Wide complex tachycardia

1. Osama Diab
Assistant prof. of Cardiology
Ain Shams University

2. What make the complex narrow ?
1- The impulse originates above the
ventricles
2- The impulse conducts to the ventricle
centrally (through the AVN-His)
3- The LBB and RBB are intact
(Simultaneous LV and RV activation)

3. What make the complex wide ?
1- The impulse originates from the
ventricles
2- The impulse conducts to the ventricle
eccentrically (through acces pathway)
3- LBBB or RBBB

4. Wide complex tachycardias
1- PVCs
2- Ventricular tachycardia
3- Antidromic AVRT
4- SVT with BBB
5- AF or flutter with antegrade
accessory pathway conduction
6- AF or flutter with BBB
7- PM mediated tachycardia

5. The ACC algorithm

6. the most commonly used algorithm. SN 89%, SP 59.2%.
1
2
3
4

7. V2
V3
V4
V1
V5
V6
Why absence of RS indicates VT ?

8. V1 V2
V3
V4
V5
V6
Why absence of RS indicates VT ?

9. V1 V2
V3
V4
V5
V6
Why absence of RS indicates VT ?
However, presence of RS does not preclude VT

10. the most commonly used algorithm. SN 89%, SP 59.2%.
1
2
3
4

11. Why RS interval 100 ms indicates VT ?
Normally ventricular activation speed up by the
virtue of Purkinje fibers
<100 ms

12. Why RS interval 100 ms indicates VT ?
Subepicardial origin of VT delay
ventricular activation
>100 ms
Again.. RS <100 ms does not preclude VT

13. the most commonly used algorithm. SN 89%, SP 59.2%.
1
2
3
4

14. Morphologic criteria
Initial R
more than
40ms
In the presence of LBBB like morphology
Capture beats
Fusion beats
Notch Any Q in V6
Rapid
downstroke
No q
LBBB
aberration

15. Morphologic criteria
In the presence of RBBB like morphology
Monophasic R in V1 Deep
RBBB

16. Ultrasimple Brugada criterion:
RW to peak Time (RWPT)
Sensitivity 60%, specificity 82.7%.
Pava LF, Perafán P, Badiel M, Arango JJ, Mont L, Morillo CA, and Brugada J. R-wave peak time at DII: a new criterion for differentiating
between wide complex QRS tachycardias. Heart Rhythm 2010 Jul; 7(7) 922-6. doi:10.1016/j.hrthm.2010.03.001 pmid:20215043

17.  Individuals with previous MI or known CAD are
approximately 4 times more likely to present with VT
rather than SVT etiologies of their WCT
 80% of all patients presenting with WCT will be
diagnosed having VT as the cause of WCT
Wide QRS complex tachycardia: ECG differential diagnosis.Brady WJ, Skiles J. Am J Emerg Med. 1999 Jul; 17(4):376-81.

18. History of prior MI, CHF, and recent angina all had
positive predictive values for VT greater than 95%
The best predictor for SVT was age less than or
equal to 35 years (positive predictive value of 70%)
 Hemodynamic instability favors VT
 Irregular cannon waves favors VT
 Variability of S1 and SBP favors VT
 Vagal maneuvers may reveal SVT
 In pt with a PM, a magnet can terminate PMT

19.  Different axis in limb leads indicates VT
 Preexisting BBB
 WPW
 P wave morphology helps recognize AV
dissociation
 IVCD
 Prior MI

20. No diagnostic technique is
100% correct and that there are
always exceptions to the rule

21. VT due to Enhanced Automaticity
General features
-Gradual onset and offset
-Can not be terminated by DC shocks
-Secondary to a causes (hypoxia, ischemia, sympathomimetic
drugs, thyrotoxicosis, electrolyte disturbance, HF, PE)
-May be idiopathic (idiopathic VT)

22. General Management
Treat the cause
If symptomatic:
-B blockers, Calcium channel blockers
-Xylocaine, mexiletine, amiodarone
-Ablation
VT due to Enhanced Automaticity

23. General Features
-Sudden onset & offset
-Fixed rate
-Can be induced by programmed extrastimulation
-Can be terminated by overdrive pacing (ATP)
-Can be terminated by DC shock
Reentrant VT
(scar related VT)

24. Reentry

25. Slow pathway
with short RP
Fast pathway
with long RP
Sinus beat
Normal sinus beat
No reentry.. No tachycardia

26. Slow pathway
with short RP
Fast pathway
with long RP
Premature beat
Too late premature beat
No reentry.. No tachycardia

27. Slow pathway
with short RP
Fast pathway
with long RP
Premature beat
Too early premature beat
No reentry.. No tachycardia

28. Slow pathway
with short RP
Fast pathway
with long RP
Premature beat
Critically timed premature beat
Reentry……..tachycardia

29. Slow pathway
with short RP
Fast pathway
with long RP
Premature beat
Critically timed premature beat
RP(fast) – RP(slow)Tachycardia zone =

30. Slow pathway
with short RP
Fast pathway
with long RP
Premature beat
Critically timed premature beat
RP(fast) – RP(slow)Tachycardia zone =

31. Slow pathway
with short RP
Fast pathway
with long RP
Premature beat
Critically timed premature beat
RP(fast) – RP(slow)Tachycardia zone =

32. RP(fast) – RP(slow)Tachycardia zone =
Critically timed premature beat
Premature beatTachycardia zone

33. Antiarrhythmic drugs
Premature beatTachycardia zone
How antiarrhythmic drugs
prevent reentrant arrhythmias?
Antiarrhythmic drugs shorten the tachycardia zone

34. Antiarrhythmic drugs
Premature beatTachycardia zone
How antiarrhythmic drugs
prevent reentrant arrhythmias?
Antiarrhythmic drugs prevent the initiating prematures

35. RP(fast) – RP(slow)Tachycardia zone =
How antiarrhythmic drugs
prevent reentrant arrhythmias?
RP(fast) RP(slow)
Tachycardia
zone
msec
RP(fast) RP(slow)
Antiarrhythmic drugs

36. RP(fast) – RP(slow)Tachycardia zone =
Critically timed premature beat
RP(fast) RP(slow)
Tachycardia
zone
msec
RP(fast) RP(slow)
Antiarrhythmic drugs
Proarrhythmic effect

37. (Medical Cardioversion)
RP RP
Drugs Drugs
How antiarrhythmic drugs terminate
reentrant arrhythmaias?

38. Overdrive pacing
Rentry

39. • Congenital Long QT Syndrome
• Acquired Long QT Syndrome
• Short QT Syndrome
• Brugada Syndrome
• Catecholaminergic Polymorphic VT
• Early repolarization syndrome
VT due to Channelopathies

40. VT
Idiopathic VT Scar related VT
Normal heart
10% of all VTs
Young, middle aged
Automatic / triggered
Commonly from outflow tracts
(adenosine sensitive)
Respond to BB, CCB
Ablation is curativs
Structural heart disease
Elderly, middle aged
Reentrant
Respond to BB, amiodarone
ICD
3D guided ablation can decrease
shocks from ICD (40%)

41. The most frequently (70%) idiopathic ventricular
arrhythmias originate from the right ventricular outflow
tract (RVOT)  multiple extrasystoles, couplets, and
even short bouts of ventriculartachycardia.
Recent reports described theoccurrence of
cardiomyopathy associated with RVOT ectopic activity
Idiopathic VT

42. Idiopathic dilated cardiomyopathy rarely is associated
with extrasystoles having a pattern of left bundle branch
block with normal or inferior axis, suggesting that RVOT
extrasystoles are unlikely a consequence of
cardiomyopathy.
More importantly,in all these reports, a dramatic
improvement of LV function occurred after RFA of
ventricular ectopy, suggesting that the cardiomyopathy
actually resulted from the ventricular arrhythmia
Idiopathic VT

44. V5
V6
LVOT-VT:
Supravalvular focus: Absent S in V5, V6
Infravalvular focus: S in V5, V6
Sensitivity 100%
Specificity 88%
Hachiya H, et al. . How to diagnose, locate, and ablate coronary cusp ventricular tachycardia. J Cardiovasc
Electrophysiol 2002;13:551-6.

45. Ablation of idiopathic VT
CARTO Conventional

46. 1- Area of conduction
block:
Scar area + MVA
2- Surviving myocardial
strands within the scar
(isthmus)
3- An outer loop of normal
myocardioum
4- Entrance
5- Exit
Components of VT reentry circuit
Non viable
Viable

47. Diastolic pathway: Entrance, isthmus, and exit
Systolic pathway: Outer loop

48. RA
Ablation of scar related VT
Scar
Outer loop
Isthmus
Scar/MVA

49. SVT with RBBB

50. Preexcited AF

51. ECG from the same pt: WPW

52. VT

53. VT

54. Atrial tachycardia with RBBB

55. VT

56. VT

57. NSVT originating from LVOT

58. VT with narrow QRS

59. Bidirectional VT (digoxin toxicity or CPMVT)

60. Long QT - Torsade

61. NSVT on Holter (slight irregularity)

62. Holter monitoring: Artifacts