1. WIDE COMPLEX TACHYCARDIA
Dr.Pradeep Sreekumar

2. Definitions
Wide QRS complex tachycardia is a rhythm with a rate of ≥100 b/m and QRS duration of ≥ 120 ms
VT – Three or more consequtive ventricular beats with rate of 100/minute or more
SVT- Tachycardia requiring participation of structures above bundle of His.

3. LBBB morphology-QRS complex duration ≥ 120 ms with a predominantly negative terminal deflection in lead V1
RBBB morphology-QRS complex duration ≥ 120 ms with a predominantly positive terminal deflection in V1

4. Why QRS is wide?
A widened QRS (≥120 msec) occurs when ventricular activation is abnormally slow
Arrhythmia originates outside of the normal conduction system (ventricular tachycardia)
Abnormalities within the His-Purkinje system (supraventricular tachycardia with aberrancy).
Pre-excited tachycardias: supraventricular tachycardias with antegrade conduction over an accessory pathway into the ventricular myocardium.

5. SVT (20%)
VT (80%)
Stewart RB. Ann Intern Med 1986

6. Causes of wide QRS complex tachycardia
Supraventricular tachycardia
- with prexsisting BBB
- with BBB due to heart rate (aberrant conduction)
- antidromic tachycardia in WPW syndrome
Ventricular tachycardia

7. Other causes.. Hyperkalemia Acidosis Antiarrhythmics-IA,IC
Ventricular pacing

8. Functional Bundle Branch Block
Functional aberration results from sudden change in cycle length when parts of the His-Purkinje system are partially or wholly inexcitable
Functional RBBB more common.

9. Linking phenomenon
Mechanism for perpetuation of functional anterograde bundle branch block due to repetitive transseptal retrograde concealed penetration by impulses propagating along the contralateral bundle.
Linking: a dynamic electrophysiologic phenomenon
in macroreentry circuits,Michael h. lehmann et al, Circulation. 1985;71:

10. LINKING PHENOMENON

11. AVRT Orthodromic AVRT – Antegrade conduction :AVnode
Retrograde conduction : Accessory pathway.
Wide QRS is produced only if aberrant conduction
(rate related or preexisting BBB)
Antidromic AVRT – antegrade conduction over the accessory pathway and retrograde conduction over the AV node .

12. AVRT

13. Mahaim fibre mediated tachycardia
Antegrade conduction : Mahaim pathway
Retrograde conduction:AV node
LBBB morphology
Left axis deviation
Pre-excitation during sinus rhythm is uncommon

15. Bundle Branch Reentrant VT

16. RBBB morphology wide QRS tachycardiaVT
Structurally normal heart
LVOT VT
Fasicular VT
Abnormal heart
LV myocardial VT
Bundle Branch Reentrant VT

17. SVT
SVT with pre existing RBBB
SVT with functional RBBB

18. LBBB morphology wide QRS tachycardiaVT
Structurally normal heart
RVOT VT
Abnormal heart
Right ventricular myocardial VT
ARVD

19. Mahaim fibre mediated tachycardia
SVT
Mahaim fibre mediated tachycardia
SVT with LBBB

20. Unique clinical challenge
Diagnosing the arrhythmia is difficult —
Diagnostic algorithms are complex and imperfect.
Urgent therapy is often required —
Patients may be unstable at the onset of the arrhythmia or deteriorate rapidly at any time.
Risks associated with giving therapy for an SVT to a patient who actually has VT

21. SVT vs VT Clinical history
Age
- ≥ 35 ys → VT (positive predictive value of 85%)
Underlying heart disease
Previous MI → 90% VT
Pacemakers or ICD
Increased risk of ventricular tachyarrhythmia
Medication
Drug-induced tachycardia → Torsade de pointes
Diuretics
Digoxin-induced arrhythmia → [digoxin] ≥2ng/l or normal if hypokalemia

22. Duration of the tachycardia — SVT is more likely if the tachycardia has recurred over a period of more than three years

23. SVT vs VT
AV dissociation
-cannon A waves
-variable intensity of S1
Termination of WCT in response to maneuvers like Valsalva, carotid sinus pressure, or adenosine favor SVT

24. Maneuvers
The response of the arrhythmia to maneuvers may provide insight to the mechanism of the WCT
Carotid sinus pressure —  Enhances vagal tone , depresses sinus and AV nodal activity

25. Carotid sinus pressure
Sinus tachycardia will gradually slow with carotid sinus pressure and then accelerate upon release.
Atrial tachycardia or atrial flutter-the ventricular response will transiently slow.
The arrhythmia is unaffected.
Paroxysmal SVT frequently terminates with carotid sinus pressure.

26. VT
Unaffected by vagal maneuvers such as carotid sinus pressure or valsalva
May slow or block retrograde conduction.
Exposes AV dissociation
Rarely, VT terminates in response to carotid sinus pressure.

27. Laboratory tests
The plasma potassium and magnesium concentrations (hypokalemia and hypomagnesemia predispose to the development of ventricular tachyarrhythmias. )
Digoxin, quinidine, or procainamide levels-to rule out drug toxicity

28. Chest x-ray Evidence suggestive of structural heart disease
Evidence of previous cardiothoracic surgery
Presence of a pacemaker or ICD.

29. Rate
Limited use in distinguishing VT from SVT.
When the rate is approximately 150 beats per minute, atrial flutter with aberrant conduction should be considered.
Ventricular rate > 200-suspect preexcitation tachycardia

30. Regularity
Marked irregularity of RR interval occurs in atrial fibrillation (AF) with aberrant conduction and polymorphic VT

31. Axis
A right superior axis (axis from -90 to ±180º)- “northwest" axis, strongly suggests VT .
(sensitivity 20%,specificity 96%)
Exception -antidromic AVRT in Wolff-Parkinson-White (WPW) syndrome .

32. Compared to the axis during sinus rhythm, an axis shift during the WCT of more than 40º suggests VT .
In a patient with a RBBB-like WCT, a QRS axis to the left of -30º suggests VT.
In a patient with an LBBB-like WCT, a QRS axis to the right of +90º suggests VT .

33. QRS duration In general, wider QRS favors VT.
In a RBBB-like WCT, a QRS duration >140 msec suggests VT
In a LBBB-like WCT, a QRS duration >160 msec suggests VT  
In an analysis of several studies, a QRS duration >160 msec was a strong predictor of VT (likelihood ratio >20:1) .

34. A QRS duration <140 msec does not exclude VT
( VT originating from the septum or within the His-Purkinje system may be associated with a relatively narrow QRS complex.)

35. Concordance
Concordance is present when the QRS complexes in all six precordial leads (V1 through V6) are monophasic with the same polarity.
Either -entirely positive with tall, monophasic R waves, or entirely negative with deep monophasic QS complexes.
If any of the six leads has a biphasic QRS (qR or RS complexes), concordance is not present.

36. Negative concordance is strongly suggestive of VT
exception:SVT with LBBB aberrancy may demonstrate negative concordance
Positive concordance -also indicates VT
exception: antidromic AVRT with a left posterior accessory pathway

37. Presence of concordance strongly suggests VT (90 percent specificity)
Absence is not helpful diagnostically (approximately 20 percent sensitivity) 
Higher specificity for Positive concordance compared to negative concordance(specificity 95% vs 90 %)

38. Negative concordance

39. Positive concordance

40. AV dissociation
AV dissociation is characterized by atrial activity that is independent of ventricular activity
Atrial rate slower than the ventricular rate diagnostic of VT.
Atrial rate that is faster than the ventricular rate - SVTs.

41. Absence of AV dissociation in VT
AV dissociation may be present but not obvious on the ECG.
The ventricular impulses conduct backwards through the AV node and capture the atrium ( retrograde conduction), preventing AV dissociation.

42. Dissociated P waves PP and RR intervals are different
PR intervals are variable
There is no association between P and QRS complexes
The presence of a P wave with some , but not all, QRS complexes

43. Fusion beats
Fusion beat-produced by fusion of two ventricular activation wavefronts characterised by QRST morphology intermediate between normal and fully abnormal beat.
Fusion beats during a WCT are diagnostic of AV dissociation and therefore of VT.
Low sensitivity(5-20%)

45. Capture beats
Capture beats, or Dressler beats, are QRS complexes during a WCT that are identical to the sinus QRS complex .
Implies that the normal conduction system has momentarily "captured" control of ventricular activation from the VT focus.
Fusion beats and capture beats are more commonly seen when the tachycardia rate is slower

47. If old ecg available…
Ideal QRS configuration between baseline and WQRST-suggest SVT(exception :bundle branch reentrant VT)
Contralateral BBB patterns in baseline vs WQRST ECGs-suggest VT
WQRST complexes narrower than baseline ECG-suggest VT(the baseline ecg must have a bundle branch block pattern)

48. Also look for…. VPCs Evidence of prior MI QT interval
ECG clues to any other structural heart disease

49. SVT vs VT ECG criteria: Brugada algorithm
Brugada P. Ciculation 1991

50. Step 1

51. Step 2

52. Step 3

53. Step 4: LBBB - type wide QRS complex
SVT VT
R wave >30ms
small R wave
notching of S wave V1
fast downslope
of S wave
> 70ms V6
Q wave
no Q wave

54. V1 in LBBB type QRS
True LBBB R-R duration <- 30 msec Interval from QRS onset to S nadir ≤70 msec (85% of SVT –A) VT R >30 msec,QRS onset to S nadir>70 msec (sensitivity-0.78,specificity 0.85,positive predictive value 0.97) Notching and slurring of QRS complex –myocardial disease

55. V6 in LBBB type QRS True LBBB Monophasic R with slow upstroke VT
qR or QS pattern

56. Step 4: RBBB - type wide QRS complex
SVT VT
rSR’ configuration
monophasic R wave
qR (or Rs) complex V1 or
R/S > 1
R/S ratio < 1
QS complex V6 or

57. V1 in RBBB type QRS
Initial ventricular activation is independent of RBB.
RBBB abberation affects only the latter QRS
True RBBB
rR’,rsR’,rSr’,rSR’ VT
qR,Rsr’,monophasic R wave
(Sensitivity 0.97,specificity 0.88)

58. VT SVT

59. V6 in RBBB type QRS RBBB abberation-small s wave. qRs or Rs pattern
RBBB type VT-
VT from left ventricle-LV and RV voltage contributes to S
qRS,qrS,rS,QS patterns seen

60. “R/S ratio in V6 rule”
R/S ratio in RBB type wide QRS tachycrdia less than one, favours VT
Sensitivity-0.73
Specificity-0.79
Positive predictive value 0.9

61. Josephson’s sign 
Notching near the nadir of the S-wave
Suggest VT

62. Wellens Criteria • QRS width > 140 msec • Left axis deviation
  •   AV dissociation
  •  Configurational characteristics of the QRS morphology

63. Ultrasimple Brugada criterion
Joseph Brugada
R wave peak time in Lead II 
Duration of onset of the QRS to the first change in polarity (either nadir Q or peak R) in lead II.
If the RWPT is ≥ 50ms the likelihood of a VT very high (positive likelihood ratio 34.8)
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)

65. Vereckei A, Duray G, Szénási G, Altemose GT, and Miller JM
Vereckei A, Duray G, Szénási G, Altemose GT, and Miller JM.  Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur Heart J 2007 Mar; 28(5)

67. aVR algorithm
Criteria looks ONLY at lead aVR (if answer is yes, then VT):
1. Is there an initial R wave?
2. Is there a r or q wave > 40 msec
3. Is there a notch on the descending limb of a negative QRS complex?
4. Measure the voltage change in the first (vi) and last 40 msec (vt). Is vi / vt < 1?
Vereckei et al, Heart Rhythm 2008

68. Sensitivity Specificity PPV NPV Brugada 89% 73% 92% 67%
Vereckei 97% % % %
Vereckei A, Duray G, Szénási G, Altemose GT, and Miller JM.  Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur Heart J 2007 Mar; 28(5)

72. Sensitivity & Specificity For VT
88% and 53% by aVR algorithm

73. VT vs AVRT ECG criteria
Brugada P. Ciculation 1991

74. THANK YOU…….