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WCT by GADISA 1

APPROACH TO WIDE QRS


COMPLEX TACHYCARDIA

Presenter :Dr Gadisa D (R1)


Moderators:Dr Zelalem/Dr
Kalkidan( EMCC Ass’t professor)
Dr Elias (EMCC R2)

10/01/2020
OUTLINES
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 Introduction
 Patientapproach
 ECG Evaluation
 SVT with abberancy or pre-excitation
 Premature ventricular tachycardia
 Ventricular tachycardia
 Torsades De Pointes
 Ventricular flutter and VF
 References
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INTRODUCTION
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INTRODUCTION
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 Wide QRS complex tachycardia (WCT) is a


rhythm often with a rate of more than 100
beats/min and a QRS duration of more than 120ms.

 A WCT represents a unique clinical challenge


for two reason:

 Diagnosing the arrhythmia is difficult.


 Urgent therapy is often required.

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EPIDEMIOLOGY

 Several arrhythmias:
 VT- 80-90%
 SVT with aberrancy- 15-20%
 SVT with pre-excitation and antidromic AVRT -1-6%
 Paced Rhythm (Pacemaker-mediated tachycardia)

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APPROACH TO THE PATIENT

o The first priority when evaluating a patient with WCT is an


assessment of patient STABILITY.
 Unstable patient:
 hypotension,
 altered mental status,
 chest pain, or
 heart failure,

o Need urgent treatment


 Emergency synchronized cardioversion is the treatment of
choice regardless of the mechanism of the arrhythmia.
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 In stable patient, a focused clinical evaluation


should include the following:

-History,
-Physical examination,
-Response to certain maneuvers, and
-Careful inspection of the ECG

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HISTORY
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 Age 
 History of heart disease
 Presence of an implantable cardioverter
defibrillator (ICD) or Presence of a pacemaker
 Duration of the tachycardia 
 Symptoms 
 Medications

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MEDICATIONS
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 Many medications have proarrhythmic effects

 directly by prolonging the QT interval or


 indirectly via alterations in electrolyte levels

 The most common drug-induced WCT is a form of


polymorphic VT called torsades de pointes
(TdP). 

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Physical Examination

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 Abnormal vital signs or o Ancillary testing:


altered mentation  Serum electrolytes
 Underlying heart disease and
 Cardiac biomarkers
 Evidence for AV dissociation
 Serum levels of certain
 Strongly suggest VT but its
drugs
absence is less helpful
 Chest x-ray
 Fluctuating BP
 Cacophony of S1
 Cannon A wave

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ECG
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EVALUATION
 VT vs Aberrantly conducted SVT
The unknown rhythm should be presumed to be VT in the absence of
contrary evidence as VT is the most devastating and also
epidemiologically common.

One has to be familiar with criteria for distinguishing VT


from SVT.

 Baseline ECG: pre-excitation and LBBB/RBBB

 ECG during the attack


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ECG PARAMETERS

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 Rate
 Regularity

 QRS duration

 QRS axis

 Pericordial QRS concordance

 QRS morphology

 DISSOCIATED P WAVES, FUSION AND

CAPTURE BEATS.
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Rate and Regularity

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 An irregular WCT usually represents atrial


fibrillation (AF) with aberrant conduction, although
polymorphic VT should also be considered.

 Monomorphic ventricular tachycardia may present


with an irregular rhythm, but only minimally
irregular as compared to an aberrantly conducted
atrial fibrillation, which ordinarily manifests
marked irregularity.

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QRS axis

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 A right superior axis is rare in SVT and strongly suggests


VT with 2 exceptions.

1. The antidromic atrioventricular reentrant tachycardia


(AVRT) seen with ventricular preexcitation.
2. The second is a biventricular pacemaker in which the
axis is often indeterminate with an initial Q wave in lead I.

 A shift of 400 from the baseline ECG is suggestive of VT.

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QRS duration:

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 In general, a wider QRS favors VT.


 In a RBBB-like WCT, a QRS duration >140 msec suggests VT;
 In a LBBB-like WCT, a QRS duration >160 msec suggests VT
 2 exceptions

1. SVT with an AV accessory pathway; the presence of drugs


capable of slowing intraventricular conduction, such as
class I antiarrhythmic drugs; and in association with
hyperkalemia.
2. A very wide QRS complex may also be seen with a dilated
cardiomyopathy

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Pericordial QRS concordance
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•Negative concordance

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Pericordial QRS concordance
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 Positive concordance

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AV dissociation:

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If AV dissociation can be quickly identified, an


atrial rate slower than the ventricular rate,
along with any fusion or capture beats,
strongly suggests VT.

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QRS morphology

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 Most WCTs can be classified as having one of two


patterns:

 RBBB-like pattern (QRS polarity is predominantly


positive in leads V1 and V2)

 LBBB-like pattern (QRS polarity is predominantly


negative in leads V1 and V2)

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RBBB
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LBBB
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SUMMARY
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ALGORITHMS
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 Diagnostic algorithms meant for differentiating


SVT and VT as a cause of WCT are complex and
imperfect.

 There is no single criteria or combination of criteria that provides complete


diagnostic accuracy in evaluating WCT.

 However VT is the most common cause WCT

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ALGORITHM 1
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 The most commonly used called Brugada


algorithm or Brugada criteria.

 Consists of four steps:


1. Absence of RS complex in pericordial leads
2. RS interval >100ms
3. AV dissociation
4. QRS morphology criteria

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VT vs Preexcited SVT
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 For cases in which preexcitation is likely, such as a


 Young pt without structural heart disease, or
Pt with a known accessory pathway, a separate algorithm has been developed by
Brugada and colleagues.

 This algorithm consists of three steps.


1. Polarity of the QRS in leads V4- V6 is defined as positive or
negative.
-If predominantly -ve, then VT 100% specific
2. Polarity of the QRS is +ve in V4-V6, the presence of a qR in one
or more of precordial leads V2- V6=VT (100%spec)
3. If a qR wave in V2-V6 is absent, the AV r/ship is then evaluated.
 Sensitivity of only 75% for the diagnosis of preexcited SVT when all three steps
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are answered negatively
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ALGORITHM 2
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 Vereckie approach
1. The presence of AV dissociation
2. The presence of an initial R wave in lead aVR
3. QRS morphology; and
4. Estimation of the Vi/Vt, determined by measuring the voltage
change on the ECG tracing during the initial 40 ms(Vi) and the
terminal 40 ms(Vt) of the same biphasic or multiphasic QRS
complex

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SPECIFIC WCT

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SVT with abberancy
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 SVT with wide complex QRS due to


BBB
Rate related
Preexicitation syndrome
drugs
The aberrant conduction is caused by
an accessory pathway or a bundle branch block

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Pre-excitation syndrome

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 The term preexcitation is depolarization of the


ventricular myocardium via an accessory pathway (or
bypass tract) linking the atria to the ventricles,
circumventing the normal AV node.

 Accessory pathways do not have the so-called brakes


or rate limits of the AV node, lending themselves to
reentry tachycardia and rapid ventricular rates.

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Wolff-Parkinson-White (WPW) syndrome
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 is the classic accessory pathway syndrome,


characterized by paroxysmal tachycardia and three
resting electrocardiographic features.
• Short PR interval (<0.12 second)
• QRS duration longer than 0.10 second
• Slurred upstroke to the QRS complex, referred
to as a delta wave

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WPW Syndrome’s ECG
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WPW
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WPW
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Atrial fibrillation in WPW
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Management
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 Procainamide is frst-line therapy for tachycardia whenever the presence of


wide QRS complexes suggests conduction down an accessory pathway;
amiodarone is an alternative???

 Agents that can enhance conduction in the accessory tract and/or block
conduction in the AV node should be avoided in WPW patients with
wide-complex, both regular and irregular tachycardias; these include
adenosine, amiodarone, β-blockers, and calcium channel blockers

 Use prompt electrical cardioversion (100–200 J) if there is


 any clinical deterioration,
 failure of pharmacologic therapy, or
 extreme tachycardia (>250 beats/min)

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Premature Ventricular
Contractions
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(PVC)

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PVC ECG Example
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TERMINOLOGIES

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 Bigeminy, trigeminy, quadrigeminy,...

 Couplet, triplet,…

 Unifocal, multifocal (multiform, polymorphic, or


pleomorphic).

 Fixed or variable coupling; that is, the interval between the


normal QRS complex and the PVC.
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When should you worry about PVCs?
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Rules of malignancy:
 Frequent PVCs

 Runs of consecutive PVCs, especially three or

more in a row
 Multiform PVCs, in which the PVCs vary in their

site of origin and hence in their appearance


 PVCs falling on the T wave of the previous beat,

called the R-on-T phenomenon.

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R on T Phenomenon
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Management
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2015 ESC Guidelines


 In most, PVCs with no
structural heart disease
doesn’t need treatment.
Reassurance
 If treatment is warranted
 Various class I, II, and III
drugs
 lidocaine, procainamide,
 BBs , amiodarone
 Ablation can be useful
 Treatment of provocative
conditions
 Electrolyte disturbance,
 hypoxia,
 drug effects
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Ventricular Tachycardia (VT)
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is the occurrence of three or more consecutive


depolarizations from a ventricular ectopic pacemaker at a rate faster than 100
beats/min.
IHD composes about 50% of all cases of symptomatic ventricular tachycardia
Ventricular tachycardia can occur in a
nonsustained vs Sustained fashion
stable vs unstable,
monomorphic (accounting for about 70% of cases
)vs polymorphic,TdP,Bidirectional
perfusing vs. pulseless as during cardiac arrest

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MONOMORPHIC VT

Monomorphic VT

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POLYMORPHIC VT
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Bidirectional VT
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Non-sustained
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Site of VT origin based on QRS morphology
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Management of VT
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Management Cont’d

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Pharmacologic cardioversion of
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VT
 Historically, lidocaine, amiodarone, procainamide, and
sotalol have been used, based mostly on expert opinion.

 Lidocaine has fallen out of favor because it was shown to be


inferior to both procainamide and sotalol.

 The American Heart Association (AHA) recommends


procainamide (IIa) over amiodarone (IIb) for pharmacologic
conversion of VT, whereas the European Resuscitation
Council (ERC) favors amiodarone.

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Torsades de Pointes
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 Is literally translated as “twisting of the points”


 is a paroxysmal form of polymorphic VT that meets the
following clinical criteria:
1. Ventricular rate greater than 200 beats/min
2. Undulating QRS axis, with the polarity of the complexes
appearing to shift about the baseline
3. Paroxysms of less than 90 seconds
 Occurs in the setting of a prolonged QT
interval, a reflection of abnormal ventricular repolarization.
 Acquired or Congenital

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TdP
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 Common triggers include electrolyte


disturbances (eg, hypokalemia, hypomagnesemia) and
many different drugs (notably class IA and IC agents),and
other drugs
 The typical form is initiated by bradycardia or is pause
dependent, with a short-long-short coupling interval, ie, a
PVC (short RR interval), a compensatory pause (long RR
interval), and second PVC (short RR interval)

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TdP’s ECG
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Hypokalemia’s ECG
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Management
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 Correcting any underlying metabolic or electrolyte


abnormalities and increasing the heart rate to shorten
ventricular repolarization.
 Do not use class IA and IC antidysrhythmics.
 Empirical IV magnesium sulfate
is effective, even in the absence of
hypomagnesemia, and may prevent recurrence if
electrical cardioversion succeeds.

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Magnesium
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 is primarily used as an antiarrhythmic agent in


 known hypomagnesemia,
 QT interval prolongation,
 Polymorphic ventricular tachycardia,
 torsades de pointes.

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Ventricular Flutter and Fibrillation
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ECG features

 Both VFL and VF represent severe derangements of the


heartbeat that can terminate fatally or produce significant
brain damage within 3 to 5 minutes unless corrective
measures are undertaken promptly.

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VFL/VF

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 VFL
 sine wave in appearance, regular large oscillations
 At rate of 150 to 300 beats/minute (usually about 200)

 VF
 Irregular undulations of varying contour and
 Distinct QRS complexes, ST segments, and T waves are
absent.
 Fine-amplitude fibrillatory wavesV,F0.2
L mV with prolonged
VF.
 worse survival rates
VF

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Mechanisms

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 VF occurs in various clinical situations but, most


commonly in association with CAD and as a terminal
event
 Most frequently in the morning.
 Other causes of VF
 Antiarrhythmic drug administration,
 Hypoxia, ischemia,
 AF resulting in very Rapid ventricular rate in pts with
preexcitation syndrome;
 After electrical shock administered during cardioversion,…

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Clinical Features
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 Hemodynamic collapse is present with both VFL & VF

 Faintness, followed by LOC, seizures, apnea, and


eventually, if the rhythm continues untreated,
 Death
 BP is unobtainable, and heart sounds are usually absent.

 The atria can continue to beat at an independent rhythm for a


time.

 Eventually, electrical activity of the heart ceases


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Management
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 Basic life support and advanced cardiac life support

 Immediate nonsynchronized DC shock using 200 to 400 J


 VF,
 ventricular flutter, and
 Pulseless VT

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REFERENCES
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1. TINTINALLI’S EMERGENCY MEDICINE A COMPREHENSIVE STUDY GUIDE


9TH EDITION

2. ROSEN’S EMERGENCY MEDICINE: CONCEPTS AND CLINICAL PRACTICE,


9th EDITION

3. HARRISON’S PRINCIPLES OF INTERNAL MEDICINE 20TH EDITION

4. ONLY EKG BOOK YOU'LL EVER NEED, THE, 5TH EDITION

5. 2017 AHA/ACC/HRS GUIDELINE FOR MANAGEMENT


OF PATIENTS WITH VENTRICULAR ARRHYTHMIAS AND
THE PREVENTION OF SUDDEN CARDIAC DEATH

6. ESC 2015 VENTRICULAR ARRHYTHMIAS AND


THE PREVENTION OF SUDDEN CARDIAC DEATH

7. UP TO DATE 2018
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Thank You
WCT by GADISA 10/01/2020

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