Education in Heart
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Cardiac Electrophysiology,
Stanford University, Stanford,
California, USA
Correspondence to
Dr Nitish Badhwar, Cardiac
Electrophysiology, Stanford
University, Stanford, CA 94305,
USA; Badhwar@stanford.edu
© Author(s) (or their
employer(s)) 2020. No
commercial re-use. See rights
and permissions. Published
by BMJ.
To cite: Shah RL, Badhwar N.
Heart Epub ahead of
print: [please include Day
Month Year]. doi:10.1136/
heartjnl-2019-315304
Approach to narrow complex tachycardia: non-
invasive guide to interpretation and management
Rajan L Shah , Nitish Badhwar
INTRODUCTION
Narrow QRS complex tachycardia (NCT)
represents an umbrella term for any rapid cardiac
rhythm greater than 100 beats per minute (bpm)
with a QRS duration of less than 120 milliseconds
(ms). The operative word ‘narrow’ maintains that
regardless of the arrhythmia mechanism or atrial
activity, ventricular depolarisation is rapid via
engagement of the His-Purkinje system (HPS).
Thus, the great majority of NCT encountered
routinely are supraventricular tachycardias (SVT)
or forms of tachycardia arising above the bifur-
cation of the bundle of His (HB). These arrhyth-
mias are frequently symptomatic and often result
in recurrent or persistent palpitations, breathing
disturbances, exercise intolerance, lightheaded-
ness and/or chest pain,1 2 and symptomatic patients
require medical attention.3 4 As many as 20% of
patients have history of syncope, some may experi-
ence hypotension or heart failure, and rarely (2%)
patients can present with non-lethal cardiac arrest.5
Cardiologists, as well as Family, Internal and
Emergency Medicine practitioners regularly care
for patients with NCT. Although documentation
of NCT via 12-lead ECG is considered the gold
standard, identification of the specific arrhythmia
mechanism can be made with telemetry, ambulatory
Holter ECG, implantable loop recorders, as well
as novel wearable technologies including adhesive
patch recorders and smartwatch/smartphone-based
applications.6 Using one or more of these tools, a
comparison during tachycardia and sinus rhythm
(NSR) may in fact reveal the aetiology of the
arrhythmia. The purpose of this current document
is to offer clinicians: (a) a survey of involved mech-
anisms, (b) a systematic approach to the differential
diagnosis and (c) management options for NCT.
MECHANISMS
A basic understanding of mechanisms involved in
arrhythmia initiation can be used to assist in the
evaluation of NCT and support the provider in
choosing therapies, as well as counselling patients.
Mechanisms include (A) Enhanced automaticity,
(B) Triggered activity, and (C) Re-entry (figure 1).7
The most common mechanism for NCT is re-entry.
Re-entry describes functional and/or anatomic
abnormalities in conduction or impulse propaga-
tion, which can be thought of as a self-propagating
micro-circuit or macro-circuit. The criteria neces-
sary for reentry are: (1) at least two functionally or
anatomically distinct potential pathways that join
proximally and distally to form a circuit of conduc-
tion; (2) unidirectional block in one pathway; (3)
slow conduction down the unblocked pathway,
Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304
Learning objectives
► Differential diagnosis of narrow complex
tachycardia (NCT).
► ECG diagnosis of different causes of NCT.
► Management of NCT.
allowing the previously blocked pathway time to
recover excitability.
Classifications and hints
Several constructs for ECG classification are imper-
ative in supporting a mechanism and facilitating a
stepwise approach to the diagnosis (figure 2). (A)
Regular versus irregular: refers to the consistency
of R to R intervals during NCT; variability greater
(ABES). Protected by copyright.
than 20 ms should be considered irregular and
may mechanistically suggest various atrial locations
firing (multifocal atrial tachycardia (MAT)), or vari-
able degrees of atrioventricular (AV) block during
an otherwise regularly activated atrial arrhythmia.
(B) Ventricular-atrial (VA) relationship: 1:1 rela-
tionship versus an atrial rate greater than ventric-
ular rate; refers to the number of P waves identified
per QRS complex and allows inferences regarding
the role of AV nodal conduction on propagation
of arrhythmia. NCT with atrial rates greater than
ventricular rates are non-AV node (AVN) depen-
dent; 1:1 VA is not specific. (C) The RP relationship
should be determined when a 1:1 VA relationship
is present: short RP versus long RP refers to the
interval between the R wave (ventricular depolari-
sation) to the subsequent P wave (atrial depolarisa-
tion). By figuratively splitting the interval between
two QRS complexes in half, if the P wave following
the preceding QRS complex falls within (1) the
first half it is referred to as a short RP tachycardia;
(2) the second half, a long RP tachycardia. (D) P
wave morphology: a baseline comparison of atrial
activation during NCT with NSR is key to distin-
guish mechanisms such as ectopic focal firing (atrial
tachycardia (AT)), macro-reentrant tachycardia
(F waves in atrial flutter (AFL)), versus mecha-
nisms that involve retrograde (negative P waves in
II, III and avF) atrial activation (AV nodal re-en-
trant (AVNRT), AV re-entrant (AVRT), junctional
tachycardia (JT)). Sinoatrial depolarisation results
in right followed by left atrial depolarisation,
producing upright P wave in leads I, II, III, aVL
and negative P wave in aVR.8 Further helpful hints
towards the diagnosis of NCT can be seen by exam-
ining the: (1) mode of initiation of tachycardia;
(2) effect of bundle branch block or ventricular
1
 Education in Heart

Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
(ABES). Protected by copyright.
Figure 1 Arrhythmia mechanisms causing narrow complex tachycardia. AVN, atrioventricular node; AP, accessory pathway; AVNRT, atrioventricular
nodal re-entrant tachycardia; AVRT, atrioventricular re-entrant tachycardia; AT, atrial tachycardia; AFL, atrial flutter; A. fib, atrial fibrillation; MAT,
multifocal atrial tachycardia; NCT, narrow complex tachycardia.

Figure 2 Algorithm for differential diagnosis of narrow complex tachycardia. AV, atrioventricular; AVNRT, atrioventricular nodal re-entrant
tachycardia; AVRT, atrioventricular re-entrant tachycardia; AVB, atrioventricular block; JT, junctional tachycardia.
2 Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304

premature depolarisation on tachycardia; (3) effect
of drugs or AV dissociation or variable conduction
on tachycardia.
NARROW COMPLEX TACHYCARDIA
Atrioventricular nodal re-entrant tachycardia
AVNRT accounts for the majority of regular NCT
in humans,9 10 excluding appropriate sinus tachy-
cardia. It is usually seen in young adults without
structural heart disease, and the majority of cases
are observed in females.9 AVNRT is rarely life
threatening.5 11 It is a form of micro-reentrant
tachycardia involving two functional pathways,
generally referred to as alpha and beta, that make
up a micro-circuit limited to the AVN and perinodal
tissue.12 13
Typical AVNRT
‘Typical’ AVNRT is synonymous with ‘slow–fast’
AVNRT in which the alpha pathway represents
the antegrade limb of the perinodal circuit and has
slow conduction properties, while the beta pathway
represents the retrograde limb with fast conduction
properties. Conduction via the retrograde limb is
so rapid that ventricular and subsequent atrial acti-
vation occur simultaneously (referred to as ‘A on
V’). As such, typical AVNRT manifests as a short RP
tachycardia with buried or very discrete, abnormal
P waves representing retrograde conduction seem-
ingly within or immediately after the QRS in a 1:1
VA relationship. Blending of the P wave with the
tail of the QRS complex can distort the QRS and
result in pseudo S waves in the inferior leads, or
pseudo R waves in V1; these are not present in NSR
(figure 3).
During NSR, patients classically conduct ante-
grade through the AVN via the fast pathway and the
presence of dual AV nodal pathways may be mani-
fested by different PR intervals. Holter monitoring
may demonstrate atrial premature depolarisations
(APD) and isolated atrial echo beats (‘single beat’
form of AVNRT where antegrade conduction down
one limb is followed by retrograde conduction via
the second resulting in P wave or atrial depolarisa-
tion, but is unable to turn around antegrade to form
a subsequent QRS, most commonly due to refracto-
riness) between episodes. Further Holter evidence
can be seen on initiation of NCT with an APD14
that results in sudden prolongation of PR interval,15
characteristic of block in the fast pathway and shift
in antegrade conduction to the slow pathway (figure
3B). P wave morphology of the initial ectopic APD
usually differs from the subsequent retrograde P
waves during tachycardia. Ventricular premature
depolarisations (VPD) rarely induce typical AVNRT
due to refractoriness of the HPS prohibiting an early
VPD from retrogradely reaching the AVN. During
tachycardia, spontaneous VPDs or development of
bundle branch block will have no effect on tachy-
cardia cycle length given neither the ventricle or
bundles are required for propagation of the circuit.
Tachycardia terminating with atrial depolarisation
(P wave) in the setting of spontaneous or induced
Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304
Education in Heart
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AV block supports AVNRT or AVRT; this is unchar-
acteristic of AT.
Atypical AVNRT
‘Atypical’ AVNRT denotes less common forms of
perinodal micro-reentry and their circuits can be
further classified as ‘fast–slow’ and ‘slow–slow’
subtypes in which the antegrade limb may be either
a fast conduction or slow conducting pathway,
respectively, and a distinct slow pathway charac-
terises the retrograde limb of the circuit in both.
A regular, 1:1 VA relationship is maintained on
ECG, however, the slow conducting property of
the retrograde limb results in separation of the P
wave from the preceding QRS complex, classifying
the NCT as a long RP tachycardia (figure 4). The
differential diagnosis of this long RP tachycardia
with such P wave morphology is: (1) AT arising
from a region near the HB, such as the coronary
sinus ostium, and (2) Slowly conducting accessory
pathway tachycardia, referred to as permanent
reciprocating junctional tachycardia (PJRT), which
is often incessant. Holter may demonstrate APDs
and isolated echo beats during NSR similar to
slow–fast AVNRT, though is less likely to demon-
strate dramatically different PR intervals. NCT is
(ABES). Protected by copyright.
often similarly initiated by an APD with a distin-
guished P wave morphology from subsequent retro-
grade P waves during tachycardia. Atypical forms of
AVNRT are more likely than typical to be initiated,
and terminated, by a VPD in which the impulse
timely conducts retrograde via the slow pathway
(meeting either an excitable or refractory antero-
grade pathway, respectively).
Dual AV nodal non-reentrant tachycardia
(DAVNNT)
DAVNNT is an uncommon arrhythmia manifesting
as NCT that occurs in the presence of dual AVN
physiology without re-entry.16 To cause this entity,
a single atrial impulse conducts antegrade down
both the beta and alpha (fast and slow) pathways
producing a ‘double fire’ ventricular response;
resultant NCT can occur during NSR. On ECG,
a single P wave is followed by two narrow QRS
complexes causing an irregular R–R tachycardia
(figure 5) and identification of the recurring pattern
is critical to distinguish DAVNNRT from irregu-
larly irregular NCT, most importantly, atrial fibril-
lation17; differential diagnosis includes NSR with
echo beats versus junctional bigeminy.
AV re-entrant tachycardia
AVRT is generally considered the second most
common regular SVT,9 yet overall is not frequent-
appearing in the population. Gender influences
have been reported and suggest that SVT involving
an accessory pathway (AP) tends to be more
frequent in males.18 It usually occurs in young
adults without structural heart disease, however an
association with congenital disease, namely Ebstein
anomaly, has been demonstrated.19 One distinct,
clinically relevant feature of AVRT is a documented
3
 Education in Heart

Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
(ABES). Protected by copyright.
Figure 3 Typical AVNRT (micro-reentry, dual AVN). (A) Holter of normal sinus rhythm for baseline comparison. Antegrade conduction via fast
pathway resulting in baseline PR interval. (B) In same patient, NCT initiating with sudden prolongation of PR interval, characteristic of block in the
fast pathway and shift in antegrade conduction to the slow pathway; retrograde conduction via fast pathway back to the atrium producing pseudo R
waves (*; a on V), not present in sinus (ø). AVN, atrioventricular node; AVNRT, atrioventricular nodal re-entrant tachycardia.

Figure 4 Atypical AVNRT (micro-reentry, dual AVN): ECG of long RP tachycardia with retrograde (negative) P waves in II/III/aVF; slow–slow atypical
AVNRT is depicted. AVN, atrioventricular node; AVNRT, atrioventricular nodal reentrant tachycardia.
4 Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304
 Education in Heart

Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
Figure 5 DAVNNT (non-reentry, dual AVN): ECG of irregular NCT; P waves are present (vertical arrow) and each is followed by two narrow QRS
complexes consistent with sinus rhythm and ‘double fire’. AVN, atrioventricular node; DAVNNT, dual AV nodal non-reentrant tachycardia; NCT, narrow
complex tachycardia.

association with syncope, presyncope and sudden connections include atrio-nodal, atrio-fascicular,

(ABES). Protected by copyright.

death.3 4
AVRT is a form of macro-reentry, in which the
pathways of the circuit consist of a limb of conduc-
tion over the AVN, and a second limb of conduc-
tion via an AP typically connecting atrial and
ventricular tissue directly.20 21 The pathway may be
right or left sided, may conduct impulses bidirec-
tionally, and commonly has conduction properties
distinct from those of the AVN —namely, rapid
and non-decremental. Other septal-located AP
nodo-fascicular and nodo-ventricular. Orthodromic
AVRT (ORT) refers to antegrade conduction down
the AVN-HPS limb manifesting as an NCT; this
form comprises 90%–95% of AVRT (figure 6B).19
Conduction during tachycardia in an opposite
direction (antegrade down an atrial–ventricular
bypass tract) results in a wide complex tachycardia
and signifies antidromic AVRT.19 22 During NSR,
manifest antegrade conduction via an AP produces
a short PR interval and widened, fused QRS with

Figure 6 AVRT (macro-reentry, AP): (A) ECG of sinus rhythm with pre-excitation: short PR interval and delta wave. (B) ECG of short RP NCT in the
same patient. Orthodromic AVRT: antegrade down the AVN, retrograde up the AP resulting in retrograde P waves (*). AVN, atrioventricular node; AVRT,
atrioventricular re-entrant tachycardia; AP, accessory pathway; NCT, narrow complex tachycardia.
Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304 5
 Education in Heart

Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
(ABES). Protected by copyright.
Figure 7 AVRT (macro-reentry): ECG of short RP (>90 ms) NCT with development of spontaneous left bundle branch block (ø); retrograde P waves
(*). Tachycardia slows by 40 ms during bundle branch block and equally accelerates on return to narrow; Coumel’s sign. AVRT, atrioventricular re-
entrant tachycardia; NCT, narrow complex tachycardia; RB, right bundle; LB; left bundle.

presence of a delta wave (figure 6A); this is referred
to as pre-excitation and localisation of the AP based
on such pre-excitation has been described.23 24 A
concealed bypass tract refers to the absence of pre-
excitation on ECG (indistinguishable narrow QRS)
in a patient with an existing AP; concealment may
be related to: weak antegrade conductive properties
of the bypass tract, unidirectionality of conduction
in retrograde fashion only, or distant location of AP
in relation to sinoatrial and AV nodes.
Whether a patient presents in or out of tachy-
cardia, a resting ECG revealing pre-excitation
elevates the suspicion for AVRT. During ORT,
the narrow QRS complex results from antegrade

Figure 8 Atrial tachycardia (automaticity): Holter beginning with sinus rhythm followed by ectopic APD (similar morphology to NCT) initiating AT.
Spontaneous AV block with marching ectopic P waves (*), followed by 1:1 long RP NCT. AV, atrioventricular; APD, atrial premature depolarisations; AT,
atrial tachycardia; NCT, narrow complex tachycardia.
6 Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304
 Education in Heart

Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
Figure 9 Multifocal atrial tachycardia (automaticity): ECG of irregular NCT with >3 distinct P waves (*).

conduction via the AVN and HPS; retrograde time, hence, the RP is generally not shorter than
conduction, from ventricle back up to the atrium 90 ms.25 Retrograde conduction involving a slowly
via bypass tract, is typically rapid generating a conducting decremental pathway (PJRT) results

(ABES). Protected by copyright.

short RP tachycardia. Though ORT and typical
AVNRT both produce regular, narrow complex,
short RP tachycardia, the timing of atrial activa-
tion compared with ventricular activation is funda-
mentally different in each arrhythmia and can be
noted on ECG. In AVNRT, activation of ventricle
and atrium occur in parallel (A on V); this explains
why the P wave may be hidden or reveal itself only
in the tail end of the R wave. In ORT, activation
of ventricle and atrium occur in series as in first
ventricle then bypass tract to atrium requiring some
in long RP NCT26 that is often incessant and can
lead to heart failure. On Holter, tachycardia may be
initiated by either APD or VPD.27 An APD initiates
ORT by blocking in the AP and conducting to the
ventricles in antegrade fashion through the AVN
to HPS, ventricle and then travels back to the atria
through the AP to complete the circuit. A VPD will
block in the HPS and conducts retrograde to atria
via AP. During NCT, sudden aberration or develop-
ment of bundle branch block with resultant delay
in R–P interval and slowing of tachycardia cycle

Figure 10 Junctional tachycardia (automaticity): (A) ECG of sinus rhythm. (B) NCT with AV dissociation; sinus P waves (positive II/III/aVF) indicated
by arrows marching through. Permission granted from Springer Nature - Cardiac Electrophysiology Review 2002;6:431–435.
Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304 7
 Education in Heart
Figure 11 AFL (macro-reentry, isthmus). (A) Rhythm strip of regular NCT with F waves yielding ST segment deviation; 1:1 A:V ratio. (B) ECG of AFL
with 2:1 ratio. (C) ECG of AFL with 4:1 ratio; negative F waves in II/III/aVF and positive F waves in V1 consistent with typical atrial flutter. NCT, narrow
complex tachycardia; AFL, atrial flutter.
length (R–R intervals) is consistent with ORT and
further localises the AP to the side of the functional
block (figure 7); termination of tachycardia with
spontaneous VPDs also supports AVRT.
Atrial tachycardia
AT is a relatively infrequent form of NCT and is
classically characterised by activation from a point
source within the atrium. It may occur in young
adults without structural heart disease but also can
support atrial enlargement in the setting of struc-
tural heart disease;3 4 AT is not associated with an
increased risk of syncope or sudden death.
The underlying mechanism for focal AT is prin-
cipally abnormal automaticity from an ectopic
source, and less commonly triggered activity or
micro-reentry;28 regardless, the aetiology cannot
be distinguished easily on surface electrogram.
Due to its automatic nature, ectopic atrial firing
occurs independent of the AVN or ventricular acti-
vation, thus can present as an A>V tachycardia
(figure 8) with atrial rates ranging 100–230 bpm.28
A 1:1 tachycardia can also be maintained, based
on vagal tone and AVN conduction, and a long RP
tachycardia will chiefly be depicted; the RP rela-
tionship is not fixed, therefore, A on V and short
RP NCT are also possible. Assessment of P wave
morphology during tachycardia, in comparison
with NSR, is fundamental for localisation of the
source.29 Focal atrial tachycardias tend to cluster in
areas including the crista terminalis, coronary sinus
ostium, tricuspid annulus, pulmonary veins and
mitral annulus. P waves similar to sinoatrial acti-
vation suggest appropriate or inappropriate sinus
tachycardia, sinus nodal re-entrant tachycardia,30
or a focal AT arising close to the sinus node. On
Holter, tachycardia may be initiated by an APD
8 Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304
Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
and the morphology of the initial ectopic P wave
(ABES). Protected by copyright.
is often identical to the subsequent P waves during
NCT. A ‘warm up’ and ‘cool down’ phenomenon
of gradual acceleration and deceleration of tachy-
cardia between NSR may be visible. Unlike AVNRT
and AVRT, AT may spontaneously terminate with a
QRS complex though most often atrial activity will
continue to fire in the presence of spontaneous AV
block. Administration of adenosine during AT can
result in AV block with marching ectopic P waves
and/or terminate the tachycardia due to cyclic AMP
triggered activity.
Multifocal atrial tachycardia
MAT is a rare form of NCT seen in a variety of clin-
ical disorders, most commonly identified in elderly
patients and in patients with pulmonary disease.4
Multiple areas of organised atrial activity, due to
abnormal automaticity or triggered activity, result
in the characteristic electrocardiographic feature of
three or more different P wave morphologies, with
associated irregular PR and R–R intervals (figure 9).
Junctional tachycardia
JT is a rare form of focal NCT that arises from the
AV junction tissue and the mechanism is similar
to focal AT (abnormal automaticity or triggered
activity). It is most commonly seen in paediatric
patients where it can present as congenital JT or
postoperative JT.31 Incessant JT in these patients
can lead to heart failure.32 Less commonly, JT
is seen in adults in whom it presents de novo as
a paroxysmal, A on V (short RP) NCT with heart
rate varying between 100–250 bpm. There can be
1:1 VA relationship with retrograde conduction
(inverted P morphology in II/III/aVF) from the
focus to the atrium giving an appearance on ECG
 Education in Heart

Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
Figure 13 Example of short RP NCT captured during a patient-activated transmission using a wearable, digital health sensor; AppleWatch (Apple,
Cupertino, California, USA) single-lead ECG application. Afib, atrial fibrillation; NCT, narrow complex tachycardia.

that is similar to typical AVNRT. Alternatively, JT Atrial flutter

can manifest in adults after catheter ablation for Atrial flutter is a macro-reentrant AT that is char-

(ABES). Protected by copyright.

AVNRT. In this form there is often AV dissoci-
ation during NCT which is supported by sinus P
waves marching through NCT on ECG (figure 10).
Other causes of NCT with VA dissociation include
AVNRT with block to atrium and concealed nodo-
fascicular/nodo-ventricular tachycardia. Initiation
of JT is usually with junctional beats and is not
dependent on critical PR prolongation. Periods of
warming up and cooling down can be noted. Focal
JT often terminates with adenosine suggesting trig-
gered activity as the mechanism.3 4
acterised electrocardiographically by an atrial rate
between 250–350 bpm. It can arise from either
atrium and is suggestive of structural heart disease
or previous surgery or ablation.33 It is classified as
either typical or atypical based on the ECG pattern
and morphology of flutter or F waves (atrial depo-
larisations). ‘Typical’ AFL is the most common form,
occurring in 90% of patients with this arrhythmia.29
The circuit of this arrhythmia involves an area of
critical tissue (isthmus) between the coronary sinus
ostium and the tricuspid valve. The impulse travels

Figure 12 Adenosine administration during NCT: results are diagnostic and/or therapeutic. AVNRT, atrioventricular nodal re-entrant tachycardia;
AVRT, atrioventricular re-entrant tachycardia; AT, atrial tachycardia; AFL, atrial flutter; CHB, complete heart block; JT, junctional tachycardia; ST, sinus
tachycardia; SVT, supraventricular tachycardia.
Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304 9
Education in Heart
in a counter-clockwise fashion in the right atrium
around the tricuspid annulus giving rise to the
following ECG pattern: negative flutter waves in
the inferior leads (II, III, AVF), commonly referred
to as a ‘sawtoothed’ pattern, and positive flutter
waves in V1 (figure 11C). ‘Atypical’ AFL is not
dependent on the cavo-tricuspid isthmus and may
develop around (A) an area of the atrium affected
by previous surgical procedures (Mustard/Senning/
Fontan/Atrial septal defect repair, etc.)34 referred to
as incisional flutter; and/or (B) de novo atrial scar
or that related to prior catheter ablation, especially
ablation for atrial fibrillation. Atypical left AFL
can be mitral annular, roof dependent, or revolve
around the pulmonary veins.35 AFL can present with
any degree of AV conduction, including 1:1, 2:1,
3:1, 4:1 (figure 11A,B,C), etc., as well as variable
block within the same patient. A diagnosis of 2:1
AFL should be considered in NCT with ventricular
rates of/close to 150 bpm; close examination of the
ECG will reveal F waves buried in the ST segment.
Adenosine administered during AFL will cause
AV block and help identify the flutter waves. AFL
usually does not convert with AV nodal blocking
drugs and catheter ablation is first line therapy.
Treatment
A patient with NCT and haemodynamic instability
should be electrically cardioverted without delay.3 4
NCT is however, generally haemodynamically toler-
ated and manoeuvres to augment vagal tone can be
useful for (A) slowing down tachycardia rate and (B)
terminating the arrhythmia. Techniques including
Valsalva manoeuvre, modified Valsalva manoeuvre,36
and carotid sinus massage temporarily slow AVN
conduction and can be readily performed in the
emergency department, clinic office and by a well-
informed patient. When ineffective, medications
to replicate vagal slowing of AVN conduction and
prolong refractoriness should be considered with
cardiac monitoring. The mainstay is adenosine.37
Administration of adenosine during tachycardia can
not only be therapeutic, it is often diagnostic of the
involved tachycardia mechanism (figure 12). If AV
block occurs with adenosine administration and
without termination of tachycardia, AVN-dependent
mechanisms, namely, AVNRT and AVRT are ruled
out. Adenosine causing AV block in AT, ST and AFL
will unmask dissociated P waves and confirm a non-
AVN dependent mechanism. Adenosine terminates
NCT due to AVNRT and AVRT given the role of
the AVN within each circuit.38 However, termina-
tion of AT39 and JT has also been documented with
adenosine suggestive of triggered activity. Therefore,
all mechanisms should be considered when abrupt
termination is demonstrated and rhythm strips
should be carefully examined for all aforementioned,
distinguishing clues. If adenosine is ineffective or
NCT is frequently occurring, escalation to intrave-
nous calcium channel blocker or beta blocker can be
considered in the absence of left ventricular systolic
dysfunction.
10 Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304
Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
Long-term management and prevention of recur-
rent, symptomatic NCT is best personalised to the
individual patient and should be directed in consul-
tation with Cardiovascular Medicine specialists.
Treatment with beta blocker or calcium channel
blocker medications by mouth, or primary anti-
arrhythmic strategies may be indicated. Inhaled
agents are on the horizon and may offer a conve-
nient ‘pill in the pocket’ option.40 41 Counselling
and assurance require an understanding of patient
symptoms and an appreciation for potential anxiety
with NCT recurrence, chronic medications, as well
as invasive testing. Definitive treatment of AVNRT
or AVRT with catheter ablation is supported by a
greater than 95% success rate.3 4 42 43 A detailed
explanation of the procedure includes discussion
of benefits and associated 1% or less risk of major
complication. Beyond improvement in quality of
life, catheter ablation also reduces risk of mortality
in specific populations (Wolff-Parkinson-White
syndrome (WPW)). Thus, the following scenarios
warrant consideration for referral to an electro-
physiologist: (1) Debilitating or severe symptoms;
(2) Pre-excitation or WPW syndrome; (3) Intoler-
ance or resistance to drug therapy. A more detailed
summary of treatment algorithms and strategies,
with available evidence, can be found in committee
(ABES). Protected by copyright.
guideline statements.3 4 A specific therapy for NCT
is chosen by the patient and responsible health
professional, and is based on various, patient-
centred factors.
FUTURE DIRECTIONS
While 12-lead ECG recording remains the gold-
standard for diagnosis of NCT, its yield is most
significant when episodes are persistent or patients
present in tachycardia. For paroxysmal symptoms,
the diagnosis can be fleeting and other forms of
cardiac monitoring may be necessary. New tech-
nologies44 45 for more readily obtainable and even
continuous monitoring of the cardiac rhythm
are available through wearable and application-
based sensors. These tools create an opportunity
for patient-driven investigation of de novo symp-
toms (figure 13), as well as surveillance following
provider-initiated therapies.46 47 Motion and noise
artefacts pose small limitation,48 and continuous
monitoring wearables often allow autotriggering
to store looped recording before and after an
episode49 which may assist in capturing mechanistic
clues, as described in this review. With over 1000
wearable devices available to the consumer,50 dedi-
cated large prospective trials,51 FDA-cleared detec-
tion algorithms for atrial fibrillation52 and rising
attraction towards machine learning and deep
neural networks,49 53 54 a new era of NCT detection
has already begun.55 56 Nonetheless, the ultimate
responsibility for identification and accurate diag-
nosis of NCT, along with appropriate counselling
and management of such patients, remains that of
the clinician.

Key points
► A comparison of rhythm strip or ECG during narrow complex tachycardia
(NCT) with sinus rhythm may reveal the aetiology of the arrhythmia. Beyond
ECG, an evaluation of available telemetry, wearable or implanted recorders
and smartwatch/smartphone-based ECG applications can provide helpful
hints in the analysis of NCT.
► A stepwise approach to the diagnosis of NCT includes assessment of: (A)
R–R regularity; (B) ventricular–atrial relationship; (C) RP duration; (D) P wave
morphology; (E) mode of initiation of NCT; (F) effect of bundle branch block
or ventricular premature depolarisation on tachycardia; and (G) effect of
spontaneous or induced AV block during tachycardia
► After Vagal manoeuvres, intravenous bolus of Adenosine is the mainstay
early treatment for NCT; administration of adenosine can be both therapeutic
and diagnostic of the tachycardia mechanism involved. Management of NCT
with oral medications may decrease the regularity of patient symptoms,
however, complete suppression is not common. Catheter ablation for NCT is
often curative.
CME credits for Education in Heart
Education in Heart articles are accredited for CME by various providers. To
answer the accompanying multiple choice questions (MCQs) and obtain your
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CONCLUSION
NCT encompasses a heterogeneous group of
arrhythmias originating above the HB, with distinct
electrophysiological characteristics. The differen-
tial diagnosis of NCT includes atrial fibrillation,
atrial flutter and paroxysmal SVT (AVNRT, AVRT
and AT). Knowledge of involved mechanisms is
imperative in guiding management and counsel-
ling patients. The approach to non-invasive ECG
diagnosis includes examination of R–R regularity,
VA relationship, RP duration, and morphology of
P waves. Initiation and termination of tachycardia
also provide important clues to the diagnosis, as
does the perturbation of tachycardia by APDs,
VPDs and bundle branch block. Adenosine admin-
istration during tachycardia can elucidate the mech-
anism and lead to termination of certain forms of
NCT. Catheter ablation is curative for most forms
of NCT.
Twitter Nitish Badhwar @BadhwarNitish
Contributors Each author contributed equally to the conception,
design, drafting, revision and final approval of this manuscript.
Funding The authors have not declared a specific grant for this
research from any funding agency in the public, commercial or
not-for-profit sectors.
Competing interests NB receives honoraria from Abbott and
Biosense Webster for fellows’ education; these relationships do not
conflict with or influence the contents of this paper.
Shah RL, Badhwar N. Heart 2020;0:1–12. doi:10.1136/heartjnl-2019-315304
Education in Heart
Heart: first published as 10.1136/heartjnl-2019-315304 on 17 April 2020. Downloaded from http://heart.bmj.com/ on April 17, 2020 at Agence Bibliographique de l Enseignement Superieur
Patient and public involvement Patients and/or the public
were not involved in the design, or conduct, or reporting, or
dissemination plans of this research.
Patient consent for publication Not required.
Provenance and peer review Commissioned; externally peer
reviewed.
Data availability statement There are no data in this work
Author note References which include a * are considered to be
key references.
ORCID iDs
Rajan L Shah http://orcid.org/[0000-0002-3603-7345
Nitish Badhwar http://orcid.org/0000-0002-3233-6305
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