$th part of cardiac Electrophysiology basics

1. Basics of Electrophysiologic
Study, (part4)
Dr. Salah Atta, MD
Cosultant Electrophysiologist, SBCC
Professor of Cardiology
Assiut University, Egypt

2. Role of EPS in the Diagnosis and
Management of Arrhythmias

3. Mechanisms of Arrhythmia
 Abnormal automaticity
 automatic impulse generation from unusual site
or overtakes sinus node
 Triggered activity
 secondary depolarization during or after
repolarization
 Dig toxicity, Torsades de Pointes
 Reentry
 90 % of arrhythmias

4. Reentry
 Most common
mechanism
 Requires two separate
paths of conduction
 Requires an area of
slow conduction
 Requires unidirectional
block

6. EP diagnosis of narrow QRSEP diagnosis of narrow QRS
tachycardiatachycardia

7. Differential Dx of Regular SVT
 Short RP tachycardia
 AV nodal reentrant
tachycardia (AVNRT)
 ORT( Orthodromic
reciprocating
tachycardia)= AVRT
 atrial tachycardia when
associated with slow AV
nodal conduction
Short RP interval

8. Differential Dx of Regular SVT
 Long RP tachycardia
 Atrial tachycardia
 Sinus node reentry
 Sinus tachycardia
 Atypical AV nodal
reentrant tachycardia
 Permanent form of
junctional reciprocating
tachycardia (PJRT) =
AVRT over a slow
retrograde conducting
AP.
Long RP interval

9. Forms of abnormal Sinus
Tachycardia
 Sinus node reentrant
 abrupt onset and offset
 P wave complex same as
sinus
 Amenable to calcium
channel blockers, much
less responsive to beta
blockers
 Amenable to catheter
ablation
 Syndrome of
inappropriate sinus
tachycardia
 typical sinus tachycardia
with lowest rate on Holter
of 130 bpm
 Treated with high dose
beta blockers
 Poor results with catheter
ablation

10. Regular SVT in adults
 90% reentrant, 10 % non reentrant
 60% AV nodal reentrant tachycardia (AVNRT)
 30% orthodromic reciprocating tachycardia
(ORT)
 10% Atrial tachycardia

11. Supraventricular Tachycardias
Diagnosis
 ECG is cornerstone
 Observe zones of transition for clues as to
mechanism:
 onset
 termination
 slowing, AV nodal block
 bundle branch block

12. Stepwise assessment of the induced tachycardia:Stepwise assessment of the induced tachycardia:
Once the tachycardia is induced, the followingOnce the tachycardia is induced, the following
observations help establish the mechanism:observations help establish the mechanism:
• Mode of initiation and termination.Mode of initiation and termination.
• A-V relationship: 1:1 or variable, V-A relation andA-V relationship: 1:1 or variable, V-A relation and
intervalinterval
• Atrial activation sequence, AV relationship,Atrial activation sequence, AV relationship,
ventricular activation sequence during theventricular activation sequence during the
tachycardia.tachycardia.
• Cycle length , Effect of pacing maneuvers andCycle length , Effect of pacing maneuvers and
drugs on the tachycardiadrugs on the tachycardia
• Other specific tests related to each type.Other specific tests related to each type.

13. AV Nodal Reentrant
Tachycardia
 2 pathways within or limited
to perinodal tissue
 anterograde conduction
down fast pathway blocks
with conduction down
slow pathway, with
retrograde conduction up
fast pathway.
 May have very short RP
interval with retrograde P
wave visible as an R’ in lead
V1 or psuedo-S wave in
inferior leads in 1/3 of cases .
No p wave seen in 2/3
Slow pathway
Fast pathway

14. AVNRT Mechanism

15. AV Nodal Reentrant
Tachycardia
 Responds to vagal maneuvers
in 1/3 cases
 Very responsive to AV nodal
blocking agents such as beta
blockers, CA channel
blockers, adenosine.
 Recurrences are the norm on
medical therapy
 Catheter ablation 95%
successful with 1% major
complication rate

16. EPS Diagnostic criteria of AVNRT:
 1-The initiation of AVNRT is dependent on a
critical delay in the AH interval (AH jump).
 2- The occurence of atrial activation
simultaneously with or before the ventricular
activation

18. AVNRTAVNRT

20. EPS diagnosis of AVNRT
 3- Retrograde VA during AVNRT is earliest on
HBE with a VA interval ≤70 msec.
 4- Inability of His synchronous ventricular
extrastimuli to pre-excite the atria during
AVNRT.
 5- BBB block has no effect on the tachycardia
cycle length.

22. WPW syndrome
ECG criteria:
 Accelerated AV conduction PR <120 msec
 Prolonged QRS > 120 msec
 Abnormal slurred upstroke of QRS ( delta wave)
 Abnormal depolarization and repolarization may
lead to pseudoinfarction pattern

23.  WPW

24. WPW epidemiology
 Present in 0.3% of the
population
 Risk of sudden death 1 per
1000 patient-years
 Sudden death due to atrial
fibrillation with rapid
ventricular conduction
 Atrial fibrillation often
induced from rapid ORT
ORT(orthodromic reciprocating
tachycardia

25. WPW pathophysiology
 Short AV conduction
 early excitation of ventricle
at site of accessory pathway
 Bizarre upstroke of QRS
 abnormal initial site of
depolarization
 Wide QRS
 early initiation of
ventricular depolarization
The result is fusion of both normal and
accessory conduction
No
conductio
n
delay
AV
node Accessory
pathway

27. EP criteria of Manifest pre-excitation:
Shows the following electrophysiologic criteria:
 In sinus rhythm, the AH interval is normal while the
HV interval is shorter than 35 msec.
 The anterograde curve is non decremental showing a
fixed AV interval, with closer atrial extrastimuli with
increasing pre-excitation, till the ERP of the AP is
reached and the AP conduction is blocked. At this
coupling interval the QRS complex normalizes as the
impulse is blocked in the AP and is conducted
exclusively over the AV node.
 the eccentericc ventricular activation sequence

30. EPS of WPW

32. Antegrade ERP of the AP

33. Safe AP

34. Concealed pre-excitation
(unidirectional retrograde
conduction over the AP):
 Has the same electrophysiologic properties of
manifest APs in the retrograde direction.
Anterogradely, conduction is decremental as the
impulses proceed over the AV node.

35. Orthodromic Reciprocating
Tachycardia
 Anterograde over AV node and
retrograde conduction of an
accessory pathway.
 RP interval short but longer than
AVNRT due to required
conduction through ventricle
prior to conduction up accessory
pathway
 Frequently presents in patients
with WPW patients as narrow
complex tachycardia
Up
accessory
pathway
Conduction down AVnode

36. ORT
 Amenable to AV nodal
blocking agents in
absence of WPW
syndrome (anterograde
conduction of pathway)
 Amenable to catheter
ablation with 95%
success and 1% rate
major complication
Conduction down AVnode
Up
accessory
pathway

37.  AVRT is induced and terminated by VPD, APDs or
pacing.
 The retrograde atrial activation sequence during AVRT
is eccentric and fixed independent of the SVT cycle
length.
 During ventricular pacing with extrastimulation, the
retrograde curve is also non decremental. The
retrograde atrial activation sequence simulates that
during orthodromic AVRT.
 ParaHisian pacing: constant V-A interval.
EPS of AVRT

39.  Both the atrium and the ventricle are necessary
for initiation and continuation of AVRT. AV or
VA block would interrupt the AVRT.
 His synchronous VPDs, during AVRT, either
terminates the tachycardia or conducts up the
AP pre-exciting (advancing) the atria.
 In case of free wall AP: Epsilateral BBB
produces prolongation of the SVT Cycle length
and the VA by 35 msec or more.
EPS of AVRT

40. His synchronized ventricular ES

41. EP criteria of AVRT
 The shortest VA interval during AVRT is generally
greater than 60 milliseconds and QRS to HRA interval
of at least 95 milliseconds.
 In the presence of septal AP the VA interval during RV
pacing tends to be similar to the VA interval during
AVRT.
 In AVNRT, VA during RV pacing tends to be longer
than during tachycardia. In AVNRT there is simult-
aneous antegrade and retrograde conduction from the
AVN, resulting in a short VA interval.

42. Orthodromic AVRTOrthodromic AVRT

44. Atrial Fibrillation and WPW
 AV nodal blocking agents
may paradoxically
increase conduction over
accessory pathway by
removing concealed
retrograde penetration
into accessory pathway.
Concealed penetration into the pathway
causes intermittent block of pathway
conduction

46. Management of Atrial
Fibrillation with WPW
 Avoid AV nodal blockers
 IV procainamide to slow accessory pathway
conduction
 Amiodarone if decreased LVEF
 DC cardioversion if symptomatic with
hypotension

47. Management of Patients with
WPW
 All patients with symptomatic AF & WPW
should be evaluated with EPS
 Accessory pathways capable of conducting faster
than 240 BPM should be ablated (ERP<250ms)
 Patients with inducible arrhythmias involving
pathway should be ablated
 WPW patients in high risk professions should be
evaluated.

48. Differentiation by pacing during
the SVT

49. What is entrainment?
 It is widely taught that a His-refractory ventricular premature
beat (VPB) can advance atrial timing during AVRT. The VPB
depolarizes the ventricles earlier than the tachycardia wavefront
would have, and this in turn advances atrial activation so that the
AVRT circuit is reset. If this rather basic electrophysiologic
concept is well understood, then entrainment, which is nothing
more than thecontinual resetting of such a circuit by a series of
consecutive VPB's (ie. a pacing train slightly faster than the
tachycardia), should be easily understood also.
 Tachycardia reappearnce after pacing cessation with same sequence,
morphology and cycle length is a mandatory condition for the definition of
entrainment.

51. Concealed entrainment (QRS complex is that of a paced beat) is different
from entrainment with concealed fusion (QRS complex is that of the native tachycardia). This
subtle distinction in nomenclature is commonly overlooked .
During orthodromic AVRT, the overdrive ventricular pacing site most likely
to result in entrainment with fusion is at the base, near the insertion of the AP.
Thus,
entrainment with concealed fusion indicates that the pacing site is close to the
ventricular insertion of the AP and can be used to map the AP.
On reappearance of the tachycardia after stopping pacing, certain criteria can be checked for
diagnosis of the re-entry circuit and nature of the SVT.....
Differentiation by pacing during
the SVT

52. A cPPI-TCL (post pacing interval – tachycardia cycle length) >
110 ms is consistent with AVNRT,
while a cPPI-TCL < 110 ms is consistent with AVRT employing
a non-left sided AP.
A cPPI-TCL > 110 ms can occur with AVRT employing a
left sided AP simply because the RVA pacing site is far
from such a circuit. During a long RP interval SVT, a
cPPI-TCL > 110 ms should also prompt conside-ration
of orthodromic AVRT employing a slowly conducting
AP with decremental conduction properties.*
Differentiation by pacing during
the SVT

53.  *In these challenging situations, fusion during
entrainment by ventricular pacing and delay of atrial
timing by a His refractory VPB should be considered
proof of the involvement of an AP regardless of the
PPI-TCL value.
 SA-VA(Stimulus to Atrium – Ventricle to A) differences <
85 ms are consistent with AVRT, while SA-VA differences >
85 ms are consistent with AVNRT.
 the cPPI-TCL and SA-VA differences may be unreliable during
SVTs with marked spontaneous beat-to-beat variation in TCL
(>40 ms).
Differentiation by pacing during
the SVT

54. Differentiation by pacing during
the SVT

55. Differentiation by pacing during
the SVT

56. A proposed algorithm to arrive at a diagnosis for regular sustained SVT based on the results of overdrive
ventricular pacing. Non-diagnostic responses may contain partial diagnostic information and include (i) termination
with conduction to the atria, (ii) termination of SVT with septal VA ≥ 70 ms by a VPB prior to His bundle
refractoriness that does not conduct to the atrium (excludes AT), and (iii) dissociation of the ventricles from the
tachycardia (excludes AVRT). A=atrium; V=ventricle; AT=atrial tachycardia; AVNRT=atrioventricular node
reentry tachycardia; AVRT=atrioventricular reciprocating tachycardia; S=stimulus; PPI=post pacing interval;
TCL=tachycardia cycle length; HRVPB=His refractory ventricular premature beat.

57. Atrial Flutter
An atrial flutter (Macrore-entry in the right
atrium with atrial rate: 300/min) with two
to one conduction to the ventricles with
LBBB aberration was evident.

62. Atrial Tachycardia
 Most are due to abnormal
automaticity and have
right atrial focus
 May be reentry
particularly in patients
with previous atriotomy
scar, such as CABG or
congenital repair patients

63. Atrial Tachycardia
 Atrial rate between 150 and 250 bpm
 Does not require AV nodal or infranodal
conduction as the origin is atrial.
 P wave morphology different than sinus
 P-R interval > 120 msec differentiating from
junctional tachycardia
 Origin inferred from P wave morphology.

64. Atrial tachycardia
 P wave upright lead V1 and negative in aVL
consistent with left atrial focus.
 P wave negative in V1 and upright in aVL
consistent with right atrial focus.
 Adenosine may help with diagnosis if AV block
occurs and continued arrhythmia likely atrial
tachycardia
 70-80% will also terminate with adenosine.

65. Atrial Tachycardia Therapy
 Frequently treated with antiarrhythmics
 Class 1 agents procainamide, quinidine, flecainide
may be used in patients without structural heart
disease.
 Class III agents sotalol, amiodarone, dofetilide may
be used with caution according to specific side effects
 AV Nodal blocking agents for rate control.
 Catheter ablation effective in 70-80%

67. EP Diagnosis of
Wide-Complex Tachycardia
(WCT)
Basic EPS

68. Definition:
Tachycardia with a QRS duration > 120 msec, which is related to an
asynchronous, or sequential activation of the ventricular
myocardium.
Wide Complex Tachycardia (WCT(
It comprises a broad range of cardiac rhythm abnormalities:
•Supraventricular tachycardia (SVT), with
permanent or functional BBB.
•Pre-excited tachycardia including:
•Antidromic tachycardia
•SVT with a by stander accessory pathway
•Ventricular tachycardia.

69. WCT
Causes of WCT

70. WCT
Causes of WCT in structually normal heart patients
(Eckardt et al., Heart 2006;92;704-711(

71. WCT
Causes of WCT in structually normal heart patients
(Eckardt et al., Heart 2006;92;704-711(

72. WCT
Many diagnostic clues have been proposed to
differentiate between SVT with aberration, and VT,
starting with
•History,
•Physical examination,
•ECG analysis and
•EPS: being the most definitive way for diagnosis.
The diagnosis of WCT starts from outside the EP laboratory:

73. Intracardiac Electrocardiography (EPS) of
WCT
Basic EPS

74. --Identifies whether broad-complexIdentifies whether broad-complex
tachycardias are ventricular ortachycardias are ventricular or
supraventricular in origin:supraventricular in origin:
which is the leading the atrium or thewhich is the leading the atrium or the
ventricle ?!ventricle ?!
During the CulpritDuring the Culprit
arrhythmiaarrhythmia?!

77. Basic EPS
Fahmy T, Hammouda M, Mokhtar M, 2001

78. Basic EPS
Fahmy T, Hammouda M, Mokhtar M, 2001

79. Thank you