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9
6
Broad QRS Tachycardias
Hein J.J. Wellens
Recognition of Atrioventricular Dissociation. . . . . . . .
Mechanisms of Widened QRS During
Supraventricular Tachycardia . . . . . . . . . . . . . . . . . .
Electrocardiographic Diagnosis of Wide QRS
Tachycardia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Configurational Characteristics of the
QRS Complex . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2007
2008
2009
Localizing the Site of Origin of
Ventricular Tachycardia . . . . . . . . . . . . . . . . . . . . . .
Etiology of Ventricular Tachycardia. . . . . . . . . . . . . . . .
Value of the ECG During Sinus Rhythm . . . . . . . . . . .
The Practical Approach . . . . . . . . . . . . . . . . . . . . . . . . . .
Summary. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2012
2014
2016
2017
2017
2011
Key Points
• Ninety percent of broad QRS tachycardia patients presenting to the emergency room are ventricular tachycardias (VTs).
• Atrioventricular dissociation in VT is characterized by
irregular cannon A waves in the jugular venous pulse,
varying intensity of the first heart sound, beat-to-beat
changes in the systolic blood pressure.
• Independent beating of atria and ventricles during VT
can result in “capture” or “fusion beats.”
• Ninety percent of cases of VT have a QRS duration of
more than 0.14 second and virtually all supraventricular
tachycardias (SVTs) with aberrant conduction have a
QRS duration of <0.14 second.
• Most VTs have a prior myocardial infarction as their
etiology.
• Idiopathic VTs may have their origin in the RV or LV.
• When a wide QRS tachycardia is not tolerated hemodynamically, emergent cardioversion should be
performed.
Because a drug given for the treatment of supraventricular
tachycardia (SVT) may be deleterious to a patient with a
ventricular tachycardia (VT),1,2 the differential diagnosis in
broad QRS tachycardia is critical. Although 90% of broad
QRS tachycardias presenting in the emergency room are VT,
errors are often made because physicians wrongly consider
VT unlikely if the patient is hemodynamically stable,3 and
they are frequently unaware that certain findings on physical
examination and on the electrocardiogram (ECG) may
quickly and accurately lead to the correct diagnosis.
The possible causes of a broad (wide) QRS tachycardia are
as follows (corresponding to A to F in Fig. 96.1):
1. Supraventricular tachycardia with preexisting or functional bundle branch block (BBB). This includes sinus tachy-
cardia, atrial tachycardia, atrial flutter, atrial fibrillation, and
atrioventricular (AV) nodal reentrant tachycardia.
2. Orthodromic circus movement tachycardia using the
AV node in the anterograde direction and an accessory
pathway in the retrograde direction with preexisting or functional BBB.
3. Supraventricular tachycardia with conduction over an
accessory AV pathway.
4. Antidromic circus movement tachycardia using an
accessory pathway in the anterograde direction and the AV
node or another accessory pathway in the retrograde
direction.
5. Atrioventricular reentrant tachycardia using a nodoventricular fiber in the anterograde direction and the bundle
of His or another accessory pathway in the retrograde
direction.
6. Ventricular tachycardia.
Recognition of Atrioventricular Dissociation
In addition to careful evaluation of the ECG, examination
of the patient should include a search for physical signs of
AV dissociation. Atrioventricular dissociation is present in
approximately 50% of all VTs. The other 50% show some
form of retrograde conduction to the atria.4 Therefore,
the finding of AV dissociation is an important diagnostic
clue.
The physical signs of AV dissociation are as follows5:
1. Irregular cannon A waves in the jugular pulse
2. Varying intensity of the first heart sound
3. Beat-to-beat changes in systolic blood pressure
Any one of these three clues indicates AV dissociation.
However, in the absence of such clues, VT cannot be ruled
out; there remains the possibility of coexistent atrial
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96
Mechanisms of Widened QRS During
Supraventricular Tachycardia
As shown in Figure 96.1, BBB may be one of the causes of a
wide QRS tachycardia. This block may be preexistent (also
present during sinus rhythm) or functional. Functional BBB
during SVT may occur because of phase 3 block or retrograde
invasion into the bundle branch.
Phase 3 Block
FIGURE 96.1. Possible causes of wide QRS tachycardia. See text for
explanation.
fibrillation or ventriculoatrial conduction, in which case
none of the signs of AV dissociation would be present. In
theory, it is also possible for an AV junctional tachycardia
with retrograde block to have AV dissociation; however, in
view of the rarity of such a rhythm, AV dissociation remains
a valuable diagnostic clue for VT.
The Jugular Pulse
In VT with independent beating of atria and ventricles, the
atria occasionally beat against closed AV valves, resulting in
retrograde blood flow into the jugular vein, producing the
so-called cannon A wave. Inspection of the jugular vein
reveals the characteristic occasional expansive pulsation.
Phase 3 (tachycardia-dependent) aberration usually occurs in
the right bundle branch because that bundle commonly has
the longest refractory period.6 Left bundle branch block (LBBB)
aberration accounts for approximately one third of cases of
aberrant ventricular conduction. It may occur in normal fiber
if the impulse is premature enough to reach the cell when
the membrane has not fully repolarized. This form of aberration is commonly observed at the beginning of paroxysmal
SVT (Fig. 96.2). Phase 3 aberration is promoted by a long-short
cycle sequence because the refractory period of the bundle
branch of the beat following the long cycle is prolonged.
Concealed Retrograde Conduction
Although the mechanism of QRS widening at the onset of
SVT commonly is phase 3 aberration, the sustaining mechanism is often concealed retrograde conduction up one of the
bundle branches.6,7 Figure 96.3 is a schematic representation
of how, during sinus rhythm, LBBB aberration is initiated by
the premature atrial beat that also initiates SVT. This phase
3 block of the left bundle is followed by conduction over the
right bundle and retrograde invasion into the left bundle
branch. This makes the left bundle branch refractory when
the next supraventricular impulse passes through the AV
node. The impulse is conducted down the right bundle
branch and then in a retrograde direction again up the left
bundle branch. This mechanism is responsible for continua-
Varying Intensity of the First Heart Sound
The first heart sound marks the onset of ventricular systole
and is caused by the closing of the mitral and tricuspid
valves. During AV dissociation, there is a beat-to-beat change
in the loudness of the first heart sound, owing to the varying
position of the AV valves at the time of ventricular contraction. Therefore, the first heart sound varies in intensity
during VT and in complete heart block, as well as during AV
Wenckebach and atrial fibrillation.
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V1
Changes in Systolic Blood Pressure
During AV dissociation, ventricular filling from the atria
varies, depending on the time interval between atrial and
ventricular contraction. These differences in ventricular
filling lead to a beat-to-beat change in systolic stroke volume
into the aorta, which in turn causes beat-to-beat changes in
systolic blood pressure. This sign of AV dissociation can
easily be detected at the bedside by use of the blood pressure
recorder. Thus, a typical fi nding in VT with AV dissociation
is that the rhythm is regular, whereas the systolic blood pressure differs from beat to beat.
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V4
V6
400 ms
FIGURE 96.2. Phase 3 aberration. In a patient with supraventricular tachycardia (SVT) and 2 : 1 atrioventricular (AV) conduction (left),
there is a sudden change in 1 : 1 AV conduction. This sudden increase
in ventricular rate is accompanied by widening of the fi rst three
QRS complexes (left bundle branch block, LBBB). Note that the third
QRS shows less widening than the first and second QRS complexes.
This sequence is typical of phase 3 aberration.
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2009
Retrograde concealed conduction into one of the bundle
branches is a common mechanism of perpetuation of aberration during SVT.6
His
RBB
Electrocardiographic Diagnosis of Wide
QRS Tachycardia
LBB
A
A 12-lead ECG is required for the correct diagnosis of wide
QRS tachycardia on the basis of morphology. The physician
should examine the ECG systematically, looking for the
presence of AV dissociation and analyzing QRS characteristics, such as width, axis, and configuration.
Atrioventricular Dissociation
B
FIGURE 96.3. (A,B) Schematic representation of initiation of left
bundle branch (LBB) block aberration and perpetuation of aberration
by concealed retrograde invasion into the left bundle branch. These
critical time relations are interrupted by a ventricular premature
beat resulting in normalization of the QRS complex during the
SVT.
tion of LBBB during SVT. Retrograde invasion into the left
bundle branch continues until it is disrupted by a ventricular
premature beat. Figure 96.4 gives a clinical example of the
latter mechanism during SVT with right bundle branch
block.
A
B
Traditionally (and correctly), dissociation between atrial and
ventricular activity during tachycardia has been considered
a hallmark of VT. As pointed out previously, however,4 some
form of ventriculoatrial conduction is frequently present
during VT. Identification of atrial activity during VT can be
difficult or impossible on the 12-lead ECG. Recognition of
the P wave in a wide QRS tachycardia is important, however,
because of the diagnostic value of AV dissociation. Independent beating of atria and ventricles during a VT can result
in “capture” or “fusion” complexes (Fig. 96.5). This occurs
when the ventricular rate during VT is such that an appropriately timed atrial impulse is able to traverse the AV node
to depolarize the ventricles completely (capture) or partially
(fusion). In the latter situation, fusion occurs because of concomitant ventricular activation from the VT focus (Fig. 96.5).
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I
II
II
III
aVR
III
aVR
aVL
aVL
aVF
V1
V2
V3
V4
aVF
V1
V2
V3
V4
V5
V5
V6
400 ms
85473
FIGURE 96.4. (A) Example of widening of the QRS complex during
tachycardia by retrograde invasion into the right bundle branch. The
critical time relations required for perpetuation of retrograde invasion into the right bundle branch are disrupted by a right-sided
ventricular premature beat. (B) Same patient during sinus rhythm.
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V6
991203
400 ms
FIGURE 96.5. An example of a ventricular tachycardia with ventricular fusion and capture beats. The narrow QRS complex of beat
5, is a fusion complex. The last narrow QRS complex during the
tachycardia terminates VT because of invasion into the reentry
circuit of the VT. Note that the patient has extensive scarring of the
anterior wall from a previous myocardial infarction.
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I
aVR
V1
V4
II
aVL
V2
V5
III
aVF
V3
V6
96
V1
II
FIGURE 96.6. Marked widening of the QRS in a patient
with an atrial tachycardia who is on flecainide
medication.
V5
The occurrence of a narrower QRS during VT is not always
the result of a conducted supraventricular beat; it may also
result from fusion with a ventricular depolarization arising
in the ventricle contralateral to the ventricle in which the
tachycardia originates, or when fusion occurs with a ventricular echo beat when a retrogradely conducted impulse
during VT travels to the AV node and reenters the
ventricle.8
a right axis deviation is very likely to be VT. In discussing
the importance of the axis in the frontal plane in the differential diagnosis of wide QRS tachycardia, it is important
to realize that a markedly abnormal axis can occur in
A
B
I
I
II
II
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Width of the QRS Complex
When we compared the width of the QRS complex in 100
cases of VT and 100 cases of SVT with aberrant conduction,
we found that all cases of SVT with aberrant conduction
had a QRS width of less than or equal to 0.14 second,
whereas 95% of cases of VT had a QRS width of more
than 0.14 second.4 These findings indicate that a QRS width
of more than 0.14 second is highly suggestive of a ventricular origin of the tachycardia. The cause of a VT also plays
a role in the width of the QRS complex. As reported by
Coumel and associates9 in coronary artery disease, the
average QRS complex is wider during VT than the QRS
complex of the patient with idiopathic VT (171 vs. 135 ms).
There are three situations in which an SVT can have a QRS
width of more than 0.14 second. The first occurs when the
patient has an SVT in the presence of preexistent bundle
branch block. The second involves an SVT with AV conduction over an accessory pathway. The third is marked QRS
widening during SVT because of the use of antiarrhythmic
drugs that prolong intraventricular conduction, most commonly flecainide. A typical example of the latter is given in
Figure 96.6.
III
III
aVR
aVR
aVL
aVL
aVF
V1
V1
V2
V2
V3
Most patients with VT secondary to a previous myocardial
infarction have a markedly abnormal QRS axis in the frontal
plane. Especially in right bundle branch block (RBBB)-like
VT, the axis usually points superiorly, in contrast to SVT
with RBBB, in which the axis is to the right. Patients with
idiopathic VT can have a normal QRS axis in the frontal
plane, but the two most common types of idiopathic VT
may have marked left-axis or right-axis deviation (Fig. 96.7).
In fact, an LBBB-shaped tachycardia with a vertical axis or
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V4
V4
The QRS Axis
aVF
V5
V5
V6
V6
400 ms
FIGURE 96.7. The two most common forms of idiopathic ventricular tachycardia. (A) The origin is in the outflow tract of the right
ventricle. The QRS shows an LBBB-shaped QRS and a vertical axis.
(B) The origin is in the inferoseptal portion of the left ventricle. The
QRS shows a right bundle branch block (RBBB) shape and left axis
deviation.
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patients with preexistent BBB during SVT and in patients
who, during tachycardia, have AV conduction over an accessory pathway. In the latter situation, marked left-axis deviation can be found during anterograde conduction over a
right-sided or posteroseptal accessory bundle and marked
right-axis deviation in cases of a left lateral accessory
pathway.
Configurational Characteristics
of the QRS Complex
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II
III
V1
Bundle Branch Block–Shaped QRS Complexes
An SVT with RBBB aberration is recognized because of a
triphasic rSR in lead V1 and a triphasic qRS pattern in lead
V6.4,10 In lead V1, the initial r wave reflects normal septal
activation, the S wave left ventricular activation, and the R
wave delayed activation of the right ventricle. Lead V6 shows
a narrow q wave as the result of normal septal activation and
an R/S ratio of more than 1. A typical example of RBBB aberration during SVT is shown in Figure 96.4. In VT with an
RBBB-like QRS contour, lead V1 usually shows a monophasic
or biphasic R wave. The presence of a deep S wave in lead V6
(R : S ratio <1) supports the diagnosis of VT. An R : S ratio <1
in V6 is more common when left axis deviation is present
(Fig. 96.8). The differential diagnosis of an LBBB-shaped VT
A
I
II
B
C
84237
III
aVR
V6
400 ms
FIGURE 96.9. Ventricular tachycardia (left panel) with an LBBB
shape showing initial positivity of the QRS in lead V1 (>0.04 second),
slurring of the S wave in lead V1 and a distance from the beginning
of the QRS to the nadir of the S wave in lead V1 of 140 ms. Lead V6
shows a qR complex. The right panel shows the electrocardiogram
during sinus rhythm.
and SVT with LBBB aberration is made in lead V1 and V2 and
in lead V6. If an R wave is present in either lead V1 or V2, it
is small and narrow (<0.04 second) in LBBB aberration, and
the down stroke of the S wave is clean and swift (no slurs or
notches). Because of the narrow R wave and/or the clean
down stroke, the distance from the beginning of the QRS to
the nadir of the S wave is 0.07 second or less. In contrast, an
R wave of more than 0.04 second, with a slurred down stroke
and a delayed S nadir in V1 and/or V2 (>0.07 second) supports
the diagnosis of VT.11 A q wave in lead V6 confirms VT
(Fig. 96.9).
aVL
Presence of Q Waves During Tachycardia
aVF
Coumel and associates9 demonstrated the value of QR complexes during a wide QRS tachycardia as pointing to a ventricular origin for the arrhythmia. This is typically found in
VT in patients with a localized ventricular scar because of
a previous myocardial infarction. An example is given in
Figure 96.8.
V1
V2
V3
V4
Duration of the Onset of R to Nadir S in
Precordial Leads
V5
V6
84258
400 ms
FIGURE 96.8. Two types of ventricular tachycardia (VT) in a
patient with an old anteroseptal myocardial infarction (C). Both VTs
(A,B) have an RBBB shape and clearly show AV dissociation. Note
the effect of the frontal plane axis on the R : S ratio in lead V6 in
RBBB shaped VT. An R : S <1 is present in the case of a superior axis
(B), but R : S >1 with an inferior QRS axis (A). Note also the presence
of QR complexes during VT (in III, aVF, V1, and V6 in A, and in V2
and V3 in B), indicating the presence of a scar from a previous myocardial infarction.
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This distance is increased in VT. As pointed out by Brugada
et al.,12 the presence of an RS interval of more than 100 ms
in one or more precordial leads is highly suggestive of
VT. However, such a duration may occur in SVT with AV
conduction over an accessory pathway, in SVT with preexistent BBB (especially LBBB), and in SVT during the administration of drugs that slow intraventricular conduction
(Fig. 96.6).
Table 96.1 lists all the limitations of these different electrocardiographic findings.
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TABLE 96.1. Limitations of electrocardiographic signs suggestive of a ventricular origin for a wide QRS tachycardia
Sign
Limitations
AV dissociation
VA conduction may occur during VT
AV junctional rhythm with BBB and AV dissociation
Preexistent BBB (especially LBBB)
SVT with AV conduction over an accessory pathway
Use of drugs slowing intraventricular conduction (class Ia, class Ic, amiodarone)
Not helpful in LBBB-shaped QRS
SVT with AV conduction over a right-sided or posteroseptal accessory pathway
SVT during use of class IC drugs
Not helpful in RBBB-shaped QRS
Only in VT with localized myocardial scarring or infiltration (sarcoidosis, or
amyloidosis)
Positive concordancy may occur during SVT with AV conduction over a left
posterior accessory pathway
SVT on drugs slowing conduction
SVT with AV conduction over an accessory pathway
Preexistent BBB (especially LBBB)
Occurs only at relatively slow VT rates
R/O fusion with a contralateral VPC during VT
R/O fusion with a ventricular echo beat
Requires availability of ECG during sinus rhythm
R/O atrial premature beat with aberrant conduction
Left-axis deviation (to the left of −30 degrees)
Right-axis deviation (to the right of +90 degrees)
Presence of q(Q)R complexes in leads other than AVR
Concordant pattern in precordial leads
R-nadir S >100 ms in one or more intraventricular
precordial leads
Presence of a supraventricular impulse able to
depolarize the ventricles completely (“capture
beat”) or partially (fusion complex)
Presence of premature beats during sinus rhythm
with the same QRS configuration as during wide
QRS tachycardia
AV, atrioventricular; BBB, bundle branch block; ECG, electrocardiogram; LBBB, left bundle branch block; MI, myocardial infarction; R/O, rule out; SVT, supraventricular tachycardia; VA, ventriculoatrial; VPC, ventricular premature complex; VT, ventricular tachycardia.
LBBB Versus RBBB-Like Configuration
Localizing the Site of Origin
of Ventricular Tachycardia
An LBBB-shaped VT indicates that the origin of the arrhythmia is in the right ventricle resulting in delayed activation
of the left ventricle. The reverse is true when the site of
origin of the VT is in the left ventricle. Then the right
ventricle is activated last, resulting in an RBBB-like QRS
complex (Fig. 96.10).
The ability to treat VT by removing the site of origin, or
interrupting the reentrant pathway of the arrhythmia,
stresses the necessity to identify (when possible) the site of
origin of VT.13 The ECG can be helpful in doing so by looking
at the configuration, the width, and the axis (in the frontal
and horizontal) plane of the QRS complex of the VT.
I
II
III
aVR
I aVL
aVF
V1
III
II
VT origin right ventricle
QRS: LBBB shape
I
II
V2
III
aVR
V3
aVL
I
aVF
V4
V5
V6
V1
V2
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V3
400 msec
III
VT origin left ventricle
QRS: LBBB shape
II
V4
V5
V6
84237b
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FIGURE 96.10. Ventricular tachycardia origin
and shape of the QRS complex. Left panel: An
origin in the right ventricle produces an LBBBlike shape. Right panel: A left ventricular
origin gives an RBBB-like QRS configuration.
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I
II
III
aVR
aVL
I aVF
V1
III
FIGURE 96.11. Ventricular tachycardia origin
and QRS width. Left panel: An origin close to
the interventricular septum results in more
simultaneous right and left ventricular activation and therefore a more narrow QRS complex.
In contrast (right panel), a VT origin in the
lateral ventricular wall results in sequential
ventricular activation and a wider QRS
complex.
V2
I
V3
II
III
V4
II
VT origin close to interventriclar
septum
more simultaneous
ventricular activation
more
narrow QRS.
I aVR
aVL
V5
aVF
V1
V6
84237A
400 msec
V2
III
II
V3
VT origin far from interventriclar
V4
septum
septal ventricular
V5
activation
wide QRS.
V6
The Width of the QRS Complex
94359c
400 msec
The QRS Axis
When as shown in Figure 96.11, the origin of the VT is close
to the interventricular septum, more simultaneous left and
right ventricular activation occurs, leading to a more narrow
QRS complex. In contrast, a VT origin in the lateral wall of
the origin results in sequential ventricular activation and a
wider QRS complex.
The Frontal Plane
As shown in Figure 96.12, a VT origin in the apical part of
the ventricle, has a superior axis (to the left of −30 degrees).
An inferior axis is present when the VT has an origin in the
basal area of the ventricle.
I
II
III
aVR
aVL
I aVF
I
V1
III
II
VT origin infero-apical
frontal QRS axis
II
V2
III
V3
aVR
V4
I aVL
V5
aVF
V6
V1
400 msec
V2
V3
FIGURE 96.12. Ventricular tachycardia
origin and QRS axis in the frontal plane.
An apical origin results in a superiorly
directed axis (left panel). In contrast, a
basal origin leads to an inferior QRS axis
(right panel).
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VT origin antero-basal
frontal QRS axis
II
V4
V5
V6
9914a
400 msec
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96
B
I
I
II
posterior
LV
RV
III
II
aVR
III
aVL
aVF
aVR
aVL
posterior
V6 V
1
V1
anterior
V2
V1
anterior
V3
V4
V4
V5
V6
FIGURE 96.13. A concordant pattern in
localizing the VT origin in the horizontal plane. Left panel: A VT arising in the
apical area of the left ventricle resulting
in a negative concordancy of all precordial leads. Right panel: Ventricular
activation starts in the posterior area,
resulting in positive concordancy of all
precordial leads. The latter can be found
in left posterior VT but also in SVT with
AV conduction over a left posterior
accessory AV pathway.
RV
V2
V3
V6
LV
aVF
V1
V5
86665a
V6
94359a
400 ms
The Horizontal Plane
As shown in Figure 96.13, when a VT arises in the anteroapical area of the ventricle, all precordial QRS complexes will
be negative (negative concordancy). When ventricular activation starts in the left posterior area, all precordial QRS complexes will be positive (positive concordancy). As pointed out
before, positive concordancy can also be found when a supraventricular tachycardia with AV conduction over a left posterior accessory pathway is present.
The ECG for localizing VT is most reliable when there is
little or no cardiac damage. When scar tissue is present in
the ventricle (as after myocardial infarction), localizing VT
origin by ECG is often difficult, and intracardiac mapping
will be necessary especially when catheter ablation of VT is
considered (see Chapter 102).
from the endocardially located idiopathic VT’s. (See also
Chapter 102.)
Idiopathic left VTs all have an RBBB-like shape because
of an origin in the left ventricle. Figure 96.16 shows three
A
B
I
I
II
II
III
III
aVR
aVR
Etiology of Ventricular Tachycardia
aVL
aVL
Most VTs have a previous myocardial infarction as their etiology, and a QR complex during VT can be very helpful to
make that diagnosis. However, characteristic ECG patterns
can also be found in idiopathic VT14 and VT in patients with
arrhythmogenic right ventricular dysplasia (ARVD).15 Figure
96.14 shows two patterns of idiopathic VT arising in or close
to the outflow tract of the right ventricle. Both have an LBBBlike QRS complex indicating a right ventricular origin. In
panel A the frontal QRS axis is +70 and lead I shows a positive QRS complex, indicating an origin of the tachycardia in
the lateral part of the outflow tract of the right ventricle. In
panel B the frontal QRS axis is inferior and the QRS is negative in lead I pointing to an origin on the septal site in the
right ventricular outflow tract. Recently, it has become clear
that ventricular tachycardias may originate in the root of the
pulmonary artery and the aorta.16–19 In those patients, epicardially located muscle fibers run to the base of the right or
left ventricle. An example is given in Figure 96.15. These
tachycardias require a different catheter ablative approach
aVF
aVF
V1
V1
V2
V2
V3
V3
V4
V4
V5
V5
V6
V6
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Septal side RVOT
FIGURE 96.14. Two patterns of idiopathic VT arising in or close to
the outflow tract of the right ventricle. See text.
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aorta
LV
RV
FIGURE 96.15. Two examples of idiopathic VTs arising in the aortic root. The
one on the left has its origin close to the
right coronary cusp and is connected by
a muscle band to the epicardium of the
outflow tract of the right ventricle. The
one on the right is originating close to
the left coronary cusp and is connected
to the posterior part of the left ventricular outflow tract.
A
I
V1
II
V2
III
V2
III
V3
aVR
V4
aVL
V5
aVF
V6
V4
aVL
V5
aVF
V6
C
01004
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5
V6
95165
400 ms
FIGURE 96.16. Three types of left ventricular idiopathic VT. See
text.
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aVR
B
99325
V1
V3
I
93152a
I
types. The most common one is shown in panel A. The
frontal QRS axis shows left axis deviation. The site of origin
of the VT is in or close to the posterior fascicle of the LBB.
In panel B, the frontal QRS axis is further leftward (a socalled northwest axis). This tachycardia arises more anteriorly, close to the interventricular septum. The least common
idiopathic left VT is the one shown in panel C. Now, the
frontal QRS axis is inferiorly directed. This VT originates in
the anterior fascicle of the LBB.
In ARVD, there are three predilection sites in the right
ventricle: the inflow and outflow tracts, and the apex. While
the first two sites have a QRS configuration during tachycardia that is difficult to differentiate from right ventricular
idiopathic VT, left axis deviation in a young person with an
LBBB-shaped VT should immediately lead to the suspicion
of ARVD. In fact, there is an important rule in LBBB-shaped
VT with left axis deviation that cardiac disease should be
suspected and that idiopathic right ventricular VT is
extremely unlikely. Figure 96.17 gives an example of an
LBBB-shaped VT in a patient with ARVD. The typical ECG
features found in ARVD both during VT and during sinus
rhythm can be found elsewhere.15
When the broad QRS is identical during tachycardia and
sinus rhythm, one has to differentiate SVT with preexistent
BBB from bundle branch reentrant tachycardia.20 In diseased
hearts, especially when the bundle branches and the interventricular septum are involved, a tachycardia may occur
based on a circuit with anterograde conduction down one
bundle branch or one of the left-sided fascicles, and, after
septal activation, retrograde conduction over another branch
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A
96
95058
B
85252
I
I
II
II
III
III
aVR
aVR
aVL
aVF
V1
V2
V3
aVL
aVF
V1
V2
V4
V3
V5
V4
V6 85305
400 ms
FIGURE 96.17. A VT in a patient with diffuse arrhythmogenic right
ventricular dysplasia. (A) A VT with an LBBB-like shape and a
frontal QRS axis of −60 degrees. The QRS width is 200 msec. (B)
Characteristic ECG fi ndings during sinus rhythm such as T-wave
inversion in leads V1 to V3 and a different QRS width in V1 and V2
(120 ms) and V6 (90 ms).
V5
V6
MACVU 002C
400 ms
FIGURE 96.19. Example of bundle branch reentrant ventricular
tachycardia in a patient with a previous anteroseptal myocardial
infarction. During VT the impulse goes down over the left anterior
fascicle and back up over the right bundle branch. The tachycardia
is shortly interrupted by two paced ventricular beats, but resumes
immediately after three conducted sinus beats. The sinus beats also
show that anterograde conduction to the ventricle went by way of
the left anterior fascicle because of anterograde block in the left
posterior fascicle and the right bundle branch.
of the bundle branch system (Fig. 96.18). Figure 96.19 gives a
clinical example in a patient with a previous anteroseptal
myocardial infarction. Bundle branch reentry tachycardia
may occur in patients with anteroseptal myocardial infarction, idiopathic dilated cardiomyopathy, myotonic dystrophy, after aortic valve surgery, and after severe frontal chest
trauma.
Value of the ECG During Sinus Rhythm
FIGURE 96.18. The tachycardia circuit in bundle branch or fascicular reentrant tachycardia. On top, the situation during sinus rhythm
with anterograde block in the right bundle and the left posterior
fascicle. During VT the impulse uses either the right bundle branch
(bundle branch reentry) or the posterior fascicle (fascicular reentry)
for retrograde conduction.
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The ECG during sinus rhythm may show changes such as
preexistent BBB, ventricular preexcitation, or an old myocardial infarction, which are very helpful in correctly interpreting the ECG during broad QRS tachycardia. Also, the presence
of AV conduction disturbances during sinus rhythm make it
very unlikely that a broad QRS tachycardia in that patient
has a supraventricular origin, and, as shown in Figure 96.20,
a QRS width during tachycardia more narrow than during a
sinus rhythm points to a VT.
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broa d qr s tach yc a r di a s
A
I
II
III
FIGURE 96.20. Tachycardia QRS smaller than QRS during sinus rhythm. On
the left, sinus rhythm is present with a
very wide QRS because of an anterolateral myocardial infarction and pronounced delay in left ventricular
activation. On the right, a VT arising on
the right side of the interventricular
septum results in more simultaneous
activation of the right and left ventricle
than during sinus rhythm and therefore,
a smaller QRS complex.
aVR
aVL
V1
It is important not to panic when one is confronted with
a wide QRS tachycardia. Statistically, VT is much more
common than SVT, also when the tachycardia is hemodynamically well tolerated. The patient should be examined for
clinical signs of AV dissociation, and the 12-lead ECG should
be systematically evaluated. When the tachycardia is hemodynamically not tolerated, emergent cardioversion should be
performed. If the tachycardia is tolerated but the diagnosis
is in doubt, the patient should not be treated with adenosine
or verapamil; procainamide should be given instead.
Summary
Most wide QRS tachycardias have a ventricular origin.
Correct diagnosis, which includes the identification of underlying heart disease, has important prognostic and therapeutic implications. In ventricular tachycardia, treatment during
the arrhythmia depends on the hemodynamic tolerance of
the arrhythmia.
When underlying heart disease is present, it should be
corrected when possible. Currently, implantable cardiodefibrillator (ICD) implantation is often required (see Chapter
98). In some VT patients, cure can be obtained by catheter
ablation (see Chapter 102).
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V5
aVF
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V2
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