1. DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA

2. Wide Complex Tachycardia(WCT)-a rhythm with QRS duration ≥ 120 ms and heart rate > 100/min
VT-WCT originating below the level of His bundle
SVT…at or above the level of His bundle

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 predominant terminal deflection in V1
LBBB & RBBB morphology denote morphological appearance of QRS complex- result from direct myocardial activation

4. REGULAR WCT (1)VT - MC cause of WCT in general population (80%) -95% of WCT in pts with structural heart disease (2)SVT with abnormal intraventricular conduction(15% to 20% of WCT) -SVT with BBB/aberration (fixed/functional) -Mahaim pathway mediated tachycardia -Antidromic AVRT

6. IA, Ι C,amiodarone,tricyclic antidepressants
(3)SVT with a wide complex due to abnormal muscle spread of impulse
RBBB in pts undergone rt.ventriculotomy
LBBB in pts with DCM
(4)SVT with wide complex due to drug or electrolyte induced changes
IA, Ι C,amiodarone,tricyclic antidepressants
Hyperkalemia
(5)Ventricular paced rhythms
LBBB with left axis
(6)Post resuscitation

8. Irregular WCT
Any irregular supraventricular rhythm(AF,EAT or atrial flutter with varying conduction) with aberrant ventricular conduction
AF with ventricular preexcitation-if the ventricular rate in AF is >220/min or shortest R-R int is <250 msec, bypass tract should be considered
Polymorphic VT / Torsade de pointes

9. SVT vs VT- history and physical examination
History of prior heart disease favour VT
Prior MI,angina or CCF
Each factor -95% PPV for VT
H/o similar episodes for >3 yrs - SVT more likely
First episode of WCT after MI - VT more likely
Older age grp > 35 yrs-VT more likely

10. Findings of AV dissociation - favour VT
Cannon a waves
Variable intensity of S1
Variable SBP
AV dissociation can be brought out by carotid sinus massage,adenosine
Termination in response to CSM, adenosine, valsalva-suggest SVT

11. ECG FEATURES
QRS morphology
SVT with aberrancy-QRS complex must be compatible with some form of BBB or FB
If not, diagnosis by default is VT

12. Specific QRS morphologies
V1 with RBBB
SVT with aberration-
initial portion of QRS not affected by RBBB aberration
Triphasic complex (rabbit ear sign) with rt peak taller
r S R (r-septal activation,S-activation of LV,R-activation of RV)
pattern s/o VT
Monophasic R
Broad(>30 msec)initial R qR
Triphasic complex with lt.peak taller

14. V6 with RBBB
SVT with aberration
qRs,Rs,RS(R/S>1)
Delayed RV activation produces a small S wave in V6
pattern s/o VT
rS,QS,Qrs,QR
RS with R/S<1
Large S due to RV component of ventricular activation+depolarisation of some portion of LV as activation propagates away from V6

16. V1 –LBBB
SVT with aberrancy
rS, QS
Rapid initial forces(narrow r & rapid smooth descent to nadir of S)
Initial forces are relatively preserved VT
Broad R/deep S
QS with a slow descent to S wave nadir
Initial R >30 msec s/o VT; wider the R , greater the likelihood
Notch in downstroke of S
Interval from onset of QRS to nadir of S >60 msec
Taller R during WCT than sinus rhythm

17. V6 –LBBB
SVT with aberrancy
Lacks initial Q wave
Monophasic R or RR’ VT
QR,QS,QrS,Rr’
Patterns consistent with SVT may be seen

19. Width of the QRS
Site of origin
lateral free wall of the ventricle  very wide QRS.
close to the IVS  Smaller QRS
When during tachycardia, the QRS is more narrow than during sinus rhythm, VT should be diagnosed.
other factors that play a role in the QRS width
scar tissue (after MI)
ventricular hypertrophy
muscular disarray (as in HCM).

21. QRS complex duration
VT probable when QRS duration >140 ms with RBBB morphology ; >160 ms with LBBB morphology
QRS duration > 160 msec  a strong predictor of VT regardless of bundle--branch block morphology
QRS duration < 140 msec does not exclude VT…If the tachycardia originates in the proximal part of the His­Purkinje system, duration can be relatively short—as in fascicular VT, where QRS duration ranges from 0.11 s to 0.14 s.

22. QRS axis
Identify site of origin of VT and aetiology
VT from apical part of the ventriclesuperior axis
VT from basal area of the ventricle  Inferior axis
The presence of a superior axis in patients with RBBB shaped QRS very strongly suggests VT.
The presence of an inferior axis in LBBB shaped QRS tachycardia RVOT VT
Extreme axis deviation ( -30 to -180) suggest VT.

24. QRS axis
Mean QRS axis in the normal range favors SVT with aberrancy
Right superior axis -90 to ± 180° suggests VT
Axis shift during WCT of > 40° favors VT
LBBB morphology with RAD - almost always due to VT
RBBB with a normal axis - uncommon in VT

25. Concordant pattern
Concordant precordial R wave progression……High specificity for VT (90%)
Low sensitivity(observed in only 20% of VTs)
Negative concordance .. Apical VT
Positive concordance .. (ventricular activation begins left posteriorly) … seen in VT originating in Lt post wall or SVT using a left posterior accessory pathway for AV conduction

27. Concordance of the limb leads - predominantly negative QRS complex in limb leads s/o VT

28. AV DISSOCIATION
Most useful ECG feature
Complete AV dissociation seen in 20 to 50 % of VT(sensitivity 20 to 50% ,specificity 100%)
15 to 20% of VT has 2nd degree VA block

29. Variation in QRS complex altitude during WCT - due to summation of p wave on the QRS complex –clue to presence of AVD
30% of VT has 1:1 retrograde conduction - CSP or adenosine used to block retrograde conduction to diagnose VT
When the atrial rate < ventricular rate - s/o VT
Atrial rate > ventricular rate s/o SVT with conduction block

30. Evidences of AV dissociation
Fusion beat – when one impulse originating from the ventricle and a second supraventricular impulse simultaneously activate the ventricular myocardium. Morphology intermediate b/w sinus beat & pure ventricular complex
Rarely in SVTs with aberration….PVCs can produce fusion beats
Capture beat – normal conduction momentarily captured control of ventricular activation from the VT focus

32. Onset of tachycardia
Episode initiated by a premature p wave - SVT
If it begins with a QRS - can be ventricular or supraventricular

33. Presence of Q waves during a WCT – s/o old MI - s/o VT
Patients with post MI VT maintain Q wave in the same territory as in NR
DCM- Q waves during VT, which was not there in sinus rhythm
Pseudo Q –retrograde p deforming the onset of QRS

34. QRS complex during WCT narrower than NR
In presence of BBB during NR, a WCT with a narrower complex indicate VT
Contralateral BBB in NR and in WCT s/o VT
QRS alternans-
alternate beat variation in QRS amplitude > 0.1 mV
occurs with equal frequency in WCT due to VT & SVT,but greater no. of leads show this (7 vs 4) in SVT with aberrancy(Kremer et al; AJC )

35. Multiple WCT configurations-
More than one QRS configuration during a WCT –VT more likely
51% of pts with VT,8% with SVT in one series

37. Importance of sinus rhythm ECG
Differentiation between VT and SVT with antegrade conduction over accessory pathway
Aberrancy…. ? rate related or pre existing
Presence of premature complexes in sinus rhythm
?Old MI ; ?pre excitation
QT interval
ECG clues to any other structural heart disease
rule out ECG artifacts which may be misdiagnosed as WCT

38. VT vs Preexcited tachycardia
Predominantly negative QRS complexes in V4-V6
Presence of a QR complex in one or more leads V2-V6
More QRS complex than P
75% sensitivity & 100% specificity for VT (Stierer et al)

39. Criteria for diagnosis-VT vs SVT with aberrancy
Griffith et al;1991
QRS morphology in V1 & aVF, change in QRS axis >40 from normal rhythm & h/o MI
Predictive accuracy greater than 90% in detecting VT
Kremer et al ;1988
Precordial concordance, NW axis, monophasic R in lead V1

40. BRUGADA CRITERIA
Brugada et al analysed 554 cases of WC tachycardias with a new algorithm(circulation 1991)
Sensitivity of the four consecutive steps was 98.7% & specificity was 96.5%
Four criteria for VT sequentially evaluated
If any satisfied-diagnosis of VT made
If none are fulfilled-SVT

42. EVALUATION OF RS COMPLEXES

43. Measurement of RS interval

44. New aVR algorithm
Vereckei et al;Heart Rhythm 2008
483 WCT (351 VT, 112 SVT, 20 preexcited tachycardia) analysed
Greater sensitivity for VT diagnosis than Brugada algorithm(96.5% vs 89.2%, P .001)
Greater specificity for diagnosing SVT compared with Brugada criteria

46. Reasons for using aVR
During SVT with aberrancy,initial septal activation and main ventricular activation are directed away from lead aVR  negative QRS complex
Exception - inferior MI- initial r wave (rS complex) during NSR or SVT
Initial dominant R suggest VT typically originating from inferior or apical region
SVT with aberrancy-initial activation is rapid
VT-initial ventricular activation slow due to muscle to muscle spread of activation

48. Vi/Vt (ventricular activation velocity ratio)
Vi –initial ventricular activation velocity
Vt –terminal ventricular activation velocity
Both measured by the excursion (in mV) ECG during initial (Vi) and terminal (Vt) 40 msec of QRS complex

51. THANK YOU

56. Mahaim pathway mediated tachycardia
antegrade conduction through mahaim(nodoventricular) pathway and retrograde through AV node
Tachycardia with LBBB morphology and left axis
episodes of pre-excited tachycardia without exhibiting pre-excitation during sinus rhythm
Wide QRS complex tachycardia occur because absence of retrograde conduction over accessory pathway