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Differential diagnosis of broad complex tachycardia

Differential diagnosis of broad complex tachycardia. Dr.Deepak Raju. Definitions. Wide Complex Tachycardia(WCT)-a rhythem with QRS duration ≥ 120 ms and heart rate > 100 bt /min Ventricular tachycardia-a WCT originating below the level of His bundle

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Differential diagnosis of broad complex tachycardia

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  1. Differential diagnosis of broad complex tachycardia Dr.DeepakRaju

  2. Definitions • Wide Complex Tachycardia(WCT)-a rhythem with QRS duration ≥ 120 ms and heart rate > 100 bt/min • Ventricular tachycardia-a WCT originating below the level of His bundle • SVT-tachycardia dependent on participation of structures at or above the level of His bundle • LBBB morphology-QRS complex duration ≥ 120 ms with a predominantly negative terminal deflection in lead V1

  3. RBBB morphology-QRS complex duration ≥ 120 ms with a predominantly positive terminal deflection in V1 • LBBB&RBBB morphology denote morphological appearance of QRS complex-result from direct myocardial activation

  4. Causes of regular WCT • Ventricular tachycardia- • Most common cause of WCT in general population(80%) • 95% of WCT in pts with structural heart disease • Supraventricular tachycardia with abnormal interventricular conduction(15% to 30% of WCT) • SVT with BBB aberration; • fixed(present during normal rhythem) • functional(present only during WCT)

  5. Functional aberration results from sudden change in cycle length when parts of the His-Purkinje system are partially or wholly inexcitable • Functional RBBB commoner because of longer refractoriness • Linking phenomenon -Functional BBB may persist for several successive impulses because the bundle branch that is blocked antegradely may be activated trans-septally via its contralateral counterpart

  6. AV reentrant tachycardia (AVRT) • Orthodromic AVRT – antegrade conduction over the AV node and retrograde conduction through accessory pathway.WCT occurs in aberrant conduction,either rate related or preexisting • Antidromic AVRT – antegrade conduction over the accessory pathway and retrograde conduction over the AV node result in WCT • Pre-excited tachycardia- SVT with ventricular activation occurs predominantly via accessory pathway

  7. 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

  8. SVT with a wide complex due to abnormal muscle spread of impulse • RBBB in pts undergone rt.ventriculotomy • LBBB in pts with DCM • SVT with wide complex due to drug or electrolyte induced changes • Ι A, Ι C,amiodarone,tricyclic antidepressants • Hyperkalemia • Ventricular paced rhythems • LBBB with left axis

  9. Causes of irregular WCT • Any irregular supraventricularrhythem(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

  10. 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

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

  12. 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

  13. Specific morphologies of QRS • 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

  15. V1 -LBBB • SVT with aberrancy • r S, 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 likelihood • Notch in downstroke of S • Interval from onset of QRS to nadir of S >60 msec • Taller R during WCT than sinus rhythem

  16. 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

  17. QRS complex duration • 69% of VT had QRS duration >140 ms-Wellens et al • 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

  18. 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 rt axis deviation-almost always due to VT • RBBB with a normal axis-uncommon in VT

  19. Concordant pattern • Concordant precordial R wave progression pattern(all precordial leads predominantly positive or predominantly negative) • High specificity for VT (90%) • Low sensitivity(observed in only 20%of VTs) • Exception –antidromic AVRT w/ a left posterior accessory pathway-positive concordance

  20. Concordance of the limb leads-predominantly neg QRS complex in limb leads s/o VT

  21. A V dissociation • Most useful ECG feature • Complete AV dissociation seen in 20 to 50 % of VT(sensitivity .2 to .5,specificity 1) • 15 to 20% of VT has 2nd degree V A block • Lewis leads-p waves seen better with arm leads at various levels on opposite sides of sternum • Psudo p waves-contour of terminal portion of QRS may resmble p-inspect simultaneous recording in other leads

  22. 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

  23. 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 • Capture beat – normal conduction momentarily captured control of ventricular activation from the VT focus

  24. Onset of tachycardia • Episode initiated by a premature p wave-SVT • If begins with a QRS-can be ventricular or supraventricular • If first wide QRS preceded by a sinus p with a shorter PR int.-usually VT

  25. 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 rhythem • Psudo Q –retrograde p deforming the onset of QRS

  26. 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,butgrterno.of leads show this (7 Vs 4) in SVT with aberrancy(Kremer et al;Am J Cardiol)

  27. 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

  28. Importance of sinus rhythem ECG • Differentiation between VT and SVT with antegrade conduction over accessory pathway • Aberrancy is rate related or pre existing • Presence of premature complexes in sinus rhythem • Old MI • QT interval • ECG clues to any other structural heart disease

  29. rule out ECG artifacts which may be misdiagnosed as WCT

  30. VT Vs preexcited tachycardia • Characteristics specific for 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)

  31. Criteria for diagnosis • Griffith et al;1991 • QRS morphology in V 1&aVF,change in QRS axis grter than 40 from normal rhythem&h/o MI • Predictive accuracy greater than 90% in detecting VT • Kremer et al ;1988 • Precordialconcordance,NWaxis,monophasic R in lead V1

  32. 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

  33. Evaluation of RS complexes

  34. Measurement of RS interval

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