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MEHDI BAKHSHI
MSN,CCN
PHD CANDIDATE
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Importance of diagnosis of WCT
 -Correct diagnosis is important both for acute
management and also subsequent management.
 -If we inject verapamil to a patient with VT and
low EF , prolonged hypotension and
hemodynamic deterioration happens.
 -Non of the criteria is perfect but they can be
helpful.
 -The clinical situation of the patient with WCT
usually don’t allow leisurely analysis of ECG ,so the
criteria must be not only accurate but easily
applied and easily remembered.
Definitions
 -WCT :Rate equal or more than 100 and QRS duration
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of at least 120 msec.
-VT :a WCT originating below the level of His bundle.
-SVT : a tachycardia dependent on participation of
structures at or above the level of His bundle.
-LBBB morphology: QRS duration more than 120 with
predominantly negative terminal deflection in V1.
-RBBB morphology : QRS duration more than 120 and
a terminal positive deflection in V1.
-LBBB and RBBB morphology denote the appearance
of QRS , without implying actual His-Purkinje disease.
Top 10 reasons for WCT*
 1. Ventricular
 6. VT
Tachycardia
 2. Ventricular Tach
 3. VT
 4. VT
 5. VT
 7. VT
 8. VT
 9. SVT with preexisting
BBB
 10. SVT with aberrant
conduction
* Ken Grauer. A Practical Guide to ECG Interpretation. 2nd
Diagnostic methods
 12-lead electrocardiogram ! ! !
 Post-op atrial/ventricular pacing wires
 Esophageal pacing leads
 Adenosine can be diagnostic
 Invasive electrophysiology study
Diagnostic methods
 Always
 Always
 Always record a rhythm strip during any intervention
(adenosine, cardioversion, Valsalva, etc.)
Differential Diagnosis of WCT
 -Ventricular tachycardia (about 80% of cases ).
 -SVT with abnormal interventricular conduction (15-20 %):
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*SVT with BBB aberration (fixed or functional).
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*Pre-excited SVT (SVT with ventricular activation occurring
over an anomalous AV connection ).Their ECG can be
indistinguishable from VT originating at the base of ventricle.(15 % of all)
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*SVT with wide QRS due to abnormal muscle-muscle spread
of impulse.( surgery, DCM)
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*SVT with wide complex due to drug or electrolyte-induced
changes. (hyperkalemia. Class Ia ,Ic drugs or Amiodarone)
 -Ventricular paced rhythms .(small but growing percentage )
1. VT is more common than SVT with aberrancy
2. In patients with structural heart disease, particularly prior
infarction, VT is much, much more common than SVT with
aberrancy
3. If SVT is misdiagnosed as VT for the purposes of acute
treatment, no harm will come to the patient
4. If VT is misdiagnosed as SVT for the purposes of acute
treatment, a cardiac arrest can be precipitated
SVT vs VT
History
 -The majority of patients with VT have structural heart
disease, In SVT they may or may not have.
 -Patient with VT are older.
 -Patients with SVT more often have history of previous
similar episodes .(cutoff of 3 years)
Factors Favoring VT
 Concordance across all V leads (+/-)
 ERAD axis deviation
 QRS > .16 sec
 AV dissociation
 Suggestive QRS morphology
SVT vs VT
ECG criteria
 -A fundamentally simple approach: If WCT is due
to SVT with aberration, the QRS must be
compatible with some form of BBB or FB.
 -QRS duration:70% of VTs have QRS duration
>140, but no SVT has it. VT is probable when
QRS> 140 with RBBB and >160 with LBBB
pattern.Anti arrhythmic drugs may prolong QRS.
Some patients with VT may have QRS of 120-140
specially in those without structural heart disease.
SVT vs VT
ECG criteria contd,
 -QRS
axis:
 *The more leftward the axis , the more probable
VT.
 * The quadrant between -90 and 180 (northwest
)can’t be achieved with any combination of FB or
BBB.
 *Some has suggested that if the axis in sinus
rhythm is more than 40 degrees different with
WCT the diagnosis is VT , but it is not widely
accepted.
SVT vs VT
ECG criteria contd
 -Specific morphologies ;
 If with RBBB pattern:
 *In V1:During aberration there is no change in
initial portion of QRS so we may see rSr’ ,rR’ , rsr’
or rSR’. But a monophasic R wave , or a broad (> 30
msec) R with any following terminal QRS forces or
qR are highly suggestive of VT.
 * In V6 :During aberration qRs , Rs ,or RS (with
R/S ratio >1) are seen but in VT we may see rS,Qrs ,
QS or QR or monophasic R wave. If RS pattern is
present R/S must be less than 1.
SVT vs VT
ECG criteria contd
 LBBB pattern:
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* In V1 :Either rS or QS with rapid initial forces (narrow R
with rapid smooth descent to S )is seen in LBBB type
aberration. Any other pattern such as broad R/deep S or QS
with slow descent to S wave nadir will imply VT.
 If the initial R is wider than 30 msec it suggest VT , the
wider the R , the greater the likelihood of VT.
 Notching in the down-stroke of S or interval from the onset
of QRS to the S wave nadir greater than 60 msec strongly
suggest VT.
 *In V6 :In aberrancy there is no initial Q wave and we see
RR’, or monophasic R. During VT common patterns are QR
,QS ,QrS ,or Rr’ although patterns compatible with SVT
may also be seen.
SVT vs VT
ECG criteria contd
 Combination of LBBB and RAD is almost always
due to VT .
 RBBB with a normal axis is very uncommon in VT.
 Concordant pattern in precordial leads is
uncommon in SVT ,with the exception of preexcited tachycardia .The specificity of concordant
pattern for VT is >90% but sensitivity is low(20%).
 Negative concordance in limb leads is another way
of describing NW axis and suggests VT.
QRS duration > 140 ms
Concordant pattern in all precordial leads
Absence of RS complex in all precordial leads
R-to-S interval >100 ms in one precordial lead
SVT vs VT
ECG criteria contd
 Q waves during WCT show old MI and are in favor of
VT. Generally patients with old Q waves maintain it
during WCT .
 Some patients with DCM may have Q during VT while
they don’t show it in SR.
 Pseudo Q waves may be seen in some SVTs with
aberrancy. (AVNRT or pre-excited with a posterior AV
connection ).
AV
Dissociation
AV dissociation
 Is the most useful criteria.
 Complete AVD is seen in 20-50% of all VTs and practically no SVTs.
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(specificity near 1)
15-20 %of VTs have second degree VA block.
Another clue to the presence of AVD is variation in QRS amplitude.
(summation of p on QRS or variable ventricular filling).
30% of VTs have 1:1 retrograde conduction. Faster VTs are less likely to
have 1:1 conduction but there is no cut-off.
Carotid pressure or adenosine can cause transient VA block and show
VT.
Fusion beats imply the presence of AVD (most often seen during slow
tachycardias). It is most reliable when it is a clear fusion and not a
simply change in morphology. Which can be due to PVC during VT.
PVCs can fuse with SVT beats which can erroneously be taken as VT.
Narrow QRS complex VT
 VT can have QRS duration less than the cutoff of 140
msec. Possible explanations are:
 1-Septal origin of VT.
 2- Early penetration in the His- Purkinje system.
Atrial Fibrillation with
Rapid Conduction Via Accessory
Pathway
Antidromic AVRT
AF +WPW
Sustained Aberrant
Conduction
V1
Polymorphic
VT
V1
“Torsade de Pointes”
(Polymorphic VT Associated with
Prolonged Repolarization)
Sustained VT: Degeneration to VF
Atrial Fibrillation with Rapid Conduction
Via Accessory Pathway: Degeneration to
VF
Regular Wide QRS Tachycardia:
VT or SVT with Aberrant
Conduction?
More R-Waves Than P-Waves Implies
VT!
II
Artifact Mimicking “Ventricular
Tachycardia”
QRS complexes “march through”
the pseudo-tachyarrhythmia
Artifact
precedes
“VT”
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