Differential diagnosis of broad complex tachycardia Dr Deepak

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 • 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 V 1

• RBBB morphology-QRS complex duration ≥ 120 ms with a predominantly positive terminal deflection in V 1 • LBBB&RBBB morphology denote morphological appearance of QRS complexresult 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 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)

• 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

• 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

– 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

– 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

Causes of irregular WCT • Any irregular supraventricular rhythem(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

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 S 1 • 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 morphologies of QRS • V 1 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 q. R Triphasic complex with lt. peak taller

V 6 with RBBB • SVT with aberration – q. Rs, RS(R/S>1) – Delayed RV activation produces a small S wave in V 6 • pattern s/o VT – r. S, 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 V 6

V 1 -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

V 6 -LBBB • SVT with aberrancy – Lacks initial Q wave – Monophasic R or RR’ • VT – QR, QS, Qr. S, Rr’ – Patterns consistent with SVT may be seen

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

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

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

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

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 2 nd 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

• Variation in QRS complex altitude during WCTdue 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 • 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 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

• 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

• 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 m. V – 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 likely – 51% of pts with VT, 8% with SVT in one series

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

• rule out ECG artifacts which may be misdiagnosed as WCT

VT Vs preexcited tachycardia • Characteristics specific for VT – Predominantly negative QRS complexes in V 4 -V 6 – Presence of a QR complex in one or more leads V 2 -V 6 – More QRS complex than P • 75% sensitivity&100%specificity for VT(Stierer et al)

Criteria for diagnosis • Griffith et al; 1991 – QRS morphology in V 1&a. VF, 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 – Precordial concordance, NW axis, monophasic R in lead V 1

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 a. VR 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 a VR – Duriing SVT with aberrancy, initial septal activation and main ventricular activation directed away from lead a. VR, so negative complex – Exception-inferior MI-initial r wave (r. S complex) during NSR or SVT – Initial dominant R suggest VT typically originating from inferior or apical region

• VT originating from other sites-show a slow initial upward vector f/b main vector pointing downward and creates a predominantly negative QRS in lead a. VR. • Exception-VT originating from the most basal septum or free wall

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

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