Commentary Supraventricular Tachycardia

Supraventricular Tachycardia: Electrocardiogram

Diagnosis and Clinical Management for the
Non-electrophysiologist
Andreas A Boehmer, Moritz Rothe, Christina M Soether, Bernhard M Kaess and Joachim R Ehrlich
Division of Cardiology, St Josefs-Hospital, Wiesbaden, Germany

DOI: https://doi.org/10.17925/EJAE.2021.7.1.4

S
upraventricular tachycardia (SVT) is a common cause of hospital admissions and should be correctly diagnosed and treated by
any physician involved. Diagnosis and acute treatment are, nevertheless, sometimes difficult for the non-electrophysiologist.
Both diagnosis and clinical management of SVTs have recently been the focus of the new, and very detailed, European Society
of Cardiology (ESC) guidelines. This paper serves as a support to non-electrophysiologists in electrocardiogram (ECG)-based detection,
differentiation and treatment of SVT. While vagal manoeuvres, or the application of adenosine, may be performed after 12-lead ECG recording
in haemodynamically stable patients for further diagnosis and treatment, haemodynamically unstable patients should be cardioverted
immediately. Concerning sinus rhythm maintenance after initial termination of tachycardia, catheter ablation is preferred to antiarrhythmic
therapy. This review covers aspects of ECG diagnosis and the differential approach to identifying various types of SVT.

Keywords Supraventricular tachycardia (SVT) occurs with a prevalence of 2–3/1,000 in the general population
Supraventricular tachycardia, catheter and is characterised by atrial rates >100 beats per minute (bpm) at rest. Per definition, SVT
ablation, electrocardiogram (ECG), vagal originates in the atria or atrioventricular (AV) node tissue above the His bundle.1,2 Diagnosis and
manoeuvres, ventricular tachycardia
clinical management of SVT have been the focus of recent European Society of Cardiology
Disclosures: Andreas A Boehmer, Moritz Rothe, guidelines, covering 65 pages, with additional supplemental material.3 It may be difficult to apply
Christina M Soether, Bernhard M Kaess and Joachim R to clinical practice for non-electrophysiologists not involved daily in the treatment of patients with
Ehrlich have no financial or non-financial relationships
or activities to declare in relation to this article. arrhythmia. Accordingly, it is the aim of the present article to summarize SVT-relevant aspects of
Acknowledgement: Leonie Friedrich is acknowledged diagnosis and management in a clinically applicable manner. For more detailed information, we
for outstanding support with artwork. refer to the specific guidelines and a position paper published by the European Heart Rhythm
Review process: Double-blind peer review. Association in 2017.1,3
Compliance with ethics: This study involves a review of
the literature and did not involve any studies with human
or animal subjects performed by any of the authors. Basis of supraventricular tachycardia
Authorship: The named authors meet the International On a cellular basis, SVT can either originate from non-re-entrant mechanisms, such as enhanced
Committee of Medical Journal Editors (ICMJE) criteria automaticity or triggered activity, or from re-entry within myocardial tissue perturbing normal
for authorship of this manuscript, take responsibility
for the integrity of the work as a whole, and have sinus rhythm.4 Occasionally, sinus rhythm itself will be dysregulated and become tachycardic by
given final approval for the version to be published. sinus node re-entry or inappropriate activation.5 This is one of the few entities in the field of
Access: This article is freely accessible at SVT probably best managed by conservative measures, such as regular physical exercise, over
touchCARDIO.com © Touch Medical Media 2021.
antiarrhythmic drugs or catheter ablation.1,3
Submitted: 23 April 2020
Accepted: 28 January 2021
Published online: 27 May 2021
Enhanced automaticity and triggered activity typically lead to focal atrial tachycardia (AT).4 Focal
Citation: European Journal of Arrhythmia
arrhythmias in patients who have not been operated on or ablated before may arise from specific
& Electrophysiology. 2021;7(1):4–11 sites with predisposition to arrhythmogenesis, such as crista terminalis or coronary sinus orifice.6,7
Corresponding author: Joachim R Ehrlich, Department Conversely, re-entrant arrhythmias commonly utilize anatomical pathways, such as the pulmonary
of Cardiology, St Josefs-Hospital, Beethovenstraße 20,
65189 Wiesbaden, Germany. E: [email protected]
veins, the cavo-tricuspid isthmus in the case of atrial flutter or scars induced by surgery, or
previous ablation in regions of the left atrium.8–10 Such substrates carry implications for specific
Support: No funding was received for therapy. For instance, peri-mitral left atrial flutter occurs frequently after radiofrequency ablation
the publication of this article.
for atrial fibrillation (AF).11

Clinical presentation and general treatment options

Most patients with SVT present with a history of rapid heart rhythm. Age at first presentation
gives important clues to the aetiology. Generally, as a rule of thumb, atrial flutter is commonly
seen in older patients (age at onset of palpitations >60 years); while AV re-entrant tachycardia
(AVRT), using an accessory pathway, is a frequent cause of palpitations in younger patients
(<40 years). AV nodal re-entrant tachycardia (AVNRT) or AT can be seen in any age stratum.

The clinical presentation of SVT may range from mild palpitations to significantly reduced quality
of life with (near) syncope or tachycardia-induced cardiomyopathy. Regarding general assessment,

4 Journal Publication Date: 2 August 2021 TOUC H ME D ICA L ME D IA

 Supraventricular Tachycardia Diagnosis and Management

Video 1: Pulsation of the jugular vein (frog sign) during tachycardias: pre-excited AF with rapid conduction over an accessory
tachycardia pathway should not be treated with adenosine.3,12 In this context, still
more rapid ventricular activation over the accessory pathway may ensue
and class-I-anti-arrhythmic drugs – such as procainamide or flecainide
– or the class-III-anti-arrhythmic drug, ibutilide, are preferred.3 However,
since patients with pre-excited AF are frequently haemodynamically
unstable, and the substances mentioned should be used with caution,
electrical cardioversion is the most important tool in the acute treatment
of this specific tachycardia.

Many patients with a longstanding history of arrhythmia find out about

vagal manoeuvres such as the Valsalva manoeuvre (representing the
most common and powerful one), drinking cold water, or sticking a finger
into the throat to activate the gag reflex. Vagal manoeuvres are simple
to perform and are readily at hand. Of note, the recording of a 12-lead
ECG during ongoing tachycardia and concomitant performance of vagal
manoeuvres is of great diagnostic value. Beyond helping importantly
in the differential diagnosis, these manoeuvres are also potentially
therapeutic (e.g. in case of AVNRT).
This video illustrates a ‘frog sign’ in a patient with atrioventricular nodal re-entrant
tachycardia. Pulsation of the internal and external jugular vein at the right side of the
neck can be seen. Key point 3
Vagal manoeuvres should be applied to diagnose or terminate SVT
physical findings are rare except for occasional visible pulsations of while recording a 12-lead ECG.
the jugular veins at the neck during tachycardia (Video 1). Vital signs
are central in order to determine if emergent treatment (electrical
cardioversion) is necessary. Full blood counts and a biochemistry profile, The Valsalva manoeuvre (forced expiration against closed mouth and
including electrolytes and thyroid function, are of value, as specific nose or blowing into a 10 mL syringe to move the plunger while bearing
disturbances may lead to tachycardia. Overall, documentation of the down as if having a bowel movement for about 10–15 seconds) is only
tachycardia in a 12-lead electrocardiogram (ECG) is of prime importance. modestly effective in terminating SVT with a success rate of 5–20%.13
A modified Valsalva manoeuvre with maintaining an oral pressure of
Key point 1 40 mmHg for 15 seconds, followed by a passive leg raise after the
Recording of a 12-lead ECG is crucial during ongoing tachycardia in Valsalva strain increased conversion rates from 17% in the standard
stable patients. treatment arm to 43% in patients in a multicentre study.13

Mechanistically, during the Valsalva manoeuvre, increased intrathoracic

Intermittent and continuous methods of ECG-monitoring, such as pressure results in reduced venous return into the thorax and thus
AliveCor® (Mountain View, CA, USA), smartwatches or implantable loop reduced right ventricular cardiac filling/output. Then, exhalation increases
recorders, have facilitated tachycardia documentation. For this reason, venous return and cardiac output. Subsequently, aortic pressure rises
there is disagreement about whether a suggestive history is enough and activates the parasympathetic cardiac nervous system, slowing the
evidence to refer to electrophysiological study with eventual catheter heart rate and AV conduction by means of baroreflex.14 A similar effect
ablation or not. A baseline ECG in sinus rhythm can further provide hints is achieved by carotid sinus massage, through which the artificially
to tachycardia mechanisms as evidenced by pre-excitation and signs of increased carotid pressure reduces the baroreceptor firing rate.15 Carotid
structural heart disease, and may be useful to help determine P-waves sinus massage should not be performed in individuals with known
in tachycardia. stenosis of the internal carotid artery, in those with previous stroke or
transient ischaemic attack or in patients with a bruit on auscultation over
In general, patients with any form of SVT (narrow or wide-complex) the carotid artery.
should be electrically cardioverted if haemodynamically unstable.3
While preparing for cardioversion, alternative measures (e.g. adenosine If simple vagal manoeuvres do not succeed, a rapidly flushed bolus
application) may be performed. of adenosine (dosed 6–18 mg intravenously, through a large-bore
antecubital cannula) will be the next step. Adenosine will briefly
Key point 2 (~10–20 seconds) interrupt – or at least slow down – AV-nodal
Patients with SVT and haemodynamic instability should be conduction and either terminate SVT or unmask atrial activity
electrically cardioverted. and help to identify P-waves.16 In sinus tachycardia, its application
may lead to a transient slowing of the heart rate. Adenosine
administration is effective in approximately 90% of cases.17
In stable patients, vagal manoeuvres or adenosine are the first Possible reasons for inefficiency of adenosine application in
recommended steps in the management of ongoing SVTs and narrow narrow-complex tachycardia may include inadequate dose, enhanced
(<120 ms QRS duration) or wide (>120 ms QRS duration) complexes.3 adrenergic tone or high-septal ventricular tachycardia (VT).

While this recommendation is valid for any narrow-complex tachycardia, Typically, VTs do not respond to vagal manoeuvres, but retrograde
there is one important exemption to this rule with wide-complex conduction of P-waves may be slowed and thus more readily identified.

E UROPEA N JOU RN A L O F ARRHYT H MIA & E LE CT RO PH YS IO LO G Y 5

Commentary Supraventricular Tachycardia

Figure 1: Systematic approach for patients with tachycardia

Haemodynamically Haemodynamically
stable unstable

12-lead ECG

Narrow QRS Wide QRS Narrow/wide QRS

Diagnosis SVT SVT with BBB AVRT VT Any

Vagal if orthodromic:
manoeuvres Adenosine CSM Adenosine CSM CSM Adenosine CSM

if orthodromic: if antidromic:
Acute
therapy Beta blockers, Beta blockers, Beta blockers, Procainamide, Procainamide,
diltiazem, verapamil diltiazem, verapamil diltiazem, verapamil ibutilide amiodarone

Long-term
therapy

This figure illustrates the general approach to a patient with tachycardia. After initial assessment of haemodynamic stability, emergent cardioversion is performed in case of
instability irrespective of QRS width. Ideally, registration of a 12-lead ECG will occur for documentation and later analysis. In the case of haemodynamic stability, narrow-QRS
tachycardia can be diagnosed/treated with vagal manoeuvres. In the case of wide-complex tachycardia, differential treatment is indicated. In most cases, catheter ablation
represents the long-term therapy of choice. Patients with sustained VT will, in a large proportion, receive an implantable cardioverter/defibrillator
AVRT = atrioventricular re-entrant tachycardia; BBB = bundle branch block; CSM = carotid sinus massage; ECG = electrocardiogram; SVT = supraventricular tachycardia;
VT = ventricular tachycardia.

Table 1: Classification of supraventricular tachycardias

Atrial tachycardias AV junctional tachycardias AV re-entrant tachycardia

Sinus tachycardia (physiological, inappropriate, re-entrant) AV-nodal re-entrant tachycardia Orthodromic/antidromic
(typical/atypical) Permanent junctional reciprocating tachycardia
Focal/multifocal atrial tachycardia Junctional ectopic tachycardia
Cavotricuspid isthmus dependent/non-cavotricuspid isthmus
dependent flutter (left/right atrial)
AV = atrioventricular.

However, some VTs may be sensitive to adenosine (e.g. fascicular outflow resulting in narrow-complex tachycardia, too. A general classification of
tract VT).18 narrow-complex tachycardias is summarized in Table 1.

Chest discomfort, dyspnoea or headache are common side effects of It is important to compare ECGs recorded during tachycardia with sinus
adenosine. Of note, adenosine has a very short half-life; thus, clinical rhythm ECGs (Figure 2). The presence of pre-excitation in a resting ECG
effects wane after a few seconds and side effects are temporary and with sinus rhythm (Figure 2D) is an important clue towards the diagnosis,
reversible. Bronchoconstriction is rarely observed in patients with even in the absence of a documented tachycardia. However, lack of
asthma and the drug is accepted in this context.19 As an alternative in pre-excitation does not rule out AVRT, as it may occur as orthodromic
patients with severe forms of asthma, verapamil may be considered, tachycardia, utilizing a so-called ‘concealed’ pathway with exclusive
but side effects, such as hypotension, may occur and – as the half-life retrograde (ventriculo-atrial) conduction, in which case, ECG features of
is much longer – will eventually need to be handled clinically.3,19 Figure AVRT are not visible (Figure 2D, inset).
1 shows a step-by-step approach to systematic diagnosis, acute and
long-term therapy of common tachycardia forms. Sudden prolongation of the PR interval occurs in typical AVNRT after
an atrial ectopic beat reflecting slow antegrade conduction through
Electrocardiogram interpretation the ‘slow’ AV-nodal pathway, which will initiate SVT (Figure 2C, inset).
Narrow-complex tachycardia An AT may also be triggered by atrial ectopic beats, as may AVRT.
SVT resulting from activation of the ventricles via the His–Purkinje Automatic ATs often present with gradual acceleration and deceleration
system will typically present as a narrow-complex tachycardia. Rarely, (‘warm-up and cool-down’). Premature ventricular beats are common
early activation of the His bundle can also occur in high-septal VT, thus triggers of atypical AVNRT (with a re-entrant pathway in the opposite

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 Supraventricular Tachycardia Diagnosis and Management

Figure 2: Schematic illustration of anatomical substrate of narrow-complex supraventricular tachycardias to exemplary

electrocardiograms during tachycardia and sinus rhythm

A B C D

Anatomic substrate

Orthodromic Antidromic

ECG during tachycadia

ECG during sinus rhythm

This schematic illustrates the anatomic substrate of narrow-complex SVT to exemplary ECGs during tachycardia and in sinus rhythm. A: This panel illustrates an atrial tachycardia
with focus in the left atrium that conducts to the ventricles. B: Atrial flutter. C: An example of typical ‘slow–fast’ AVNRT with rapid retrograde activation of the atria after QRS. The
inset in C illustrates an impulse travelling down the ‘slow’ pathway and retrogradely up to the atria via the ‘fast’ pathway of the AV node. The baseline ECG (bottom row, A–C)
does not help with the diagnosis. D: Baseline ECG shows pre-excitation and thus is helpful in differentiating this SVT from other narrow-complex tachycardias. The inset in D
demonstrates the impulse propagation in case of orthodromic or antidromic tachycardia.
AV = atrioventricular; AVNRT = atrioventricular nodal re-entrant tachycardia; ECG = electrocardiogram; SVT = supraventricular tachycardia.

direction as in typical AVNRT or AVRT), but rarely induce typical RP relationship and P-wave morphology
AVNRT. Termination of a tachycardia should be scrutinized diligently. From an ECG point of view, narrow-QRS tachycardias can be differentiated
If narrow-complex tachycardia terminates with a P-wave after the last into long- and short-RP tachycardias. Short-RP tachycardias are those
QRS, an AT is rather unlikely and AVNRT or AVRT move into the centre with RP intervals shorter than 50% of the tachycardia RR interval,
of differential diagnosis. Conversely, termination with a QRS complex whereas long-RP SVTs display RP greater than RR (Figure 4).
frequently points to AT or atypical AVNRT.
A very short RP interval usually indicates rapid retrograde activation of
The regularity of RR intervals should always be assessed. Irregular the atria as in typical (‘slow–fast’) AVNRT or, less commonly, AT. Precise
tachycardias may represent focal or multifocal AT, AF and atrial RP measurements from surface ECGs are difficult but suggest 90 ms as
flutter with varying AV conduction. Atrial flutter can have fixed AV a cut-off for differentiation between typical AVNRT and atypical AVNRT
conduction and represent a diagnostic challenge if 2:1 conduction or AVRT.21 Rapidly retrogradely conducted P-waves may present as a
is present and flutter waves are masked. In addition, SVT with re- ‘pseudo-R’ in V1 and/or ‘pseudo-S’ wave in the inferior leads, which are
entrant mechanism tends to appear regular but commonly presents absent in the resting ECG (Figure 2C). These findings are more common
with a certain irregularity caused by alternating cycle length.20 In in typical AVNRT rather than in AVRT due to an accessory pathway or AT.1
order to help differentiate these tachycardias by unmasking flutter
or P-waves, vagal manoeuvres and, if not successful, adenosine may Besides the RP relationship, P-wave morphology matters. P-waves similar
be administered. to those in normal sinus rhythm suggest appropriate or inappropriate
sinus nodal tachycardia, sinus nodal re-entrant tachycardia or AT arising
Atrioventricular re-entrant tachycardia close to the sinus node. P-waves that are different from those in sinus
In case of orthodromic tachycardia, P-waves may be buried in rhythm and conducted with a PR interval equal to or longer than the PR
QRS-complexes, or retrograde with a QRS width usually <120 ms due to in sinus rhythm are typically seen in AT. In this case, the morphology of
conduction via the AV-node (unless there is pre-existing bundle branch the P-wave can also provide clues as to the location of the AT focus. For
block [BBB]) and variation in QRS amplitude. Antidromic tachycardia example, positive P-waves in V1 and negative P-waves in lead I indicate
re-presents with wide QRS complexes due to depolarization via the left atrial origin.
accessory pathway. Specific treatment options for orthodromic and
antidromic AVRT are provided in Figure 1. AF with pre-excitation is Wide-complex tachycardia
characterized by ventricular rates between 200 and 300 bpm, possible Wide-complex tachycardias (QRS >120 ms) are frequently more difficult
beat-to-beat variation in QRS width, and RR interval (Figure 3). to analyze. SVT may present as a wide-complex tachycardia due to

E UROPEA N JOU RN A L O F ARRHYT H MIA & E LE CT RO PH YS IO LO G Y 7

Commentary Supraventricular Tachycardia

Figure 3: Electrocardiogram example of pre-excited atrial fibrillation

Heart rate 250 bpm, beat-to-beat variation in QRS width and RR interval.
bpm = beats per minute.

Figure 4: Schematic illustration of RP interval pre-existing or functionally induced BBB, drug-induced conduction
measurement and classification (short/long RP) slowing, antegrade conduction of an accessory pathway or an atrial
sensed ventricular paced rhythm in patients with pacemakers. SVT with
wide-complex also can be induced by drug or electrolyte disturbances.
Among the drugs leading to QRS widening, antiarrhythmic substances
Short RP tachycardia are common.22,23 Functional right BBB (RBBB) during tachycardia occurs
more frequently than functional left BBB (LBBB) because of the longer
R P R
refractoriness of the right bundle branch.24 BBB can occur with any SVT
or with sinus tachycardia.

Differentiation between supraventricular tachycardia

with aberrancy and ventricular tachycardia
Differentiation between SVT with aberrancy and VT may be very challenging,
50% RR
interval
even to the expert eye. An effective solution for electrophysiologists and
non-electrophysiologists lies in the systematic analysis of the traditional
four-step Brugada algorithm.25 Brugada et al. reported a sensitivity and
Long RP tachycardia
specificity of the four consecutive steps of 98.7% and 96.5%, respectively,
for VT diagnosis.25
R P R
In accordance with the Brugada algorithm, VT can be assumed if at least
one of the following four questions is answered positively:
1. Is there an absence of an RS complex in any precordial lead (V1–V6,
are all complexes completely upright or completely downward)?
2. Is the RS interval >100 ms?
50% RR
interval 3. Is AV dissociation present?
AV dissociation is one of the most important ECG criteria for
the diagnosis of VT and is characterized by atrial activity that is

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 Supraventricular Tachycardia Diagnosis and Management

Figure 5: Morphology criteria for supraventricular tachycardia/ventricular tachycardia in precordial leads V1 and V6

Leads RBBB LBBB

SVT VT SVT VT

Triphasic: Mono-/biphasic: • QS/rS with r <40 ms • R ≥40 ms (A)

rSR’, rsR’, rR’ R, qR, Rr’ (rabbit ear) • S-downstroke <70 ms • notching in S-downstroke (B)
V1/(2) • Onset QRS to s-nadir
R’ r ≥70 ms (C)
R’
R R R
r
r B
s r’
A
s q QS S C

Triphasic: Mono-/biphasic: Absence of q-wave QR, QS

qRs, R/S > 1 R, QS or QR, R/S < 1
R
R
R R R’
(no q, s, r’)
V6 s
R/S > 1 R R Q

q R/S < 1
s

Q
S

This schematic illustrates the morphological criteria in V1 and V6 used in the Brugada algorithm25 and EHRA consensus guidelines1 to differentiate between SVT with aberrancy and VT.
EHRA = European Heart Rhythm Association; LBBB = left bundle branch block; RBBB = right bundle branch block; SVT = supraventricular tachycardia; VT = ventricular
tachycardia.

independent of ventricular activity. Once properly identified, it QRS duration and QRS axis during tachycardia
strongly suggests the presence of VT (some rare exceptions may VT is more likely in wide-complex tachycardia with QRS duration
include sinus tachycardia with dual AV conduction or AVNRT). The >140 ms with RBBB or >160 ms with LBBB pattern. Also, QRS axis may
relation between atrial and ventricular events is 1:1 or greater help with diagnosis. In patients with SVT with aberration pattern, the
(more P-waves than QRS complexes) in most cases of SVT. Although QRS axis is frequently confined between -60 degrees and +120 degrees
ventriculo–atrial conduction can be found in up to 50% of patients (Figure 7). Therefore, wide-QRS tachycardias with a QRS axis outside
with VT and a 1:1 relation is possible, most VTs have a relation this range are likely to be VT. In particular, extreme axis deviation to
<1:1 (more QRS complexes than P-waves). Recognition of AV -90 degrees to +180 degrees (‘north-west’ axis or ‘no-man’s-land’ in the
dissociation may be difficult as P-waves are often hidden by circle of Cabrera) strongly suggests VT both in the presence of RBBB and
wide-complex and T-waves during a wide-QRS tachycardia. LBBB patterns.27 Thus, predominantly negative QRS complexes in leads I,
P-waves are usually best recognized in inferior and precordial II and III (representing this extreme axis deviation) are a useful criterion
chest leads.26 for identifying VT.
4. Are the morphology criteria for VT present both in precordial leads V1
and V6 (Figure 5)?1,25 Key point 4
In wide-complex tachycardia AV dissociation, fusion or capture beats,
An example of SVT with aberrancy (LBBB morphology), in which the or abnormal QRS ‘north-west’ axis is suggestive of VT.
application of the Brugada algorithm allows differentiation from VT,
is shown in Figure 6. Further points, which serve to diagnose VT in
particular, are the presence of fusion or capture beats, and the analysis The differential diagnosis of wide-complex QRS tachycardia on
of QRS duration and the QRS axis. 12-lead ECGs may be very challenging. The discussion of more detailed
morphological criteria and various applicable algorithms is beyond
Fusion and capture beats the scope of this paper. Acute management includes analyses of
Occasionally, in particular in VT with rates ~100–120 bpm, sporadic sinus haemodynamic stability and indication for electrical cardioversion. In the
beats that are conducted to the ventricles are identified and change the absence of an established diagnosis despite careful evaluation, patients
appearance of QRS complexes. During repetitive ventricular activation presenting wide-complex tachycardia should be treated for VT.1
in VT there are minor excitable gaps within the activation that can be
captured or fused (hence its name) by individual sinus rhythm beats. The Indication for ablation or medical treatment
appearance of these beats will represent features of both morphology of In general, catheter ablation is an efficient cure for the majority of
the VT and the underlying sinus rhythm (Figure 7). arrhythmias at a very low risk of complications. This is especially true for

E UROPEA N JOU RN A L O F ARRHYT H MIA & E LE CT RO PH YS IO LO G Y 9

Commentary Supraventricular Tachycardia

Figure 6: Electrocardiogram example of supraventricular tachycardia with aberrancy (left bundle branch block
morphology)

Note absence of RS complex in V6, RS interval <100 ms, lack of AV dissociation, typical morphological criteria in V1 and V6 and normal QRS axis.
AV = atrioventricular.

Figure 7: Electrocardiogram example of a patient during ventricular tachycardia and sinus rhythm

A. B.

This figure illustrates 12-lead ECGs from the same patient with ischaemic cardiomyopathy. A: Recorded during sustained VT (HR ~120 bpm). B: Recorded during normal sinus
rhythm (HR ~60 bpm). There are several VT diagnostic features in A readily visible. There is AV dissociation. Fewer P-waves than QRS complexes can be identified (* in V1). Two
fusions beats can be recognized (arrows). These have strikingly different QRS axis in the frontal plane (similar to that in B). The QRS axis of VT complexes points to ‘north-west’ in
A, and left axis deviation in sinus rhythm in B. Finally, QRS of fusion beats (arrow) are narrower than other QRS complexes. The VT QRS complexes have a duration >140 ms with
RBBB, and thus are suggestive of VT.
AV = atrioventricular; bpm = beats per minute; ECG = electrocardiogram; HR = heart rate; RBBB = right bundle branch block; VT = ventricular tachycardia.

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 Supraventricular Tachycardia Diagnosis and Management

AVNRT and AVRT. Catheter ablation is more effective than medication, AV-nodal conduction and thus may be a useful option for patients
and quality of life in treated patients is increased to a greater extent;28,29 with SVT leading to a 2:1 conduction. In the case of uncertainty, any
therefore, it is preferred over medical therapy in the majority of cases.3 wide-complex tachycardia should be treated as VT, meaning that no
However, since catheter ablation does not always represent the only verapamil should be applied. If this drug is given to patients with VT
therapy option, patients who are potential candidates for ablation should misdiagnosed as SVT, it can have deleterious effects.30
be referred to an electrophysiologist in order to determine the necessity
for, and interindividual benefits of, ablation. Pregnant patients in the first trimester and patients with inappropriate
sinus tachycardia, postural orthostatic tachycardia syndrome and
Class I indications for ablation include recurrent focal AT (IB), symptomatic multifocal AT represent exceptions to this common approach.1
recurrent cavotricuspid isthmus dependent flutter (IA) and non-cavotricuspid Anti-arrhythmic drugs should be avoided during the first trimester of
isthmus-dependent flutter (IB), symptomatic recurrent AVNRT (IB), pregnancy. Thereafter, typically beta blockers or flecainide can be used.
symptomatic recurrent AVRT (IB) and tachycardia-induced cardiomyopathy Radiation-free ablation using 3D navigation systems is recommended in
due to SVT (IB). In this context, AV nodal ablation with subsequent pacing experienced centres.31
(biventricular or His-bundle pacing) is recommended if the SVT responsible
for tachycardia-induced cardiomyopathy cannot be ablated or controlled by Key point 5
antiarrhythmic drugs (IC).3 In general, catheter ablation is recommended and preferred over
medical therapy for treatment of SVT.
Asymptomatic patients with pre-excitation should always be referred to
an experienced electrophysiological centre for evaluation of high-risk
properties and indications for catheter ablation.3 Summary
Many patients can be helped with the adequate diagnosis and
Differential pharmacological management of SVTs comprises substances treatment of arrhythmias, and the management of patients with SVT
such as verapamil, class I (ajmaline, procainamide, flecainide) or class is an important field of involvement for any physician, in particular
III (amiodarone, ibutilide) antiarrhythmic drugs.3 Verapamil slows non-electrophysiologists. q

1. Katritsis DG, Boriani G, Cosio FG, et al. European Heart Rhythm 10. Stevenson IH, Kistler PM, Spence SJ, et al. Scar-related right 21. Letsas KP, Weber R, Siklody CH, et al. Electrocardiographic
Association (EHRA) consensus document on the management atrial macroreentrant tachycardia in patients without prior differentiation of common type atrioventricular nodal reentrant
of supraventricular arrhythmias, endorsed by Heart Rhythm atrial surgery: electroanatomic characterization and ablation tachycardia from atrioventricular reciprocating tachycardia
Society (HRS), Asia-Pacific Heart Rhythm Society (APHRS), outcome. Heart Rhythm. 2005;2:594–601. via a concealed accessory pathway. Acta Cardiol.
and Sociedad Latinoamericana de Estimulacion Cardiaca y 11. Chae S, Oral H, Good E, et al. Atrial tachycardia after 2010;65:171–6.
Electrofisiologia (SOLAECE). Europace. 2017;19:465–511. circumferential pulmonary vein ablation of atrial fibrillation: 22. Crijns HJ, Kingma JH, Gosselink AT, et al. Sequential bilateral
2. Orejarena LA, Vidaillet H Jr., DeStefano F, et al. Paroxysmal mechanistic insights, results of catheter ablation, and risk bundle branch block during dofetilide, a new class III
supraventricular tachycardia in the general population. factors for recurrence. J Am Coll Cardiol. 2007;50:1781–7. antiarrhythmic agent, in a patient with atrial fibrillation.
J Am Coll Cardiol. 1998;31:150–7. 12. Gupta AK, Shah CP, Maheshwari A, et al. Adenosine induced J Cardiovasc Electrophysiol. 1993;4:459–66.
3. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines ventricular fibrillation in Wolff-Parkinson-White syndrome. 23. Crijns HJ, van Gelder IC, Lie KI. Supraventricular tachycardia
for the management of patients with supraventricular Pacing Clin Electrophysiol. 2002;25(4):477–80. mimicking ventricular tachycardia during flecainide treatment.
tachycardia. The Task Force for the Management of Patients 13. Appelboam A, Reuben A, Mann C, et al. Postural modification Am J Cardiol. 1988;62:1303–6.
with Supraventricular Tachycardia of the European Society of to the standard Valsalva manoeuvre for emergency treatment 24. Chilson DA, Zipes DP, Heger JJ, et al. Functional bundle branch
Cardiology (ESC). Eur Heart J. 2020;41:655–720. of supraventricular tachycardias (REVERT): a randomised block: discordant response of right and left bundle branches to
4. Antzelevitch C, Burashnikov A. Overview of basic controlled trial. Lancet. 2015;386:1747–53. changes in heart rate. Am J Cardiol. 1984;54:313–6.
mechanisms of cardiac arrhythmia. Card Electrophysiol Clin. 14. Mancia G, Bonazzi O, Pozzoni L, et al. Baroreceptor control of 25. Brugada P, Brugada J, Mont L, et al. A new approach to the
2011;3:23–45. atrioventricular conduction in man. Circ Res. 1979;44:752–8. differential diagnosis of a regular tachycardia with a wide QRS
5. Gomes JA, Hariman RJ, Kang PS, Chowdry IH. Sustained 15. Wehrwein EA, Joyner MJ. Regulation of blood pressure by the complex. Circulation. 1991;83:1649–59.
symptomatic sinus node reentrant tachycardia: incidence, arterial baroreflex and autonomic nervous system. 26. Alzand BS, Crijns HJ. Diagnostic criteria of broad QRS complex
clinical significance, electrophysiologic observations and Handb Clin Neurol. 2013;117:89–102. tachycardia: decades of evolution. Europace. 2011;13:465–72.
the effects of antiarrhythmic agents. J Am Coll Cardiol. 16. Belardinelli L, Linden J, Berne RM. The cardiac effects of 27. Wellens HJ, Bar FW, Lie KI. The value of the electrocardiogram in
1985;5:45–57. adenosine. Prog Cardiovasc Dis. 1989;32:73–97. the differential diagnosis of a tachycardia with a widened QRS
6. Kalman JM, Olgin JE, Karch MR, et al. “Cristal tachycardias”: 17. DiMarco JP, Miles W, Akhtar M, et al. Adenosine for paroxysmal complex. Am J Med. 1978;64:27–33.
origin of right atrial tachycardias from the crista terminalis supraventricular tachycardia: dose ranging and comparison 28. Katritsis DG, Josephson ME. Classification, electrophysiological
identified by intracardiac echocardiography. J Am Coll Cardiol. with verapamil. Assessment in placebo-controlled, multicenter features and therapy of atrioventricular nodal reentrant
1998;31:451–9. trials. The Adenosine for PSVT Study Group. Ann Intern Med. tachycardia. Arrhythm Electrophysiol Rev. 2016;5:130–5.
7. Kistler PM, Fynn SP, Haqqani H, et al. Focal atrial tachycardia 1990;113:104–10. 29. Brachmann J, Lewalter T, Kuck KH, et al. Long-term symptom
from the ostium of the coronary sinus: electrocardiographic 18. Lerman BB, Stein KM, Markowitz SM. Adenosine-sensitive improvement and patient satisfaction following catheter
and electrophysiological characterization and radiofrequency ventricular tachycardia: a conceptual approach. J Cardiovasc ablation of supraventricular tachycardia: insights from the
ablation. J Am Coll Cardiol. 2005;45:1488–93. Electrophysiol. 1996;7:559–69. German ablation registry. Eur Heart J. 2017;38:1317–26.
8. Yang Y, Varma N, Keung EC, Scheinman MM. Reentry within 19. Burki NK, Alam M, Lee LY. The pulmonary effects of intravenous 30. Stewart RB, Bardy GH, Greene HL. Wide complex tachycardia:
the cavotricuspid isthmus: an isthmus dependent circuit. adenosine in asthmatic subjects. Respir Res. 2006;7:139. misdiagnosis and outcome after emergent therapy.
Pacing Clin Electrophysiol. 2005;28:808–18. 20. Jais P, Matsuo S, Knecht S, et al. A deductive mapping strategy Ann Intern Med. 1986;104:766–71.
9. Po SS, Li Y, Tang D, et al. Rapid and stable re-entry within the for atrial tachycardia following atrial fibrillation ablation: 31. Razminia M, Willoughby MC, Demo H, et al. Fluoroless catheter
pulmonary vein as a mechanism initiating paroxysmal atrial importance of localized reentry. J Cardiovasc Electrophysiol. ablation of cardiac arrhythmias: a 5-year experience.
fibrillation. J Am Coll Cardiol. 2005;45:1871–7. 2009;20:480–91. Pacing Clin Electrophysiol. 2017;40:425–33.

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