Supraventricular

Tachyc a rd i a
1
Arun Umesh Mahtani, MBBS , Devi Gopinath Nair, MD, FHRS*

KEYWORDS
 Tachycardia  Supraventricular arrhythmias  Cardiac heart diseases
 Accessory pathways  AVNRT  Radio frequency ablation

KEY POINTS
 The term paroxysmal supraventricular tachycardia encompasses a heterogeneous group
of arrhythmias with different electrophysiologic characteristics.
 Knowledge of the mechanism of each supraventricular tachycardia is important in deter-
mining management in the office, at the bedside, and in the electrophysiology laboratory.
 Such paroxysmal supraventricular tachycardias have an abrupt onset and offset, typically
initiating and terminating with premature atrial ectopic beats.
 In the acute setting, both vagal maneuvers and pharmacologic therapy can be effective in
arrhythmia termination.
 Catheter ablation has revolutionized therapy for many supraventricular tachycardias, and
newer techniques have significantly improved ablation efficacy and reduced periproce-
dural complications and procedure times.

Supraventricular tachycardia (SVT) is a common term used to describe tachycardias

with rates of more than 100 bpm, with a mechanism that involves the atrial tissue up to
the atrioventricular junction (AVJ). These include atrioventricular nodal reentrant
tachycardia (AVNRT), various types of accessory pathway-mediated atrioventricular
reentrant tachycardias (AVRT), atrial tachycardia (AT), including focal and multifocal
mechanisms, sinus tachycardia, atrial flutter, and atrial fibrillation. Paroxysmal SVT
(PSVT) is the term used for a subset of SVTs that have an abrupt onset and offset
such as AVNRT, AVRT, and AT. The prevalence of SVT in the general population is
2.29 per 1000 persons.1 When adjusted by age and sex in the US population, the inci-
dence of PSVT is estimated to be 36 per 100,000 persons per year. Compared with

Disclosure Statement: The authors have no financial relationships to disclose pertaining to the
content of this article.
Department of Cardiac Electrophysiology, St. Bernard’s Heart and Vascular Center, Jonesboro,
AR, USA
1
Present address: Unit B-306, Mantri Elegance Apartments, Bannerghatta Road, Bangalore,
Karnataka 560076, India.
* Corresponding author. 3878 Ridgewood Cv, Jonesboro, AR 72404.
E-mail address: drdevignair@gmail.com

Med Clin N Am 103 (2019) 863–879

https://doi.org/10.1016/j.mcna.2019.05.007 medical.theclinics.com
0025-7125/19/ª 2019 Elsevier Inc. All rights reserved.
864 Mahtani & Nair

patients with cardiovascular disease, those with PSVT without cardiovascular disease
are younger (37 vs 69 years; P 5 .0002) and have faster PSVT (186 bpm vs 155 bpm;
P 5 .0006). Women have twice the risk of men of developing PSVT.1 Individuals
greater than 65 years of age have more than 5 times the risk of younger persons of
developing PSVT.1
AVNRT is more common in persons who are middle aged or older, whereas in ad-
olescents, the prevalence may be more balanced between AVRT and AVNRT, or AVRT
may be more prevalent.1 The relative frequency of tachycardia mediated by an acces-
sory pathway decreases with age. The incidence of manifest preexcitation or a Wolff–
Parkinson–White syndrome pattern on electrocardiogram (ECG) tracings in the gen-
eral population is 0.1% to 0.3%. However, not all patients with manifest ventricular
preexcitation develop PSVT.2–4

CLASSIFICATION

There are different ways of classifying PSVT.

Based on site of origin

a. Impulse originating from the atrial tissue above the AVJ, without using the AVJ as
part of the circuit:
Rhythms in this category include atrial fibrillation, AT, atrial flutter with variable con-
duction, or multifocal AT (MAT).
b. Impulse using AVJ as part of circuit:
Rhythms in this category include AVNRT, AVRT, and junctional tachycardia.

Based on the RP interval (the RP interval is the interval between the onset of a
surface QRS to the onset of a visible P wave).
a. No RP tachycardia with no visible P waves:
Rhythms in this category include Typical AVNRT and AT.
b. Very short RP interval tachycardia with the RP interval of less than or equal to the
PR interval and the actual RP interval less than 90 ms:
Rhythms in this category include typical AVNRT and AT.
c. Short RP interval tachycardia with the RP interval of less than or equal to the PR
interval and the actual RP interval is 90 ms or greater:
Rhythms in this category include orthodromic AVRT, atypical AVNRT, and AT.
d. Long RP interval tachycardia where the RP interval is greater than or equal to the
PR interval: rhythms in this category include sinus tachycardia, AT, permanent
junctional reciprocating tachycardia, and atypical AVNRT.
An algorithm for the differential diagnosis of PSVT is shown in Fig. 1.

MECHANISMS OF DIFFERENT TYPES OF PAROXYSMAL SUPRAVENTRICULAR

TACHYCARDIA
Atrioventricular Nodal Reentrant Tachycardia
AVNRT accounts for most of the cases of PSVT.5 It is most commonly seen in women
who are in their fourth or fifth decade of life.6,7
AVNRT occurs in patients who exhibit dual atrioventricular nodal physiology with a
slow pathway and a fast pathway within the atrioventricular node (AVN). The slow
pathway has a slow conduction velocity but a relatively shorter refractory period,
whereas the fast pathway has a swift conduction velocity, but a significantly longer re-
fractory period. Conduction through these 2 pathways can either be in the antero-
grade or retrograde direction.8–10
 Supraventricular Tachycardia 865

Fig. 1. Algorithm for differential diagnosis of narrow complex tachycardia. A-Fib, atrial
fibrillation; PJRT, permanent junctional reciprocating tachycardia.

Typical Atrioventricular Nodal Reentrant Tachycardia

In sinus rhythm, the impulse is conducted from the atrium to the ventricles through the
fast pathway of the AVN and through the bundle of His. Typical AVNRT begins when
there is a perfectly timed premature atrial depolarization that blocks in the fast
pathway during its refractory state and propagates through the slow pathway in the
AVN, reaching the ventricles. However, if the propagation is slow enough and the
fast pathway comes out of its refractory state, the impulse can travel retrograde
into the atria creating a reentry circuit within the AVN. The antegrade limb of the circuit
is down the slow pathway and the retrograde limb of the circuit is up the fast pathway.
The atria and ventricles are depolarized simultaneously as bystanders and do not
participate in the tachycardia.

Electrocardiogram characteristics of typical atrioventricular nodal reentrant

tachycardia
As the first premature impulse travels over the slow pathway in the antegrade direc-
tion, there is evidence of a prolonged PR interval in the initiating beat of the tachy-
cardia. During reentry, there is simultaneous activation of the atria and ventricles.
Hence, the P wave and the QRS complex occur almost simultaneously resulting in
a no RP or very short RP tachycardia (Fig. 2). The P wave will be negative in leads
II, II, and aVF as the impulse travels retrograde from the low to the high atrium. The
P waves also have smaller width suggesting septal activation.
866 Mahtani & Nair

Fig. 2. ECG of a typical AVNRT, with a very short RP/no RP tachycardia.

Atypical Atrioventricular Nodal Reentrant Tachycardia

There is a role reversal in atypical AVNRT. A perfectly timed premature ventricular de-
polarization activates the slow pathway in a retrograde fashion, depolarizing the atria;
the ventricles are activated thereafter through the fast pathway in an antegrade
fashion. Atypical AVNRT occurs in about 10% of all patients having AVNRT.6

Electrocardiogram characteristics of atypical atrioventricular nodal reentrant

tachycardia
In atypical AVNRT there is a clear separation between the P waves and the QRS com-
plexes. Tachycardia is usually initiated by a premature atrial or ventricular contraction.
The PR interval is normal as the impulse travels antegrade through the fast pathway,
as it would in sinus rhythm. However, the RP interval, which represents retrograde
conduction of the electrical signal through the slow pathway, is prolonged, resulting
in a long RP tachycardia. The P wave continues to remain negative in leads II, III,
and aVF as the impulse travels in the atrium from bottom to top, and the vector is
therefore directed away from these leads (Figs. 3 and 4). The P waves also have
smaller width, suggesting septal activation.

Atrioventricular Reentrant Tachycardia

AVRT is the second most common PSVT in clinical practice,5 usually seen in a younger
population.9 In AVRT, the circuit includes the AVN and an accessory pathway con-
necting the atria and ventricles that allows for antegrade and/or retrograde
conduction.
An accessory pathway is an abnormal band of conducting tissue that can transmit
impulses anterograde, retrograde, and or both. When an impulse is transmitted anter-
ograde across this pathway,9 the region of the ventricle connected to this pathway is
excited/depolarized earlier than the rest of the ventricle, known as ventricular preex-
citation, resulting in the characteristic delta wave and a short PR interval. This type of
pathway is called a “manifest” pathway, because it is clearly visible while in sinus
rhythm. Manifest accessory pathways can conduct retrograde as well. Accessory
 Supraventricular Tachycardia 867

Fig. 3. Initiation of atypical AVNRT.

pathways that can only conduct impulses in a retrograde direction are called “con-
cealed” accessory pathways, because there is no ventricular preexcitation and no ev-
idence of ECG changes while in sinus rhythm.11,12

Orthodromic Atrioventricular Nodal Reentrant Tachycardia

This is the most common mechanism of AVRT among patients with accessory
pathway.13 It starts with a perfectly timed premature atrial contraction that travels
through the AVN and the His-Purkinje system to cause ventricular depolarization.
The impulse then travels retrograde through the accessory pathway to the atria form-
ing a reentrant circuit.

Electrocardiogram characteristics of orthodromic atrioventricular nodal reentrant

tachycardia
Tachycardia is usually initiated by a premature atrial or ventricular contraction. During
reentry, there is activation of the ventricles through the AVN in an antegrade fashion,

Fig. 4. ECG of atypical AVNRT with long RP tachycardia.

868 Mahtani & Nair

Fig. 5. ECG of orthodromic AVRT with a short RP (RP >80 ms) tachycardia.

resulting in a narrow QRS tachycardia, after which the atria are activated retrograde
through the accessory pathway. Hence, the P wave follows the QRS complex resulting
in a short RP (much less frequently a long RP) depending on the site and conduction
properties of the accessory pathway. The P wave morphology depends on the site of
the accessory pathway (Fig. 5).

Antidromic Atrioventricular Nodal Reentrant Tachycardia

This entity is rare compared with orthodromic AVRT and is usually seen in about 10%
of the patients with manifest accessory pathway.14–21 Here, the premature impulse
travels anterograde through the accessory pathway and reentry into the atria is via
the Hisian system and the AVN. It is more common among patients with multiple
accessory pathways.15

Electrocardiogram characteristics of antidromic atrioventricular nodal reentrant

tachycardia
Tachycardia is usually initiated by a premature atrial or ventricular contraction. During
reentry, there is activation of the ventricles by the accessory pathway in the antegrade
fashion following which the atria are activated later through the AVN via the retrograde
approach. Owing to the maximum preexcitation of the ventricles, this is a wide com-
plex tachycardia and the QRS morphology depends on the site of the accessory
pathway (Fig. 6).

Permanent Junctional Reciprocating Tachycardia

Permanent junctional reciprocating tachycardia is a type of orthodromic AVRT usually
seen in pediatric population or young adults using a slowly conducting concealed
accessory pathway. Permanent junctional reciprocating tachycardia is usually inces-
sant22 and if left untreated, patients will have a deterioration of cardiac function owing
to cardiomyopathy that can ultimately lead to heart failure.23 This pattern results in a
long RP tachycardia with a P wave morphology that is typically negative in the inferior
leads, but varies depending on the location of the accessory pathway.

Atrial Tachycardia
AT is the least common of the PSVTs. It accounts for 10% of the total number of cases
of PSVT.24,25 AT originates in the atrial tissue and does not require another part of the
 Supraventricular Tachycardia 869

Fig. 6. ECG of antidromic AVRT; wide complex tachycardia with maximum preexcitation.

conduction system for its propagation. There are 2 types of AT that can cause SVT,
unifocal AT and MAT.

Unifocal Atrial Tachycardia

In unifocal AT, the electrical impulse originates from one site located anywhere in the
atria. The P wave pattern on the ECG depends on the site of origin of the ectopic im-
pulse. The patient could have 1:1 AV conduction or there could be more atrial impulses
than ventricular impulses. Unifocal AT can be due to reentry or enhanced automaticity
within an atrial focus. AT occurring owing to reentry is usually paroxysmal and is asso-
ciated with underlying structural heart disease.26 In contrast, enhanced automaticity is
incessant and can occur in the setting of a structurally normal heart.26 Treating the
incessant variety is of utmost importance as failure to treat can lead to
tachyarrhythmia-associated cardiomyopathy and ultimately heart failure.

Multifocal Atrial Tachycardia

In MAT, there are multiple foci located in the atria that have enhanced automaticity.27
The diagnosis of MAT is usually based on an ECG criterion. It requires 3 or more
different P wave morphologies, each representing a separate atrial focus, along with
an average heart rate 100 beats per minute or more. Unlike atrial fibrillation, MAT
has the presence of isoelectric periods between P waves. A wandering atrial pace-
maker has a similar ECG appearance. The only difference is that the average heart
rate is 100 beats per minute or less. A strong association has been found between
MAT and various pulmonary diseases.27

Rare Types of Permanent Junctional Reciprocating Tachycardia

Sinoatrial reentrant tachycardia
Sinoatrial reentrant tachycardia is a rare cause of PSVT with a reentrant circuit origi-
nating within the sinus node.28–31 Because the reentrant circuit is in the sinus node
the P wave morphology remains identical to a normal sinus P wave. The only way
to identify SART is to look for a prolonged RP interval when compared with a PR inter-
val. In contrast with inappropriate sinus tachycardia, which is an automatic tachy-
cardia, sinoatrial reentrant tachycardia starts and stops abruptly.
870 Mahtani & Nair

Clinical presentation
PSVTs have an impact on quality of life, which varies according to the frequency of the
episodes, the duration of the SVT, and whether symptoms occur not only with exer-
cise ,but also at rest. Modes of presentation includes documented SVT in 38%, pal-
pitations in 22%, chest pain in 5%, syncope in 4%, atrial fibrillation in 0.4%, and
sudden cardiac death in 0.2%.32 PSVT is often misdiagnosed as panic or anxiety dis-
order, particularly in patients with a prior history of psychological illness.33 As
mentioned, early diagnosis and management is of paramount importance because
incessant types of SVT can progress to cardiomyopathy and heart failure.
On physical examination tachycardia may be the only finding. However, in some
cases of PSVT elevated jugular venous pressure also known as the frog’s sign may
be observed.32 This sign occurs when the atrium contracts against a closed tricuspid
valve causing blood to flow retrograde into the venous system.

Diagnosis
As with every arrhythmia, an ECG is warranted to identify the type of PSVT. In most
cases of PSVT the QRS complex is narrow. However, wide QRS complexes can oc-
casionally be seen.34 It is important to look for characteristics like P wave morphology,
QRS morphology, PR interval, and RP interval. Clinically, this is important because the
treatment options vary for each type of PSVT. Other investigations to consider are an
echocardiogram to look for underlying structural heart disease, electrolyte abnormal-
ities, and serum thyroid-stimulating hormone levels because they can all be triggers
for the PSVT. The importance of pulmonary disease in the setting of a structurally
normal heart should be emphasized. Patients with many pulmonary diseases,
including asthma, chronic obstructive disease, and obstructive disease, are at a higher
risk of developing atrial tachyarrhythmias. Cardiac monitoring, including continuous
ambulatory monitoring using an external or implantable monitor, is sometimes
required to capture the PSVT. Occasionally an invasive electrophysiological study
might be required, usually in conjunction with a planned ablation treatment strategy.

Treatment Options
There are a wide variety of acute and long-term treatment options available to stop
and eventually treat the PSVT.

ACUTE MANAGEMENT OPTIONS

Nonpharmacologic Methods
Nonpharmacologic treatment is usually the first step to control a PSVT episode when
there is no hemodynamic instability. The principle behind nonpharmacologic methods
is to increase vagal tone, which in turn slows conduction through the AVN. Because a
majority of PSVTs use the AVN as part of their reentry circuit, such maneuvers can
terminate the reentrant circuit. This method of treatment can also be used to diagnose
the type of PSVT35,36:
a. The Valsalva maneuver is an effective way to abort an episode of PSVT. This
method was first described in the year 1936 by Hamilton and continues to remain
an effective method to stop an episode of PSVT. This can be done by bearing
down, coughing, or splashing cold water over the face.
b. Carotid sinus massage: The carotid sinus is an area in the carotid artery that has
pressure-sensitive receptors to maintain adequate blood pressure and control car-
diac output. It is found just below the angle of the jaw. Massaging over this area for
10 seconds causes firing of these pressure-sensitive receptors and causes a
 Supraventricular Tachycardia 871

Fig. 7. Algorithm for the acute treatment of narrow complex tachycardia.

vagally induced slowing of conduction through the AVN. Precautions while per-
forming this maneuver include performing it only over 1 side and avoiding it in
elderly patients with audible carotid bruits.35

Pharmacologic Methods
Pharmacologic therapy for acute termination of PSVT is appropriate when nonphar-
macologic maneuvers fail. The preferred initial agents are intravenous adenosine or
872 Mahtani & Nair

Fig. 8. Algorithm for the management of AVNRT.

a nondihydropyridine calcium channel blocker. Adenosine’s effects are mediated by

membrane hyperpolarization that typically occurs within 15 to 30 seconds after admin-
istration. Adenosine has a powerful effect on the AVN and is highly effective in causing
transient, complete AVN block. Transient sinus bradycardia or sinus arrests often
occur but are short lived. The ECG should be recorded continuously during adenosine
administration to document the effect of the drug on PSVT and to monitor for the rare
occurrence of proarrhythmia. Patients should be warned that they might experience
short-lived sensations of claustrophobia, dyspnea, flushing, and chest discomfort.
The initial dose of adenosine is 6 mg intravenous bolus (flushed), using a large vein.
Subsequent doses of 12 mg or even 18-mg boluses may be required. PSVT resolution
after adenosine administration establishes AVNRT or AVRT as the likely PSVT
 Supraventricular Tachycardia 873

Fig. 9. Algorithm for the management of AVRT.

mechanism, although occasionally unifocal AT will terminate with adenosine as well. In

most unifocal ATs, adenosine administration results in a transient slowing of the ven-
tricular rate, revealing the underlying atrial activity. Adenosine should be used carefully
in patients with Wolff–Parkinson–White syndrome and atrial fibrillation because it
shortens the refractory period of the accessory pathway resulting in rapid conduction
of atrial fibrillation, increasing the chances of dangerous ventricular tachyarrhythmias
from preexcited atrial fibrillation. Etripamil in the form of a nasal spray is a short acting
calcium channel blocker and has been tested for acute termination of PSVT episodes.
The rates of conversion to sinus rhythm are high and the time to conversion is less than
3 minutes, with a low side effect profile.
The use of direct current cardioversion is generally limited to cases of hemodynam-
ically unstable PSVT that do not respond to any of these methods and is a rare phe-
nomenon.37 An algorithm for the acute management of PSVT is presented in Fig. 7.
Long-Term Management
Referral to an electrophysiologist is indicated for patients with poorly tolerated or
frequently recurring arrhythmias. Most of the time, patients with AVNRT or AVRT are
874 Mahtani & Nair

Fig. 10. Algorithm for the management of AT.

referred for ablation before extended trials of drug therapy because these rhythms are
curable at least 95% of the time.

Pharmacologic Treatment
Chronic prophylactic drug therapy is an important treatment option for patients
with PSVT who have difficulty self-terminating their arrhythmia. Patient age,
frequency of PSVT, and symptom burden should all be taken into account
before considering chronic prophylactic medical therapy. Pharmacotherapy is
associated with side effects and often does not result in complete freedom from
arrhythmia.
Both long-acting calcium channel blockers and beta blockers improve symptoms in
60 to 80% of patients with PSVT.38,39 Flecainide and propafenone are class IC antiar-
rhythmic drugs that suppress automaticity and slow conduction and can thus result in
a significant decrease in duration and frequency of PSVT episodes. These drugs are
 Supraventricular Tachycardia 875

Fig. 11. Algorithm for the management of junctional tachycardia.

contraindicated in patients with known structural heart disease because of an

increased risk of ventricular arrhythmias.39,40
Class III drugs such as sotalol or dofetilide are also effective in controlling PSVT.
These drugs prolong the refractory period, prevent propagation of reentry, and sup-
press automaticity.41 Class III antiarrhythmic drugs carry the risk of long QT and
Torsades de Pointes and must be managed by an electrophysiologist. In fact,
most electrophysiologists would recommend a catheter ablation before antiar-
rhythmic drug therapy for the vast majority of PSVTs, save for atrial fibrillation.
This recommendation is because antiarrhythmic drugs expose the patient to the
real risk of proarrhythmia over the long term, in addition to other noncardiac side
effects.

Catheter Ablation
Given the high success rates and favorable safety profiles of diagnostic electrophys-
iology study followed by catheter ablation, many patients choose this option early in
their course. Guidelines recommend ablation for patients with recurrent PSVT based
on the type of SVT and known success rates.42 Complications of ablation for PSVT are
generally low, although they vary significantly depending on the arrhythmia being
treated. One large multicenter study examining patients undergoing AVNRT, AVRT,
and AVN ablation found low risks of death, stroke, myocardial infarction, tamponade,
and arterial perforation. Procedures involving ablation near the AVN are more likely to
be complicated by atrioventricular block. Other possible complications include peri-
cardial and pleural effusions, pneumothorax, and damage to the coronary vasculature
and valves, although these complications are rare.42
Ablation of AVNRT targets the slow pathway of the AVN, located along the posterior
tricuspid annulus near the coronary sinus ostium. Slow pathway modification using
876 Mahtani & Nair

radiofrequency ablation or cryoablation results in success rate of 99% for the perma-
nent cure of AVNRT (Fig. 8). However, the incidence of complete heart block remains
1.0% to 1.5%.43,44
Success rates for accessory pathway ablation for the treatment of AVRT range from
95% to 98%, with recurrence rates of AVRT as low as 2% (Fig. 9). Location of the
accessory pathway can have a significant effect on success rates,45,46 with accurate
localization of the accessory pathway being key to a successful procedure.
Unifocal AT ablation is indicated in patients with recurrent, symptomatic episodes.
The use of 3-dimensional mapping technology has significantly improved the efficacy
of focal AT ablation with success rates ranging from 69% to 100%,47 with recurrence
rates as low as 8% (Figs. 10–12).

Fig. 12. Algorithm for the management of PSVT of unknown mechanism. EP, electrophysio-
logic; SHD, structural heart disease.
 Supraventricular Tachycardia 877

SUMMARY

PSVT encompasses a heterogeneous group of arrhythmias with different electrophys-

iologic characteristics. Knowledge of the mechanism of each SVT is important in
determining management in the office, at the bedside, and in the electrophysiology
laboratory. In the acute setting, both vagal maneuvers and pharmacologic therapy
can be effective in arrhythmia termination. Catheter ablation has revolutionized ther-
apy for many SVTs, and newer techniques have significantly improved ablation effi-
cacy and reduced periprocedural complications and procedure times.

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