Download Differential diagnosis of broad complex tachycardia

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 V1
• RBBB morphology-QRS complex duration ≥
120 ms with a predominantly positive
terminal deflection in V1
• 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 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
• 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
• 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<1
– Large S due to RV component of ventricular
activation+depolarisation of some portion of LV as
activation propagates away from V6
V1 -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
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
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 deviationalmost 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 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 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 mV
– 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 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
• 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
– 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 a VR
– Duriing SVT with aberrancy,initial septal 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
• 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 aVR.
• 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 mV) ECG
during initial (Vi) and terminal (Vt) 40 msec of QRS
complex
Thank you