Differential diagnosis of broad complex tachycardia

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Differential diagnosis of broad complex tachycardia Powered By Docstoc
• Wide Complex Tachycardia(WCT)­a rhythm with
  QRS duration ≥ 120 ms and heart rate > 100/min

• VT­WCT originating below the level of His bundle
• SVT…at or above the level of His bundle
• LBBB morphology ­ QRS complex duration ≥ 120 ms with
  a predominantly negative terminal deflection in lead V1

• RBBB morphology­QRS complex duration ≥ 120 ms with a
  predominant terminal deflection in V1

• LBBB & RBBB morphology denote morphological
  appearance of QRS complex­ result from direct myocardial
(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
   • RBBB in pts undergone rt.ventriculotomy
   • LBBB in pts with DCM
(4)SVT with wide complex due to drug or electrolyte induced
   •IA, Ι 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 preexcitation­if the ventricular
   rate in AF is >220/min or shortest R­R 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 yrs­VT 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
• Termination in response to CSM, adenosine, valsalva­
  suggest SVT
QRS morphology

• SVT with aberrancy­QRS 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 (r­septal activation,S­activation of LV,R­activation of
   – pattern s/o VT
       • Monophasic R
       • Broad(>30 msec)initial R
       • qR
       • Triphasic complex with lt.peak taller
V6 with RBBB
• SVT with aberration
   –Delayed RV activation produces a small S wave in V6
• pattern s/o VT
   –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
• 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
• SVT with aberrancy
   –Lacks initial Q wave
   –Monophasic R or RR’
• VT
   –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 bundle­­branch block morphology
• QRS duration < 140 msec does not exclude VT…If the
  tachycardia originates in the proximal part of the
  His­Purkinjesystem, duration can be relatively short—as 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
• 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 progression……High
  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
• Concordance of the limb leads ­ predominantly
  negative QRS complex in limb leads s/o VT
• 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 2nd 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
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
• 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
• 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 V4­V6
   –Presence of a QR complex in one or more leads V2
   –More QRS complex than P
• 75% sensitivity & 100% specificity for VT (Stierer et
Criteria for diagnosis­VT 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
• 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 satisfied­diagnosis of VT made
• If none are fulfilled­SVT
Measurement of RS interval
New aVR algorithm
• Vereckei et al;Heart Rhythm 2008
• 483 WCT (351 VT, 112 SVT, 20 preexcited tachycardia)
• 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 aberrancy­initial activation is rapid
• VT­initial 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
–Mahaim pathway mediated tachycardia
 •antegrade conduction through
  mahaim(nodoventricular) pathway and
  retrograde through AV node
 •Tachycardia with LBBB morphology and left axis
 •episodes of pre­excited tachycardia without
  exhibiting pre­excitation during sinus rhythm
 •Wide QRS complex tachycardia occur because
  absence of retrograde conduction over accessory

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