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

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Definitions
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



Causes of regular wct
Causes of regular WCT predominantly positive terminal deflection in V1

  • 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) length when parts of the His-Purkinje system are partially or wholly

    • 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 length when parts of the His-Purkinje system are partially or wholly 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
Causes of irregular WCT impulse

  • 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


Svt vs vt history and physical examination
SVT Vs VT- history and physical examination impulse

  • 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- impulsefavour 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


Ecg features qrs morphology
ECG features-QRS morphology impulse

  • 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
Specific morphologies of QRS impulse

  • 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


V6 with rbbb
V6 with RBBB impulse

  • 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


V1 lbbb
V1 -LBBB impulse

  • 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


V6 lbbb
V6 -LBBB impulse

  • SVT with aberrancy

    • Lacks initial Q wave

    • Monophasic R or RR’

  • VT

    • QR,QS,QrS,Rr’

    • Patterns consistent with SVT may be seen


Qrs complex duration
QRS complex duration impulse

  • 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
QRS axis impulse

  • 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 pattern impulse

  • 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



A v dissociation
A V dissociation impulse

  • 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


  • 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
Evidences of AV dissociation summation of p wave on the QRS complex –clue to presence of AVD

  • 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
Onset of tachycardia summation of p wave on the QRS complex –clue to presence of AVD

  • 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 summation of p wave on the QRS complex –clue to presence of AVD

  • 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 summation of p wave on the QRS complex –clue to presence of AVD

    • 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)


  • Multiple WCT configurations- summation of p wave on the QRS complex –clue to presence of AVD

    • 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
Importance of sinus summation of p wave on the QRS complex –clue to presence of AVDrhythem 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



Vt vs preexcited tachycardia
VT Vs summation of p wave on the QRS complex –clue to presence of AVDpreexcited 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)


Criteria for diagnosis
Criteria for diagnosis summation of p wave on the QRS complex –clue to presence of AVD

  • 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


Brugada criteria
Brugada summation of p wave on the QRS complex –clue to presence of AVD 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
Evaluation of RS complexes summation of p wave on the QRS complex –clue to presence of AVD


Measurement of rs interval
Measurement of RS interval summation of p wave on the QRS complex –clue to presence of AVD


New avr algorithm
New summation of p wave on the QRS complex –clue to presence of AVDaVR 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 summation of p wave on the QRS complex –clue to presence of AVD

    • Duriing SVT with aberrancy,initialseptal activation and main ventricular activation directed away from lead aVR, so negative 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



  • Vi/ vector f/b main vector pointing downward and creates a predominantly negative QRS in lead 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


Thank you
Thank you vector f/b main vector pointing downward and creates a predominantly negative QRS in lead


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