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
slide3

RBBB morphology-QRS complex duration ≥ 120 ms with a predominantly positive terminal deflection in V1

  • LBBB&RBBB morphology denote morphological appearance of QRS complex-result from direct myocardial activation
causes of regular wct
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)
slide6

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
slide7

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
slide9

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
slide10

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
  • 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
  • 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
slide13

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
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
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-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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
slide31

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
  • 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
  • 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
slide35

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
slide36

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,butgrterno.of leads show this (7 Vs 4) in SVT with aberrancy(Kremer et al;Am J Cardiol)
slide37

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
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
vt vs preexcited tachycardia
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
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
    • Precordialconcordance,NWaxis,monophasic R in lead V1
brugada criteria
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
new avr algorithm
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
slide52

Reasons for using a VR

    • 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
slide53

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
slide57

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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