WIDE COMPLEX TACHYCARDIA
Dr.Pradeep Sreekumar
Definitions

Wide QRS complex tachycardia is a rhythm with a
rate of ≥100 b/m and QRS duration of ≥ 120 ms

VT – Three or more consequtive ventricular beats
with rate of 100/minute or more

SVT- Tachycardia requiring participation of
structures above bundle of His.

LBBB morphology-QRS complex duration ≥ 120 ms
with a predominantly negative terminal deflection in
lead V1

RBBB morphology-QRS complex duration ≥ 120 ms
with a predominantly positive terminal deflection in V1
Why QRS is wide?

A widened QRS (≥120 msec) occurs when
ventricular activation is abnormally slow
 Arrhythmia originates outside of the normal
conduction system (ventricular tachycardia)
 Abnormalities within the His-Purkinje system
(supraventricular tachycardia with aberrancy).
 Pre-excited tachycardias: supraventricular
tachycardias with antegrade conduction over an
accessory pathway into the ventricular
myocardium.
SVT (20%)
VT (80%)
Stewart RB. Ann Intern Med 1986
Causes of wide QRS complex tachycardia

Supraventricular tachycardia
- with prexsisting BBB
- with BBB due to heart rate (aberrant conduction)
- antidromic tachycardia in WPW syndrome

Ventricular tachycardia
Other causes..




Hyperkalemia
Acidosis
Antiarrhythmics-IA,IC
Ventricular pacing
Functional Bundle Branch Block

Functional aberration results from sudden change in
cycle length when parts of the His-Purkinje system
are partially or wholly inexcitable

Functional RBBB more common.
Linking phenomenon
Mechanism for perpetuation of functional anterograde
bundle branch block due to repetitive transseptal
retrograde concealed penetration by impulses
propagating along the contralateral bundle.
Linking: a dynamic electrophysiologic phenomenon
in macroreentry circuits,Michael h. lehmann et al, Circulation.
1985;71:254-265
LINKING PHENOMENON
AVRT

Orthodromic AVRT –
Antegrade conduction
:AVnode
Retrograde conduction
: Accessory pathway.
Wide QRS is produced only if aberrant
conduction
(rate related or preexisting BBB)

Antidromic AVRT – antegrade conduction over
the accessory pathway and retrograde conduction
over the AV node .
AVRT
Mahaim fibre mediated
tachycardia
 Antegrade
conduction : Mahaim pathway
 Retrograde
 LBBB
 Left

conduction:AV node
morphology
axis deviation
Pre-excitation during sinus rhythm is
uncommon
Bundle Branch Reentrant VT
RBBB morphology wide QRS
tachycardia
VT
Structurally normal heart

LVOT VT
 Fasicular VT

Abnormal heart
LV myocardial VT
 Bundle Branch Reentrant VT


SVT
SVT with pre existing RBBB
SVT with functional RBBB
LBBB morphology wide QRS
tachycardia
VT
Structurally normal heart


RVOT VT
Abnormal heart
Right ventricular myocardial VT
 ARVD


SVT
Mahaim fibre mediated tachycardia
SVT with LBBB
Unique clinical challenge
Diagnosing the arrhythmia is difficult —
Diagnostic algorithms are complex and imperfect.
Urgent therapy is often required —
Patients may be unstable at the onset of the
arrhythmia or deteriorate rapidly at any time.
Risks associated with giving therapy for an SVT to a
patient who actually has VT
SVT vs VT
Clinical history
Age
- ≥ 35 ys → VT (positive predictive value of 85%)
Underlying heart disease Previous MI → 90% VT
Pacemakers or ICD
Increased risk of ventricular tachyarrhythmia
Medication
Drug-induced tachycardia → Torsade de pointes
Diuretics
Digoxin-induced arrhythmia → [digoxin] ≥2ng/l or
normal if hypokalemia

Duration of the tachycardia — SVT is more likely if
the tachycardia has recurred over a period of more
than three years
SVT vs VT

AV dissociation
-cannon A waves
-variable intensity of S1

Termination of WCT in response to maneuvers like
Valsalva, carotid sinus pressure, or adenosine favor
SVT
Maneuvers

The response of the arrhythmia to maneuvers may
provide insight to the mechanism of the WCT

Carotid sinus pressure — Enhances vagal tone ,
depresses sinus and AV nodal activity
Carotid sinus pressure

Sinus tachycardia will gradually slow with carotid
sinus pressure and then accelerate upon release.

Atrial tachycardia or atrial flutter-the ventricular
response will transiently slow.
The arrhythmia is unaffected.

Paroxysmal SVT frequently terminates with carotid
sinus pressure.
VT

Unaffected by vagal maneuvers such as carotid sinus
pressure or valsalva

May slow or block retrograde conduction.
Exposes AV dissociation
Rarely, VT terminates in response to carotid sinus
pressure.
Laboratory tests

The plasma potassium and magnesium concentrations
(hypokalemia and hypomagnesemia predispose to the
development of ventricular tachyarrhythmias. )

Digoxin, quinidine, or procainamide levels-to rule
out drug toxicity
Chest x-ray

Evidence suggestive of structural heart disease

Evidence of previous cardiothoracic surgery

Presence of a pacemaker or ICD.
Rate

Limited use in distinguishing VT from SVT.

When the rate is approximately 150 beats per minute,
atrial flutter with aberrant conduction should be
considered.

Ventricular rate > 200-suspect preexcitation
tachycardia
Regularity
Marked irregularity of RR interval occurs in
atrial fibrillation (AF) with aberrant conduction and
polymorphic VT
Axis

A right superior axis (axis from -90 to ±180º)“northwest" axis, strongly suggests VT .
(sensitivity 20%,specificity 96%)

Exception -antidromic AVRT in Wolff-ParkinsonWhite (WPW) syndrome .

Compared to the axis during sinus rhythm, an axis
shift during the WCT of more than 40º suggests VT .

In a patient with a RBBB-like WCT, a QRS axis to
the left of -30º suggests VT.

In a patient with an LBBB-like WCT, a QRS axis to
the right of +90º suggests VT .
QRS duration

In general, 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

In an analysis of several studies, a QRS duration
>160 msec was a strong predictor of VT (likelihood
ratio >20:1) .

A QRS duration <140 msec does not exclude VT
( VT originating from the septum or within the HisPurkinje system may be associated with a relatively
narrow QRS complex.)
Concordance

Concordance is present when the QRS complexes in
all six precordial leads (V1 through V6) are
monophasic with the same polarity.

Either -entirely positive with tall, monophasic R
waves, or entirely negative with deep monophasic
QS complexes.

If any of the six leads has a biphasic QRS (qR or RS
complexes), concordance is not present.

Negative concordance is strongly suggestive of VT
 exception:SVT with LBBB aberrancy may
demonstrate negative concordance

Positive concordance -also indicates VT
 exception: antidromic AVRT with a left posterior
accessory pathway

Presence of concordance strongly suggests VT (90
percent specificity)

Absence is not helpful diagnostically (approximately
20 percent sensitivity)

Higher specificity for Positive concordance compared
to negative concordance(specificity 95% vs 90 %)
Negative concordance
Positive concordance
AV dissociation

AV dissociation is characterized by atrial activity that
is independent of ventricular activity

Atrial rate slower than the ventricular rate diagnostic
of VT.

Atrial rate that is faster than the ventricular rate SVTs.
Absence of AV dissociation in VT

AV dissociation may be present but not obvious on the
ECG.

The ventricular impulses conduct backwards through
the AV node and capture the atrium ( retrograde
conduction), preventing AV dissociation.
Dissociated P waves

PP and RR intervals are different

PR intervals are variable

There is no association between P and QRS
complexes

The presence of a P wave with some , but not all,
QRS complexes
Fusion beats

Fusion beat-produced by fusion of two ventricular
activation wavefronts characterised by QRST
morphology intermediate between normal and fully
abnormal beat.

Fusion beats during a WCT are diagnostic of AV
dissociation and therefore of VT.

Low sensitivity(5-20%)
Capture beats
Capture beats, or Dressler beats, are QRS complexes
during a WCT that are identical to the sinus QRS
complex .
Implies that the normal conduction system has
momentarily "captured" control of ventricular
activation from the VT focus.
Fusion beats and capture beats are more commonly
seen when the tachycardia rate is slower
If old ecg available…

Ideal QRS configuration between baseline and
WQRST-suggest SVT(exception :bundle branch
reentrant VT)

Contralateral BBB patterns in baseline vs WQRST
ECGs-suggest VT

WQRST complexes narrower than baseline ECGsuggest VT(the baseline ecg must have a bundle
branch block pattern)
Also look for….

VPCs

Evidence of prior MI

QT interval

ECG clues to any other structural heart disease
SVT vs VT
ECG criteria: Brugada algorithm
Brugada P. Ciculation 1991
Step 1
Step 2
Step 3
Step 4: LBBB - type wide QRS complex
VT
SVT
R wave >30ms
notching of S wave
small R wave
V1
fast downslope
of S wave
> 70ms
Q wave
V6
no Q wave
V1 in LBBB type QRS
True LBBB
R-R duration <- 30 msec
Interval from QRS onset to S nadir ≤70 msec
(85% of SVT –A)
VT
R >30 msec,QRS onset to S nadir>70 msec
(sensitivity-0.78,specificity 0.85,positive predictive value
0.97)
Notching and slurring of QRS complex –myocardial
disease
V6 in LBBB type QRS

True LBBB
Monophasic R with slow upstroke

VT
qR or QS pattern
Step 4: RBBB - type wide QRS complex
VT
SVT
rSR’ configuration
V1
or
R/S > 1
V6
qR (or Rs) complex
monophasic R wave
R/S ratio < 1
QS complex
or
V1 in RBBB type QRS
Initial ventricular activation is independent of RBB.
RBBB abberation affects only the latter QRS

True RBBB
rR’,rsR’,rSr’,rSR’

VT
qR,Rsr’,monophasic R wave
(Sensitivity 0.97,specificity 0.88)
VT
SVT
V6 in RBBB type QRS


RBBB abberation-small s wave.
qRs or Rs pattern
RBBB type VTVT from left ventricle-LV and RV voltage
contributes to S
qRS,qrS,rS,QS patterns seen
“R/S ratio in V6 rule”

R/S ratio in RBB type wide QRS tachycrdia less than
one, favours VT
Sensitivity-0.73
Specificity-0.79
Positive predictive value 0.9
Josephson’s sign


Notching near the nadir of the S-wave
Suggest VT
Wellens Criteria
• QRS width > 140 msec
• Left axis deviation
• AV dissociation
• Configurational characteristics of the QRS
morphology
Ultrasimple Brugada criterion

Joseph Brugada - 2010

R wave peak time in Lead II

Duration of onset of the QRS to the first change in
polarity (either nadir Q or peak R) in lead II.

If the RWPT is ≥ 50ms the likelihood of a VT very
high (positive likelihood ratio 34.8)
Pava LF, Perafán P, Badiel M, Arango JJ, Mont L, Morillo CA, and Brugada
J. R-wave peak time at DII: a new criterion for differentiating between wide complex QRS
tachycardias. Heart Rhythm 2010 Jul; 7(7) 922-6.
Vereckei A, Duray G, Szénási G, Altemose GT, and Miller JM.
Application of a new algorithm in the differential diagnosis of wide QRS
complex tachycardia. Eur Heart J 2007 Mar; 28(5) 589-600.
aVR algorithm
Criteria looks ONLY at lead aVR (if answer is
yes, then VT):
1. Is there an initial R wave?
2. Is there a r or q wave > 40 msec
3. Is there a notch on the descending limb of a
negative QRS complex?
4. Measure the voltage change in the first (vi) and
last 40 msec (vt). Is vi / vt < 1?
Vereckei et al, Heart Rhythm 2008
Sensitivity Specificity PPV
NPV

Brugada
89%
73%
92%
67%

Vereckei
97%
75%
93%
87%
Vereckei A, Duray G, Szénási G, Altemose GT, and Miller JM.
Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur
Heart J 2007 Mar; 28(5) 589-600.
Sensitivity & Specificity For VT

88% and 53% by aVR algorithm
VT vs AVRT
ECG criteria
Brugada P. Ciculation 1991
THANK YOU…….