DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA.

DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA

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 SVTat or above the level of His bundle

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

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

(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 I A, C,amiodarone,tricyclic antidepressants Hyperkalemia (5)Ventricular paced rhythms LBBB with left axis (6)Post resuscitation

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

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

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

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

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

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

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

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

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).

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 VTIf the tachycardia originates in the proximal part of the HisPurkinje system, duration can be relatively shortas in fascicular VT, where QRS duration ranges from 0.11 s to 0.14 s.

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.

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

Concordant pattern Concordant precordial R wave progressionHigh 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

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

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 2 nd degree VA block

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

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

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

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

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 )

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

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

VT vs Preexcited 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)

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

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

EVALUATION OF RS COMPLEXES

Measurement of RS interval

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

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

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

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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

DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA.

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