REVIEW

Supraventricular Arrhythmias: Clinical

Framework and Common Scenarios for
the Internist
Christopher V. DeSimone, MD, PhD; Niyada Naksuk, MD;
and Samuel J. Asirvatham, MD

Abstract

Supraventricular arrhythmias can cause uncomfortable symptoms for patients. Often, the first point of
contact is in the primary care setting, and thus, it is imperative for the general internist to have a clinical
framework in place to recognize this cluster of cardiac arrhythmias, be familiar with immediate and long-
term management of supraventricular tachycardias, and understand when cardiac electrophysiologic
consultation is necessary. The electrocardiographic characteristics can have subtle but important clues to
the diagnosis and initial management. An understanding of the mechanisms of these arrhythmias is
essential to provide proper therapy to the patient. In addition, there are common practice strategies that
should be emphasized to avoid common misperceptions that could pose risk to the patient. In this review,
we provide a framework to more easily recognize and classify these arrhythmias. We also illustrate the
mechanism for these arrhythmias to provide an understanding of the interventions generally used.
ª 2018 Mayo Foundation for Medical Education and Research n Mayo Clin Proc. 2018;nn(n):1-17

flutter. In addition, irregular, narrow complex

S
upraventricular tachycardia (SVT) is an
encompassing term referring to fast
heart rhythms that involve cardiac tissue
above (supra) the ventricles.1 A ventricular
rate that exceeds 100 beats/min along with a
narrow QRS complex (QRS width, <120 ms)
is, in broad strokes, the general way SVTs
are identified. Less commonly, a wide QRS
complex (QRS width,
120 ms) can also
result from an SVT; the increased QRS width
is due to concomitant aberrancy of the normal
conduction system, such as that associated
with bundle branch block. Alternatively,
SVTs with a wide QRS complex can involve
supraventricular tissue with conduction to
the ventricle via abnormal myocardial fibers,
such as in the case of an accessory pathway
connection.2
Supraventricular tachycardias are classi-
cally clustered as regular, narrow complex
tachycardias that include atrioventricular
nodal reentrant tachycardia (AVNRT), atrio-
ventricular reentrant tachycardia (AVRT), and
atrial tachycardia (AT)3,4 (Figure 1). As SVTs
include rhythms with origin above the
ventricle, regular, narrow complex tachycar-
dias also include sinus tachycardia and atrial
tachycardias (Figure 2) can be seen and classi-
fied as SVTs. This includes atrial fibrillation From the Department of
(AF), multifocal AT, and atrial flutter with Cardiovascular Diseases
(C.V.D., N.N., S.J.A.) and
variable block. Department of Pediatrics
In this review, we discuss each of these and Adolescent Medicine
(S.J.A.), Mayo Clinic,
rhythms independently to focus on the patho- Rochester, MN.
physiologic basis and mechanism of each
arrhythmia (section I). In section II, we provide
a classification schema for these arrhythmias
and focus on electrocardiographic (ECG) clues
and recommend an approach to recognize these
rhythms. In section III, we provide a simplified
approach to clinical management and inter-
weave clinical pearls into the discussion. In sec-
tion IV we discuss the management of SVTs.
SECTION I: PATHOPHYSIOLOGIC BASIS OF
SVTS
Atrioventricular Nodal Reentrant
Tachycardia
Atrioventricular nodal reentrant tachycardia is
the most common of the classical SVTs in the
general population,5 and its frequency is likely
rooted in the origins and anatomical basis of
the tachycardia circuit. For example, it is likely

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ARTICLE HIGHLIGHTS
d The internist requires a fundamental knowledge of the mecha-
nisms and management of these arrhythmias.
d The electrocardiographic characteristics can have subtle but
important clues to the diagnosis and initial management.
d Patient management may require rate or rhythm control,
electrical cardioversion, or even catheter ablation.
d Understanding downstream therapies helps the internist pro-
vide initial counseling to the patient and recognize when to refer
to cardiac electrophysiology.
that many patients are born with 2 atrial
myocardial inputs into the atrioventricular
(AV) node, which have been termed as path-
ways to the AV node: (1) a slow pathway and
(2) a fast pathway6 (Figure 3). Because these
pathways set up at least 2 means into and
out of the AV node, a reentry circuit can occur
under certain conditions. During sinus
rhythm, conduction from the atria to the AV
node travels down both the fast and slow
pathways. However, the fast pathway conduc-
tion continues to the AV node and further
down the conduction system and it also con-
ducts in a retrograde manner into the slow
pathway to extinguish its conduction; this is
termed concealed (as it is not manifested on
ECG) penetration into the slow pathway.7
Atrioventricular nodal reentrant tachy-
cardia occurs under certain conditions, which
create the setup for a reentrant circuit8
(Figure 4). For example, a premature atrial
contraction can create an electrical wavefront
that can travel antegrade down the slow
pathway while the fast pathway is still refractory
(unable to conduct) to electrical stimuli from
the previous sinus impulse.9 Retrograde con-
duction to atrial tissue can occur if the fast
pathway has recovered from refractoriness and
thus allows electrical activation back toward
the atrium. The atrial activation wavefront can
again conduct antegrade back down the slow
pathway and thus create a reentrant loop for
tachycardia to sustain10,11 (Figure 4).
Atrioventricular Reentrant Tachycardia
Atrioventricular reentrant tachycardia is
dependent on the presence of an electrical
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MAYO CLINIC PROCEEDINGS
connection between the atrium to the ventricle
in addition to that of the normal conduction
system and AV node (which serves to slow
conduction from the atrium to the ventricle).12
This is a connection of the atrium to the
ventricle via muscle fibers and is termed an
accessory pathway. These muscle fibers are
located across the valvular annuli and can
occur at several locations. This connection by-
passes the normal conduction system (and is
thus sometimes referred to as a bypass tract),
and most importantly the AV node. These
muscle fibers can conduct electrical activity
in an antegrade manner from the atrium to
the ventricle, or in a retrograde manner from
the ventricle to the atrium, and some can
conduct in both directions.13
Tachycardias related to an accessory
pathway can occur from a reentrant circuit us-
ing the normal AV conduction system as one
limb and an accessory pathway as the other
limb of the circuit.8,11 If the electrical wave-
front travels down the AV node to reach the
ventricle and returns to the atria via an acces-
sory pathway connection, the tachycardia is
termed orthodromic reentrant tachycardia
(ORT) (Figure 3). If the antegrade limb is
down the accessory pathway to reach the
ventricle and returns to the atrium in a retro-
grade fashion from the conduction system,
the tachycardia is termed antidromic reentrant
tachycardia (ART) (Figure 3). Of note, ART,
which bypasses the AV node (normal conduc-
tion system) to reach the ventricle, causes a
wide QRS complex tachycardia. Alternatively,
ORT engages the conduction tissue to reach
the ventricle, and then returns to the atrium
via the pathway, and thus presents on the
ECG as a narrow complex tachycardia. In
practice, ORT is much more common than
ART.11
Atrial Tachycardia
Although AT may at times be a nonspecific
term, it is generally used to refer to focal spon-
taneous depolarization of the atria at a site not
at the sinus node14,15 (Figure 3). Focal AT can
be caused by stressors to the body, which
heightens autonomic tone and thus firing of
a specific collection of cells/tissue located in
the atria.14 Alternatively, these can originate
from abnormal cells that can automatically
fire, similar to the normal pacemaker cells
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SUPRAVENTRICULAR ARRHYTHMIAS FOR THE INTERNIST

Regular, narrow complex tachycardia

(QRS width <120 ms, HR >100 beats/min)

Long RP interval Short RP interval

RP interval
V1
I RP interval

Sinus tachycardia AVNRT

Sinus P-wave morphology
(positive P waves in leads II, III,
and aVF; biphasic P wave with
terminal negative deflection in
lead V1)
Focal atrial tachycardia
Non-sinus P-wave morphology
Pseudo-R' in leads V1 or pseudo-S' in
leads II, II, and aVF
ORT
Possible retrograde P waves (negative P
waves in leads II, III, and aVF)

FIGURE 1. Supraventricular tachycardias (SVTs) with regular, narrow QRS complexes. SVTs with suc-
cessive QRS complexes that are regular and have a narrow QRS width (<120 ms) with a heart rate (HR)
greater than 100 beats/min are further subclassified on the basis of the RP interval. The RP interval
represents the time from ventricular activation (R from the QRS complex) to atrial activation (P wave).
The long RP tachycardias (including sinus tachycardia and focal atrial tachycardia) are separated from SVTs,
which have a short RP interval (atrioventricular nodal reentrant tachycardia [AVNRT] and orthodromic
reciprocating tachycardia [ORT]). Note that SVTs with short RP intervals involve the atrioventricular node
as part of the tachycardia circuits and thus provide an initial insight into tachycardia mechanisms. Sinus
tachycardia has a P wave morphology reflective of the site of the sinus node, with the P wave being
positive in leads II, III, and aVF and biphasic in lead V1 with a terminal negative deflection. Focal atrial
tachycardias have P waves that can be subtly or vastly different from those of the sinus node, depending
on the site of origin. Close inspection reveals that AVNRT can sometimes have a “pseudo-R0 ” wave in
lead V1 and a “pseudo-S0 ” wave in leads II, III, and aVF. In ORT, clues may include negative P waves in leads
II, III, and aVF, which represent retrograde activation of the atria from the ventricle.

located in the sinus node.14 The origin of this
arrhythmia can technically be anywhere above
the ventricle, but common locations include
the crista terminalis, coronary sinus, pulmo-
nary veins, tricuspid or mitral annulus, or
atrial septum.16
It is important to differentiate AT from si-
nus tachycardia, which is a normal physiologic
response1 and treatment is aimed at correcting
the underlying cause (anemia, fever, infection,
hyperthyroidism, hypoxia, etc).17 The origin
of sinus tachycardia is at the sinus node,
located in the superior posterolateral aspect
of the right atrium.
Multifocal AT
Multifocal AT is usually seen in patients with
chronic lung conditions such as chronic
obstructive pulmonary disease as a result of
right atrial enlargement, hypercapnia,
decreased oxygen, or, in other cases, drugs
used to treat lung diseases, such as inhaled
b-agonists, that cause cellular firing at multiple
sites of the atrium.18 Digoxin toxicity can also
produce multifocal AT, specifically with AV
block. It is because of these multiple areas of
the atrium firing that the criterion for this
arrhythmia is met by giving 3 or more
P wave morphologies on the ECG or telemetry
monitoring strip.1
Atrial Flutter
Atrial flutter is a reentrant circuit that occurs
because of a region of tissue with slowed
conduction by either anatomical constraints
or tissue characteristics of regions of slowed

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 MAYO CLINIC PROCEEDINGS

include this CTI region for its circuit is called

Irregular, narrow complex tachycardia a noneCTI-dependent flutter and is termed
(QRS width <120 ms, HR >100 beats/min) atypical flutter. This delineation is extremely
important to recognize because of the implica-
tions for catheter ablation (discussed below).
Absent P waves P waves present
Atrial Fibrillation
Atrial fibrillation Atrial fibrillation is the most common
arrhythmia and is characterized by an irregu-
≥3 P-wave
II aVL
Sawtooth P waves
morphologies
larly irregular rhythm. Atrial fibrillation can
III aVF lead to progressive atrial remodeling, atrial
II CTI-dependent flutter Multifocal atrial cardiomyopathy, and persistent AF. This has
Absence of a distinct P-wave with variable block tachycardia led to the concept of AF begets further AF.
inscription on the ECG
III aVF
II
There are multiple hypotheses and layers of
V1
complexities as to the cause and natural
II

V6
progression of AF.3,22,23 We refer the reader
VI

Negative P waves in inferior

At least three different ≥3 P-wave
morphologies on the ECG
leads (II, III, and aVF) and
positive P wave in lead V1
FIGURE 2. Supraventricular tachycardias (SVTs) with irregular, narrow QRS
complexes. SVTs with successive QRS complexes that are irregular but with
a narrow QRS width (<120 ms) are separated from the regular, narrow
complex tachycardias. Further subclassification involves identifying the
presence and morphology of P waves. The absence of a distinct P wave
with intervening isoelectric intervals is reflective of chaotic activation of the
atrium underlying atrial fibrillation. The presence of continuous activity
above or below the isoelectric line is characteristic of a reentry circuit
reflective of continuous atrial flutter activation. Note that the characteristic
flutter waves in cavotricuspid isthmus (CTI)edependent flutter are negative
in leads II, III, and aVF and positive in lead V1. Note that in multifocal atrial
tachycardia, there are at least 3 P wave morphologies. These are reflective
of atrial activation origination at multiple sites in the atria. ECG ¼ elec-
trocardiogram; HR ¼ heart rate.
conduction velocity. It is because of one or a
combination of these that a reentrant circuit
can form and continue to propagate
throughout the atria with 1:1 or variable con-
duction to the ventricle. This type of SVT is
divided into 2 types: (1) Typical flutter, which
is dependent on the myocardial fibers that
exist at a location in the right atrium between
the inferior vena cava and the tricuspid valve
called the cavotricuspid isthmus (CTI).1,19 It is
because of the constraint of this muscle lying
in between 2 electrically inert structures (infe-
rior vena cava and tricuspid valve annulus)
that this tachycardia can easily occur.20 It is
also the reason for the high chance of success-
ful ablation of this arrhythmia at this
location.21 (2) Atrial flutter that does not
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4 Mayo Clin Proc.
to several excellent reviews, including a recent
publication in Mayo Clinic Proceedings by
Morin et al for a more in-depth discussion in
this topical area.22,24,25 Generally, patients
who initially present with paroxysms of AF
are thought to have inciting triggers for AF
from ectopic firing from the muscle sleeves
that reside in the pulmonary veins. The rapid
firing that occurs from the pulmonary vein
muscle and enters the atria can lead to
fibrillation.26
SECTION II: CLASSIFICATION SCHEME OF
SVTS BASED ON ECG CHARACTERISTICS
Particular attention to key ECG characteristics
during the tachycardia on the 12-lead ECG,
ECG Holter strip, or telemetry monitoring
strip may permit differentiation of SVT and
thus aid in clinical management. This under-
scores the importance of recording the tachy-
cardia, especially while the patient is having
symptoms.
We recommend that the clinicians first focus
on key aspects of the ECG such as (1) narrow vs
wide QRS complex, (2) regular vs irregular SVTs,
(3) relationship between P waves and QRS com-
plexes (atrial and ventricular depolarization),
and (4) morphology of the P wave on the
12-lead ECG.
Narrow vs Wide QRS Complex
When reviewing a tachycardia on the ECG, the
initial step is to classify it into a narrow or
wide complex tachycardia. This is done by
measuring the width of the QRS complex;
these complexes are defined as narrow if the
QRS width is less than 120 milliseconds and
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SUPRAVENTRICULAR ARRHYTHMIAS FOR THE INTERNIST

FIGURE 3. Classical supraventricular arrhythmias and mechanisms. Top left panel, Critical components of the atrioventricular nodal
reentrant tachycardia (AVNRT) circuit. A right atrial oblique view of the heart is shown to illustrate the atria, conduction system,
ventricle, and highlights of the AVNRT circuit. Note that there are 2 inputs into the atrioventricular (AV) node: the slow pathway and
fast pathway inputs. Electrical activation occurs antegrade into the AV node and retrograde from the AV node back to the atrium as
part of the reentry circuit. Electrical activity continues down the normal conduction system to the ventricle. Top right panel, Focal
atrial tachycardia arising in the right atrium with focal origination of activation (yellow waves). This serves as the atrial impulse, which
then conducts to the rest of the atria and down to the ventricles. This is different from the sinus node, which would be higher and
more posterior in the right atrium. The P wave in this location would exhibit a less positive P wave in leads II, III, and aVF. This is
because the focus of activation is lower in the right atrium than in the sinus node. Because the focus favors the right atrium, the P wave
duration would be almost the same. Bottom panel, Accessory pathwayemediated tachycardias. In orthodromic reciprocating
tachycardia (ORT) and antidromic reciprocating tachycardia (ART), the circuit includes an accessory pathway, which is comprised of
muscle fibers that connect the atrium to the ventricle across the valvular annuli. In ORT, the circuit travels from the atria down
through the normal conduction system down to the ventricle. The electrical activity travels from the ventricle across the accessory
fibers to bypass the AV node and reach the atria. The QRS complex is therefore narrow in this tachycardia as it uses the normal
conduction system to activate the ventricle. In ART, the circuit travels from the atria and bypasses the normal conduction system via
the accessory pathway and activates the ventricular muscle directly and this myocardial cell-to-myocardial cell connection is slower
than the normal conduction system and creates a wide QRS complex (as it takes longer to activate) on the electrocardiogram. Note
that both these tachycardias involve the AV node and also require an atrioventricular connection via muscle fibers at the annulus.

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wide if the QRS width is 120 milliseconds or
more.
It should be noted that wide complex
tachycardias can include all the SVTs if there
is concomitant aberrant ventricular conduc-
tion such as in intermittent or permanent
bundle branch block (which makes the QRS
complex wide) or antidromic conduction
down an accessory pathway (ART). Impor-
tantly, wide complex tachycardias should alert
the clinician to consider ventricular tachy-
cardia, artifact, or a paced rhythm.27
Regular vs Irregular SVTs
Once the clinician has filtered down the
possible tachycardia from the ECG by triaging
narrow vs wide QRS complex, the next step in
characterization involves the regularity or
irregularity of successive QRS complexes.
The differential diagnosis of regular, narrow
complex tachycardias includes sinus tachy-
cardia, atrial flutter, AVNRT, AVRT (ORT),
and focal AT1 (Figure 1). Irregular, narrow
complex tachycardias include AF and multi-
focal AT (Figure 2). Atrial flutter can present
as a regular, narrow complex tachycardia,
but can be irregular because of variable AV
conduction block.
Relationship Between P Waves and QRS
Complexes
The ECG should next be scrutinized for the
presence of P waves and their correlation
with QRS complexes. A reasonable classifica-
tion strategy is to define the SVT as a short
RP tachycardia (short duration between the
P wave and the QRS complex) or a long
RP tachycardia (long duration between the
P wave and the QRS complex)28 (Figure 1).
The RP interval reflects the difference in time
between activation of the ventricle and activa-
tion of the atrium. A short RP tachycardia has
an RP interval that is shorter than the PR inter-
val, and correspondingly, a long RP tachy-
cardia has an RP interval that is longer than
the PR interval. In general, AVNRT and
AVRT are short RP tachycardias.29,30 In
AVNRT, the RP interval can be short or even
negative because there is near-simultaneous
activation of the atria and ventricles from a
common point near the AV node.28 In addi-
tion, AT with first-degree AV block can
present as a short RP tachycardia. This is
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MAYO CLINIC PROCEEDINGS
because of prolongation in the PR interval,
and thus the subsequent P wave is closer to
the QRS complex because of the delay.
Although short, the RP interval in ortho-
dromic AVRT (Figure 1) is almost never less
than 90 milliseconds because of the necessary
time it takes for electrical activation to occur in
series from the ventricular tissue to the acces-
sory pathway and from the accessory pathway
to the atrium.29,30
Atrial tachycardias or sinus tachycardias
are classified as long RP tachycardias. This oc-
curs because of the short PR interval associated
with these rhythms (Figure 1).
SECTION III: ECG CLUES TO AID IN
DIAGNOSING SUPRAVENTRICULAR
ARRHYTHMIAS
The characteristics of SVT based on different
mechanisms are summarized in Figures 1
and 2. Electrocardiographic findings are based
on narrow vs wide QRS complexes, regularity
of successive QRS complexes, relationship be-
tween RP intervals (short vs long), and the
morphology of the P wave.
Atrioventricular Nodal Reentrant
Tachycardia
Typical AVNRT has nearly simultaneous or
superimposed P waves and QRS complexes.
This produces a relatively short PR interval,
pseudo-R0 wave in lead V1, or pseudo-S0
wave in the inferior leads (leads II, III, and
aVF)30 (Figure 5). The reason for P waves
and QRS complexes occurring so close
together is the parallel activation of the atria
and ventricles from the AVNRT circuit.
Accessory PathwayeRelated Tachycardias
(ORT and ART)
Accessory pathways with antegrade conduc-
tion to the ventricle (or ART) can manifest as
a delta wave in the early portion of the QRS
complex31 (Figure 6). This occurs because of
early activation of the ventricle via an acces-
sory pathway. The depolarization of the
ventricle occurs in a myocardial cell-to-
myocardial cell conduction manner rather
than via the specialized conduction system
(which itself produces a narrow QRS
complex).
The presence of an accessory pathway on the
surface ECG is called a Wolff-Parkinson-White
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FIGURE 4. Slow and fast pathways (SP and FP) during sinus rhythm, premature atrial contraction, and atrioventricular nodal reentrant
tachycardia (AVNRT). Top left panel, In sinus rhythm, conduction travels antegrade down both the SP (red dotted) and the FP (blue
dotted). The FP continues down the normal conduction system to the ventricles and also conducts retrograde back up the SP to
block further conduction. This is manifested on the electrocardiogram (ECG) as a normal PR interval (bottom left panel). Top middle
panel, When a premature atrial contraction (PAC) occurs (green star), it is able to conduct down toward the FP (blue dotted) and SP
(green dotted). However, it is not able to conduct via the FP, as it is refractory to further electrical stimulation. This allows conduction
to continue from the SP (green dotted) down to the ventricles. This is manifested on the ECG as a long PR interval (bottom right
panel) compared to sinus rhythm, as the PR interval reflects SP conduction from the atria to the ventricle. Top right panel, Because the
PAC conducts down the SP but not the FP, there is unidirectional block and thus a setup for a reentrant circuit (green arrows).
However, retrograde conduction back to the atrial tissue can occur via the FP once it recovers from refractoriness. Electrical activity
can then continue as a reentrant arrhythmia via both the SP and the FP as limbs of the AVNRT circuit. This is noted as a short RP
interval with almost simultaneous P waves and QRS complexes inscribed on the ECG (bottom right panel).

pattern.32 If a patient has both an ECG pattern
and a tachycardia, the diagnosis is Wolff-
Parkinson-White syndrome. Antidromic recip-
rocating tachycardia results in a regular
tachycardia with a wide QRS complex on the
surface ECG because conduction is via ventricu-
lar myocardial tissue and not through conduc-
tion system tissue.
Evidence of accessory pathways may be
concealed from inscription on the ECG, and
the QRS complex may appear to be of normal
width and the delta wave may be absent.33
However, a tachycardia circuit called ORT
can still occur via an accessory pathway. This
can occur when the activation of the conduc-
tion system to the ventricles occurs in an
antegrade fashion and returns to the atria via
an accessory pathway. In ORT, the RP interval
is at least 90 milliseconds because of the
necessary time it takes for the impulse to

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FIGURE 5. Electrocardiographic (ECG) clues suggestive of atrioventricular nodal reentrant tachycardia (AVNRT). The ECG exhibits a
regular, narrow QRS complex tachycardia. P waves are difficult to discern from the QRS complexes as these are nearly simultaneous.
Close inspection of certain leads such as lead V1 reveals the presence of a sharp deflection just after the QRS complex, which is
termed an R0 wave. Close inspection of the inferior leads II, III, and aVF reveals a small sharp deflection after the QRS complex, which
is termed an S0 wave. These sharp deflections superimposed on the QRS complex represent activation of the P wave and are
classically seen in AVNRT.

conduct in series through the ventricular
tissue to reach the accessory pathway and,
then via the pathway, activate the atria in a
retrograde fashion.29,30
Sinus Tachycardia
This arrhythmia can be noted on the ECG
on the basis of the P wave morphology,
which is reflective of the location of the
sinus node origin. The generation of the
P wave inscription reflects activation of
the superior posterolateral portion of the
right atrium, which then travels to the rest
of the right atrium and across to the
left atrium, as well as inferiorly. Thus, the
P wave is noted to be wide and has a posi-
tive deflection in the inferior leads II, III,
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8 Mayo Clin Proc.
and aVF, and lead I is positive. The terminal
portion of the P wave in lead V1 has a nega-
tive deflection, as the left atrium is in the
chamber adjacent to that which contains
the sinus node (right atrium), and the
wave front is moving away from lead V1
and toward the left atrium. The P wave
morphology in sinus tachycardia will there-
fore resemble the P wave morphology
during sinus rhythm.
Atrial Tachycardia
This arrhythmia is recognized on the ECG
with a noted change from a classical P wave
that originates from the sinus node region.16,34
For example, an AT that arises from the
ostium of the coronary sinus will have a
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FIGURE 6. Electrocardiogram (ECG) of a patient with Wolff-Parkinson-White syndrome exhibiting preexcited QRS complexes. This
ECG exhibits characteristic inscriptions noted in patients with accessory pathways that manifest on the recording strips. Note the
“delta wave,” which is a deflection that occurs as the initial part of the QRS complex. This represents early activation or preexcitation
of the ventricle via conduction antegrade down an accessory pathway. Another key feature on the ECG of these patients is a short PR
interval, as the delta wave is occurring at the same time and thus masking the normal conduction time.

narrower P wave duration. This is because Atrial Flutter

activation begins in between both atria and
because activation of the right and left atria be-
gins at a common central region.16 This is in
contrast to sinus node activation, which begins
in the superior and posterior aspects of the
right atrium and activates the right atrium first
and then the left atrium. An AT originating
from the low right atrium (as opposed to the
high right atrium as in sinus rhythm) along
the crista terminalis would have a negative
P wave axis in the inferior leads II, III, and
aVF (as opposed to a positive axis that is
seen in sinus).16
Sometimes it is almost impossible to
distinguish between AT and sinus tachycardia.
However, the clinical history and ECG moni-
toring are critical to the diagnosis, as findings
of an abrupt onset and rate that is higher than
the physiologic range can be useful in
differentiation.15
Multifocal AT
By definition, there should be organized atrial
activity yielding P waves with 3 or more
different morphologies to diagnose multifocal
AT (Figure 1).1
Typical atrial flutter involves the CTI.19 The
key is to observe an opposite direction of
P or flutter waves in the inferior leads (II, III,
and aVF) and lead V1. In the more common
form, counterclockwise CTI-dependent atrial
flutter, P waves are positive in lead V1 and
negative in leads II, III and aVF, producing a
sawtooth pattern (Figure 1). In clockwise
CTI-dependent atrial flutter, the opposite
orientation will be observed, that is, positive
flutter waves in the inferior leads and negative
in lead V1.1
Atrial Fibrillation
The characteristic ECG finding is the absence
of a distinct P wave inscription on the ECG
because of rapid oscillations (fibrillatory
waves) that vary in amplitude, shape, and
timing35,36 (Figure 2). Electrical activation of
the atrial muscle is chaotic and signals of low
amplitude may not generate sufficient voltage
to manifest on the surface ECG. The QRS
complexes will be irregularly irregular. Some-
times P waves in lead V1 may appear organized;
however, careful inspection will find irregular-
ity and ill-defined P waves in other leads.

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This is in contrast to atrial flutter, in which
there is constant cyclical atrial activity during
the flutter circuit. Lead V1 is usually over the
right atrial appendage and this may have
more organization than the rest of the atrium
and thus confuse the clinician, especially
when other leads suggest fibrillation.35 Thus,
if there is evidence of AF in any lead, then
the patient’s rhythm is AF.
SECTION IV: MANAGEMENT OF SVTS
Immediate Treatment of SVT
Immediate management of regular SVT is fairly
standardized and aimed to stabilize the patient
who presents with narrow complex tachy-
cardia (summarized in Figure 7). The primary
objective in a patient with regular and stable
SVT is to slow conduction through the AV
node and to terminate AVNRT or ORT.1 Vagal
maneuvers can be attempted, which could
include Valsalva maneuvers, carotid sinus
massage, or application of a cold/wet towel
to the face.8 If vagal maneuvers are ineffective,
the next step is typically administration of
intravenous adenosine.37,38 Other second-line
treatments include AV nodeeslowing agents,
such as b-blockers, diltiazem, or verapamil,
and can be considered if the above are ineffec-
tive or contraindicated.1
In irregular SVT, especially AF with preex-
cited tachycardia, facilitation of conduction
down the accessory pathway can lead to
precipitation of ventricular fibrillation. Thus,
AV nodal blocking agents are absolutely contrain-
dicated in this situation as this can be fatal.
Clinical Pearl 1: Perturbation of the AV Node
Can Assist in Defining a Tachycardia
If one cannot distinguish between atrial flutter,
AF, and AT, cardiac monitoring and perturba-
tion of the conduction system can be of great
use.39 Reviewing tracings that include periods
of varying AV block, which can be caused by
vagal maneuvers, carotid massage, or AV
node blockade, could provide the ability to
see atrial activity, that is, chaotic baseline
(AF) or regular sawtooth pattern (atrial
flutter), and provide diagnostic insight. In
this regard, adenosine, which has an extremely
short half-life, can be administered to help
narrow the differential diagnosis of SVT. In
addition, if the tachycardia circuit breaks
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10 Mayo Clin Proc.
MAYO CLINIC PROCEEDINGS
with perturbation of the AV node, this is indic-
ative of its necessary role in the tachycardia
circuit. For example, this can include ORT, us-
ing the antegrade limb of the circuit in ORT.
This can also be seen with AVNRT. In AT,
AV nodal blockers may sometimes terminate
the arrhythmia because of effects on abnormal
atrial tissue, or alternatively it can create tran-
sient AV block with ongoing atrial activity, and
thus aid in diagnosis.
Clinical Pearl 2: Unstable SVT May Require
Cardioversion
Although SVT is usually hemodynamically
tolerated, certain patients, particularly when
already ill and hospitalized, may quickly
decompensate in tachycardia. In these situa-
tions, synchronized electrical cardioversion
should be performed. However, even in this
scenario, vagal maneuvers and adenosine can
be attempted first while preparation for car-
dioversion is ongoing. Intravenous adenosine
is short acting and works on the AV node to
create slowing or block in conduction. If the
tachycardia involves the AV node, adenosine
can serve to break the tachycardia circuit.
Specific Treatment Options for SVT Based
on the Tachycardia Mechanism
Atrioventricular Nodal Reentrant Tachy-
cardia. Long-term treatment is focused on
symptomatic management, which is dictated
by severity, frequency, and patient preference.
The treatment of this arrhythmia can be
noninvasively done by performing vagal ma-
neuvers or with the use of AV nodal blockers
such as b-blockers, which can interrupt this
circuit.40 These are sometimes effective,
though sometimes these medications are not
well tolerated.41 Catheter ablation typically
involving ablation of the slow pathway offers a
potential for curing AVNRT with an almost
95% success rate.42,43
Accessory PathwayeRelated Tachycardia
(ORT and ART). The treatment of these
pathway-related tachycardias is typically abla-
tion,44 although in those averse to invasive
procedures, AV nodal blocking agents or
antiarrhythmic agents that slow conduction in
the atria as well as accessory pathway tissue,
such as class 1C antiarrhythmic agents, for
example, flecainide, can be trialed.1 However,
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SUPRAVENTRICULAR ARRHYTHMIAS FOR THE INTERNIST

Regular, narrow complex tachycardia Irregular, narrow complex tachycardia

(QRS width <120 ms, HR >100 beats/min) (QRS width <120 ms, HR >100 beats/min)

Hemodynamically Hemodynamically Hemodynamically Hemodynamically

unstable stable unstable stable

1. Electrical Electrical
Atrial fibrillation
cardioversion cardioversion
2. Adenosine can be
tried but should not
delay cardioversion RP interval
Anticoagulationa
Rate or rhythm
controlb
Risk factor
modification
Long RP interval Short RP interval

Treat the underlying AVNRT

Sinus tachycardia
cause ORT

1. β-Blockers/ 1. Vagal maneuvers

calcium channel Focal atrial 2. Intravenous Multifocal atrial Treat underlying
blockers tachycardia adenosine tachycardia lung disease
2. Catheter ablation 3. β-Blockers/
calcium channel
blockers Atrial flutter with
Treat like AF Atrial flutter 4. Catheter ablation Treat like AF
variable block

aCHA DS VASc
2 2 score ≥2, AF >48 h, not actively bleeding
If >48 hours, not receiving anticoagulation and/or unsure of anticoagulation compliance use TEE guidance before cardioversion
Anticoagulation required for a minimum of 4–6 wk after cardioversion

bCan be accomplished by rate control (β-blocker/calcium channel blocker, and digoxin) or rhythm control
(amiodaron, flecainide, propafenone, sotalol, and dofetilide) and/or catheter ablation

FIGURE 7. Treatment algorithm for supraventricular arrhythmias. Treatment schema for supraventricular tachycardias (SVTs) is
delineated according to the classification schema used in this review. The first decision step depends on the hemodynamic stability of
the patient. If the patient is hemodynamically unstable, electrical cardioversion is recommended for regular, narrow as well as irregular,
narrow complex tachycardias. Of note, in regular, narrow complex tachycardias, adenosine can be tried for diagnostic and therapeutic
purposes during preparation for cardioversion but should not delay therapy. With regular, narrow complex SVTs and hemodynamic
stability, the RP interval is treated on the basis of subclassifications. Note that antidromic reentrant tachycardia/orthodromic recip-
rocating tachycardia, which involve the atrioventricular node, include therapies to perturb this structure, such as intravenous adenosine
or vagal maneuvers. Atrial flutter is generally treated like atrial fibrillation (AF) in terms of rate/rhythm control and importantly
anticoagulation. Please note that atrial flutter is difficult to treat with rate controlling agents. Thus, especially if it is CTI-dependent
flutter, catheter ablation is a viable strategy. AVNRT ¼ atrioventricular nodal reentrant tachycardia; HR ¼ heart rate; ORT ¼
orthodromic reciprocating tachycardia; TEE ¼ transesophageal echocardiogram.

there are a few issues that merit additional
consideration. First, AV nodal agents should
not be used in patients with documented pre-
excited tachycardias, which conduct antegrade
across an accessory pathway, such as those
who experience ART or AF with preexcitation
(Figure 8). This could be life-threatening
because of 1:1 atrial to ventricular con-
duction and degeneration to ventricular
fibrillation.1 In the immediate setting, elec-
trical cardioversion, intravenous procaina-
mide, or intravenous ibutilide can be

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 MAYO CLINIC PROCEEDINGS

FIGURE 8. Electrocardiographic (ECG) characteristics in a patient with preexcited atrial fibrillation. Notable ECG findings in a patient
with preexcited atrial fibrillation are annotated on the ECG. A delta wave is present at the onset of the QRS complex. In addition, the
QRS complex is wide because of myocardial cell-to-myocardial cell conduction, which is slower than if it travels via conduction tissue.
In atrial fibrillation, which is an irregular chaotic atrial rhythm, conduction to the ventricle is also irregular. With ECG findings such as
these, atrioventricular nodal blockers are completely contraindicated.

administered. Procainamide and ibutilide have preexcitation during resting or ambulatory

a short half-life, slow conduction down the
accessory pathway, and have the additional
benefit of potential AF termination.45 Second,
it is important to ensure that the pathway is
not a high-risk pathway for the patient, that is,
one with rapid antegrade accessory pathway
conduction that predisposes the patient to the
risk of sudden cardiac death.46 In a
population-based study in Olmsted County,
Minnesota, the incidence of sudden cardiac
death was found to be approximately 0.15%
per year.47 In addition, in a parallel cohort of
patients who underwent radiofrequency abla-
tion vs those who did not, an incidence of
sudden cardiac death/ventricular fibrillation of
2.4 cases per 1000 person-years was reported
for those who did not undergo catheter
ablation.48
Risk stratification can be either observed
on the resting or exercise ECG or at the time
of electrophysiology study. Clues for low-risk
pathways include intermittent loss of
n n
12 Mayo Clin Proc.
monitoring as well as abrupt loss of conduc-
tion of preexcitation during exercise.1 During
electrophysiology study, the antegrade and
retrograde conduction characteristics of the
pathway can be defined. In addition, the
patient can be put into AF to evaluate how
fast the pathway conducts to the ventricles if
future AF were to occur.1 If the pathway is
weakly conducting, it is safe to avoid ablation.
If the pathway is of high risk, ablation can be
performed during the same procedure. It is
also safe to use AV nodal blockers if the
pathway is weakly conducting.
Clinical Pearl 3: Do Not Use AV Node
Blocker Agents for Tachycardia With
Preexcitation and an Irregular Rhythm
In the case of a conducting antegrade pathway
with preexcitation on the ECG and irregular
QRS complexes, Valsalva maneuvers, adeno-
sine, b-blockers, or calcium channel blockers,
that is, those that block the AV node and
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SUPRAVENTRICULAR ARRHYTHMIAS FOR THE INTERNIST
facilitate pathway conduction, should not be
attempted.1 The concern is that conduction
would be preferentially shifted from down the
AV node to the pathway, which may not
have any decremental properties, and thus
conduct rapidly. Thus, if the AV node is
blocked but atrial activity occurs rapidly (eg,
in AF), it is possible for 1:1 atrial to ventricular
conduction via an accessory pathway to occur.1
This could degenerate into ventricular fibrilla-
tion. The clinician will note AF because of the
lack of P waves and irregularly irregular rate
of subsequent QRS complexes. Of note, QRS
morphologies will have various degrees of
preexcitation and fusion between ventricular
excitation from the normal conduction system
and preexcitation from the antegrade pathway.
Clinical Pearl 4: Electrical Cardioversion
or Procainamide for Tachycardia With
Preexcitation and Irregular Rhythm
As stated above, if the preexcited rhythm
looks irregular, this is particularly a dire
circumstance and most likely AF with rapid
ventricular conduction via an accessory
pathway. Atrioventricular nodal blockers
such as adenosine, b-blockers, and calcium
channel blockers should not be administered.1
In these cases, intravenous procainamide can
be given or, if hemodynamically unstable,
electrical cardioversion is warranted.45
It is particularly these situations that we
want to identify early and these patients should
be referred for electrophysiologic consultation for
further laboratory study and possible ablation.
Specific pacing maneuvers are performed in a
controlled setting to see how fast the pathway
conducts to risk stratify the patient. High-risk
patients are to undergo catheter ablation of
these pathways during the same study.1
Similarly, weakly conducting pathwaysd
those in which preexcitation is intermittent,
or not present, especially at heart rates below
100 beats/mindare unlikely to be of concern
and AV nodal blockers can still be used.
Atrial Tachycardia. The approach to long-
term management is dictated by the
frequency and severity of symptoms. A medi-
cal approach may include oral b-blockers,
diltiazem, verapamil, or antiarrhythmic agents.
Catheter ablation is also an appropriate initial
treatment.1
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For sinus tachycardia and multifocal AT,
treatment is aimed at treating the underlying
cause.49 In the case of sinus tachycardia, this
can be of multiple stressors such as anemia,
hypoxia, fever, or infection. In multifocal AT,
in general, the goal is to treat the underlying
lung disease.
Atrial Flutter. Cavotricuspid isthmuse
dependent atrial flutter can be targeted with a
relatively high success rate of more than 90%
via catheter ablation21,50 (Figure 9). Thus,
catheter ablation for this arrhythmia is typically
recommended. Rate-controlling agents can be
used to decrease the ventricular rate, which
may improve symptoms, although these are
not always effective.50 Atrial flutters that are
noneCTI-dependent are typically much more
difficult to ablate, and antiarrhythmic agents
may be trialed initially before engaging in a
more complex ablation procedure.
Clinical Pearl 5: Relationship Between AF
and Atrial Flutter
The trigger for AF as well as AF itself can be the
trigger for atrial flutter. Thus, it is common to
observe both arrhythmias together. In patients
with both arrhythmias recorded, catheter abla-
tion for atrial flutter can be undertaken at the
same time as that for AF.22
Atrial Fibrillation. The goal of therapies for
these patients are multitiered and include life-
style modifications to remove or reduce
triggers such as alcohol, caffeine, obstructive
sleep apnea treatment,51 weight loss in those
with obesity,52 and exercise in those with a
sedentary lifestyle.24,52-54 In addition, modifi-
cation of hypertension is essential and treat-
ment of heart failure is critical to lower the
pressure seen in the left atrium, which leads to
stretch and remodeling, and potentially scar
formation, all of which could be a setup for
AF.22 These strategies should be the basis for
every patient regardless of further therapies.
Clinical Pearl 6: Rate vs Rhythm Control
Strategy
Landmark trials including Atrial Fibrillation
Follow-up Investigation of Rhythm Manage-
ment (AFFIRM) and Rate Control versus Elec-
trical Cardioversion for Persistent Atrial
Fibrillation (RACE) observed no clinical
13

FIGURE 9. Catheter ablation of the cavotricuspid isthmus line for atrial
flutter treatment. Because of the anatomical constraint of typical atrial flutter
circuits from the electrically inert structures of the tricuspid valve (TCV)
annulus and inferior vena cava (ICV), not only is there a region for flutter to
occur but also a practical location to create a line of block with radio-
frequency catheter ablation. During catheter ablation for typical atrial flutter,
radiofrequency energy is used to create a line of tissue destruction that
creates a line of electrical block between the TCV and the ICV and thus
eliminates a necessary region for the flutter circuit.
benefits (survival or stroke prevention) regard-
less of a rhythm or rate control strategy.41,54 In
addition, both strict rate control (resting heart
rate, <80 beats/min; heart rate during moder-
ate exercise, <110 beats/min) and lenient rate
control (resting heart rate, <110 beats/min)
offer similar clinical outcomes as noted in
the RACE II trial.55 However, the results did
not account for tachycardia-induced cardio-
myopathy (see discussion below).
There are considerable limitations of trial
data evaluating rate and rhythm control. Mainly,
the AFFIRM and RACE trials were largely con-
ducted before catheter-based pulmonary vein
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14 Mayo Clin Proc.
MAYO CLINIC PROCEEDINGS
isolation was common and only limited antiar-
rhythmic drugs (ie, amiodarone and sotalol)
were used.41,54 Subsequent trials, however, are
more supportive of a catheter-based approach.
In patients with a left ventricular ejection fraction
of 35% or less who already had an implantable
cardioverter-defibrillator, catheter ablation
improved outcomes (death or hospitalization
for heart failure) and left ventricular dysfunction,
compared with conventional drug treatment in
the Catheter Ablation for Atrial Fibrillation
with Heart Failure (CASTLE-AF) trial.56
The recently reported Catheter Ablation
versus Antiarrhythmic Drug Therapy for Atrial
Fibrillation (CABABA) trial, which randomized
approximately 2200 patients with AF to either
catheter ablation or drug therapy, reported that
ablation is not superior to drugs for a composite
of cardiovascular outcomes during 5-year
follow-up. However, its preliminary results sug-
gest a reduction in cardiovascular hospitalization
and AF recurrence with a catheter ablation
approach.57 Further analysis and reports on qual-
ity of life and cost-effectiveness are underway.
Conclusively, the decisions to use a rate or
rhythm control strategy depend largely on
symptoms, as well as notable comorbidities
such as heart failure/cardiomyopathy, and on
patient preference for ablation over drug
therapy.22 It is therefore reasonable to refer
patients with AF to an electrophysiologist for
a detailed discussion about rate vs rhythm con-
trol strategy (antiarrhythmic drugs and catheter-
based ablation). Finally, it is important to
emphasize that the cornerstone of management
of AF (and atrial flutter) is stroke prevention and
the need of anticoagulation is not modified with
any treatment modalities (including ablation).
Clinical Pearl 7: Anticoagulation for Atrial
Flutter and AF
A mainstay of AF is that of stroke prophylaxis
with the use of anticoagulation. This is also
necessary in patients with atrial flutter. The
decision to initiate anticoagulation should be
based on the CHADS2-VASc risk score, and
not dependent on the duration of arrhythmias,
or treatment strategy (ie, rate, rhythm, or
ablation).58
Tachycardia-Induced Cardiomyopathy
Atrial arrhythmiaemediated cardiomyopathy
is not uncommonly seen and can have severe
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SUPRAVENTRICULAR ARRHYTHMIAS FOR THE INTERNIST
consequences because of severe decline in
ventricular function.59 These patients tend to
have slower tachycardia (and without much
symptoms), but incessant or frequent parox-
ysmal tachycardia.60 Aggressive management
of this arrhythmia is recommended. Atrial
fibrillation or flutter with poor rate control
can also cause cardiomyopathy. The general
recommendation in this scenario is to ensure
adequacy of rate control or offer a rhythm
control strategy.22
When frequent enough, any SVT can
cause cardiomyopathy. In particular, an
arrhythmia that classically causes cardiomyop-
athy is a permanent form of junctional recipro-
cating tachycardia. This is an uncommon
subtype of AVRT that involves a concealed
accessory pathway with retrograde decre-
mental conduction properties. Patients often
present with slow and incessant AVRT. Cath-
eter ablation can often successfully restore
cardiac function.61,62
CONCLUSION
Supraventricular arrhythmias can cause distress
and comorbidity to patients. These arrhythmias
are not uncommon, and the internist requires
a fundamental knowledge of the mechanisms
and management of these arrhythmias. With
an approach to reviewing the ECG and clues
to arrive at a differential SVT diagnosis, the
proper triage in patient management will be
augmented. This may require rate or rhythm
control, electrical cardioversion, or even catheter
ablation. With an understanding of downstream
therapies used, the internist will be equipped to
provide initial counseling to the patient and
recognize the importance of referral to cardiac
electrophysiology for advanced measures
including catheter ablation. These essential te-
nets are all the more important as these can
involve younger patients with life-threatening
ramifications as well as older patients who
may be at risk of heart failure progression.
Abbreviations and Acronyms: AF = atrial fibrillation; ART
= antidromic reciprocating tachycardia; AT = atrial tachy-
cardia; AV = atrioventricular; AVNRT = atrioventricular
nodal reentrant tachycardia; AVRT = atrioventricular reen-
trant tachycardia; CTI = cavotricuspid isthmus; ECG = elec-
trocardiographic/electrocardiogram; ORT = orthodromic
reciprocating tachycardia; SVT = supraventricular
tachycardia
Mayo Clin Proc. n XXX 2018;nn(n):1-17 n https://doi.org/10.1016/j.mayocp.2018.07.019
www.mayoclinicproceedings.org
Potential Competing Interests: Dr Asirvatham serves as a
consultant to Aegis, ATP, Nevro, Sanovas, Sorin Medical,
and FocusStart.
Correspondence: Address to Samuel J. Asirvatham, MD,
Department of Cardiovascular Diseases, Mayo Clinic, 200
First St SW, Rochester, MN 55905 (asirvatham.samuel@
mayo.edu).
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