DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA

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) -Mahaimpathway mediated tachycardia -Antidromic AVRT

6. (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-septalactivation,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superioraxis • 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 vsPreexcited tachycardia • VT • 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 preexcitedtachycardia) 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,initialseptal 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