differential diagnosis of broad complex tachycardia

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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 - PowerPoint PPT Presentation

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Differential diagnosis of broad complex tachycardia

Differential diagnosis of broad complex tachycardiaDr.Deepak RajuDefinitions Wide Complex Tachycardia(WCT)-a rhythem with QRS duration 120 ms and heart rate > 100 bt/minVentricular tachycardia-a WCT originating below the level of His bundleSVT-tachycardia dependent on participation of structures at or above the level of His bundleLBBB 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 V1LBBB&RBBB morphology denote morphological appearance of QRS complex-result from direct myocardial activation

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

Functional aberration results from sudden change in cycle length when parts of the His-Purkinje system are partially or wholly inexcitableFunctional RBBB commoner because of longer refractorinessLinking 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 counterpartAV 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 preexistingAntidromic AVRT antegrade conduction over the accessory pathway and retrograde conduction over the AV node result in WCTPre-excited tachycardia- SVT with ventricular activation occurs predominantly via accessory pathway

Mahaim pathway mediated tachycardiaantegrade conduction through mahaim(nodoventricular) pathway and retrograde through AV nodeTachycardia with LBBB morphology and left axisepisodes of pre-excited tachycardia without exhibiting pre-excitation during sinus rhythmWide QRS complex tachycardia occur because absence of retrograde conduction over accessory pathway

SVT with a wide complex due to abnormal muscle spread of impulseRBBB in pts undergone rt.ventriculotomyLBBB in pts with DCMSVT with wide complex due to drug or electrolyte induced changes A, C,amiodarone,tricyclic antidepressantsHyperkalemiaVentricular paced rhythemsLBBB with left axis

Causes of irregular WCTAny irregular supraventricular rhythem(AF,EAT or atrial flutter with varying conduction) with aberrant ventricular conductionAF with ventricular preexcitation-if the ventricular rate in AF is >220/min or shortest R-R int is 3 yrs-SVT more likelyFirst episode of WCT after MI-VT more likelyOlder age grp>35 yrs-VT more likelyFindings of AV dissociation-favour VTCannon a wavesVariable intensity of S1AV dissociation can be brought out by carotid sinus massage,adenosineTermination in response to CSM, adenosine,valsalva-suggest SVT

ECG features-QRS morphologySVT with aberrancy-QRS complex must be compatible with some form of BBB or FBIf not,diagnosis by default is VT

Specific morphologies of QRSV1 with RBBBSVT with aberration-initial portion of QRS not affected by RBBB aberrationTriphasic complex (rabbit ear sign)with rt peak tallerr S R (r-septal activation,S-activation of LV,R-activation of RV) pattern s/o VT Monophasic R Broad(>30 msec)initial RqRTriphasic complex with lt.peak taller

V6 with RBBB SVT with aberrationqRs,Rs,RS(R/S>1)Delayed RV activation produces a small S wave in V6 pattern s/o VTrS,QS,Qrs,QRRS with R/S30 msec s/o VT,wider the R greater likelihoodNotch in downstroke of SInterval from onset of QRS to nadir of S >60 msecTaller R during WCT than sinus rhythem

V6 -LBBBSVT with aberrancyLacks initial Q waveMonophasic R or RRVTQR,QS,QrS,RrPatterns consistent with SVT may be seen

QRS complex duration69% of VT had QRS duration >140 ms-Wellens et alVT probable when QRS duration >140 ms with RBBB morphology ,>160 ms with LBBB morphologyQRS duration > 160 msec-a strong predictor of VT regardless of bundle--branch block morphology QRS duration < 140 msec does not exclude VT

QRS axisMean QRS axis in the normal range favors SVT with aberrancyRight superior axis -90 to 180 suggests VTAxis shift during WCT of > 40 favors VTLBBB morphology with rt axis deviation-almost always due to VTRBBB with a normal axis-uncommon in VTConcordant patternConcordant 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

Concordance of the limb leads-predominantly neg QRS complex in limb leads s/o VTA V dissociationMost useful ECG featureComplete 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 blockLewis leads-p waves seen better with arm leads at various levels on opposite sides of sternumPsudo p waves-contour of terminal portion of QRS may resmble p-inspect simultaneous recording in other leads

Variation in QRS complex altitude during WCT-due to summation of p wave on the QRS complex clue to presence of AVD30% of VT has 1:1 retrograde conduction-CSP or adenosine used to block retrograde conduction to diagnose VTWhen the atrial rateventricular rate s/o SVT with conduction blockEvidences of AV dissociationFusion 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

Onset of tachycardiaEpisode initiated by a premature p wave-SVTIf begins with a QRS-can be ventricular or supraventricularIf first wide QRS preceded by a sinus p with a shorter PR int.-usually VTPresence of Q waves during a WCT s/o old MI-s/o VTPatients with post MI VT maintain Q wave in the same territory as in NRDCM-Q waves during VT,which was not there in sinus rhythemPsudo Q retrograde p deforming the onset of QRS QRS complex during WCT narrower than NRIn presence of BBB during NR,a WCT with a narrower complex indicate VTContralateral BBB in NR and in WCT s/o VTQRS alternans-alternate beat variation in QRS amplitude>0.1 mV occurs with equal frequency in WCT due to VT &SVT,but grter no.of leads show this (7 Vs 4) in SVT with aberrancy(Kremer et al;Am J Cardiol)Multiple WCT configurations-More than one QRS configuration during a WCT VT more likely51% of pts with VT,8% with SVT in one series

38Importance of sinus rhythem ECGDifferentiation between VT and SVT with antegrade conduction over accessory pathwayAberrancy is rate related or pre existingPresence of premature complexes in sinus rhythemOld MIQT intervalECG clues to any other structural heart diseaserule out ECG artifacts which may be misdiagnosed as WCT

VT Vs preexcited tachycardiaCharacteristics specific for VTPredominantly negative QRS complexes in V4-V6Presence of a QR complex in one or more leads V2-V6More QRS complex than P75% sensitivity&100%specificity for VT(Stierer et al)Criteria for diagnosisGriffith et al;1991QRS morphology in V 1&aVF,change in QRS axis grter than 40 from normal rhythem&h/o MIPredictive accuracy greater than 90% in detecting VTKremer et al ;1988Precordial concordance,NW axis,monophasic R in lead V1Brugada criteriaBrugada 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 evaluatedIf any satisfied diagnosis of VT madeIf none are fulfilled-SVT

Evaluation of RS complexes

Measurement of RS interval

New aVR algorithm Vereckei et al;Heart Rhythm 2008483 WCT (351 VT, 112 SVT, 20 preexcited tachycardia)analysedGreater sensitivity for VT diagnosis than Brugada algorithm(96.5% vs 89.2%, P .001)Greater specificity for diagnosing SVT compared with Brugada criteriaReasons for using a VRDuriing SVT with aberrancy,initial septal activation and main ventricular activation directed away from lead aVR, so negative complexException-inferior MI-initial r wave (rS complex) during NSR or SVTInitial dominant R suggest VT typically originating from inferior or apical regionVT originating from other sites-show a slow initial upward vector f/b main vector pointing downward and creates a predominantly negative QRS in lead aVR. Exception-VT originating from the most basal septum or free wall

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

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