Electrophysiology study of AVNRT arrhythmia in heart

1. EP STUDY
REENTRY
AVNRT

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. AND NOW…
TACHYARRHYTHMIA MECH
REENTRY MECH
SVT
AVNRT

4. TACHYARRHYTHMIAS

5. • Basic mechanisms of tachyarrhythmias
– Enhanced impulse formation
– Abnormal conduction

6. • Enhanced impulse formation
– Abnormal automaticity (Phase 4)
• Least affected by Extrastimulus testing
• Overdrive pacing – either overdrive suppression or
No effect

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. • Abnormal conduction – impulse propagation
– Reentry
• Pathway - Anatomic, Functional, Both

9. REENTRY

10. 3 conditions for reentry
• Atleast 2 functional (or anatomic) distinct
pathways
• Joining proximally and distally
• Forming a closed circuit of conduction

11. 3 conditions for reentry
• Unidirectional block in 1 of the pathways

12. 3 conditions for reentry
• Slow conduction down the unblocked
pathway – allowing the previously blocked
pathway time to recover excitability

13. 3 characteristics of reentry
• Initiated by timed extrastimulus – more
effectively than rapid pacing
• Programmed stimulation can also terminate
Tachy

14. 3 characteristics of reentry
• No direct relation of pacing cycle length to the
tachy cycle length

15. 3 characteristics of reentry
• Extrastimulus can reset or entrain the Tachy in
presence of fusion
Reentry is the MC mech of SVTs

16. EP EVALUATION OF SVT

17. 6 TENETS

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. 2
• Atrial activation sequence
• P-QRS relation

20. 3
• Effect of BBB during Tachy
– Spontaneous or induced BBB
– On cycle length
– V-A conduction time

21. 4
• Requirement of atria, HB, Ventricle
– in initation and maintenance of tachy
– Effect of AV dissociation on tachy

22. 5
• Effect of atrial or ventricular stimulation
during tachy
• Differentiates AT, AVNRT, CBT
• EXCITABLE GAP

23. 6
• Effect of drugs or physiological maneuvers
during Tachy

24. AVNRT

25. • MC SVT
• >50% SVTs
• Concept by Mines in 1913
• Moe demonstrated on rabbit AVN! – Dual AVN
pathways

26. Typical or Common AVNRT

27. Typical or Common AVNRT
Alpha Beta

28. Atypical or uncommon AVNRT

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. Definition of Dual AVN pathway

31. Definition of ‘JUMP’

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 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!

37. 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

39. 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!

41. • AV nodal conduction delay (A-H) is of prime
importance in AVNRT – Not coupling interval
of AES
‘CRITICAL AV DELAY’ or ‘CRITICAL AH INTERVAL’

42. 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

43. AES from CS vs HRA
• Dual pathway conduction and AVNRT
• EASIER to induce from HRA

44. 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

45. Induction
If single AES doesn’t increase AH sufficiently
– Double APC
– Atrial pacing
– Shorter drive cycle length
– Isoproterenol, Atropine
– CS stimulation

46. Induction
85% Typical AVNRT
Dual pathway seen in response to single HRA AES

47. Induction
85% Typical AVNRT
Dual pathway seen in response to single HRA AES
Using all above methods
Dual Pathway seen in 95% patients

48. Induction
5-10% show MULTIPLE pathways
Multiple jumps of >50 ms with shorter
coupling intervals
AVNRT of different rates

49. Induction
Upto 25% Non-AVNRT population also – Dual
pathway seen by these protocols
But
Only ‘JUMP’ seen

50. 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

51. 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

52. 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

53. 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

54. 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

55. Induction by V Pacing – Mechanism
• FP retrograde refractory period > Slow
pathway
– Dual AV pathway seen
– Atypical AVNRT induced

58. DETERMINANTS OF INDUCTION OF AVNRT

59. DETERMINANTS OF INDUCTION OF AVNRT
• Rapid retograde conduction in FP
– Typical AVNRT patients – 1:1 VA conduction at
<400ms PCL

60. 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

61. 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

62. DETERMINANTS OF INDUCTION OF AVNRT
Low inducibility
No VA conduction
VA conduction worse than AV – VA WCL at PCL
> 500 ms

63. 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!

64. AVNRT: SURFACE ECG AND EPS

65. AVNRT HBE
• 70% - atrial activation before or at onset of
QRS
• 25% - buried within QRS

66. AVNRT Surface ECG

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 Surface ECG
• <5% AVNRTs
• R-P / P-R is >1
• Difference from bypass tract needed
• More Common in Post ablation pts.

72. EFFECT OF BBB ON AVNRT

73. Effect of BBB on AVNRT
• No effect on A-A of AVNRT
• No effect on H-H of AVNRT

74. 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

75. 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

77. Atria not needed
• Retrograde VA blocks
• 2:1 block
• AV dissociation
• No atrial activation at all

82. Response to APC during SVT

85. Excitable GAP

86. Pharmacology/Maneuvers
• Propranolol
• Isoproterenol/Atropine
• Vagal maneuvers

87. 6 TENETS

88. 1
• Mode of initiation
Relation of
– Basic drive cycle length
– ES coupling interval
– Onset of tachy
– Tachy cycle length
• Differentiates triggered activity from reentry

89. 2
• Atrial activation sequence
• P-QRS relation

90. 3
• Effect of BBB during Tachy
– Spontaneous or induced BBB
– On cycle length
– V-A conduction time

91. 4
• Requirement of atria, HB, Ventricle
– in initation and maintenance of tachy
– Effect of AV dissociation on tachy

92. 5
• Effect of atrial or ventricular stimulation
during tachy
• Differentiates AT, AVNRT, CBT
• EXCITABLE GAP

93. 6
• Effect of drugs or physiological maneuvers
during Tachy

94. TO BE CONTINUED….

95. ….NEXT presentations
• AVRT
• Ventricular Pre-excitation
• Atrial Tachycardia
• Ventricular arrhythmias
• Catheter ablation