy
  79. 79. 5 • Effect of atrial or ventricular stimulation during tachy • Differentiates AT, AVNRT, CBT • EXCITABLE GAP
  80. 80. 6 • Effect of drugs or physiological maneuvers during Tachy
  81. 81. TO BE CONTINUED….
  82. 82. ….NEXT presentations • AVRT • Ventricular Pre-excitation • Atrial Tachycardia • Ventricular arrhythmias • Catheter ablation

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