The document discusses wide complex tachycardia, providing definitions and discussing the differential diagnosis, ECG diagnosis, and electrophysiological approach. It notes that wide complex tachycardia can be ventricular tachycardia or supraventricular tachycardia with aberrancy or preexcitation. The ECG is important for diagnosis but often inconclusive. An electrophysiology study can help determine the site of origin through evaluating AV dissociation, measuring HV intervals, and inducing arrhythmias.

1. Dr Awadhesh Kumar Sharma
DM 2nd YR

2.  Wide Complex Tachycardia(WCT) often presents a
diagnostic dilemma for the physician particularly in
determining its site of origin, which can be either
ventricular or supraventricular.
 Correct diagnosis is important both for acute management
and also subsequent management.
 In one series, only 32% of clinicians correctly diagnosed
ventricular tachycardia (VT) in patients who presented
with WCT.
 The surface ECG is the standard and most clinically used
tool for identifying the underlying cause of wide complex
tachycardia.
Ann Int Med. 1988;109; 905-912.

3.  Definition of WCT
 Differential Diagnosis of wide complex
tachycardia
 ECG diagnosis of wide complex tachycardia
 EP Approach of wide complex tachycardia

4.  Wide complex tachycardia (WCT) refers to a
cardiac rhythm of more than 100 beats per
minute with a QRS duration of 120 ms or
more on the surface electrocardiogram
(ECG).

5.  Regular wide complex tachycardia
includes three major categories
1-Ventricular tachycardia (VT)
2-Supraventricular tachycardia (SVT) with
aberrancy
3-Preexcited tachycardia.
Irregular WCT
1- Afib + pre-excitation, Afib + BBB,
Aflutter + BBB, MAT + BBB, polymorphic
Vtach (torsades)

6.  AV dissociation.
 Width of the QRS complex.
 QRS axis in the frontal plane.
 Configurational characteristics of the QRS
complex( morphological criteria).
 Value of the ECG during sinus rhythm.
 Vagal maneuvers

7. SA
Node
Ventricular
Focus
ATRIA AND VENTRICLES
ACT INDEPENDENTLY
AV
Dissociation

8.  Presence off this largely establishes the
diagnosis of VT but its absence is not helpful
 May sometimes not be evident on ECG
 Some cases of VT, the ventricular impulses
conduct retrograde through the AV node and
capture the atrium, preventing dissociation

16. Many diagnostic clues have been proposed to
differentiate between SVT with abberation &
VT starting with-------
History
Physical examination
ECG analysis
EPS

18.  Class I
Patients with wide QRS complex tachycardia
in whom correct diagnosis is unclear after
analysis of available ECG tracings and for
whom knowledge of the correct diagnosis is
necessary for patient care
 Class II
None
ACC/AHA Guidelines for Clinical Intracardiac
Electrophysiological and Catheter Ablation
Procedures 1995

19.  Class III
Patients with VT or supraventricular tachycardia
with aberrant conduction or preexcitation
syndromes diagnosed with certainty by ECG
criteria and for whom invasive
electrophysiological data would not influence
therapy.
However, data obtained at baseline
electrohysiological study in these patients might
be appropriate as a guide for subsequent
therapy.

20. Cycle length = 60.000/ HR length of time bet. Heart beats
V
A
V
SCL
P

21.  SCL= interval bet. 2 successive A waves
 AH interval ( 50—120 msec) AVN
 HV interval (35 – 55 msec) His- purk
 His deflection (cond. Via His bundle)

22. 1-VA /AV Dissociation
2-Measurement of HV during tachycardia
3-Measurement of His-atrial (HA) during
tachycardia and during RV pacing
4-Introduction of premature atrial extra stimuli
during tachycardia
5-Atrial overdrive pacing
6-Response to Adenosine
Josephson M,clinical cardiac electrophysiology,2002,322-424

23. Relationship between atrial and ventricular
activity-
 Placing a catheter within the atrium provides
unequivocal evidence for the timing of atrial
activity.
 If atrial activity is independent of or
intermittently associated with ventricular
activity, atrioventricular dissociation is present
and ventricular tachycardia overwhelmingly
becomes the most likely diagnosis.

25.  There are two very rare conditions in which true AV
dissociation can be observed in the setting of wide
complex tachycardia other than VT.
 The first is a tachycardia arising from the AV node region
associated with both retrograde block and bundle branch
block aberrancy.
 The second is a reentrant circuit using a nodo ventricular
accessory pathway.
 The best way to rule these unusual arrhythmias out is to
identify the presence of dissociation between ventricular
signals and His bundle signals.

26.  The situation is much more difficult in the setting of a 1 :
1 ventricular and atrial relationship.
 There are several strategies that can be tried, but the
most commonly used approach is to use adenosine to
produce retrograde block within the AV node and evaluate
whether the wide complex tachycardia terminates.
 Continuation of wide complex tachycardia in the presence
of transient ventriculo atrial block establishes the likely
diagnosis of ventricular tachycardia

27.  Delievering an atrial premature stimulus
during tachycardia-can preexcite the
ventricle in VT OR AVRT although a change in
QRS morphology expected in VT
 Right atrial pacing– minimal or no
preexcitation in case of left sided accessory
pathway
 Coronary sinus pacing—preexcitation
increased in case of left accessory pathway

28.  His –synchronous atrial extrastimulus cannot
preexcite the ventricle if the mechanism of
tachycardia is AVNRT with aberrancy but
could preexcite the ventricle during SVT with
a bystander AP changing the QRS morphology.

31.  The sequence of His and Right bundle
branch(RBB)activation during tachycardia
 RBB activation preceds H activation- favours
VT or antidromic AVRT
 AV dissociation- rules out antidromic AVRT

32.  Comparing H-A during tachycardia to H-A
during RV pacing-
AVRT,VT-same H-A during both phase
AVNRT with aberration – HA tachy < HA
RV pacing

33.  Atrial overdrive pacing- development of
constant QRS fusion seen in-
1-VT in the presence of
bystander AP
2- AVRT with multiple AP
3- BBRT
Not in-----
1-Antidromic AVRT without
another AP
2- Aberrant SVT

35. JT BBRT VT(MYOCARDIAL)
HB act Antegrade Retrograde Retrograde
BB act Preceeding V Before &
after
Obscured (after V)
H-H/V-V H-H preceeds
V-V
H-H
preceeds V-
V
V-V preceeds H-H

36. Fahmy T,Hammouda M, Mokhtar M,2001

37. Fahmy T,Hammouda M, Mokhtar M,2001

38. THANKS

39.  The method for induction and termination of
ventricular tachycardia provides clues for the
mechanism of tachycardia.
 Most patients with structural heart disease due
to myocardial infarction develop ventricular
tachycardia caused by reentrant circuits that use
protected channels of viable tissue within scar.
Premature beats will block in one portion of the
channel, propagate slowly in another channel,
and set up a reentrant circuit.

40.  The ability to induce a ventricular arrhythmia
with premature ventricular beats strongly
suggests reentry as a mechanism.
 In contrast, automatic ventricular tachycardias
often require infusion with a beta-agonist
(isoproterenol is usually used in the
electrophysiology laboratory) and are related to
high ventricular rate either by atrial pacing or by
ventricular pacing.

41.  The electrophysiologic properties of accessory
pathways can vary significantly
 Most commonly accessory pathways are
composed of tissue histologically and
electrophysiologically like atrial or ventricular
tissue, with a rapid phase 0 upstroke and a
plateau phase.
 Accessory pathways can usually conduct in both
directions, from atrium to ventricle and from
ventricle to atrium.
 However, some accessory pathways can only
conduct in one direction,usually from ventricle
to atrium.

42.  These accessory pathways are often called
―concealed,‖ because their presence is not
observed during sinus rhythm (no
atrioventricular activation) but they can
participate in supraventricular tachycardia
because of robust ventricle-to-atrium
depolarization.
 Some accessory pathways conduct very
slowly, more like AV node tissue.

43.  Three types of arrhythmias can develop in
the presence of an accessory pathway .
 The most common type of tachycardia is
orthodromic atrioventricular reentrant
tachycardia (orthodromic AVRT), in which a
reentrant circuit develops that activates the
AV node in the normal fashion (ortho is
Greek for regular), and, after activating
ventricular tissue, the wave of depolarization
travels retrogradely over the accessory
pathway to depolarize the atria.

44.  This arrhythmia is often described as
reciprocating or ―circus movement‖
 The ECG during orthodromic reciprocating
tachycardia will display a regular narrow
complex tachycardia, because the ventricles
are activated normally via the AV node.
 In some cases the presence of a retrograde P
wave can be seen in the ST segment

45.  Patients can also develop antidromic
atrioventricular reentrant tachycardia
(antidromic reciprocating tachycardia), in which
the direction of the reentrant circuit is reversed
and the ventricles are activated via the
accessory pathway and the atria are activated by
the AV node.
 Antidromic reciprocating tachycardia is
characterized by a regular wide complex
tachycardia (since the ventricles are depolarized
by the accessory pathway).
 Sustained antidromic tachycardia is very rare.

46.  Finally, patients can develop atrial
fibrillation with rapid ventricular activation.
 If atrial fibrillation develops in the presence
of an accessory pathway, the ventricles can
be depolarized very rapidly.
 In fact the triad of an irregular, very fast,
wide complex rhythm should always arouse
suspicion for the presence of an accessory
pathway and atrial fibrillation.

47.  It is generally agreed by most investigators
that sudden death occurs in patients with
accessory pathways because of rapid
ventricular activation from atrial fibrillation
initiating ventricular fibrillation.

48.  Baseline evaluation
 Electrophysiology studies can help delineate
the properties of accessory pathways and
evaluate risk for sudden cardiac death and
mechanisms of arrhythmia initiation.
 At baseline, the HV interval will be very
short and in some cases negative.
 The PR interval is significantly shortened and
that the beginning of the QRS actually
precedes His bundle depolarization (H) for a
negative HV interval.

49.  With progressively more rapid atrial
pacing, the delta wave will become more
prominent as more of the ventricle is
activated via the accessory pathway
 With more rapid atrial pacing the observed
response will depend on the relative
refractory properties of the AV node and the
accessory pathway.
 If the refractory period in the accessory
pathway is reached first, the QRS will
suddenly normalize due to conduction down
the AV node alone.

50.  As the atrial pacing rate is increased, and the
refractory period of the AV node is
reached, eventually an atrial paced beat without
a QRS complex will be seen.
 Patients with accessory pathways who develop
sudden cardiac death often have a shorter
accessory pathway refractory period, since a
shorter refractory period means that more rapid
ventricular depolarization can occur.
 Most experts suggest that risk of sudden cardiac
death is increased in those patients with
accessory pathway refractory periods of less
than 270 ms.

51.  With ventricular pacing in a patient with an
accessory pathway, retrograde depolarization
of the atria can occur via two routes: the AV
node and the accessory pathway.

52.  Ventricular tachycardia in the setting of no
structural heart disease is almost always due
to abnormal automaticity or triggered
activity.
 In contrast, in patients with structural heart
disease reentry is the most common
mechanism for ventricular tachycardia, due
to the presence of ―patchy scars‖ that
increase the likelihood of ―protected
channels‖ forming the substrate for reentry.

53.  Electrophysiology testing can provide clues to
the mechanism for tachycardia.
 Induction of ventricular tachycardia with
premature ventricular extra stimuli suggests an
underlying reentrant mechanism, although
triggered activity can also be initiated this way.
 Initiation of ventricular tachycardia due to
automaticity is often rate-related and is usually
performed by ventricular pacing or atrial pacing
at a constant rate.
 In addition, isoproterenol is often required to
initiate the tachycardia.

54.  A stepwise stimulation protocol for initiation of
sustained VT.
 After ventricular pacing for 8 to 15 beats, a
single extra stimulus is used to scan electrical
diastole until it encounters refractoriness or
reaches a very short coupling interval (<200 ms).
 Second, third, and, in some cases, fourth stimuli
are then added.
 Two or more different basic pacing rates (drive
cycles) typically are used (e.g., 100 and 150
beats/min) before premature stimulus delivery.

55.  If pacing at the right ventricular apex fails to
induce VT, pacing at a second right ventricular
site (e.g., the right ventricular outflow tract)
generally is used.
 In general, pacing with up to three extrastimuli
at two cycle lengths and two sites induces VT in
approximately 90% of patients who have had this
arrhythmia spontaneously after MI.
 The addition of rapid burst pacing, left
ventricular stimulation, and programmed
stimulation during isoproterenol infusion further
increases sensitivity.

56.  As the number of extrastimuli increases, the
risk of initiating nonspecific, polymorphic VT
or VF increases.
 Limiting the closest coupling interval to
greater than 200 ms reduces the risk of
initiating ventricular fibrillation
 VT initiated by isoproterenol infusion or with
rapid burst pacing during isoproterenol
administration, but not in response to
coupled extrastimuli, is believed to be more
likely caused by abnormal automaticity
rather than by re-entry.

57.  In contrast to ECGs, in which atrial activity
may be difficult to detect, direct recordings
from the atrium always allow clear
delineation of whether AV dissociation is
present.
 When AV dissociation is present, the
diagnosis is VT, with the rare exception of
junctional ectopic tachycardia with
ventriculoatrial (VA) block or rare forms of
SVT without atrial tissue participation.

58.  When AV dissociation is present and
depolarization of the bundle of His does not
precede each QRS complex, the diagnosis of
VT is unequivocal.

59.  Polymorphic VT indicates a continually
changing ventricular activation sequence.
 Spontaneous polymorphic VT is most
commonly caused by myocardial ischemia or
TdP associated with Q-T interval
prolongation.
 Polymorphic VT also occurs in idiopathic
VF, Brugada syndrome, and hypertrophic
cardiomyopathy as well as other
cardiomyopathies.

60.  Sustained polymorphic VT (lasting >30 seconds or
requiring termination) is initiated less commonly
in normal hearts and usually requires aggressive
stimulation (three or more extrastimuli and
relatively short stimulus coupling intervals of
<200 ms).
 Initiation of polymorphic VT is of possible
relevance in patients with suspected Brugada
syndrome.
 Polymorphic VT, often induced with two or fewer
extrastimuli, is induced in approximately 80% of
patients with Brugada syndrome who have been
resuscitated from cardiac arrest

61.  In patients with hypertrophic
cardiomyopathy, sustained VT (usually
polymorphic) is inducible in 66% of those who
had a prior cardiac arrest compared with 23%
of patients without a history of cardiac arrest
or syncope

62.  A bundle of His deflection is consistently present
before each QRS during an uncommon type of VT
caused by re-entry through the bundle branches
 The re-entry wave front circulates up the left
bundle branch, down the right bundle
branch, and then through the intra ventricular
septum to re-enter the left bundle.
 Ventricular depolarization proceeds from the
right bundle, giving rise to a tachycardia with an
LBBB configuration.


63.  Rarely, the circuit revolves in the opposite
direction (down the left bundle and back up
the right bundle) or is confined to the
fascicles of the left bundle branch
system, giving rise to a tachycardia with an
RBBB configuration.
 The diagnosis is confirmed by showing that
the atria can be dissociated but that the
bundle of His depolarization is closely linked
to the circuit.

64.  Electrophysiologic study in
ventricular tachycardia. (Re
entry type from previous MI)
 (a) A single extrastimulus (S2)
after an 8 beat drive at
550ms cycle length (S1 S1)
initiates sustained
monomorphic ventricular
tachycardia (VT) . Note the
presence of atrioventricular
dissociation and the absence
of a His potential before the
QRS. (b) A burst of rapid
ventricular pacing (RVP) is
used to restore normal sinus
rhythm (NSR).

65.  Electrophysiologic findings in
bundle branch re entry. The
tracings shown are surface
ECG leads 1, aVF and V1, and
intracardiac recordings from
the high right atrium (HRA),
the bundle of His (HBE) and
the right ventricular apex
(RVA). The surface leads
show the typical pattern of
left bundle branch block. The
intracardiac recordings show
atrioventricular dissociation
and a His potential preceding
each ventricular
depolarization .