Approach to Wide complex tachycardia /cardiology

Wide Complex Tachycardia:
Approach To Diagnosis
Moderator
Dr. Vikas Agrawal
Speaker
Dr. Awdhesh Chaudhary

ARRHYTHMIAS
• Classified on basis of impulse generation or conduction
– Origin
• SA node, Atria, AV node, Ventricle
– Conduction
• Normal anterograde, retrograde
• Accessory pathway, bundle branch block
• AV block
– both
• 2 basic types:
– Fast pulse, >100 bpm (tachyarrhythmia)
– Slow pulse, < 60 bpm (bradyarrhythmia)
Harrison`s principles of internal medicine 20th edition

TACHYARRHYTHMIAS
• Tachyarrhythmias
– on basis of QRS duration
• Narrow complex (QRS <120 milliseconds)
• Wide complex (QRS ≥120 milliseconds)
– On basis of origin of impulse
• Supraventricular (sinus node, atria, AV node, or His
bundle)
• Ventricular (ventricular tissue or Purkinje fibres )

Tachycardia
Narrow QRS
(QRS< 0.12 sec)
Regular rhythm Irregular rhythm
Wide QRS
(QRS>0.12 sec)
Regular rhythm Irregular rhythm
•Sinus Tachycardia
•AVNRT(artriovent
ricular nodal
reentry
tachycardia)
•AVRT(artrioventri
cular reentry
tachycardia)
•Focal AT
•Atrial flutter
•Atrial fibrillation
•Multifocal atrial
tachycardia
•Focal atrial
tachycardia with
variable block
•Atrial flutter with
variable AV block
•Ventricular
tachycardia
(Monomorphic).
•SVT with aberrant
conduction
•Antidromic AVRT
with antegrade AV
conduction via
ascessory
pathway(i.e. WPW
syndrome)
•AF with aberrant
conduction.
•AF with antegrade
AV conduction via
ascessory
pathway(i.e. WPW
syndrome)
•Polymorphic VT
modified from Braunwald`s heart disease 11th edition

APPORACH TO ARRHYTHMIA
• The evaluation of patients with suspected
cardiac arrhythmias is highly individualized,
however two key features
• History and ECG.
• In general, more severe presenting symptoms
the more aggressive evaluation and
treatments is required.

ASSESS PATIENT FOR
CLINCAL STABILITY
UNSTABLE PATIENT
(i.e, PULSELESS,
HEMODYNAMICALY
UNSTABLE)
STABLE PATIENT
IMMEDIATE
TREATMENT
HISTORY & PHYSICAL
EXAMINATION AND
ECG SHOULD BE
SYSTEMATICALLY
REVIEWED
Primary goal is
to determine
etiology and
type of
arrhythmias
INITIAL APPROACH

HISTORY
• Age : > 35 or less than 35 years
• Previous history
– of myocardial ischemia, heart failure, structural heart
disease, dyselectrolytemia
• Family history
• H/o cardiac arrhythmia in past
• H/o pacemaker implantation
• H/o persistent atrial fibrillation
• Drug history of proarrhythmic drugs
• Previous old ECG

HISTORY
• Common presenting symptoms include
– palpitations
– dizziness
– exercise intolerance
– episodes of light-headedness
– syncope
– sudden cardiac arrest leading to sudden death.
– Chest pain
– Can be asymptomatic also.
• Syncope is a concerning symptom, that can be due to
an episode of VT that produces severe hypotension.

EXAMINATION AND LABORATORY TEST
• EXAMINATION: cannon A waves, variable intensity of S1, pulse,
focus on evidence of heart disease
• ANCILLARY TESTING: Termination of Arrhythmia in response to
maneuvers like Valsalva, carotid sinus pressure, and adenosine.
• LABORATORY TEST:
– 12 Lead ECG
– Event recorder
• Non-looping, patient activated recorder
• Looping event recorders
– Continuous ambulatory recording
– Holter monitor—typically used for 24–48 h
– Implanted loop recorders
– Exercise Testing
– Electrophysiologic study

COMMON TERMS RELATED TO VT
• PREMATURE VENTRICULAR COMPLEX
(PVC):
– PVC is the premature occurrence of a QRS complex
– Duration usually exceeding the dominant QRS
complex (>120 msec)
– T wave is usually large and opposite in direction to the
major deflection of the QRS.
– QRS complex is not preceded by a premature P wave
– QRS can be preceded by a non conducted sinus P wave
occurring at its expected time.
Braunwald`s heart disease 11th edition

• PVCs that originate from the same focus will
have the same QRS morphology and are
referred to as unifocal PVCs.

• PVCs from different ventricular sites have
different QRS morphologies and are referred
to as multifocal PVCs

• Bigeminy : refers to pair of complex and
indicates a normal and premature complex
• Trigeminy :indicates a premature complex that
follows two normal beats
• Quadrigeminy : a premature complex that
follows three normal beats.

• Coupling interval: Interval between the
normal QRS complex and the PVC.
• PVCs can exhibit fixed or variable coupling
interval.

Two consecutive ventricular beats are ventricular couplets.
Three successive PVCs are called as ventricular triplets.

AV DISSOCIATION, CAPTURE AND
FUSION BEATS

Concordance exists when the QRS complexes in all the chest leads are
monophasic with same polarity either predominantly positive or
predominantly negative.
The presence of concordance suggests that the tachycardia has
a ventricular origin.
Positive

Negative
If any lead has biphasic QRS (qR or RS
complex) concordance not present

 IDIOVENTRICULAR RHYTHM :
• Three or more consecutive PVCs at less than 60 beats per
minute.
 ACCELERATED IDIOVENTRICULAR RHYTHM :
• Idioventricular rhythm with rate between 60 and 100 beats per
minute.

VENTRICULAR TACHYCARDIA(VT)
• Originate from ventricular myocardium, valve
cusps, aorta, pulmonary artery or Purkinje
fibers .
• Ventricular arrhythmias are characterized by a
wide QRS complex ≥ 120 msec
• VT is three or more consecutive beats(PVCs)
at a rate faster than 100 beats/min with ST-T
vector pointing opposite the major QRS
deflection.
HARRISON`S 20th e

NON-SUSTAINED VT :
• VT that terminates spontaneously within 30
second is non-sustained VT.
• Non-sustained VT is usually monomorphic with
rates <200 beats/min and typically lasting <8
beats.
SUSTAINED VT:
• VT that persists for >30 seconds OR;
• terminated by an active intervention, such as
administration of an intravenous medication,
external cardioversion, or pacing or a shock from
an implanted cardioverter defibrillator.
In conventional rate of 25mm/sec, 30 sec =150 large square on ecg

• MONOMORPHIC VT: VT with stable single QRS
morphology from beat to beat.
• POLYMORPHIC VT: VT with changing or multiform
QRS morphology from beat to beat.
• BIDIRECTIONAL VT: VT with a beat-to-beat
alternation in the QRS frontal plane axis.
– seen in the setting of digitalis toxicity or
catecholaminergic polymorphic VT(CPVT).

LBBB TYPE AND RBBB TYPE
MORPHOLOGY OF VT
• LBBB morphology :
– QRS>120 msec with
prominent negative
deflection in V1.
• RBBB morphology :
– QRS>120 msec with
prominent positive
deflection in V1.

Localizing Origin Of Ventricular Beats
• VT (PVCs) that have a dominant S-wave in V1, referred to as
LBBB configuration originate from the right ventricle or
interventricular septum.
• Those with a dominant R-wave in V1 originate from the left
ventricle and has RBBB configuration.
• A superior frontal plane axis (negative in II, III, AVF)
indicates initial depolarization of the inferior wall
(diaphraghmatic aspect of the heart)
• An inferior frontal plane axis (positive in II, III, AVF)
indicates an origin in the cranial aspect of the heart.

Causes of wide complex tachycardia
1) Ventricular Tachycardia (80%)
2) SVT with abnormal intra-ventricular conduction (15- 25%)
 SVT with aberrant conduction via His-Purkinje system( 15-20%)
 With pre existent (fixed) BBB or functional BBB
 Pre-excited SVT (with anterograde conduction via an accessory pathway)
 Antidromic AVRT
 Atrial tachycardia, Atrial flutter or AVNRT with bystander accessory
pathway
 SVT with intra-myocardial conduction delay
 Ventricular hypertrophy and /or dilation
 Cardiomyopathy
 Congenital heart disease
 SVT with wide QRS
 due to drug toxicity (class 1A, 1C, Amiadarone)
 electrolyte disturbance (e.g. hyperkalemia)
3) Ventricular pacing (<1%)
4) Artifact Current Cardiology Reviews, 2014, Vol. 10, No. 3 by András Vereckei .et al

SUSTAINED VT
• Rapid VT, >200 beats/min, usually causes hypotension that
may present as syncope.
• Patients with normal cardiac function might tolerate rapid
VT, and those with severe left ventricular (LV) dysfunction
may experience symptoms of hypotension, even if VT is
slower than 150 beats/min.
• Monomorphic VT that is rapid or associated with structural
heart disease may deteriorate to ventricular fibrillation
(VF), which may be the initial cardiac rhythm recorded at
the time of resuscitation of a cardiac arrest.

VT vs SVT
• There is difference in prognosis and management of SVT and VT, so
distinction between SVT and VT is critical.
• VT carries much graver prognosis, usually implies the presence of
significant heart disease result in more profound hemodynamic
compromise, it require immediate attention and measures to
revert back to normal sinus rhythm.
• A number of ECG criteria have been evaluated to distinguish
supraventricular tachycardia with aberrancy from VT.
• Wide complex tachycardias without a typical LBBB/RBBB
configuration, particularly if different from the QRS in sinus rhythm,
and especially in patients with a history of MI, are almost always VT.

VT vs SVT
• A QRS morphology that is identical to that present during sinus rhythm,
even if abnormal, suggests that the tachycardia is supraventricular.
• The presence of AV dissociation is usually a reliable marker for VT but P-
waves can be difficult to define.
• A monophasic R wave or Rs complex in aVR OR concordance from V1 to V6
of monophasic R or S waves are also relatively specific for VT.
• Presence of capture beats and fusion beats favors VT.
• A P-wave following each QRS does not exclude VT because 1:1 conduction
from ventricle to atrium can occur.

VT SCORE
• The VT score method was based on seven ECG features:
1. Initial R wave in V1
2. Initial r > 40 ms in V1/V2
3. Notched S in V1
4. Initial R in aVR
5. Lead II R wave peak time ≥50 ms
6. No RS in V1-V6,
7. Atrioventricular dissociation.
• Atrioventricular dissociation was assigned two points, and
each of the other features was assigned one point.
• Score ≥3 is definitive for VT
VT SCORE SPECIFICITY
1 83%
2 88%
3 99.6%
4 100%
The ventricular tachycardia score: a novel approach to electrocardiographic diagnosis of
ventricular tachycardia… Marek Jastrzebski. et al ,2015

Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia,That
Remains the QuestionJohn B Garner1 and John M Miller Arrhythmia & Electrophysiology Review

A: QRS duration <140 ms; B: QRS configuration is rSR’; C: R/S ratio in V6 >1; D: R–S duration in
precordial lead with RS complex <100 ms; E: aVR with sharp Q followed by R wave; F: QRS onset
to peak in lead II <50 ms. Each of these criteria correctly point to a diagnosis of SVT

POLYMORPHIC VENTRICULAR
TACHYCARDIA (P-VT)
• P-VT has continually changing QRS morphology indicating a
changing ventricular activation sequence.
• Typically seen in association with acute myocardial infarction
or ischemia (MI), ventricular hypertrophy, and a number of
genetic mutations that affect cardiac ion channels.
• Polymorphic VT and VF that occur within the first 48 h of
acute MI are associated with greater in-hospital mortality.
• Usually degenerates into ventricular fibrillation (VF).

Normally conducted sinus beat  a premature ventricular contraction (PVC) 
compensatory pause  long RR interval. PVC after the next sinus beat initiates VT.
This is the classic “pause dependent” mode of initiation of torsades des pointes VT with
long–short intervals.
The VT has a characteristic initiation sequence of a
premature ventricular beat that induces a pause, followed by
a sinus beat that has a longer QT interval and interruption of
the T-wave by the premature ventricular contraction (PVC)
that is the first beat of the polymorphic VT (“pause-
dependent”).

TORSADES DE POINTES
• Torsades de pointes is polymorphic VT that occurs in
the setting of a long QT interval and is characterized by
a waxing and waning QRS amplitude.
• The twisting of the points, although characteristic,
may not always be seen, especially if the episode is
non-sustained or if only a limited number of leads are
available.

Ventricular flutter
• Very rapid (150-300 bpm, usually 200 bpm) mono-
morphic VT that has a sinusoidal appearance is called
as ventricular flutter
• It is not possible to distinguish the QRS complex from
the T wave.
• Relatively slow sinusoidal VTs have a wide QRS
indicative of slowed ventricular conduction are caused
by drugs
– Hyperkalemia, toxicity from excessive effects of drugs that
block sodium channels (e.g., flecainide, propafenone, or
tricyclic antidepressants) and severe global myocardial
ischemia are causes

Ventricular flutter.
Sinusoidal VT due to electrolyte
disturbance or drug effects.

Ventricular Fibrillation
• VF is characterized by disordered electrical
ventricular activation without identifiable QRS
complexes.(chaotic rythm)
• Spiral wave reentry and multiple circulating
reentry wavefronts are possible mechanisms.
• Sustained polymorphic or monomorphic VT
that degenerates to VF is a common cause of
out of hospital cardiac arrest.
• Rate is indeterminate.

If patient is fully stable then its artifact

 ELECTRICAL STORM or Ventricular Tachycardia
(VT) storm
• Occurrence of three or more episodes of VT or
ventricular fibrillation (VF) within 24 hour.
INCESSANT VT:
• VT is designated incessant when VT continues to recur
shortly after electrical, pharmacologic, or
spontaneous conversion to sinus rhythm.
• Typically, VT is monomorphic.

ACCESSORY PATHWAYS AND THE WOLFF-
PARKINSON-WHITE SYNDROME
• Accessory pathways (APs) occur in 1 in 1500–2000 people
• APs are since birth are due to failure of complete partitioning
of atrium and ventricle by fibrous ring.
• AP occur most frequently between left atrium and free wall of
left ventricle
• Variety of arrhythmias can occur through APs
– narrow-complex PSVT
– wide-complex tachycardia

• Most patients have structurally normal hearts, but APs are
associated with Ebstein’s anomaly and forms of hypertrophic
cardiomyopathy.
• APs are abnormal connections that allow conduction between
the atrium and ventricles across the AV ring.
• Wolff-Parkinson-White (WPW) syndrome is defined as a
preexcited QRS during sinus rhythm and episodes of PSVT.
• Concealed APs allow only retrograde conduction, from
ventricle to atrium, so no preexcitation is present during sinus
rhythm, but SVT can occur.

• Fasciculoventricular connections between the His
bundle and ventricular septum produce
preexcitation but do not cause arrhythmia,
probably because the circuit is too short to
promote reentry.
• Atriofascicular pathways (Mahaim fibers) connect
the right atrium to fascicles of the Right bundle
branch that produce a wide complex tachycardia
having a LBBB configuration.

Morphology of QRS and delta wave is determined by AP location and
degree of fusion between the excitation wavefronts from conduction over
the AV node and conduction over the AP.
•LBBB
Morphology
•Marked
preexication –due
to proximity to SA
node
RBBB
morphology
Negative delta wave
Negative delta wave

•Short PR (<0.12 s)
•Slurred initial QRS (delta wave)
•Prolonged QRS
 produced by slow conduction
through direct activation of
ventricular myocardium over
the AP. Harrison`s principles of internal medicine 20th edition
Most common
RP<PR
Qrs <.12 sec

Tremor Induced Pseudo-VT And True
VT
• Huang et al have proposed a tested ECG algorithm to
differentiate tremor induced pseudo-VT and true VT.
• Sinus sign: Sinus rhythm is observed in a frontal or
limb lead.
• Notch sign : A notch is present on a QRS complex and
represents the length of the sinus cycle.
• Spike sign: Small spikes found within QRS complexes.
• Any of the three characteristic signs will exclude true
VT as the diagnosis.
• Absence of all three signs will diagnose of true VT
correctly in 97.3% of cases.
Huang CY, Shan DE, Lai CH, et al. An accurate electrocardiographic algorithm for differentiation of tremor-
induced pseudo-ventricular tachycardia and true ventricular tachycardia. Int J Cardiol. 2006;111(1):163–165.

Question and discussion
??????

Respiratory sinus arrhythmia. The rate of the sinus pacemaker is relatively slow at the
beginning of the strip during expiration, then accelerates during inspiration and slows again
with expiration.
P wave morphology=same and stable PR interval: Sinus arrhythmia
irregularly irregular:
Causes of irregularly irregular arrhythmia
Sinus arrhythmia, AF,MAT

AF in patient with the WPW syndrome and antegrade conduction down the bypass tract
leading to a wide complex tachycardia. Rhythm is “irregularly irregular,” and rate is extremely
rapid (about 230/min). Not all beats are preexcited.
f wave

WPW preexcitation pattern, with triad of short PR, wide QRS, and delta waves.
Polarity of the delta waves (slightly positive in leads V1 and V2 and most positive in lead
II and lateral chest leads) is consistent with a right-sided bypass tract.

MONOMORPHIC VT
RBBB morphology in V1 ,the R:S ratio <1 in V6

AF with LBBB. The ventricular rhythm is erratically irregular. Coarse fibrillatory waves are best
seen in lead V1, with a typical LBBB pattern.

Atrial flutter with 2:1 AV conduction (block) and LBBB, not to be mistaken for VT.
Typical atrial flutter activity is clearly present in lead II, at a cycle rate of about 320/min,
yielding an effective ventricular rate of about 160/min

Monomorphic VT ,AVR Dominant R WAVE, RBBB type morhpology, R TO S >100 mili sec

.
artifactual ventricular tachycardia , A “wandering” baseline and variations in the amplitude of
apparent QRS complexes were noted. normal QRS complexes were detected in chest leads V3
to V6

Spike sign , normal rhythm in lead 1 that is sinus sign===== artifact

VT Associated with Different
Forms of Heart Disease

https://ecgwaves.com/introduction-electrocardiography-ecg-
book/retledningssystemet-7/

Brugada Syndrome
• Brugada syndrome (BrS) is
characterized by an ECG
pattern consisting of coved-
type ST-segment elevation
(≥2 mm) followed by a
negative T wave in the right
precordial leads V1 through
V3 (often referred to as
type 1 Brugada ECG
pattern).
• Increased risk for SCD
resulting from episodes of
polymorphic ventricular
tachyarrhythmias.

Electrocardiographic abnormalities in resting rhythm that suggest potential for
arrhythmia. Lead V1 is shown in each example; a normal complex is presented

Approach to Wide complex tachycardia /cardiology

Approach to Wide complex tachycardia /cardiology

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