This document discusses electrophysiological diagnosis and management of atrioventricular reentrant tachycardia (AVRT). It describes the historical discovery of Wolff-Parkinson-White syndrome and mechanisms of tachyarrhythmias including reentry. Characteristics of orthodromic and antidromic AVRT are provided along with techniques for evaluating accessory pathways including baseline observations, programmed stimulation, and catheter ablation. Precise localization of accessory pathways is important for successful ablation.

1. Electrophysiological
diagnosis and
management of AVRT
Satyam Rajvanshi

3. W
P
W

4. Louis Wolff
John Parkinson
Paul Dudley White

5. • In 1930, published article
describing 11 patients
who suffered from
attacks of tachycardia
associated with a sinus
rhythm with pattern of
bundle branch block with
a short PR interval
• Later k/a WPW
syndrome!
Louis Wolff
John Parkinson
Paul Dudley White

6. MECHANISMS OF
TACHYARRHYTHMIAS

7. • Disorders of Impulse formation
• Disorders of impulse conduction
• Combination of both

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

9. • 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

10. • Disorders of Impulse formation
• Automaticity
• Triggered activity – EAD/DAD
• Disorders of impulse conduction
• Reentry
• Combination of both

11. • Disorders of impulse conduction
– Reentry
• Pathway - Anatomic, Functional, Both
• MC mechanism of SVTs

12. REENTRY

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

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

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

16. Sites of re-entry in SVT

17. AVRT: INTRODUCTION

18. AVRT
• Reentrant tachycardia with an anatomically defined
circuit that consists of two distinct pathways, the
normal AV conduction system and an AV accessory
pathway, linked by common proximal (the atria) and
distal (the ventricles) tissues.
• Other arrhythmias can utilize the accessory pathway
for conduction from the anatomic site of tachycardia
origin to other regions of the heart (like AF/AFL)
• But AVRT is a specific reentrant tachycardia in which
the accessory pathway is necessary for initiation and
maintenance of the tachycardia

19. AVRT
• Accessory pathway maybe
Manifest/WPW Concealed

20. AVRT
• Accessory pathway maybe
Manifest/WPW
• Can conduct both Antegrade
(A to V) & Retrograde (V to A)
• Abnormal ECG baseline
• Variable degrees of pre-
excitation
• Higher risk with atrial
fibrillation
Concealed
• Retrograde (V to A)
conduction only
• Normal ECG baseline
• No pre-excitation
• Atrial fibrillation not an
issue

21. AVRT
• Accessory pathway maybe
Manifest/WPW
• Antidromic AVRT ±
Orthodromic AVRT
Concealed
• Only Orthodromic AVRT
possible
• 20-40% SVTs in patients
without pre-excitation

22. AVRT
• Accessory pathway maybe
Manifest/WPW
• Antidromic AVRT ±
Orthodromic AVRT
Concealed
• Only Orthodromic AVRT
possible
• 90% - Fast conducting
• 10% - Slow (decremental)
conduction - PJRT

23. AV conduction in concealed AP
Vn – normal ventricular activation

24. AV conduction in manifest AP
Vn – normal ventricular activation
Vp – ventricular activation via AP

25. AV conduction in manifest AP
with AV nodal delay
Vn – normal ventricular activation
Vp – ventricular activation via AP

26. Pre excitation syndromes
• Preexcitation
– Exists when in relation to atrial events, all or some
part of ventricle is activated sooner than would be
expected if the impulse reached ventricle by
normal AV conduction

27. Pre excitation syndromes
• Old classification – various eponyms
– Kent fibre (A-V)
– James fibre (Atrio-nodal)
– Mahaim fibre (Atrio-Fasc or Nodo-Fasc)
• Antidromic AVRT with LBBB + superior axis
• Progressive increase in the AV interval in response to atrial
overdrive pacing (oppositeto the behavior of the usual AP, in
which preexcitation occurs with short AV intervals)
– WPW syndrome
– LGL syndrome

28. Pre excitation syndromes
• New classification – No eponyms
– Atrioventricular bypass tract
– Nodoventricular bypass tract
– Fasciculoventricular bypass tract
– AV nodal bypass tract – atrionodal/atriofascicular

29. Pre excitation syndromes
• New + Old classification
– Atrioventricular bypass tract: WPW syndrome
– Nodoventricular bypass tract: WPW variant
– Fasciculoventricular bypass tract: WPW variant
– Atrionodal bypass tract: LGL syndrome

30. WPW in Sinus Rhythm

31. Pre-excitation 12-Lead ECG
PR interval < 120 ms
Normal P wave vector (not ectopic atrial rhythm)
Delta wave
QRS duration > 100 ms

32. Orthodromic AVRT
Initiated by a closely coupled APC or
VPC
Blocks in the accessory pathway but
conducts through the AV node
Retrograde conduction via accessory
pathway
Inverted P wave produced by
retrograde conduction visible in the
inferior ECG leads

33. Antidromic AVRT
• Retrograde conduction via AV node
• Antegrade via AP

34. Orthodromic AVRT: 12-Lead ECG
Ventricular rate typically 150 – 250/min (or greater) beats per minute, regular
Narrow QRS complexes (in the absence of underlying IVCD)
Inverted P waves with an RP interval usually <50% the tachycardia RR interval (RP < PR)
Constant RP interval regardless of the tachycardia cycle length
Beat-to-beat oscillation in QRS amplitude (QRS alternans) sometimes occurs, most
commonly seen when the rate is very rapid

35. Antidromic AVRT: 12 lead ECG
Ventricular rate typically 150 – 250/min (or greater) beats per minute, regular
Wide QRS complexes (similar or wider than baseline pre-excitation)
Inverted P waves with an RP interval usually >50% the tachycardia RR interval (RP > PR)
Constant RP interval regardless of the tachycardia cycle length

36. AP Location
• Anywhere along the muscular portion of the posterior and lateral
aspects of the mitral and tricuspid annuli.
Schematic from base of heart From LAO view

37. AP Location
• None of the various algorithm is perfect
• Simplest algorithm, Fitzpatrick -

38. EP DIAGNOSIS OF AVRT

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

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

41. The 3 characteristics of reentry
• Extrastimulus can reset or entrain the
Tachycardia in presence of fusion

42. 6 TENETS OF SVT EVALUATION

43. 1
• Mode of initiation
Relation of
– Basic drive cycle length
– ES coupling interval
– Onset of tachy
– Tachy cycle length
• Differentiates triggered activity from reentry

44. 2
• Atrial activation sequence
• P-QRS relation

45. 3
• Effect of BBB during Tachy
– Spontaneous or induced BBB
– On cycle length
– V-A conduction time

46. 4
• Requirement of atria, HB, Ventricle
– in initation and maintenance of tachy
– Effect of AV dissociation on tachy

47. 5
• Effect of atrial or ventricular stimulation
during tachy

48. 6
• Effect of drugs or physiological maneuvers
during Tachy

49. AVRT: Baseline observation during NSR
• H-V < 35 ms, may be negative
• His potential can be buried in the local ventricular EGM
• Site of earliest ventricular activation is near the
ventricular insertion site of the AP (i.e., near the
tricuspid annulus or mitral annulus at the base of the
heart)
• Slowing of conduction in the AVN by carotid sinus
massage, AVN blockers, or rapid atrial pacing unmasks
and increases the degree of preexcitation, because
these maneuvers do not affect the conduction over the
AP.

50. • HV -11 ms at AES 600 ms
• HV -65 ms at AES 440 ms

51. • HV -93 ms at AES 350 ms
• Less preexcitation on sinus beat

52. AES during NSR
• In the presence of a manifest AV-AP, atrial stimulation from any
atrial site can help unmask preexcitation if it is not manifest during
NSR caused by fast AVN conduction.
• Incremental rate atrial pacing and progressively premature AES
produce decremental conduction over the AVN (but not over the
AP), increasing the degree of preexcitation and shortening the HV
interval, until the His potential is inscribed within the QRS.
• The His potential is still activated anterogradely over the AVN until
anterograde block in the AVN occurs; the QRS then becomes fully
preexcited, and the His potential becomes retrogradely activated
• Atrial stimulation close to or at the AV AP insertion site results in
maximal preexcitation and the shortest P-delta Interval

53. • Retrograde His activation and echo beat

54. AES during NSR
• The failure of atrial stimulation to increase the
amount of preexcitation can be caused by
– markedly enhanced AVN conduction
– presence of another AV-AP
– pacing-induced block in the AV AP because of a
long ERP of the AP (longer than that of the AVN)
– total preexcitation already present at the basal
state caused by prolonged or absent AVN-HPS
conduction, and/or decremental conduction in the
AP

55. VES during NSR
Indicators of the presence of a retrogradely conducting
AV AP
• VES resulting in retrograde VA conduction – eccentric
atrial activation sequence
• VES delivered when the HB is refractory that results in
atrial activation
However, if a VES delivered when the HB is refractory
does not result in atrial activation, this does not
necessarily exclude the presence of a retrogradely
conducting AP, because such a VES can be associated
with retrograde block in the AP itself, or presence of
unidirectional (anterograde-only) APs

56. VES during NSR
• In the presence of a retrogradely conducting AV BT
(whether manifest or concealed), VES during NSR can result
in VA conduction over the BT, AVN, both, or neither
• Conduction over the AP alone is the most common pattern
at short pacing CLs or short VES coupling intervals. In this
case, the VA conduction time is constant over a wide range
of pacing CLs and VES coupling intervals, (in the absence of
intraventricular conduction abnormalities or additional
Aps)
• On the other hand, retrograde conduction over the BT and
HPS-AVN is common when RV pacing is performed in the
presence of a left-sided BT at long pacing CLs or long VES
coupling intervals

57. • A- Retrograde atrial activation by both AVN and AP
• B- retrograde atrial activation by AP alone – Eccentric
activation

58. • Type of eccentric atrial activation on location of AP
• Left lateral AP

59. • Right lateral AP – A in HRA before CS

60. • Posterosepatal AP – A in PCS before HBE

61. AVRT induction: Orthodromic AVRT
Initiation of orthodromic AVRT with an AES requires
• Anterograde block in the AV-BT
• Anterograde conduction over the AVN-HPS
• Slow conduction over the AVN-HPS, with adequate delay to allow for the recovery
of the atrium and AV BT
• Subsequent retrograde conduction over the BT
• The reason this occurs is because, whereas the BT conducts more rapidly than the
AVN, it has a longer ERP, so the early atrial impulse blocks anterogradely in the BT
but conducts over the AVN.
• The site of AV delay is less important; it is most commonly in the AVN, but it can
occur also in the HB, bundle branches, or ventricular myocardium.
• BBB ipsilateral to the AV BT provides an additional AV delay that can facilitate
tachycardia initiation.
• Induction of orthodromic AVRT is easier with AES near the AV BT insertion site; the
closer the stimulation site to the BT, the easier it is to encroach on the refractory
period of the BT and achieve block

62. If SVT induction fails by AES
• use of multiple AESs
• Rapid atrial pacing
• pacing closer to the BT
would achieve block in the BT and produce adequate AV delay

63. • Orthodromic AVRT in patients with concealed BTs is identical to that in
patients with WPW.
• The only difference is that in patients with concealed BTs anterograde
block in the BT is already present.
• Because the AV BT does not conduct anterogradely, the only condition
needed to induce orthodromic AVRT is adequate AV delay
• Therefore, orthodromic AVRT initiation requires less premature coupling
intervals of the AESs in patients with concealed BTs than in patients with
WPW.
AVRT is more easily induced by VES

64. Orthodromic AVRT:
Tachycardia features
• Atrial activation sequence – first activation closest to AP insertion site
• Fast conduction in AP - Short RP interval (50-120 ms) but longer than
AVNRT
• BBB much more common in AVRT (than AVNRT or AT) – 90% of sustained
SVTs with BBB – AVRT
• CSM can terminate orthodromic AVRT by gradual slowing and then block
in the AVN.
• Adenosine, digoxin, CCB, and BB terminate orthodromic AVRT by block in
the AVN - therefore, SVT terminates with a P wave not followed by a QRS

65. Antidromic AVRT:
Tachycardia features
• RP > PR interval – PR short and fixed
• Rest features similar to Orthodromic AVRT

66. AES/VES during tachycardia
• Close coupled AES/VES affect AVRT
– Entrainment
– Fusion
– Termination
• Ability of AES/VES to affect the SVT depends on the distance
between site of stimulation to the AP and coupling interval

67. Exclusion of AVNRT
PPI – post pacing interval

68. Location of AP
• Pacing from Multiple Atrial Sites. The closer the pacing site
to the BT atrial insertion, the more rapidly the impulse will
reach the BT relative to the AVN and thus the greater the
degree of preexcitation and the shorter the P-delta interval.
• Effects of Bundle Branch Block During Orthodromic AVRT
• Earliest atrial and ventricular activation sites
• Direct recording of BT potential

69. ABLATION

70. Criteria of Successful Ablation Sites during
Anterograde Activation Mapping

71. Additional criteria during retrograde
Activation Mapping

72. AVRT: Catheter Ablation Of Accessory Pathway
• Radio frequency ablation of the accessory
pathway is often indicated in patients with
WPW who are at risk of sudden death due
to atrial fibrillation with a rapid ventricular
response via the bypass tract.
• Note the disappearance of the pre-
excitation delta wave in the QRS with
catheter ablation.

73. AVRT: Catheter Ablation
Retrograde ablation of
left side AP, RAO
Ablation of right side AP

74. • Precise location of the accessory pathway is determined by the rove catheter. Retrograde conduction over the AP is seen as a
small spike between the V and A waves. These "Kent potentials" are so named because of the original denomination of
accessory pathways as "Kent bundles," after the investigator Stanley Kent, who first proposed the existence of accessory AV
connections.
AVRT: Catheter Ablation - Location of
AP

75. Ablation technique
• If preexcitation present (Manifest AP) – ablation performed
during NSR or, preferably, atrial pacing – allows detection of
delta wave
• For concealed AP – Ablation during ventricular pacing,
allows for detection of an eccentric atrial activation
sequence.
• RF energy delivery during AVRT avoided because of
potential catheter dislodgment from its critical position on
abrupt tachycardia termination – can cause transient loss of
conduction in AP for a variable period of time without
resulting in permanent damage to the AP
• For incessant AVRT, energy may be delivered during
ventricular pacing entraining the tachycardia

76. Ablation technique
• 4 mm tip ablation catheter sufficient
• Power 50 W
• Temperature 60 degree
– AP functional loss at 50 degrees
– AP permanent loss at 60 degrees – do not stop till 55-60
degrees is achieved by good contact (larger tip catheter
are rarely needed)

77. Ablation technique
• Loss of BT conduction is expected within 1 to 6 seconds of RF
application (once the target temperature and power delivery
have been reached) for most successful lesions.
• If no effect is seen after 15 seconds of RF delivery, energy
delivery should be discontinued because it is unlikely to be
beneficial, and mapping criteria and catheter contact should
be reexamined.
• If BT conduction is eliminated during the application, RF
delivery should be continued for up to 60 seconds.

78. Ablation technique
• If BT function is not eliminated at a site with apparent favorable
electrographic features, catheter contact with the tissue may be
inadequate.
• Adequacy of catheter contact can be verified by evaluating the
electrode temperature, catheter stability on fluoroscopy,
electrogram stability, and ST elevation on the unipolar electrogram.
• If electrode temperature is consistently more than 50°C with more
than 25 W energy delivered to the tissue during the RF application -
good catheter contact
• If electrode temperature is lower than 20°C with more than 25 W
energy – bad catheter contact
• If electrode temperature reaches more than 50°C but with very low
power (less than 10 W) - coagulum at the catheter tip

79. AVRT: Catheter Ablation

80. ENDPOINTS OF ABLATION

81. Successful ablation
• Confirmation of complete loss of BT function, and not just
noninducibility of tachycardias, is essential.
• Confirmation of complete loss of anterograde BT function using AES
and atrial pacing – no preexcitation
• Marked prolongation of the local AV interval at the ablation site.
• Confirmation of complete loss of retrograde BT function using VES
and ventricular pacing - concentric and decremental retrograde
atrial activation – normal VA conduction over the AVN
• Marked prolongation of the local VA interval at the ablation site.

82. OUTCOME

83. • RF ablation is a highly effective and curative treatment for
AVRT (more than 90%)
• Initially successful RF ablation is persistent and late
recurrence of BT conduction after ablation is rare (4%)
• Short runs of palpitations are frequent post RFA, usually
caused by isolated or short runs of PACs or PVCs and not by
recurrence of BT conduction, and can be easily managed with
symptomatic treatment without further investigation.

84. • Recurrence of AP-mediated tachycardia is usually observed
during the first month after ablation
• Later symptoms (palpitations appearing more than 3 months
after the ablation) are highly suggestive of SVTs not related to
the ablated AP – 10 to 30% patients with AVRT have multiple
pathways for tachycardias

85. • Repeat procedures 2-4%
• Serious complication (e.g., cardiac tamponade, AV block,
coronary artery injury, retroperitoneal hemorrhage, stroke)
<1%
• Mortality – 0.02%

86. Right free wall BT
Success rate of 93% to 98%, a recurrence rate of 21%, and a
complication rate less than that with other BT locations.
Posteroseptal BTs
Success rate (98%) and a recurrence rate of 12%.

87. Transaortic ablation of left free wall BTs
Success rate 86% to 100%, recurrence rate is 2% to 5%, less
frequent than for BTs at other locations.
Complications of this approach include vascular
complications (50% of all complications: groin hematoma,
aortic dissection, and thrombosis), cardiac tamponade,
stroke, coronary dissection (from direct catheter trauma),
injury to the left circumflex coronary artery (from
subannular RF application), valvular damage, and systemic
embolism
The transseptal approach
Success rate of 85% to 100%, a recurrence rate of 3%
to6.6%, and a complication rate of 0% to 6%