Wide Complex Tachycardia (WCT)

Rose Lillo
Peninsula health
2010- revised 2011/2013
 Puzzled task
When wide complex tachycardia may be

SV or Ventricular in origin
Types of wide complex tachycardia
SVT
Regular With preexisting BBB
With aberrancy
Irregular AF with aberrancy/ pre-excitation
AF with preexisting block

Vs

VT
Regular monomorphic
irregular polymorphic (Torsades vs non torsades)
It is important to make a differential
diagnosis as:
Wide complex tachycardia do have different causes,
management & prognosis

Danger in misdiagnosing VT as SVT

Diagnostic mistakes are frequent

Inappropriate treatment could be fatal

Some patients can tolerate VT for hours & some patients

with SVT decompensate quickly
That is why you treat it as VT until
proven otherwise

This the safest option as

80% of WCT will be VT
Review
 Normal conduction system & axis

Mean cardiac vector is normally directed downward and leftward

(It sits on + 60◦). Axis deviation toward NML is seen in VT
QT & Refractory Period

QT interval
Represent ventricular depolarisation & repolarisation
 Refractory period (RP)

RP is proportional to the length of the preceding cycle; the longer the

cycle & the slower the rate, the longer the RP & vice versa
The RBB tends to have slightly longer RP than does the LBB
 Conducted atrial ectopic

If an early impulse finds both Bundle Branches recovered

then it will be conducted through the ventricles in a normal
fashion
Non conducted atrial ectopic

If an early impulse find both bundle branches refractory, it will

not be conducted at all
Aberrancy
 Refers to the temporary, abnormal conduction of
supraventricular impulses through the AVN with
delay or block

 Occurs when a premature supraventricular beat is

conducted to the ventricles before ventricular
repolarisation has been completed causing the
impulse to be conducted abnormally

 It produces a wide, bizarre QRS

Cont
 Ventricular aberrancy may result
from:
a shortening of the immediate cycle
a lengthening of the preceding one, or
a combination of both
Atrial ectopic conducted aberrantly

If an early atrial impulse arises it may find the RBB refractory but the
LBB recovered and able to conduct the impulse. Therefore early beats
which are conducted aberrantly often have a defined RBBB pattern
An arrhythmia arising from the atria
or AVN will produce a broad
complex if associated with
ventricular pre-excitation syndrome
or BBB
 Monomorphic & polymorphic VT

Monomorphic VT is the commonest form of sustained VT

In polymorphic VT there is a wide beat to beat ≠ in QRS morphology
Torsades de points (TDP)
 Associated with long QT syndrome
 A type of polymorphic VT
 Cardiac axis rotates over a sequence of 5-20
beats, changing from one direction to another
and back again
 Pre-excitation syndrome (WPWS)

 WPWS may present either as

an antidromic AV re-entrant
tachycardia or in association
with AF or AFlutter
The impulse is conducted from the
atria to the ventricles via an
accessory pathway
The resulting tachycardia has
broad, bizarre QRS complexes
Commonly a regular arrhythmia,
but at times may be irregular
(if AF)
Pre-excitation syndrome (WPWS)
 WPWS may present
either as an antidromic
AV re-entrant
tachycardia or in (Bundle of Kent)
association with AF or
AFlutter
The impulse is conducted
from the atria to the
ventricles via an
accessory pathway
The resulting tachycardia has
broad, bizarre QRS
complexes
Commonly a regular
arrhythmia, but at times
may be irregular (if AF)
Mechanism for pre-excitation syndrome

The impulse passes through two pathways

A PAC finds the accessory pathway refractory &

it is conducted via the AVN

The accessory pathway is recovered & able to

conduct the impulse back to the atrium
WCT due to antidromic AV re-entry

WCT due to AF and WPWS

Definitions (VT)
 VT = 3 or more VE’s in succession at a rate
of more than 120/min. If it lasts more
than 30 secs it is ‘sustained’.

 It is caused by re-entry,↑♥ automaticity

(around ischaemic/ fibrotic area) or drugs

 AIVR = ventricular rhythm at a rate of

100-120 beats/min
Causes for sustained VT
 CAD
 Dilated/hypertrophic cardiomyopathy
 RV dysplasia
 Long QT syndrome
 Electrolyte abnormalities
 Antiarryhthmics drugs
 Infiltrate heart disease (sarcoid, amyloid)
 Valvular heart disease
Criteria for diagnosis

Clues in patient’s history / physical

examination
&
ECG criteria
Clues in patient’s history
Supporting VT
 If patient has Hx of PVC’s, AMI, HF, or other structural ♥
disease, is on Antiarryhthmics or is old the WCT is most likely VT
(90% predictive)
 Hx of 1st AVB favors VT (AVN conduction slowed down)
 Age > 35 yo

Supporting SVT with aberrancy

 Use of caffeine or other stimulants (recreational drugs)
 History of WPW syndrome, BBB or hyperthyroidism
 History of PAC’s, AF, Aflutter
 Younger patients
 Often no structural heart disease (unless i.e. accessory pathway)
Important questions to be asked

Has the patient had a prior AMI?

Did the symptoms of tachyarrhythmia start

only after the AMI?
Clues in physical assessment
Tip-offs that the rhythm is VT:

 Alternating intensity of S¹ (caused by AV

dissociation) and ↑JVP
 Cannon waves in CVP trace (AV
dissociation)

the absence of these findings, however, does not

exclude the diagnosis
ECG findings in monomorphic
VT
(diagnosis)
Clues in previous ECG’s
 The QRS morphology hardly changes
between the SR with BBB and the SVT
 The QRS morphology in VT will be
different to that in SR & similar to VE’s
from previous ECG’s
 If pt has known BBB look at previous QRS’s
if matches > likely SVT.
if ≠ > likely VT
if QRS ≈ PVC > likely VT
 Rate & rhythm
 Rate is usually 120-300 beats/min
(Rate is not helpful discriminator )

 Rhythm is regular or almost regular

(< 0.04 s beat to beat variation) unless capture or
fusion beats
if the rhythm is grossly irregular the most likely
diagnosis is AF with either aberrant conduction
or pre-excitation
Axis change
 Indeterminate axis favors VT (-90 to +/- 180)

 Axis changes of more than 40º to the Right or to

the Left is suggestive of VT.

 A +(ve) QRS in AVR suggests an extremely

abnormal axis to the R) or L)

 A totally +(ve) AVR (NML axis) favors VT

(get lead I & AVF on monitor; if both –(ve)
most likely the rhythm is VT)
QRS morphology
QRS shape

QRS may have a RBBB or LBBB – like

pattern depending on origin.
 V1 positive- RBBB pattern (source Conover,
2003, p.187)
VT SVT with aberrancy
V1 Monophasic
V1
Triphasic rSR
V1
Biphasic
V1
Taller left peak
Triphasic qRS
rS with R:S < 1 V6
V6
If LAD

QRS > 0.14 sec QRS < / = 0.14

V1 negative – LBBB pattern (source Conover,
2003, p.182)
 VT  SVT with aberrancy
rS with 1 or
V1-2 V1-2 Small, narrow
more
‘ r’ wave
Fat Rw > 0.03 sec
Sleek, quick
Notch or slurred Sw
S downstroke
Delayed S nadir
(> 0.06 sec)
V6 V6
No Q or q wave
Any Q (or q) wave
When V1 is –(ve)

QRS > 0.16 sec/ RAD

If broad tachycardia has a RBBB pattern
(source Edhouse, J., and Morris, F. (2002).
A ventricular origin is suggested if:
 QRS duration > .14 sec
 Axis deviation (LAD)
 A single R or biphasic (QR or RS) R wave in lead V1
 A triphasic R wave in lead V1 with initial R wave
taller than secondary R wave and S wave that passes
through the isoelectric line
 QS complex or predominantly negative complex in
V6
 Positive concordance
If broad tachycardia has LBBB pattern in V1-
(source Edhouse, J., and Morris, F. (2002).
A ventricular origin is suggested if:
 QRS complex duration > 0.16 sec
 Axis deviation (RAD)
 rS complex in lead V1
 QS or predominantly negative complex in
lead V6
 Negative concordance
concordance
Concordance: all QRS’s in precordial
leads are +ve or –ve.
-ve concordance definitely favors VT
+ve concordance = a marker of VT
(highly suggestive of VT)
Positive concordance
Negative concordance
Bed side tip for concordance
Monitor pt in V1 & V6 (to ≠
BBB or WPWS/ VT) and
look for Concordance

How?
Keep V1 lead in place
Move LL lead to V6 position
Get V1 & Lead III (V6) on
the monitor screen
Look for concordance
QRS width
 QRS width supporting VT
〉0.14 seconds (if V1 positive)
〉0.16 seconds ( if V1 negative)
Wider with VT due to ischaemia as opposed to
idiopathic VT
usually > 0.16 s = VT
 Look at V6:
if VAT or nadir ≥ 0.07 sec (VT in 90%)
if VAT or nadir < 0.05 sec > likely SVT
QRS width cont.
 QRS width supporting SVT:
≤ 0.14 seconds
Unless- antiarrhythmics
antidromic circus movement tachycardia
pre-existing BBB
Direct evidence of independent
atrial activity – AV dissociation
 Atrial contraction independent of atrial activity ∴
the ‘p’ waves are dissociated from the QRS’s and
are +ve in leads I and II

 Atrial rate usually slower than ventricular rate.

Its presence is conclusive of VT (98%
specific)/ its absence does not exclude VT & does
not support SVT

 Beat to beat ≠, specially on ST segment suggests

independent atrial activity
Direct evidence of AV dissociation
Indirect evidence of independent
atrial activity - Capture beats
 The AVN accepts an atrial impulse ∴
normal conduction and a narrow QRS,
sandwiched among the wide complexes
 Capture beats suggests AV dissociation
 It suggests that AVN is intact ∴ making
WCT with aberrancy unlikely
 Uncommon/ it supports VT/ its absence
does not exclude VT
Capture beats
Indirect evidence of independent
atrial activity - Fusion beats
 When a sinus beat fuses with a beat
arising in the ventricles
 Ventricles depolarised partly by ‘normal’
AVN conduction & ventricular impulse ∴
the QRS has an appearance ½ between a
normal beat and a tachycardia beat
 Uncommon / supports VT/ its absence
does not exclude VT
Fusion beat
Treatment of WCT depends on the
wellbeing of the patient and the
origin of the arrhythmia
In Acute Setting
 Treat it as VT unless evidence of
SVT

 Treating SVT as if it were VT is less

likely to lead to deterioration than
treating VT as SVT
Tachyarrhythmia algorithm (with pulse)
If sure the broad tachycardia is of
supraventricular origin:
If compromised;
 amiodarone (300 mg over 20 min). Follow with IV
amiodarone infusion (900 mg over 24/24)

 Vagal stimulation (carotid sinus massage/ Valsalva

maneuver) may terminate re-entrant tachycardia/ will not
affect tachycardia of ventricular origin. Only to be done if
sure of supraventricular origin

 Verapamil, digoxin and adenosine (block the AVN) should be

avoided as they can produce an extremely rapid ventricular
response and diminish any possibility of normal conduction
through the AVN
 Cardioversion
 Antiarrhythmic
Amiodarone is the choice for treating WCT of
unknown origin & SVT (Na+, Ca+ and K+ channels,
plus α& β- adrenergic blocking properties). Also
less proarrhythmic effects

 Find out & treat reversible causes

Long term
 Prevent sudden death
 EPS
 Consider AICD if poor LVF (pts with
EF < 40% )
ECG # 1
ECG # 1 cont. Valsalva/ CSM/ adenosine
ECG # 1 cont. SVT with pre-excitation
syndrome
ECG # 2
References
Boes, S., and Nikolic, J. (2000). Broad complex
tachycardia in a young man. Heart & lung. 29 (2),
pp 149-151.
Cannom, D., and Prystowsky, E. (1999). Management
of ventricular arrhythmias: detection, drugs, and
devices. JAMA, 281 (2), pp
172-179
Conover, M. B. (2003). Understanding
electrocardiography. (8th ed.). St. Louis: Mosby.
Delacretaz, E (2006). Supraventricular tachycardia.
The new England journal of medicine, 354 (10), pp
1039- 1051.
 Edhouse, J., and Morris, F. (2002). ABC of clinical
electrocardiography: Broad complex tachycardia –
part 1. BMJ, 324 (7339), pp 719- 722.
 Edhouse, J., and Morris, F. (2002). ABC of clinical
electrocardiography: Broad complex tachycardia –
part 2. BMJ, 324 (7340), pp 776-779
 Fisch, C., (2001). Wide QRS tachycardia.
Cardiology in review. 9 (4), p 186.
 Glanville, D., and Behan, J. (2005). Wide complex
tachycardia: differential diagnosis. Lecture notes. The
University of Melbourne
References cont.
 Marriot, H. (1987). Practical
electrocardiography (reprinted seventh
edition). Maryland: Williams & Wilkins
 Snowberger, P., and Metules, T. (2001). VT
or SVT? You can tell at the bedside. RN,
64(2), pp 26-32.