Broad Complex Tachy
Broad Complex Tachy
Broad Complex Tachy
doi:10.1093/europace/euq430
Received 8 September 2010; accepted after revision 26 October 2010; online publish-ahead-of-print 3 December 2010
Broad QRS complex tachycardia still presents a diagnostic challenge when confronted with a 12-lead electrocardiogram (ECG). The ECG
differential diagnosis includes ventricular tachycardia vs. supraventricular tachycardia with functional aberration, pre-existing bundle branch
* Corresponding author. Tel: +31 43 3876543, Email: alzand@hotmail.com (B.S.N.A.), hjgm.crijns@mumc.nl (H.J.G.M.C.)
Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2010. For permissions please email: journals.permissions@oup.com.
466 B.S.N. Alzand and H.J.G.M. Crijns
Electrocardiographic detection of
atrioventricular dissociation
In our experience, AV dissociation is generally detectable in a lead
Figure 1 Lewis lead (B): during BCT (A), the presence of
where the P-wave is most prominent whether anterograde or ret-
atrioventricular dissociation is indicated by vertical black bars.
rograde. This lead is usually one of the inferior leads considering Reproduced with permission from the publisher.20
and are followed by a fully compensatory pause; the authors were complex is present in one or more precordial leads, the next
well aware that such beats are indistinguishable from AV nodal step is to measure the longest RS interval. If an RS interval is
extrasystoles with aberration and no retrograde conduction. Mar- longer than 100 ms, the diagnosis of VT is made. If not, the next
riott15 and Marriott and Sandler18 also noticed that ‘concordant’ step of the algorithm is to consider whether AV dissociation is
precordial patterns, whether entirely upright or entirely inverted, present. If so, the diagnosis of VT is made. If absent, the classical
were almost diagnostic for ventricular origin. Positive concordance morphology criteria for VT are used (Figure 3). If both lead V1
may also occur during antidromic tachycardia using a left posterior and V6 fulfil the criteria for VT, the diagnosis of VT is made. If
or left lateral accessory pathway. Negative concordance is nearly not, the diagnosis of SVT with aberrant conduction is made by
always VT. However, Volders et al. 23 published a case report of exclusion of VT.
a 17-year-old male with pectus excavatum and SVT with left
BBB (LBBB) resulting in a BCT with negative concordance. Mar- The aVR ‘Vereckei’ algorithm
riott also introduced in 1971 the term ‘Rabbit ears’ for a double- In 2007, a new algorithm analysed in 287 patients with a high accu-
peaked R-wave in lead V1. Whereas a ‘good rabbit’ with a taller racy27 has been proposed by Vereckei et al. 28 They found that the
right peak being typical for RBBB aberrancy, a ‘bad rabbit’ with a following criteria were suggestive of VT: (i) the presence of AV dis-
taller left peak suggests ventricular origin. In 1972, Swanick sociation; (ii) the presence of an initial R-wave in lead aVR, and (3)
et al. 24 continued the differentiation between right VEB and supra- measuring the voltage during the initial 40 ms (Vi), the terminal
ventricular beats showing LBBB and found that (i) the presence of 40 ms (Vt), their ratio (Vi/Vt), and that Vi/Vt ≤ 1 was suggestive of
S-wave in V4 greater in depth than the S in lead V1, (ii) a wide VT (Figure 5). In 2008, the same group presented a simplified algor-
r-wave ≥0.03 s in lead V1, and (iii) negative QRS polarity in lead ithm using only lead aVR, analysed in 313 patients with the same
I, all favour ventricular origin. In 1978, Wellens et al. 12,13 used His- accuracy29 as their first algorithm. Criteria for VT in lead aVR
bundle recording for the first time to determine the site of origin were (i) the presence of an initial R-wave, (ii) width of an initial
of tachycardia with broad QRS complex and create the so-called r- or q-wave .40 ms, (iii) notching on the initial downstroke of
‘classical criteria’ (Figure 3).25 Later, Coumel et al.26 showed that a predominantly negative QRS complex, and (4) Vi/Vt ≤ 1
a QR pattern in leads other than aVR or a QS pattern in V5–6 (Figure 6).
during VT was present in 89% of the patients with old MI, while
constantly absent in patients with idiopathic VT. Other criteria
Griffith et al.30,31 performed in 1991 a multivariate analysis in 102
The Brugada algorithm patients to identify which of 15 clinical or 11 ECG variables are inde-
In 1991, Brugada et al.27 analysed 554 BCTs and produced simple pendent predictors of VT. They found that (i) the history of previous
criteria in a stepwise approach irrespective of the QRS complex MI, (ii) in lead aVF, a predominant negative deflection was suggestive
morphology, whether RBBB- or LBBB-like, with a sensitivity and of VT especially when Q-wave was present in RBBB pattern tachy-
specificity of 0.987 and 0.965, respectively. The algorithm cardia. In LBBB pattern tachycardia, a QS or qR waveform in lead
(Figure 4) begins with the identification of an RS complex in any aVF is highly suggestive for VT, whereas an Rs complex was specific
precordial lead, if failed the diagnosis of VT is made. If an RS for SVT, (iii) in RBBB pattern tachycardia, a monophasic or biphasic
468 B.S.N. Alzand and H.J.G.M. Crijns
Figure 4 Three hundred and forty-eight VTs and 170 SVTs with aberrant conduction were included in the comparison. None of the patients
were on antiarrhythmic drugs (the Brugada algorithm27).
Figure 7 Two-lead ECG monitor tracing of an artefact simulating a BCT. The rhythm strip was misdiagnosed as VT by 58% of the cardio-
logists surveyed. From Knight et al.37 Reproduced with permission from the publisher.
(AAD) treatment are difficult to diagnose by using the morphologi- QRS complex during aberration is characterized by a QRS dur-
cal criteria, as most of the studies did not include these patients in ation between 180 and 240 ms and bizarre RBBB with a right or
the differentiation. In this section, we will discuss some of these northwest axis, or atypical LBBB with left axis, mimicking VT.
conditions. The explanation of the occurrence of bizarrely shaped BBB
during treatment with class Ic AADs, particularly flecainide, is yet
uncertain. A possible explanation is the occurrence of use-
Broad QRS complex tachycardia dependent conduction delay especially in the myocardium
occurring during anti-arrhythmic drug beyond the block.39 In contrast, conduction is relatively unham-
treatment pered in areas activated by way of the His–Purkinje system, pre-
Antiarrhythmic drugs especially those that slow conduction like serving the initial part of the QRS complex unchanged. That
class Ic drugs may cause proarrhythmia represented by monomor- conduction delay due to flecainide is more pronounced in the ven-
phic VT. On the other hand, class Ic AADs may cause bizarre aber- tricular myocardium than in the His–Purkinje system has been
rant conduction during SVT which may mimic VT38 (Figure 8). The suggested by animal experiments. In contrast to the situation
470 B.S.N. Alzand and H.J.G.M. Crijns
during a straightforward BBB, this may result in an exaggerated in the right precordial leads, indicating that initial ventricular acti-
asynchrony of activation of the various parts of the heart, giving vation occurs through the specific conduction system.
rise to a bizarre type of BBB.38 Interfascicular tachycardia has been less commonly reported.
Class III AADs, especially pure IKr blockers like dofetilide may This tachycardia usually has an RBBB morphology. The orientation
also cause atypical aberrant conduction and sequential bilateral of the frontal plain axis is variable and may depend on the direction
BBB which may be easily misdiagnosed as multiple monomorphic of the reentrant circuit. Anterograde activation over the left
VTs.40,41 This relates to the fact that class III AADs prolong the anterior fascicle and retrograde through the posterior fascicle
refractory period in the Purkinje system much more than in would be associated with right-axis deviation and the reversed acti-
the ventricular myocardium. In addition, differential effects within vation sequence with left-axis deviation.46
the Purkinje system (left vs. right, distal vs. proximal, left posterior
vs. left anterior fascicular region) may cause bizarre QRS com- Fascicular ventricular tachycardia
plexes, whereas QRS duration is not terribly prolonged. The This relatively narrow QRS complex VT presents usually in young
sequential bilateral block patterns mimicking multiple monomor- patients. It can be classified into three subtypes: the common orig-
phic VTs are due to cycle length-dependent changes in refractory inating from the left posterior fascicle with an RBBB configuration
periods among bundle branches. Misdiagnosis is enhanced not only and superior axis; the uncommon type originating from the left
by atypical BBB morphologies and the repetitive multimorphology anterior fascicle with RBBB configuration and right-axis deviation;
BCT, but also by an atypically long coupling interval before the and the rare type originating in the upper septal fascicle with a
onset of these BCTs as well as the relatively long cycle length narrow QRS complex and a normal axis.11 The diagnosis of fascicu-
during BCTs (Figure 9). lar tachycardia is difficult due to the relatively narrow complexes
and the young age of the patients with no evidence of structural
Bundle branch and interfascicular reentry heart disease. Capture beats and fusion beats may be present,
tachycardia suggesting the diagnosis of VT rather than SVT. The QRS duration
These are uncommon forms of VT usually seen in patients with an in fascicular tachycardia can vary from 100 to 140 ms. The RS dur-
acquired heart disease and significant conduction system impair- ation in the precordial leads is ,80 ms, which is in contrast with VT
ment. The surface ECG in SR characteristically shows intraventri- associated with structural heart disease where the RS interval is gen-
cular conduction defects with or without PR interval erally .100 ms.47 Fascicular and bifascicular VT with an alternating
prolongation. A relatively narrow baseline QRS complex suggests focus between the anterior and the posterior fascicle can be seen in
a role of functional conduction delay in the genesis of bundle patients with digitalis intoxication or Andersen– Tawil syndrome.
branch reentry. The QRS morphology during VT is a typical BBB
pattern, usually LBBB, and may be identical to that in SR.42 – 45 In Pre-excited supraventricular tachycardia
contrast to VT of myocardial origin, bundle branch reentry with No morphological differentiation is theoretically possible between
a LBBB pattern characteristically shows rapid intrinsicoid deflection VT and SVT with AV conduction over an accessory pathway.12,35 In
Diagnostic criteria of BCT 471
Conclusion
Broad complex tachycardia often exhibits, especially at higher fre-
quencies, an indistinct morphology to make a certain diagnosis.
Despite all available morphological criteria, BCTs are still misdiag-
nosed or remain undiagnosed. To achieve a high positive predictive
value of more than 95% to identify VT, we prefer combining three
clinical criteria; any of the morphological criteria, AV dissociation
Figure 10 Ventricular tachycardia vs. pre-excited SVT;
detected clinically through the ECG or echocardiography, and
adapted from Steurer et al.48
the past history of myocardial disease (MI, cardiomyopathy, conge-
nital heart disease, and previous surgery). If the diagnosis is still
uncertain and typical BBB morphology is missing, VT should be
1994, Steurer et al.48 studied 149 VT, 113 with previous MI, and diagnosed by default. Procainamide prolongs the refractory
118 pre-excited SVT to differentiate between them. They designed period of the myocardium, the accessory pathway, and the retro-
a stepwise approach with three ECG criteria (Figure 10). The cri- grade conduction of the fast AV nodal pathway and therefore,
teria favouring VT were: (i) the presence of predominantly negative when in doubt, may be given, thus avoiding drugs with potentially
QRS complex in leads V4–6. (ii) The presence of a QR complex in harmful effects.49
472 B.S.N. Alzand and H.J.G.M. Crijns
Conflict of interest: all authors have read and approved the compared with 70 cases of idiopathic ventricular tachycardia. Eur Heart J 1984;
5:792 – 805.
manuscript, and no part of this manuscript is being published or
27. Brugada P, Brugada J, Mont L, Smeets J, Andries EWI. A new approach to the
under consideration for publication elsewhere. There are no con- differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation
flicts of interest for any of the authors. 1991;83:1649.
28. Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. Application of a new
algorithm in the differential diagnosis of wide QRS complex tachycardia. Eur
References Heart J 2007;28:589 –600.
1. Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia: misdiagnosis and
29. Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. New algorithm using
outcome after emergent therapy. Ann Intern Med 1986;104:766 –71.
only lead aVR for differential diagnosis of wide QRS complex tachycardia.
2. Dancy M, Camm AJ, Ward D. Misdiagnosis of chronic recurrent ventricular tachy-
Heart Rhythm 2008;5:89 –98.
cardia. Lancet 1985;2:320 –3.
30. Griffith M, de Belder MA, Linker NJ, Ward DE, Camm AJ. Multivariate analysis to
3. Biaggioni I, Killian TJ, Mosqueda-Garcia R, Robertson RM, Robertson D. Adeno-
simplify the differential diagnosis of broad complex tachycardia. Br Heart J 1991;
sine increases sympathetic nerve traffic in humans. Circulation 1991;83:1668 – 75.
66:166.
4. Buxton AE, Marchlinski FE, Doherty JU, Flores B, Josephson ME. Hazards of intra-
31. Griffith M, de Belder MA, Linker NJ, Ward DE, Camm AJ. Difficulties in the use of
venous verapamil for sustained ventricular tachycardia. Am J Cardiol 1987;59:
electrocardiographic criteria for the differential diagnosis of left bundle branch
1107 –10.
block pattern tachycardia in patients with structurally normal heart. Eur Heart J
5. ECC Committee, Subcommittees and Task Forces of the American Heart
1992;13:478 –83.
Association. 2005 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Circulation 2005;112:IV1 –203. 32. Griffith MJ, Garatt CJ, Mounsey P. Ventricular tachycardia as default diagnosis in
6. Pelleg A, Pennock RS, Kutalek SP. Proarrhythmic effects of adenosine: one decade broad complex tachycardia. Lancet 1994;343:386 –8.
of clinical data. Am J Ther 2002;9:141 –7. 33. Grimm W, Menz V, Hoffmann J, Maisch B. Value of old and new electrocardio-
7. Baerman JM, Morady F, DiCarlo LA Jr, de Buitleir M. Differentiation of ventricular graphic criteria for differential diagnosis between ventricular tachycardia
tachycardia from supraventricular tachycardia with aberration: value of the clinical and supraventricular tachycardia with bundle branch block. Z Kardiol 1996;85: