DIFFERENTIAL DIAGNOSIS OF WIDE COMPLEX TACHYCARDIA
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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
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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
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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
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(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
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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
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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
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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
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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
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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
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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
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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
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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).
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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.
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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.
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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
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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
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Concordance of the limb leads - predominantly negative QRS
complex in limb leads s/o VT
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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
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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
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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
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Onset of tachycardia Episode initiated by a premature p wave -
SVT If it begins with a QRS - can be ventricular or
supraventricular
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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
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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 )
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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
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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
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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)
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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
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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
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EVALUATION OF RS COMPLEXES
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Measurement of RS interval
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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
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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
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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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THANK YOU
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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