CME CARDIOLOGY
Diagnosis and management of ventricular tachycardia
Authors: John Whitaker, A Matthew J WrightB and Usha TedrowC
Ventricular tachycardia (VT) describes rapid heart rhythms
ABSTRACT
originating from the ventricles. Accurate diagnosis of VT
is important to allow prompt referral to specialist services
for ongoing management. The diagnosis of VT is usually
made based on electrocardiographic data, most commonly
12-lead echocardiography (ECG), as well as supportive
cardiac telemetric monitoring. Distinguishing between VT
and supraventricular arrhythmias on ECG can be difficult.
However, the VT diagnosis frequently needs to be made
rapidly in the acute setting. In this review, we discuss the
definition of VT, review features of wide-complex tachycardia
(WCT) on ECG that might be helpful in diagnosing VT, discuss
the different substrates in which VT can occur and offer
brief comments on management considerations for patients
found to have VT.
Introduction
During normal atrioventricular (AV) conduction,
supraventricular impulses are conducted through the cardiac
conduction system (CCS) comprising the AV node, penetrating
AV bundle, right and left bundle branches and fascicles,
which subsequently activate Purkinje cells of the peripheral
ventricular conduction system (PVCS), typically located in the
subendocardial tissue of the ventricle, and then the contractile
ventricular myocardium itself.1 The fascicular system comprises
the penetrating AV bundle, which arises from the AV node
and penetrates the aorto-ventricular membrane, or central
fibrous body, following which it separates into the right and
left bundles. 2 The bundles subdivide into the distal fascicles,
which, in the left ventricle (LV), can exhibit significant cross-
linking (or arborisation) and anatomical variation.3 Fascicular
Authors: Aclinical senior lecturer and honorary consultant
cardiologist and electrophysiologist, School of Biomedical
Engineering and Imaging Sciences at King’s College, London,
UK and Cardiovascular Directorate Guy’s and St Thomas’s NHS
Foundation Trust, London,UK; Bconsultant cardiologist and
electrophysiologist and honorary clinical senior lecturer, School
of Biomedical Engineering and Imaging Sciences at King’s
College, London, UK and Cardiovascular Directorate Guy’s and St
Thomas’s NHS Foundation Trust, London, UK; Cassociate professor
and director of clinical cardiac electrophysiology program and
ventricular arrrhythmia program, Brigham and Women’s Hospital
and Harvard Medical School, Boston, MA, USA
442
Clinical Medicine 2023 Vol 23, No 5: 442–8
tissue is likely to arise from myocytes within the developing
interventricular septum and, in maturity, comprises electrically
insulated, rapidly conducting cells, which can be distinguished
from AV nodal tissue by their rapid conduction and expression
of Connexin-40 (Cx-40) gap junction proteins.4 Purkinje cells
of the PVCS, which also express Cx-40, are derived from
trabeculations within the ventricular myocardium and connect
to the fascicular tissue during development to complete the
formation of the CCS.5
Ventricular tachycardia (VT) is defined as an arrhythmia
that originates from tissue below the penetrating AV bundle
and results in a fast (>100 beats per minute; bpm) ventricular
rate.6 These arrhythmias can arise from, or involve, specialised
conducting tissue as well as ventricular myocardium. VT can
occur in structurally normal or abnormal hearts and can be
Key points
VT is an arrhythmia with a rate >100 beats per minute arising
from the ventricular myocardium or specialised conduction
tissue below the penetrating atrioventricular bundle.
VT can present as an irregular broad complex tachycardia
and, therefore, an irregular rhythm does not exclude it as a
diagnosis.
Where there is any uncertainty, particularly in emergent
situations, a wide-complex tachycardia should be treated
as VT until proven otherwise and, ∼80% of the time, the
diagnosis will prove to be VT, especially in patients aged
>35 years.
Most VT occurs in patients with underlying heart disease but
∼10% occurs in those with structurally normal hearts, often
arising from the outflow tracts.
Management of patients with VT can involve risk stratification
for sudden cardiac death; the use of implantable cardioverter-
defibrillators; suppression of VT through the treatment of any
underlying myocardial disease; the use of anti-arrhythmic drugs;
catheter ablation; and, in refractory cases, emerging approaches,
such as cardiac stereotactic body radiation therapy.
KEYWORDS: Ventricular tachycardia, wide-complex
tachycardia, arrhythmia, ablation, ECG
DOI:10.7861/clinmed.2023-23.5.Cardio3
© Royal College of Physicians 2023. All rights reserved.

haemodynamically stable or unstable. It is not possible to
definitively distinguish between rhythms of ventricular or
supraventricular origin solely based on ventricular rate, the
presence or absence of structural heart disease, or whether a
rhythm is haemodynamically tolerated.
Diagnosis
VT forms an important differential diagnosis for any patient
presenting with a regular wide complex tachycardia (WCT), which
is a regular heart rhythm demonstrating at least three consecutive
beats with a ventricular rate >100 bpm and a prolonged QRS
duration (>120 ms) on 12-lead electrocardiogram (ECG).7 In
addition, VT can present as an irregular rhythm, although
irregularity does not exclude VT as a diagnosis. A wide QRS complex
indicates a delay in propagation of an electrical impulse throughout
the ventricular myocardium and could be the result of slowed or
absent conduction in any single portion of the CCS, or origin of a
ventricular impulse from a location where it does not engage the
CCS. In this case, propagation throughout the ventricles occurs at
a slower speed, because of conduction via contractile myocardium
as opposed to specialised conduction tissue. In addition to VT,
the differential diagnosis for a WCT includes any supraventricular
tachycardia (SVT) with associated bundle branch block,8 SVT that
is conducted to the ventricles via an accessory atrioventricular
(or related) pathway (or ‘pre-excited’ SVT), pacemaker-mediated
tachycardia, SVT conducted with a delay in myocardial propagation
(often because of medication, including class 1A, 1C and class III
anti-arrhythmic drugs)9 or systemic disturbances10 resulting in
abnormal myocardial electrical propagation.11 When possible,
comparison between a resting 12-lead ECG and the WCT is helpful,
because it enables a comparison between the morphology of a
conducted rhythm and the WCT.
It is generally accepted that the default diagnosis of a WCT on
ECG should be considered VT until proven otherwise, particularly in
urgent situations.11 This consideration is based on the importance
of avoiding administration to patients with VT of medication
commonly reserved for the treatment of SVT, which can
commonly be associated with haemodynamic deterioration when
administered during VT.12
Pre-test probability
When attempting to diagnose the cause of a WCT on ECG, it is
important to acknowledge the pre-test probability of different
aetiologies that might be responsible. It is has been reported that
∼80% of presenting WCTs are ultimately diagnosed as VT.11 In
the context of a WCT, structural heart disease (including previous
myocardial infarction, angina or heart failure) is associated with
a positive predictive value (PPV) of >95% for VT; age over 35
confers a PPV of 85% for VT; and age <35 confers a PPV of
70% for SVT. Although these observations should not prevent a
careful examination of the ECG and the clinical context in which
a tachycardia occurs, they can be helpful when considering
management options when uncertainty persists despite
consideration of the available evidence.
Diagnosis of ventricular tachycardia
A definitive diagnosis of VT requires the demonstration
of ventriculoatrial dissociation (ie ventricular activation
© Royal College of Physicians 2023. All rights reserved.
Ventricular tachycardia
that is independent of atrial activity). With extremely rare
exceptions,13 this can be considered the case when the number
of spontaneous ventricular activations exceeds the number of
atrial activations. Alternatives features that can be taken as
evidence of AV dissociation include the presence of fusion and
capture beats, which are characterised on 12-lead ECG as early
beats (ie occurring before the next expected beat of WCT would
be seen) with a typical conducted QRS morphology (capture)
compared with a 12-lead ECG in sinus rhythm or an intermediate
morphology between the WCT and a conducted beat (fusion). AV
dissociation can also be demonstrated on 12-lead ECG through
cardiac electrical implantable devices (CIED) or by invasive
electrophysiology study (Fig 1). When this phenomenon is present,
an arrhythmia can be considered ventricular in origin, which could
be helpful for guiding immediate and subsequent therapy.
Proof of atrioventricular dissociation is sometimes not possible
based on available data when a patient is being assessed and,
therefore, a judgement about the likely origin of an arrhythmia must
be made instead. Such a judgement can be based on the clinical
context in which the arrhythmia occurs, the myocardial substrate
that an arrhythmia occurs in and electrocardiographic evidence that
might be suggestive, even if not diagnostic, of a ventricular origin
for the rhythm. It might be easier to prove that an arrhythmia is not
ventricular in origin compared with proving that it is. In the absence
of contra-indications, vagal manoeuvres or adenosine can be
diagnostically helpful in that they can slow AV conduction, proving
SVT, and arrhythmias might terminate following the administration
of adenosine, which would be suggestive of a supraventricular
arrhythmia, whereas slowing of ventriculoatrial conduction could
expose VA dissociation, proving VT.9
There are ECG features that are suggestive of VT as opposed to
SVT, with some mechanism of QRS broadening. Several algorithms
have been proposed to systematically distinguish between VT and
SVT (Fig 2).9 They typically depend on several principles to indicate
the likely origin of a WCT, which include:
> Similarity of QRS morphology to a typical pattern of aberrant
conduction: if the QRS complex has a ‘typical’ bundle branch or
fascicular block appearance, there is a higher likelihood that the
arrhythmia is an aberrantly conducted SVT. If the appearance
is not consistent with any combination of bundle branch or
fascicular blocks, then the diagnosis is most likely that of
pre-excited SVT or VT.
> Ventricular activation speed: this can be considered as the
speed of initial ventricular propagation, as defined by the
steepness of the initial QRS deflection. A rhythm that is
conducted via the CCS will usually be associated with rapid
early deflection in the QRS complex. By contrast, impulses
arising from a ventricular focus remote from the CCS will
usually propagate slowly initially, giving rise to a less steep
initial portion of the QRS complex. This has been quantified
as an RS interval in any precordial lead of >100 ms (Brugada
algorithm)14 or an R-wave in V1 of >30 ms or >60 ms from
QRS onset to the nadir of the S-wave in V1 or V2 (Kindwall
criterion).15 In addition, overall QRS duration >140 ms in a RBBB
configuration or >160 ms in a LBBB configuration favours VT.16
> Relative rapidity of the early portion of ventricular activation
compared with the late portion of ventricular activation: this is
based on the principle that, during aberrantly conducted SVT,
the initial ventricular activation would be rapid, with conduction
delay occurring later in the ventricles, whereas, in VT, the initial
443
John Whitaker, Matthew J Wright and Usha Tedrow

Fig 1. Electrocardiographic diagnosis of ventricular tachycardia (VT). (a) 12-lead electrogram (ECG) showing wide complex tachycardia with
right bundle branch block configuration. Diagnosis is made from the regular P-waves, which are dissociated with QRS complexes and indicated by red
arrows. (b) Electrograms from an implantable cardiac device (ICD; in this case, a biventricular ICD). Top line (blue) shows nearfield electrical signal on
atrial channel, middle line (magenta) shows nearfield electrical signal on right ventricular (RV) channel and bottom line (green) shows far field electrical
signal between RV lead tip and left infra-clavicular generator, which can be thought of as a single lead ECG and is used as a discriminator channel to
differentiate conducted (ie supraventricular tachycardia; SVT) from ventricular rhythms. On the left-hand side of the panel, there are more signals on the
RV channel than on the atrial channel, which is seen to be dissociated from the signal on the ventricular channel, a pattern diagnostic of VT. The device
delivers a high-energy shock (indicated) following which the VT terminates and there is a single conducted sinus beat (Vs) followed by resumption of
biventricular pacing (BiV). The difference in morphology on the discriminator channel between both the spontaneous beat (VS) and biventricular paced
beats (BiV) can be seen. (c) Data from an electrophysiology study of a patient undergoing VT ablation for recurrent shocks in the context of a non-
ischaemic cardiomyopathy. The image demonstrates a catheter entering the left ventricle (LV) through the mitral valve. Colours on the LV shell indicate
the measured bipolar voltage and are used as an indication of the health (or otherwise) of the tissue, with purple corresponding to a voltage in the normal
range, and red representing severely reduced voltage, found in diseased tissue. A 12-lead ECG of the VT being treated is shown on the right side of the
panel. This patient was successfully treated for VT with an ablation procedure and remained free from further shocks during follow-up, which, at the time
of writing, was 25 months.

444 © Royal College of Physicians 2023. All rights reserved.

 Ventricular tachycardia

Fig 2. Features on ECG that help in the diagnosis of ventricular tachycardia. Atrioventricular (AV) dissociation is diagnostic of VT. Morphological
criteria can be applied depending on the overall similarity of the QRS complex in lead V1 to a typical ‘left bundle branch block’ or ‘right bundle branch
block’ morphology. Having differentiated between these, further criteria can be applied. As per the image, QRS duration, precordial lead concordance, and
QRS axis all suggest VT. Reproduced via a Creative Commons Attribution-NonCommercial License from Kashou et al.18

ventricular activation would be slow because of transmission in the leads in question; for example, positive concordance
through myocardial tissue, in contrast to specialised CCS describes QRS complexes that are positive throughout leads
tissue.17 V1–V6. Uncommonly, positively concordant QRS complexes can
> Ventricular activation axis: when ventricular activation arises occur in the context of pre-excited SVT because of a ventricular
from the apex, the ventricular impulse will spread away insertion around the mitral annulus. Negatively concordant QRS
from this focus, resulting in a QRS axis in the precordial complexes in the precordial leads are highly suggestive of VT.
leads between –90 and –180°, or ‘northwest’. This feature
Careful examination of the 12-lead ECG during tachycardia is
on 12-lead ECG is strongly suggestive of VT. Other QRS axis
of value for determining the aetiology of the arrhythmia. Of the
features that favour VT include left-axis deviation in RBBB
algorithms that have been published and validated, the most well
morphology tachycardias and right axis deviation in LBBB
known is the Brugada algorithm.14 Although these algorithms
tachycardias.18 The polarity of the lead aVR can also be helpful
can be extremely helpful, all are subject to misclassification,
in differentiating the aetiology of a tachycardia. During
and all can be ambiguous under some circumstances. Most
conducted rhythms, the initial ventricular activation is septal
of these have been validated almost exclusively in patients
and subsequent ventricular activation proceeds away from the
undergoing electrophysiology study with interpretation by cardiac
lead aVR, resulting in a predominantly negative QRS complex
electrophysiologists outside of the acute clinical setting in which
in the lead aVR. Therefore, rhythms with an initial R wave in
the tachycardia presented.18 This is important because it gives an
the lead aVR (indicating activation toward that lead) strongly
indication of why, despite the excellent reported sensitivity and
suggest VT.9 Finally, a significant (>40°) change in axis between
specificity of these algorithms, clinicians in the real world continue
sinus rhythm and WCT suggests VT.9
to face significant diagnostic uncertainty when interpreting ECGs of
> Precordial lead concordance: both positive and negative
WCT. Ultimately, it is likely to be most helpful to apply the principles
concordance in the precordial leads are suggestive of VT.
that the algorithms are derived from rather than to learn the
Concordance describes uniform polarity of the QRS complexes

© Royal College of Physicians 2023. All rights reserved. 445

John Whitaker, Matthew J Wright and Usha Tedrow

Fig 3. An example of ventricular tachycardia (VT) arising from the right ventricular outflow tract (a) Characteristic 12-lead electrogram (ECG)
demonstrating RVOT VT. The QRS is ‘inferiorly directed’, that is, it is predominantly positive in leads II, aVF and III. In the precordial leads, the QRS has a
left bundle branch block morphology with a precordial transition (ie the first precordial lead in which a predominantly positive QRS is seen) at lead V4. Note
is also made of a QRS complex that is predominantly positive in lead I, indicating a leftward direction of activation. (b) Activation map of the tachycardia
shown in (a). Here, the 3D surface represents the right ventricle, with the inflow and outflow valves indicated. The site of origin of the tachycardia is
indicated by the arrow, which was the site of successful ablation of the VT.

algorithms themselves and be prepared to trial several algorithms in
the case of difficulty interpreting a particular algorithm.
VT in structurally abnormal hearts
As noted above, most VTs occur in structurally abnormal hearts.
The crucial structural abnormality that underlies most VTs is the
presence of myocardial fibrosis.19 A range of pathologies can result
in the development of myocardial fibrosis. These have historically
been classified as ischaemic or non-ischaemic.20 Although
the label of non-ischaemic cardiomyopathy lacks specificity, it
continues to be helpful because it indicates likely differences in
the patterns of fibrosis that could be encountered in conditions
other than previous myocardial infarction. This is of importance
when counselling patients about prognosis, when planning for
interventions and the likely success of interventions. A detailed
discussion of the differences between substrate in ischaemic
and non-ischaemic cardiomyopathies is beyond the scope of this
article. However, in both conditions, the mechanism underlying
most VTs that are treated is re-entry, which is facilitated by the
presence of fibrosis. Re-entry describes a self-sustaining pattern
of electrical activation, and is the mechanism underlying most
SVTs, including atrial flutter, a more complex form of which also
underlies atrial fibrillation.21 A re-entrant circuit can be established
when a wave of electrical activation passes from a large body of
myocardium into a slowly conducting and electrically insulated
channel, or ‘isthmus’. As it passes through this isthmus, the
recently activated large body of myocardium has the chance to
recover excitability. When the wave of activation emerges from
the isthmus, the large body of tissue is excitable again and, thus,
the emerging wave meets excitable tissue, following which this
wave can ‘re-enter’ the isthmus, and the process is repeated. As
such, an ‘endless loop’ circuit is established that continues until
it is interrupted. Myocardial fibrosis promotes the emergence of
re-entry through the slowing of conduction as well as the electrical
isolation of myocardial cells that can then behave as an electrically
insulated isthmus through which re-entry can occur.
In addition to fibrosis, conditions associated with primary
electrical abnormalities, in the absence of structural changes,
have been associated with ventricular arrhythmias. These
conditions comprise channelopathies, including catecholaminergic
polymorphic VT (CPVT), and long-QT syndromes, as well as
others.20 These are important because, unlike it often is in overt
structural heart disease, the mechanism of VT associated with
channelopathies is less likely to be re-entry, given that they
are not typically associated with fibrosis. Management should
be undertaken in specialist centres with experience in these
conditions.
VT in structurally normal hearts
Although the presence of structural heart disease confers a higher
likelihood of VT when diagnosing an undifferentiated WCT, up
to 10% of VTs occur in the absence of an identified structural
abnormality of the heart. The most common site of origin of these
rhythms is the ventricular outflow tracts. Outflow tract VTs are
associated with characteristically tall QRS complexes in the inferior
leads.22 A variety of features on 12-lead ECG can help differentiate
a right- from left-sided origin. An example of a VT arising from the
RVOT is shown in Fig 3. Although often benign, presentation with

446 © Royal College of Physicians 2023. All rights reserved.


outflow tract arrhythmias, in the form of premature ventricular
contractions (PVCs) or VT, should prompt careful exclusion of the
possibility of an arrhythmogenic cardiomyopathy (AC). Outflow
tract arrhythmias in structurally normal hearts are often not
associated with haemodynamic compromise.23 In some cases,
they might be associated with tachycardia-induced myopathy24 or
sudden-cardiac death.24 Outflow tract arrhythmias are frequently
amenable to successful catheter ablation, which is a first-line
therapy in symptomatic patients25 and, therefore, patients with
symptomatic PVCs/VT with an outflow tract appearance should
be referred for electrophysiology consultation to discuss the merits
of invasive electrophysiology study. Another distinct arrhythmia
encountered in structurally normal hearts is that of fascicular VT.
This arrhythmia results from re-entry through a circuit including
the fascicles and Purkinje cells in the LV.3 These VTs typically have
a right bundle branch block morphology and characteristic narrow
QRS complexes with an axis dependent on the fascicle involved
in the tachycardia. These are usually haemodynamically well-
tolerated rhythms that can be treated with catheter ablation as a
first line. When identified, patients with these arrhythmias should
be referred to an electrophysiologist for consideration of catheter
ablation as a curative option.25
Management
Acute management of VT is focused on assessing and then
stabilising haemodynamic compromise resulting from the
arrhythmia. The advanced life support algorithms offer a helpful
and practical approach to managing WCT, and appropriate
parameters for determining haemodynamic compromise.26 As
has been noted, in cases of diagnostic uncertainty, arrhythmias
should be treated as ventricular in origin and the administration
of medication, such as verapamil, avoided. The most commonly
administered anti-arrhythmic drug is amiodarone because of its
efficacy and relatively safe short-term safety profile. An important
aspect of acute management that might be crucial to guide
future arrhythmia management is the acquisition (and storage) of
documentary 12-lead ECG evidence of the arrhythmia. The absence
of these data can present significant challenges for ongoing care,
including decision making around the indication for secondary
prevention implantable cardioverter-defibrillators (ICDs).
Ongoing management of patients with VT includes an
assessment of the ongoing risk of sudden cardiac death (SCD). In
general, ventricular arrhythmias that occur outside of the context of
significant systemic disturbance or a reversible cause, and which are
associated with haemodynamic instability, represent an indication
for consideration of secondary prevention ICD.20 Shared decision
making is an important aspect of this process and it is important
to discuss both quality of life and longevity alongside an individual
patient’s goals of care when discussing the option of an ICD.
Suppression of recurrent arrhythmia is another challenge that
is important for symptomatic reasons. This might be required as
a result of recurrent symptoms of palpitations or in the context
of recurrent therapies from an ICD, which can have a profound
and debilitating impact on patient wellbeing. The options for
suppressing arrhythmias include: treatment of the underlying
myocardial disease with guideline-directed medical therapy
or of structural abnormalities, such as valvular or coronary
disease; the use of anti-arrhythmic drugs; invasive catheter
ablation procedures; autonomic modulation, including the use
© Royal College of Physicians 2023. All rights reserved.
Ventricular tachycardia
of catheter-based continuous sympathetic blockade or surgical
sympathectomy; and emerging non-invasive therapies for VT, such
as cardiac stereotactic body radiation therapy (cSBRT).
Conclusion
The diagnosis of VT is made primarily using the 12-lead ECG.
Diagnostic algorithms exist to differentiate VT from other
WCTs, but uncertainty often persists despite appropriate
application of these algorithms. In this scenario, a WCT should
be treated as VT until proven otherwise. In the acute setting,
acquisition of a 12-lead ECG of the arrhythmia is vital to guide
future management. Ongoing management of VT comprises
an assessment of the associated risk of sudden cardiac death,
the use of ICDs in appropriate cases, and subsequently
suppression of VT through the treatment of any underlying
myocardial disease, the use of anti-arrhythmic drugs,
catheter ablation, and other emerging therapies. Ongoing
management of VT can be complex and ideally involves an
electrophysiologist. Early referral to an electrophysiologist is
also helpful to allow appropriate patient selection for invasive
treatment for VT. ■
References
1 Joyner RW, van Capelle FJ. Propagation through electrically
coupled cells. How a small SA node drives a large atrium. Biophys J
1986;50:1157–64.
2 McAlpine WA. Heart and coronary arteries. Berlin; Springer, 1975.
3 Kapa S, Gaba P, Desimone CV, Asirvatham SJ. Fascicular ventricular
arrhythmias: pathophysiologic mechanisms, anatomical constructs,
and advances in approaches to management. Circ Arrhythm
Electrophysiol 2017;10:e002476.
4 Christoffels VM, Moorman AFM. Development of the cardiac
conduction system. Circ Arrhythm Electrophysiol 2009;2:195–207.
5 Virágh SZ, Challice CE. The development of the conduction system
in the mouse embryo heart. Dev Biol 1977;56:397–411.
6 Al-Khatib SM, Stevenson WG, Ackerman MJ et al. 2017 AHA/
ACC/HRS Guideline for Management of Patients With Ventricular
Arrhythmias and the Prevention of Sudden Cardiac Death: A Report
of the American College of Cardiology/American Heart Association
Task Force on Clinical Practice Guidelines and the Heart Rhythm
Society. Circulation 2018;138:e272–391.
7 Brugada J, Katritsis DG, Arbelo E et al. 2019 ESC Guidelines for the
management of patients with supraventricular tachycardia The
Task Force for the management of patients with supraventricular
tachycardia of the European Society of Cardiology (ESC). Eur
Heart J 2020;41:655–720.
8 Kotadia ID, Williams SE, O’Neill M. Supraventricular tachycardia:
an overview of diagnosis and management. Clin Med (Lond)
2020;20:43–7.
9 Vereckei A. Current algorithms for the diagnosis of wide QRS
complex tachycardias. Curr Cardiol Rev 2014;10:262–76.
10 Teymouri N, Mesbah S, Navabian SMH et al. ECG frequency
changes in potassium disorders: a narrative review. Am J
Cardiovasc Dis 2022;12:112–24.
11 Katritsis DG, Brugada J. Differential diagnosis of wide QRS
tachycardias. Arrhythm Electrophysiol Rev 2020;9:155–60.
12 Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia:
misdiagnosis and outcome after emergent therapy. Ann Intern
Med 1986;104(6):766–71.
13 Csapo G. Paroxysmal nonreentrant tachycardias due to simulta-
neous conduction in dual atrioventricular nodal pathways. Am J
Cardiol 1979;43:1033–45.
447
John Whitaker, Matthew J Wright and Usha Tedrow
14 Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new
approach to the differential diagnosis of a regular tachycardia with
a wide QRS complex. Circulation 1991;83:1649–59.
15 Kindwall KE, Brown J, Josephson ME. Electrocardiographic criteria
for ventricular tachycardia in wide complex left bundle branch
block morphology tachycardias. Am J Cardiol 1988;61:1279–83.
16 Akhtar M, Shenasa M, Jazayeri M, Caceres J, Tchou PJ. Wide QRS
complex tachycardia reappraisal of a common clinical problem.
Ann Intern Med 1988;109:905–12.
17 Vereckei A, Duray G, Szenasi G, Altemose GT, Miller JM. Application
of a new algorithm in the differential diagnosis of wide QRS
complex tachycardia. Eur Heart J 2006;28:589–600.
18 Kashou AH, Noseworthy PA, DeSimone CV et al. Wide complex
tachycardia differentiation: a reappraisal of the state-of-the-art.
J Am Heart Assoc 2020;9:e016598.
19 Díez J, González A, Kovacic JC. Myocardial interstitial fibrosis in
nonischemic heart disease, part 3/4: JACC Focus Seminar. J Am
Coll Cardiol 2020;75:2204–18.
20 Zeppenfeld K, Tfelt-Hansen J, de Riva M et al. 2022 ESC Guidelines
for the management of patients with ventricular arrhythmias and
the prevention of sudden cardiac death. Eur Heart J 2022;43:
3997–4126.
21 Almendral J, Caulier-Cisterna R, Rojo-Álvarez JL. Resetting and
entrainment of reentrant arrhythmias: Part I: concepts, recognition,
448
and protocol for evaluation: surface ECG versus intracardiac
recordings. Pacing Clin Electrophysiol 2013;36:508–32.
22 Enriquez A, Baranchuk A, Briceno D, Saenz L, Garcia F. How to
use the 12-lead ECG to predict the site of origin of idiopathic
ventricular arrhythmias. Heart Rhythm 2019;16:1538–44.
23 Buxton AE, Waxman HL, Marchlinski FE et al. Right ventricular
tachycardia: clinical and electrophysiologic characteristics.
Circulation 1983;68:917–27.
24 Shimizu W. Arrhythmias originating from the right ventricular
outflow tract: how to distinguish ‘malignant’ from ‘benign’? Heart
Rhythm 2009;6:1507–11.
25 Cronin EM, Bogun FM, Maury P et al. 2019 HRS/EHRA/APHRS/
LAHRS expert consensus statement on catheter ablation of
ventricular arrhythmias. Heart Rhythm 2020;17:e2–154.
26 Soar J, Deakin CD, Nolan JP et al. Adult advanced life support
guidelines. London; Resuscitation Council UK, 2021.
Address for correspondence: Dr John Whitaker, School of
Biomedical Engineering and Imaging Sciences, King’s College
London, St Thomas’s Hospital, London, SE1 7EH, UK.
Email: john.whitaker@kcl.ac.uk
© Royal College of Physicians 2023. All rights reserved.