Wide QRS Complex

Tachycardia
Nuriza karuniawan
Definition
• Wide QRS-Complex Tachycardia defined as a rhythm with rate >100
bpm and QRS duration >120 ms
• Causes of wide QRS complex tachycardia:
1. Ventricular Arrhythmia
2. Supraventricular tachycardia with
• Aberrant conduction
• Pre-existing bundle branch block
3. Preexited supraventricular tachycardia
• AVRT with antidromic conduction
• AF with antegrade conduction via accessory pathway

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
How to differentiate wide QRS complex
tachycardia?
Important clues
• Medical backgrounds
• ECG clues
Medical backgrounds favour VT
• Most WCTs are ventricular tachycardia
• Sometimes it can be still difficult to differentiate VT and SVT with
abberant conduction as it can share similar clinical sign and symptoms
(dizziness, chest pain, dyspnoea, and altered mental status)
• Some clinical clues favour VT:
• Presence structural heart disease
• Prior MI
• Family history of channelopathies
• The presence or absence of hemodynamic instability does not favour
VT or SVT as diagnosis
2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
Jacobson J. ESC Textbook of Cardiovascular Medicine.2018
ECG clues favour VT
Hallmark ECG criteria of VT
• Atrioventricular dissociation
• Morphological configuration QRS complex
• QRS duration
• Chest lead concordance
• QRS axis
• Differences in ventricular activation velocity
• Dissimilarities compared baseline ECG

Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020

 AV Dissociation
• Classically characterized by a series QRS
complexes uncoupled from dissociated P waves
• VT may be confirmed once AV dissociation is
assuredly identified key diagnostic in several
WCT differentiation methods
• ECG clues:
• Interspersed P waves nestled between or
hidden amidst QRS complex or T waves
• Capture or fusion beats (less common)
• Pitfalls:
• Identification AV dissociation can be quite
challenging
• Its absence does not rule out VT
Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020
 Morphological Criteria
• Classical Morphological Criteria
Configuration QRS complex in V1-V2 and V6 may provide essential clues whether WCT has ventricular or
supraventricular origin
• Primary purpose: identify QRS configuration that consistent or inconsistent with aberrant conduction
• WCT with QRS configuration incompatible with RBBB or LBBB patternVT is most likely diagnosis
• WCT with QRS configuration with typical RBBB or LBBBSVT with aberrant/pre-existing BBB
• Notable exceptions: fascicular VTs rapidly engage His-Purkinje network and result in fairly typical aberrant
morphologies

Hallmark QRS morphological criteria for VT

Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020
QRS Duration
• VT commonly expresses longer QRS durations
• VT primarily relies on inefficient means ventricular
depolarization(cardiomyocyte-to-cardiomyocyte conduction)
• Cut off QRS duration for VT
• QRS > 140 ms for WCTs with RBBB pattern
• QRS > 160 ms for WCTs with LBBB pattern
• Pitfalls:
• Some supraventricular WCT can display QRS duration > 160
ms (ongoing antiarrhythmic drugs, electrolyte disturbances,
dramatic conduction delays, severe underlying structural
heart disease or cardiomyopathies)
• Fascicular VT expresses QRS durations < 120 ms

Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020

Chest Lead Concordance
• Concordance: QRS complexes in all 6 precordial leads (V1-V6)
uniformly display monophasic pattern with same polarity
• Chest lead concordance is highly specific (spec>90%) but rather
insensitive (sens<20%) diagnostic for VT
• Positive concordance (“R” QRS pattern V1-V6) : VT
originating from posterobasal LV
• Negative concordance (“QS” QRS pattern V1-V6): VT
originating from anteroapical LV
• Pitfalls: Supraventricular SVT may demonstrate concordance
patterns in rare circumstances
• Supraventricular WCT w/positive concordance: SVT with
preexcitation from left posterior or left lateral APs
• Supraventricular WCT w/negative concordance : SVT in
patients with flecainide toxicities or with chest wall
deformities

Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020

 QRS axis
VT may demonstrate a nearly limitless variety of mean electrical
vectors, many of which residing outside the expected range for
supraventricular WCT
• A scar-related VT mapped to anterolateral LV may produce WCT
with atypical RBBB pattern and rightward and superior QRS axis
• Superior QRS axis (between -90 and -180 degrees) highly
predictive VT
Vereckey : Dominant R wave in lead AVR is key diagnostic determinant
of VT
LAD in RBBB and RAD in LBBB quite specific for VT

Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020

Ventricular Activation Velocity
• Normal ventricular activation displays rapid initial QRS deflections as rapid
depolarization of myocardial segment arise from His-Purkinje system
• VT: delayed/slurred initial QRS complex (RS interval > 100 ms) due to slower
cardiomyocyte-to-cardiomyocyte conduction and more rapid terminal components
of QRS complex when VT impulse engages conduction systems and swiftly
activates remainder ventricular myocardium  ratio Vi/Vt 40 ms of QRS complex
<1

Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020

 Baseline ECG Comparison
• WCT with unchanged configurations in leads V1, II, and III compared with
the preexisting bundle branch block during SR were nearly always
Supraventricular WCT, while WCTs with noticeably different QRS
configurations were usually VT.
• Griffith et al: substantial deviation in QRS axis (ie, QRS axis change ≥40°)
compared with the baseline ECG was one of the most predictive ECG
features to diagnose VT
• Pachon et al: comparisons of QRS morphology between the WCT and the
baseline ECG as one of the weighty diagnostic determinants within their
point-based algorithm

Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020

HALLMARK ECG CRITERIA FOR VENTRICULAR TACHYCARDIA

Kasou AH, Noseworthy PA, May AM et al. J Am Heart Assoc.2020

Stepwise Approach How to Differentiate VT or SVT with abberancy
Brugada Algorithm 1. Absence of RS complex in any precordial lead  VT.
2. If a precordial RS complex is present, measure QRS onset to
nadir of S wave: R-to-S interval of greater than 100 ms
confirms VT.
3. If R–S timing is less than 100 ms, look for AV dissociation. If
1 present, this confirms VT.
4. Examine QRS complex in V1 and V6:
a. With RBBB QRS morphology:
2 i. In lead V1: monophasic R, QR, or RS favours VT.
ii. In lead V6: R/S ratio of less than 1 favours VT; QS,
QR, or monophasic R favours VT.
b. With LBBB QRS morphology:
3 i. In either lead V1 or V2: R greater than 30 ms, R-to-
S (nadir) interval of greater than 60 ms or a notched
S wave favours VT.
4 ii. In lead V6: QR or QS favours VT.
c. Note: both V1/V2 and V6 criteria need to favour VT for
the diagnosis to be made using this step.
5 5. If none of these steps favours VT, a diagnosis of SVT is made.

Brugada P, Brugada J, Mont L et al. Circulation 1991;83:1649–59

 Vereckei Algorithm (aVR)

1. Presence of an initial R waveVT

1
2. Width of an initial r or q wave greater than
40 msVT
3. Notching of the initial down stroke of a
2 negative QRS complexVT
4. Ventricular activation–velocity ratio (vi/vt)
less than or equal to 1, where v is the vertical
3 excursion (in millivolts) recorded during the
initial (vi) and terminal (vt) 40 ms of the QRS
complex.
4 5. If none of these steps favours VT, a diagnosis
of SVT is made.

Vereckei A, Duray G Szénási G, Altemose GT, et al. Heart Rhythm 2008;5:89–98

 Adenosine test for differentiating WCT

The property of adenosine to depress and block the AV nodal conduction makes it a useful diagnostic tool to
differentiate WCT supraventricular or ventricular in origin
• WCT supraventricular origin
• adenosine should terminate the arrhythmia if the AV node is involved or
• produce AV block to reveal the underlying atrial rhythm like in atrial flutter with aberrancy
• Antidromic AVRT
• Antidromic AVRT from typical APs get terminated from adenosine due to block in AV node which is
retrograde limb.
• Care should be taken as adenosine can trigger atrial fibrillation which have adverse hemodynamic
consequences in antidromic AVRT.
• Adenosine test should be avoided as diagnostic agent for irregular WCT due to pregression to VF
during pre-excited AF
• WCT ventricular origin
• Adenosine can bring out ventriculoatrial block/dissociation or
• Terminate WCT in case of idiopathic RVOT VT
• Termination of WCT is not diagnostic of SVT

Gupta A, Lokhandwala Y, Rai N, et al. Journal of Arrhythmia. 2020. doi: 10.1002/joa3.12453

Effects Adenosine on cardiac cells

• cAMP-independent (direct): activating G protein-coupled inwardly rectifying adenosine sensitive potassium

channels (IK AchAdo) efflux potassium intracellularhyperpolarizing potential membrane
• Hyperpolarized potential membrane of AV nodeInitially, leads to depression of the upstroke of action
potential in and subsequent complete abolition in AV node laterdecreased conduction in the AV node
(negative dromotropy), resulting in PR prolongation and AV block
Gupta A, Lokhandwala Y, Rai N, et al. Journal of Arrhythmia. 2020. doi: 10.1002/joa3.12453
 Termination of WCT due to adenosine in idiopathic RVOT VT

cAMP-dependent (indirect/antiadrenergic effects)

of adenosine
• inhibition of inward calcium current (ICaL) and
transient inward sodium current (Iti)
• Gα (alpha) subunit of the A1 receptor leads to
the inhibition of cAMP production, which is
responsible for the inhibition of sympathetic
response through beta receptors and inward
calcium current

Adenosine antagonizes the actions of catecholamine on L-type calcium current (ICaL), which decreases the amplitude
of delayed after-depolarizations (DADs) and suppresses triggered activity induced
 adenosine can terminate idiopathic RVOT VT dependent on cAMP-mediated triggered activity
Gupta A, Lokhandwala Y, Rai N, et al. Journal of Arrhythmia. 2020. doi: 10.1002/joa3.12453
General Evaluation of Patients with Documented or Suspected
Ventricular Arrhythmia
• History and Physical examination
• Noninvasive Evaluation
• 12-lead ECG and Exercise Testing
• Ambulatory Electrocardiography
• Implanted Cardiac Monitors
• Noninvasive Cardiac Imaging
• Biomarkers
• Genetic Considerations in Arrhythmia Syndrome
• Invasive Testing
• Invasive Cardiac Imaging : Cardiac Catheterization or CT
Angiography
• Electrophysiology Study
2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
History and Physical Examination

2017 AHA/ACC/HRS guidelines for the management of patients

with ventricular arrhythmias and prevention sudden cardiac
death. Circulation 2018
12-Lead ECG and Exercise Test
• VT is the diagnosis in most adults with wide complex
tachycardia and underlying structural heart disease
• A 12-lead ECG during tachycardia is the first diagnostic
test that should be done in patient with stable wide QRS
complex tachycardia

• For exertion-related arrhythmic symptoms, exercise in a

monitored setting may reproduce the symptoms related
arrhythmia, allowing for diagnosis if not reproducible,
long-term electrocardiographic monitoring with external
or implantable recorders
• Exercise testing is particularly important when CPVT is a
possibility.

Clue ECG in SR for VA:

• Prior MI, LV enlargement (substrate for VA)
• long QT syndrome, Brugada syndrome, and ARVC
(evidence of inherited arrhythmia disorders)
2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
Ambulatory ECG and Implanted
Cardiac Monitor • Importantly, when the suspicion of VA in patient is high,
outpatient ambulatory monitoring is appropriate as
prompt diagnosis
• It is important to accurately correlate the symptoms with
the arrhythmias detected by ambulatory ECG monitoring

Continuous or intermittent ambulatory ECG with Holter

monitor or event recorder is helpful in diagnosing suspected
arrhythmias, establishing their frequency, relating them to
symptoms, and assessing the response to therapy

• A 24-hour continuous Holter recording is appropriate

when symptoms occur at least once a day
• For sporadic symptoms, event or “looping” monitors are
more appropriate because they can be activated over
extended periods of time and increase diagnostic yield

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
Noninvasive Cardiac Imaging Echocardiography is the most readily available and
commonly used imaging technique in pts with or high risk
for VA or SCD
• Cardiomyopathy, HF, prior MI, FH cardiomyopathy or
SCD, or an inherited structural heart disease
• Assessment of global and regional myocardial function,
valvular structure and function, assessment for adult
congenital heart disease

VA or SCA can be an initial manifestation of ischemic

heart disease, cardiomyopathic processes, or myocarditis

Cardiac CT and cardiac MRI: evaluation of structural heart

disease and assessment of LV and RV function, valvular
structure and coronary anatomy (incl. anomalous coronary
origins), myocardial scar and infiltrative process (LGE MRI)

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
Biomarker and Genetic
Counselling Elevated levels of natriuretic peptides (BNP or NT-pro
BNP) associated with increased risk of SCD and
appropriate ICD therapies, even after adjustment of
LVEF and other risk factors

In young patients (<40 years of age) without structural

heart disease who have unexplained cardiac arrest,
unexplained near drowning, or recurrent exertional
syncope, genetic testing may be important to identify
an inherited arrhythmia syndrome as a likely cause

Genetic counseling generally occurs before proceeding

with genetic testing, and, from a patient’s perspective,
is optimally provided by genetic counselors

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
 Invasive Imaging and EP Study

• Coronary angiography: establishing or excluding the

presence of significant obstructive ischemic heart disease
in patients with SCA or those with life-threatening VA

• Presence of ST-elevation on preresuscitation or early post

resuscitation ECG suggests ischemia and potential ACS
warranting urgent angiography and revascularization

• ST-elevation can also result from coronary spasm or DC

shocks

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
 Invasive Imaging and EP Study

• In patients who meet criteria for ICD implantation (HF and

LVEF ≤35%), data do not support the routine use of EP study
solely for risk stratification

• Risk stratification for channelopathies is generally

made on the basis of symptoms, the exercise treadmill testing
and the results of genetic testing

• EP study does not have prognostic value for risk stratification

in patients with these cardiac channelopathies

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
Therapies for Treatment or Prevention of Ventricular Arrhytmia

Medication Therapy
• With the exception of beta blockers (eg, metoprolol succinate, carvedilol), there is no
evidence from RCTs that antiarrhythmic medications for VA improve survival when given for
the primary or secondary prevention of SCD
• Antiarrhythmic is essential in some patients to control arrhythmias and improve symptoms

Class I Prominent Sodium Channel Blockade

Specific circumstances where sodium channel blockers have been used to treat VT/ SCA include:
• intravenous lidocaine for refractory VT/cardiac arrest
• oral mexiletine for congenital long QT syndrome
• quinidine for Brugada syndrome
• flecainide for CPVT
These medications could also be used in ICD patients with drug- and ablation-refractory VT

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
Beta Blockers
First-line antiarrhythmic therapy in treating ventricular arrhythmia and reducing risk of SCD due to
excellent safety profile and affectiveness
• Reduce all-cause mortality and SCD in HFrEF
• Reduce mortality in the setting polymorphic VT after MI
• Supress ventricular arrhythmia in some patients with structurally normal heart
• First line thrapy for some cardiac channelopathies (Long QT syndrome, CPVT)
Antiarrhythmic efficacy related to effects of adrenergic-receptor blockade on sympathetically
mediated triggering mechanisms

Amiodarone
Amiodarone has wide spectrum of actions : blockade beta reseptors, sodium, calcium, and potassium
currents
• Primary prevention: amiodarone decreased the risk of SCD (RR 0.76; 95% CI: 0.66–0.88) and all-
cause mortality (RR 0.88; 95% CI: 0.78–1.00) in high-risk patients (LVEF <40%, with or without
coronary disease), but quality evidence very low
• Secondary prevention of SCD: neither risk nor benefit with amiodarone
• Intravenous amiodarone has a role in reducing recurrent VF/VF during resuscitation

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
Sotalol
Sotalol appears to reduce the defibrillation threshold, but has significant proarrhythmic effects
and has not been shown to improve survival
SWORD (Survival With Oral d-Sotalol) trial: D-sotalol increase the risk of death in patients with
heart failure
Sotalol may lead to HF decompensation so that it is generally avoid in patients with LVEF <20%

Calcium Channel Blockers

Non-DHP CCBs have no role in treating ventricular arrhythmia
For patients with a structurally normal hearts, verapamil or diltiazem can suppress some outflow
tract origin
Oral and intravenous verapamil are effective in treating idiopathic interfascicular reentrant LVT.
Calcium channel blockers should not be given to patients with VT in the settin of HFrEF

2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
2017 AHA/ACC/HRS guidelines for the management of patients with ventricular arrhythmias and
prevention sudden cardiac death. Circulation 2018
 Therapies for patients with LV dysfunction with/without
heart failure
Primary prevention of SCD

ACE inhibitor reduced mortality by 15-25% SCD-HeFT: ICD was associated with a 23% decreased risk of death
Beta-blockers reduced mortality by 35% and have [HR 0.77 (95% CI 0.62, 0.96), P 0.007] and 60%
anti ischemic properties reduction in SCD in the ICD arm and dependent NYHA class
MRA reduced mortality and SCD by 23% MADIT-II: ICD decrease of 31% in all-cause mortality [HR 0.69 (95%
CI 0.51, 0.93), P 0.016], with a larger benefit in patients whose
ESC guideline for management ventricular arrhythmia and prevention
sudden cardiac death. Eur Heart J. 2015. doi: 10.1093/eurheartj/ehv316 index myocardial infarction was more remote from randomization
PVCs in patients with LV dysfunction

PVCs and runs of NSVT in subjects with structural heart disease

contribute to an increased mortality risk SCD and
• 10 PVCs per hour or runs of NSVT are an acceptable marker
of increased risk

Amiodarone or catheter ablation should be considered:

• symptomatic PVCs or NSVTs
• PVCs or NSVTs contribute to reduced LVEF (TCM)

A high PVC burden (>24%) in patients with LV dysfunction and a

rather short coupling interval of the PVCs (<300 ms) suggest
PVC-induced cardiomyopathy
 catheter ablation can suppress PVCs and restore LV function

ESC guideline for management ventricular arrhythmia and prevention sudden cardiac death. Eur Heart J. 2015.
doi: 10.1093/eurheartj/ehv316
Sustained Ventricular Tachycardia
Patients with LV dysfunction with or without HF presenting
with sustained VT should be treated according to recently
HF guidelines
• MADIT-II: patients with ICD treated with the highest
doses of beta-blockers experienced a significant
reduction in recurrent episodes of VT or VF necessitating
ICD intervention compared with patients not taking beta-
blockers [HR 0.48 (95% CI 0.26, 0.89), P 0.02]
• OPTIC study :Amiodarone plus beta-blocker therapy
significantly reduced the risk of shock compared with
beta blocker treatment alone [HR 0.27 (95% CI 0.14,
0.52), P 0.001] and sotalol [HR 0.43 (95% CI 0.22, 0.85), P
0.02].
• SCD-HeFT: compared with conventional HF therapy, the
addition of amiodarone did not increase mortality in pts
with NYHA II-III HF with LV dysfunction

ESC guideline for management ventricular arrhythmia and prevention sudden cardiac death. Eur Heart J. 2015.
doi: 10.1093/eurheartj/ehv316
Role Catheter Ablation

In patients with VT storm, catheter ablation can acutely

terminate this potentially life-threating event and has been
shown to decrease the rate of recurrent electrical storm
episodes when compared with medical treatment only

VTACH study prospectively randomized patients with previous

myocardial infarction, reduced ejection fraction (≤50%) and
haemodynamically stable VT to catheter ablation or no
additional therapy
• The rate of survival free from recurrent VT over 24 months
was higher in the ablation group [47% vs. 29%, HR 0.61 (95%
CI 0.37, 0.99), P ¼ 0.045].
• The mean number of appropriate ICD shocks/patient/year
decreased from 3.4+9.2 to 0.6+2.1 in patients undergoing
catheter ablation (P 0.018) but did not affect mortality

ESC guideline for management ventricular arrhythmia and prevention sudden cardiac death.
Eur Heart J. 2015. doi: 10.1093/eurheartj/ehv316
Thank You