Wide complex tachycardia

Wide complex tachycardia

1. Wide Complex Tachycardia 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. How likely VT is the diagnosis?

18. Clinical clues 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. Value of previous ECGs 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 beat Tachycardia zone

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

34. Antiarrhythmic drugs Premature beat Tachycardia 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. T he most frequently (70%) idiopathic ventricular arrhythmias originate from the right ventricular outflow tract (RVOT)  multiple extrasystoles , couplets, and even short bouts of ventricular tachycardia. Recent reports described the occurrence 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

43. 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 Scar related VT Non viable Viable

47. Scar related VT 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

63. Thank You