Uptodte TSV

Skip to OutlineSkip to TopicSkip to ReferencesSkip to Help
 Ilinca SavulescuIlinca Savulescu

 CME5.0
 Log Out

 Contents
 Calculators
 Drug Interactions
 UpToDate Pathways


Find

 Patient

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 SUMMARY AND RECOMMENDATIONS
 INTRODUCTION
 INITIAL DIAGNOSTIC AND TREATMENT DECISIONS
o Is the patient clinically (or hemodynamically) unstable?
o Is the QRS complex narrow or wide? Regular or irregular?
 NARROW QRS COMPLEX TACHYARRHYTHMIAS
o Regular narrow QRS complex tachyarrhythmias
 Sinus tachycardia
 Atrioventricular nodal reentrant tachycardia (AVNRT)
 Atrioventricular reentrant tachycardia (AVRT)
 Atrial tachycardia
 Atrial flutter
o Irregular narrow QRS complex tachyarrhythmias
 Atrial fibrillation
 Atrial flutter
 Multifocal atrial tachycardia
 WIDE QRS COMPLEX TACHYARRHYTHMIAS
o Regular wide QRS complex tachyarrhythmias
 Ventricular tachycardia
 Supraventricular tachycardia with aberrant conduction
 Supraventricular tachycardia with a pacemaker
 Antidromic AVRT
o Irregular wide QRS complex tachyarrhythmias
 Polymorphic ventricular tachycardia
 Preexcited atrial fibrillation
 SOCIETY GUIDELINE LINKS
 INFORMATION FOR PATIENTS
 ACKNOWLEDGMENT
 REFERENCES
GRAPHICS view all
 Algorithms
oEvaluation narrow QRS complex tachycardias in unstable patients
oAlgorithm for tachycardia differential diagnosis after ECG
oEvaluation narrow QRS complex tachycardias in stable patients
oAdult cardiac arrest algorithm 2018 update
 Tables
oDrug Rx arrhythmias WPW
oRevised Vaughan Williams classification abridged table
RELATED TOPICS
 Acquired long QT syndrome: Definitions, causes, and pathophysiology
 Acute myocardial infarction: Role of beta blocker therapy
 Atrial fibrillation: Risk of embolization
 Atrioventricular nodal reentrant tachycardia
 Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway
 Basic principles and technique of external electrical cardioversion and defibrillation
 Brugada syndrome: Prognosis, management, and approach to screening
 Catecholaminergic polymorphic ventricular tachycardia
 Focal atrial tachycardia
 Intraatrial reentrant tachycardia
 Medical management of symptomatic aortic stenosis
 Multifocal atrial tachycardia
 Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation
 New onset atrial fibrillation
 Overview of atrial fibrillation
 Overview of atrial flutter
 Patient education: Supraventricular tachycardia (SVT) (The Basics)
 Patient education: Tachycardia (The Basics)
 Patient education: Ventricular tachycardia (The Basics)
 Sinoatrial nodal reentrant tachycardia (SANRT)
 Sinus tachycardia: Evaluation and management
 Society guideline links: Arrhythmias in adults
 Society guideline links: Atrial fibrillation
 Society guideline links: Basic and advanced cardiac life support in adults
 Society guideline links: Supraventricular arrhythmias
 Society guideline links: Ventricular arrhythmias
 Sustained monomorphic ventricular tachycardia in patients with structural heart disease:
Treatment and prognosis
 Treatment of symptomatic arrhythmias associated with the Wolff-Parkinson-White syndrome
 Unexpected rhythms with normally functioning dual-chamber pacing systems
 Vagal maneuvers
 Ventricular tachycardia in the absence of apparent structural heart disease
 Wide QRS complex tachycardias: Approach to the diagnosis
Overview of the acute management of

tachyarrhythmias
Author:
Jordan M Prutkin, MD, MHS, FHRS
Section Editors:
James Hoekstra, MD
Hugh Calkins, MD
Deputy Editor:
Gordon M Saperia, MD
Contributor Disclosures
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Sep 2020. | This topic last updated: Jan 03, 2020.
INTRODUCTION Tachyarrhythmias, defined as abnormal heart rhythms with
a ventricular rate of 100 or more beats per minute, are frequently symptomatic and often
result in patients seeking care at their provider's office or the emergency department.
Signs and symptoms related to the tachyarrhythmia may include shock, hypotension,
heart failure, shortness of breath, chest pain, acute myocardial infarction, palpitations,
and/or decreased level of consciousness. An overview of the management of these
various arrhythmias will be presented here. More complete reviews of the individual
arrhythmias are discussed separately.
INITIAL DIAGNOSTIC AND TREATMENT DECISIONS In anyone
who presents with a symptomatic tachyarrhythmia, a 12-lead electrocardiogram (ECG)

should be obtained while a brief initial assessment of the patient's overall clinical
assessment is performed. If the patient is hemodynamically unstable, it may be
preferable to obtain only a rhythm strip prior to urgent cardioversion and not wait for a
12-lead ECG. The information acquired from these initial assessments is crucial for
subsequent management of the patient.
Is the patient clinically (or hemodynamically) unstable? — The most important
clinical determination in a patient presenting with a tachyarrhythmia is whether or not the
patient is experiencing signs and symptoms related to the rapid heart rate. These can
include hypotension, shortness of breath, chest pain suggestive of coronary ischemia,
shock, and/or decreased level of consciousness.
Determining whether a patient's symptoms are related to the tachycardia depends upon
several factors, including age and the presence of underlying cardiac disease.
●Hemodynamically unstable and not sinus rhythm – If a patient has

clinically significant hemodynamic instability potentially due to the
tachyarrhythmia, an attempt should be made as quickly as possible to
determine whether the rhythm is sinus tachycardia (algorithm 1). If the rhythm
is not sinus tachycardia, or if there is any doubt that the rhythm is sinus
tachycardia, urgent conversion to sinus rhythm is recommended.
(See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis,
and evaluation", section on 'Similar to sinus rhythm' and "Basic principles and
technique of external electrical cardioversion and defibrillation" and "Wide
QRS complex tachycardias: Approach to the diagnosis", section on
'Assessment of hemodynamic stability'.)
●Hemodynamically stable – If the patient is not experiencing hemodynamic
instability, a nonemergent approach to the diagnosis of the patient's rhythm
can be undertaken [1-3]. A close examination of the 12-lead ECG should
permit the correct identification of the arrhythmia in 80 percent of cases [4].
(See 'Is the QRS complex narrow or wide? Regular or irregular?' below
and "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis,
and evaluation", section on 'Evaluation' and "Wide QRS complex tachycardias:
Approach to the diagnosis", section on 'Evaluation of the electrocardiogram'.)
Is the QRS complex narrow or wide? Regular or irregular? — Treatment of any
tachyarrhythmia depends on a variety of clinical factors. However, most treatment
decisions are made based on the width, morphology, and regularity of the QRS complex
(algorithm 2). In most patients, the differentiation between narrow and wide QRS
complex tachyarrhythmias requires only a surface ECG.
●Narrow QRS complex tachyarrhythmias have a QRS complex <120
milliseconds in duration
●Wide QRS complex tachyarrhythmias have a QRS complex ≥120
milliseconds in duration
The various types of narrow and wide QRS complex tachyarrhythmias are discussed
below. (See 'Narrow QRS complex tachyarrhythmias' below and 'Wide QRS complex
tachyarrhythmias' below.)
NARROW QRS COMPLEX TACHYARRHYTHMIAS Discussion of the
treatment of narrow QRS complex tachycardias will be divided into those with a regular
ventricular response and those with an irregular ventricular response (algorithm
3 and algorithm 1).
Regular narrow QRS complex tachyarrhythmias — The regular narrow QRS complex
tachycardias include (algorithm 2) [3]:
●Sinus tachycardia (see "Sinus tachycardia: Evaluation and management")
●Inappropriate sinus tachycardia (see "Sinus tachycardia: Evaluation and
management", section on 'Inappropriate sinus tachycardia')
●Sinoatrial nodal reentrant tachycardia (SANRT) (see "Sinoatrial nodal
reentrant tachycardia (SANRT)")
●Atrioventricular nodal reentrant tachycardia (AVNRT) (see "Atrioventricular
nodal reentrant tachycardia")
●Atrioventricular reentrant (or reciprocating) tachycardia (AVRT)
(see "Atrioventricular reentrant tachycardia (AVRT) associated with an
accessory pathway")
●Atrial tachycardia (AT) (see "Focal atrial tachycardia")
●Atrial flutter (see "Overview of atrial flutter")
●Intraatrial reentrant tachycardia (IART) (see "Intraatrial reentrant
tachycardia")
●Junctional ectopic tachycardia
●Nonparoxysmal junctional tachycardia
●Idiopathic ventricular tachycardia (see "Ventricular tachycardia in the
absence of apparent structural heart disease")
Because the vast majority of regular narrow QRS complex tachycardias are due to sinus
tachycardia, AVNRT, AVRT, AT, and atrial flutter, these conditions will be presented
here. Discussions regarding the treatment of the other less common types of regular
narrow QRS complex tachycardias are presented separately. (See "Sinus tachycardia:
Evaluation and management", section on 'Inappropriate sinus
tachycardia' and "Sinoatrial nodal reentrant tachycardia (SANRT)", section on
'Treatment' and "Intraatrial reentrant tachycardia", section on
'Treatment' and "Treatment of symptomatic arrhythmias associated with the Wolff-
Parkinson-White syndrome", section on 'Permanent junctional reciprocating
tachycardia'.)
Sinus tachycardia — The most common tachycardia is sinus tachycardia. If it is certain
that the patient's rhythm is sinus tachycardia and clinically significant cardiac symptoms
are present, management should be focused on the underlying disorder and on treating
any contributing cause of the rapid heart rate (eg, coronary ischemia, pulmonary
embolism, respiratory or cardiac failure, hypovolemia, anemia, hyperthyroidism, fever,
pain, or anxiety). This may include volume replacement or diuresis, antibiotics, anti-
pyretics, oxygen, pain control, or other treatments as appropriate. In patients with sinus
tachycardia and certain forms of heart disease, such as coronary disease or aortic
stenosis, treatment may need to be directed at the heart rate itself. In such cases,
cautious use of an intravenous beta blocker is appropriate. (See "Sinus tachycardia:
Evaluation and management" and "Acute myocardial infarction: Role of beta blocker
therapy" and "Medical management of symptomatic aortic stenosis".)
Atrioventricular nodal reentrant tachycardia (AVNRT) — Patients with AVNRT
associated with hemodynamic compromise or severe symptoms due to the tachycardia
(eg, angina, hypotension, or heart failure) require rapid termination of the arrhythmia.
(See "Atrioventricular nodal reentrant tachycardia", section on 'Initial management'.)
●For patients with AVNRT who are hemodynamically unstable related to their
arrhythmia, we recommend immediate DC cardioversion. Consideration for
using vagal maneuvers (Valsalva maneuver or carotid sinus massage) is also
reasonable if it does not delay cardioversion. (See "Vagal maneuvers".)
●For patients with AVNRT associated with severe symptoms due to the
tachycardia (eg, angina, hypotension, heart failure, or mental status changes)
in whom intravenous access is available, we suggest an initial attempt at
termination with adenosine rather than cardioversion. If adenosine cannot be
administered or is ineffective, patients should undergo immediate DC
cardioversion.
●For patients with AVNRT that is not associated with severe symptoms or
hemodynamic collapse, including patients without symptoms, we suggest the
following sequential approach to acute termination:
•Vagal maneuvers (see "Vagal maneuvers")
•IV adenosine
•IV non-dihydropyridine calcium channel blocker or an IV beta blocker
Atrioventricular reentrant tachycardia (AVRT) — Patients with any arrhythmia (ie,
orthodromic AVRT, antidromic AVRT, atrial fibrillation/flutter) involving an accessory
pathway should have a prompt initial assessment of hemodynamic status. AVRT may
result in either a narrow QRS complex tachycardia or a wide QRS complex tachycardia
depending on the direction of conduction across the accessory pathway and also the
presence of aberrant conduction. (See 'Antidromic AVRT' below and "Treatment of
symptomatic arrhythmias associated with the Wolff-Parkinson-White syndrome", section
on 'Acute treatment of symptomatic arrhythmias'.)
●For patients with AVRT who are hemodynamically unstable related to their
arrhythmia, we recommend immediate DC cardioversion. Consideration for
using vagal maneuvers is reasonable if it does not delay cardioversion.
(See "Vagal maneuvers".)
●For patients with acute symptomatic orthodromic AVRT (usually narrow
QRS complex in the absence of an underlying conduction delay) who are
hemodynamically stable, our approach is as follows (table 1):
•We recommend initial treatment with one or more vagal maneuvers
rather than pharmacologic therapy. (See "Vagal maneuvers".)
•If vagal maneuvers are ineffective, pharmacologic therapy with an AV
nodal blocking agent (ie, adenosine, verapamil, beta blockers) should be
instituted. We suggest intravenous adenosine rather than intravenous
verapamil as the initial choice based on its high efficacy and short half-life.
•If adenosine is ineffective, we proceed with intravenous verapamil as the
second-line agent. If orthodromic AVRT persists,
intravenous procainamide and beta blockers approved for intravenous
administration (propranolol, metoprolol, and esmolol) are additional
therapeutic options. Amiodarone may also be considered.
●Because most patients with acute symptomatic antidromic AVRT have a
wide QRS complex, the approach to this arrhythmia is discussed below.
(See 'Antidromic AVRT' below.)
Atrial tachycardia — Focal atrial tachycardias (AT), usually paroxysmal and self-
limited, arise from a single site or area of microreentry outside of the sinus node.
(See "Focal atrial tachycardia", section on 'Acute treatment'.)
●For patients with AT who are felt to be hemodynamically unstable related to
their arrhythmia, we recommend immediate DC cardioversion.
●For a hemodynamically stable patient with symptomatic AT, we suggest
acute treatment with an oral or intravenous beta blocker or non-
dihydropyridine calcium channel blocker (ie, diltiazem or verapamil). Such
treatment may slow the ventricular response and/or terminate the arrhythmia.
Intravenous amiodarone is an acceptable alternative that may be preferred in
a patient with borderline hypotension as amiodarone may slow the rate or
convert the rhythm back to normal sinus.
Atrial flutter — Atrial flutter usually presents as a regular narrow complex tachycardia,
though it occasionally may have an irregular ventricular response. Atrial flutter should
always be considered high on the differential diagnosis when a patient presents with a
regular narrow complex tachycardia with a ventricular response of approximately 150
beats per minute. As with atrial fibrillation, the early steps in the management of a
patient with new onset atrial flutter involve an assessment of the need for cardioversion,
ventricular rate slowing therapy, and antithrombotic therapy. Our initial approach to the
management of patients with atrial flutter is the same as our approach for atrial
fibrillation. (See 'Atrial fibrillation' below.)
Irregular narrow QRS complex tachyarrhythmias — The irregular narrow QRS
complex tachycardias include (algorithm 2):
●Atrial fibrillation (AF) (see "Overview of atrial fibrillation")
●Atrial flutter with variable conduction (see "Overview of atrial flutter")
●Focal atrial tachycardia with variable conduction (see "Focal atrial
tachycardia")
●Multifocal atrial tachycardia (MAT) (see "Multifocal atrial tachycardia")
Atrial fibrillation — Most patients with new onset (ie, first detected or diagnosed) AF
with a rapid rate present with symptoms related to the arrhythmia. Except for
embolization, the symptoms associated with new onset AF are primarily due to a rapid
and/or irregular ventricular response. The early steps in the management of a patient
with new onset rapid AF involve an assessment of the need for cardioversion, ventricular
rate slowing therapy, and antithrombotic therapy. (See "New onset atrial fibrillation",
section on 'Summary and recommendations'.)
●Urgent or emergent cardioversion should be considered for patients with
active ischemia, significant hypotension, severe heart failure, or the presence
of a preexcitation syndrome associated with rapid conduction using the
accessory pathway. (See 'Atrioventricular reentrant tachycardia
(AVRT)' above.)
●For all patients who do not require urgent or emergent cardioversion, we
recommend rate control to improve symptoms and to reduce the risk of
tachycardia-mediated cardiomyopathy. We believe a goal of less than 110
beats per minute is reasonable for an asymptomatic patient with a normal
ejection fraction. Beta blockers and non-dihydropyridine calcium channel
blockers are preferred as first-line agents in most patients, and digoxin should
only rarely be used. Intravenous preparations are preferred to oral
preparations when rapid control of rate is necessary.
●For patients with AF less than 48 hours in duration in whom cardioversion is
planned, the use of antithrombotic therapy pre-cardioversion to reduce the risk
of embolization can be considered.
●For patients with AF longer than 48 hours in duration (or of unknown
duration), we recommend four weeks of therapeutic oral anticoagulation prior
to cardioversion, as opposed to immediate cardioversion. Transesophageal
echocardiography-based (TEE) screening for the presence of atrial thrombi is
recommended if cardioversion is desired earlier than four weeks.
Anticoagulation must be continued for a minimum of four weeks after
cardioversion. Whether long-term anticoagulation is indicated depends on
assessment of the patient's thromboembolic risk profile. (See "Atrial fibrillation:
Risk of embolization".)
Atrial flutter — As with atrial fibrillation, the early steps in the management of a patient
with new onset atrial flutter involve an assessment of the need for cardioversion,
ventricular rate slowing therapy, and antithrombotic therapy. Our initial approach to the
management of patients with atrial flutter is the same as our approach for atrial
fibrillation. (See 'Atrial fibrillation' above.)
Multifocal atrial tachycardia — Multifocal atrial tachycardia (MAT) is an arrhythmia
with organized atrial activity yielding P waves with three or more different morphologies.
MAT is commonly associated with significant underlying pulmonary or cardiac illness.
(See "Multifocal atrial tachycardia", section on 'Treatment'.)
●Most episodes of MAT do not precipitate hemodynamic compromise or
limiting symptoms. Thus, therapy in patients with MAT should be aimed at the
inciting underlying disease.
●Patients with MAT and associated hypokalemia or hypomagnesemia should
undergo electrolyte repletion prior to the initiation of additional medical therapy
for MAT.
●Medical therapy for MAT is indicated only if MAT causes a sustained rapid
ventricular response that causes or worsens myocardial ischemia, heart
failure, peripheral perfusion, or oxygenation. Options for medical therapy for
patients with symptomatic MAT requiring ventricular rate control include non-
dihydropyridine calcium channel blockers and beta blockers. For patients
without heart failure or bronchospasm, we suggest initial therapy with a beta
blocker, usually metoprolol, before calcium channel blockers. Conversely, for
patients with severe bronchospasm, we suggest initial therapy with a non-
dihydropyridine calcium channel blocker, usually verapamil, rather than a beta
blocker. Beta blockers may be used cautiously in patients with stable heart
failure. Rate control therapy is typically unsuccessful, however, without
treating the underlying disorder.
WIDE QRS COMPLEX TACHYARRHYTHMIAS Discussion of the
treatment of wide QRS complex tachycardias, similar to narrow QRS complex

tachycardias, can be divided into those with a regular or irregular ventricular rate.
Regular wide QRS complex tachyarrhythmias — The regular wide QRS complex
tachycardias include (algorithm 2):
●Monomorphic ventricular tachycardia (VT) (see "Sustained monomorphic
ventricular tachycardia in patients with structural heart disease: Treatment and
prognosis" and "Ventricular tachycardia in the absence of apparent structural
heart disease")
●Supraventricular tachycardia with aberrant conduction, underlying conduction
delay, conduction over an accessory pathway (eg, AVNRT with right bundle
branch block), or a paced ventricular response
●Supraventricular tachycardia in a patient on certain antiarrhythmic
medications or with significant electrolyte abnormalities
●Antidromic AVRT
The most concerning potential cause of a wide QRS complex tachycardia is VT, and, in
the majority of patients, the arrhythmia should be assumed to be VT until proven
otherwise.
Immediate assessment of patient stability takes precedence over any further diagnostic
evaluation. (See "Wide QRS complex tachycardias: Approach to the diagnosis", section
on 'Summary and recommendations'.)
●A patient who is unresponsive or pulseless should be treated according to
standard advance cardiac life support (ACLS) algorithms (algorithm 4).
●In a patient who is unstable but conscious, we recommend immediate
synchronized cardioversion with appropriate sedation when possible.
●In a stable patient, a focused diagnostic evaluation may proceed to determine
the etiology of the arrhythmia and guide specific therapy.
Ventricular tachycardia — In stable patients with known or presumed VT, we
recommend the following approach (see "Wide QRS complex tachycardias: Approach to
the diagnosis", section on 'Summary and recommendations'):
●We recommend synchronized external cardioversion, following appropriate
sedation, as the initial therapy for most patients with stable VT. If the patient
has an implantable cardioverter-defibrillator, it may be possible to terminate
the arrhythmia by antitachycardia pacing prior to an attempted cardioversion.
●In patients with refractory or recurrent wide complex tachycardia (WCT), we
suggest an intravenous class I or III antiarrhythmic drug (table 2), such
as amiodarone, lidocaine, or procainamide.
●In selected patients known to have one of the syndromes of VT in the setting
of a structurally normal heart, we suggest calcium channel blockers or beta
blockers be used for arrhythmia termination or suppression. However, the
decision to use these drugs in this setting should be made in consultation with
a cardiologist experienced in arrhythmia management.
Supraventricular tachycardia with aberrant conduction — The narrow complex
supraventricular tachycardia (SVT) rhythms may present with a wide complex in the
setting of aberrant conduction or conduction over an accessory pathway (not including
AVRT).
●In stable patients with a WCT that is known to be an SVT, initial
management is similar to that of an SVT with a narrow QRS complex. A
continuous rhythm strip should be obtained during any intervention that is
intended to slow or terminate the arrhythmia. (See 'Regular narrow QRS
complex tachyarrhythmias' above.)
●For AVNRT or AVRT, or an SVT in which the specific arrhythmia
is unknown, we suggest the following sequence of interventions in order to
terminate the arrhythmia or to slow ventricular response and facilitate
diagnosis in stable patients:
•Vagotonic maneuvers (eg, valsalva or carotid sinus pressure)
•Intravenous adenosine
•Intravenous calcium channel blockers or beta blockers
•Cardioversion in selected persistent cases, or if the patient is unstable
Supraventricular tachycardia with a pacemaker — Regular wide QRS complex
tachycardias in patients with a pacemaker may be due to tracking of one of the typical
supraventricular tachycardias (eg, sinus tachycardia, atrial flutter, etc) or may be due to
endless loop tachycardia (ELT, also referred to as pacemaker-mediated tachycardia
[PMT]). (See "Unexpected rhythms with normally functioning dual-chamber pacing
systems", section on 'Pacemaker-mediated tachycardia'.)
●In patients with tracking of a native supraventricular tachyarrhythmia, the
pacemaker usually should automatically mode switch to a non-tracking mode.
If it does not, placing a magnet on the pacemaker will lead to asynchronous
pacing at a fixed and lower rate, and the pacemaker settings can be adjusted
to prevent rapid pacing.
●If the rhythm is due to ELT, retrograde conduction from the ventricle to the
atrium is sensed by the pacemaker and serves as a trigger to pace the
ventricle, which again conducts back to the atrium and perpetuates the
tachycardia. Placing a magnet on the pacemaker leads to asynchronous
pacing and will stop the tachycardia. Most pacemakers have algorithms to
prevent or treat ELT, but pacemaker settings can usually be reprogrammed if
they are ineffective.
Antidromic AVRT — For patients with acute symptomatic antidromic AVRT (regular
and wide QRS complex) who are hemodynamically stable, our approach is as follows
(see "Treatment of symptomatic arrhythmias associated with the Wolff-Parkinson-White
syndrome", section on 'Acute termination of antidromic AVRT'):
●We treat with intravenous procainamide in an effort to terminate the
tachycardia or, if the tachycardia persists, slow the ventricular response. This
is because it is often difficult to correctly determine that the rhythm is due to
antidromic AVRT and not ventricular tachycardia.
●If the rhythm is definitely known to be antidromic AVRT,
then adenosine, verapamil, or IV beta blockers may be considered, but
monitoring should be continued to ensure that there is not a rapid ventricular
rate if atrial fibrillation (AF) subsequently develops after SVT termination.
Irregular wide QRS complex tachyarrhythmias — The irregular wide QRS complex
tachycardias include (algorithm 2):
●Polymorphic VT, including torsades de pointes (see "Acquired long QT
syndrome: Definitions, causes, and pathophysiology", section on 'Torsades de
pointes')
●Irregular narrow complex tachycardias with aberrant conduction, antegrade
conduction over an accessory pathway (eg, preexcited AF), or underlying
conduction delay (eg, AF with right bundle branch block)
●Ventricular fibrillation
Polymorphic ventricular tachycardia — Polymorphic (or polymorphous) ventricular
tachycardia (VT) is defined as an unstable rhythm with a continuously varying QRS
complex morphology in any recorded electrocardiographic (ECG) lead. Polymorphic VT
is generally a rapid and hemodynamically unstable rhythm, and urgent defibrillation is
usually necessary. In addition to immediate defibrillation, further therapy is intended to
treat underlying disorders and to prevent recurrences. The specific approach depends
upon whether or not the QT interval on the baseline ECG is prolonged. Polymorphic VT
that occurs in the setting of QT prolongation in sinus rhythm is considered as a distinct
arrhythmia, called torsades de pointes. (See "Acquired long QT syndrome: Definitions,
causes, and pathophysiology", section on 'Torsades de pointes'.)
●Prompt defibrillation is indicated in patients with hemodynamically unstable
torsades de pointes.
●In the conscious patient with recurrent episodes of torsades de pointes:
•Intravenous magnesium sulfate (initial dose of 1 to 2 grams IV over 15
minutes, may be followed by an infusion) is first-line therapy, as it is highly
effective for both treatment and prevention of recurrence of long QT-
related ventricular ectopic beats that trigger torsades de pointes. The
benefit is seen even in patients with normal serum magnesium
concentrations at baseline.
•Temporary transvenous overdrive pacing (atrial or ventricular) at about
100 beats per minute is generally reserved for patients who do not
respond to intravenous magnesium.
•In those with congenital long QT syndrome, beta blockers may be used
to reduce the frequency of premature ventricular contractions and shorten
the QT interval.
•For patients with polymorphic VT triggered by pauses or
bradycardia, isoproterenol (initial dose 0.05 to 0.1 mcg/kg per minute in
children and 2 mcg/minute in adults, then titrated to achieve a heart rate
of 100 beats per minute) can be used as a temporizing measure to
achieve a heart rate of 100 beats per minute prior to pacing.
●For patients with polymorphic VT and a normal baseline QT interval, the most
likely cause is myocardial ischemia. Treatments may include:
•Prompt defibrillation in the hemodynamically unstable patient.
•Beta-blockers if blood pressure tolerates. Metoprolol 5 mg intravenously
every five minutes, to a total of 15 mg, may be given.
•IV amiodarone may prevent a recurrent episode.
•Urgent coronary angiography and possible revascularization.
•Short-term mechanical circulatory support.
•Magnesium is less likely to be effective for polymorphic VT if the baseline
QT interval is normal.
●If the polymorphic VT is due to catecholaminergic polymorphic ventricular
tachycardia (CPVT), beta blockers should be used. If it is due to Brugada
syndrome, isoproterenol should be initiated. (See "Catecholaminergic
polymorphic ventricular tachycardia", section on 'Initial
management' and "Brugada syndrome: Prognosis, management, and
approach to screening".)
Preexcited atrial fibrillation — For patients with acute symptomatic preexcited AF who
are hemodynamically stable, our approach is as follows:
●We suggest initial medical therapy with rhythm control versus rate control.
While there is no clear first-line medication for rhythm control, options
include ibutilide and procainamide. (See "Treatment of symptomatic
arrhythmias associated with the Wolff-Parkinson-White syndrome", section on
'Acute treatment of atrial fibrillation with preexcitation'.)
●For all patients with preexcited AF, we recommend not using standard AV
nodal blocking medications (ie, beta blockers, non-dihydropyridine calcium
channel blockers [verapamil and diltiazem], digoxin, adenosine, amiodarone).
Blocking the AV node may result in increased conduction of atrial impulses to
the ventricle by way of the accessory pathway, increasing the ventricular rate
and potentially resulting in hemodynamic instability and development of
ventricular fibrillation.
●While preexcited AF conducts down a bypass pathway, in contrast to AVRT,
the rhythm is irregularly irregular and wide complex.
SOCIETY GUIDELINE LINKS Links to society and government-sponsored
guidelines from selected countries and regions around the world are provided
separately. (See "Society guideline links: Atrial fibrillation" and "Society guideline links:
Arrhythmias in adults" and "Society guideline links: Ventricular arrhythmias" and "Society
guideline links: Basic and advanced cardiac life support in adults" and "Society guideline
links: Supraventricular arrhythmias".)
INFORMATION FOR PATIENTS UpToDate offers two types of patient
education materials, "The Basics" and "Beyond the Basics." The Basics patient
education pieces are written in plain language, at the 5 th to 6th grade reading level, and
they answer the four or five key questions a patient might have about a given condition.
These articles are best for patients who want a general overview and who prefer short,
easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10 th to 12th grade
reading level and are best for patients who want in-depth information and are
comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you
to print or e-mail these topics to your patients. (You can also locate patient education
articles on a variety of subjects by searching on "patient info" and the keyword(s) of
interest.)
●Basics topics (see "Patient education: Tachycardia (The

Basics)" and "Patient education: Ventricular tachycardia (The
Basics)" and "Patient education: Supraventricular tachycardia (SVT) (The
Basics)")
SUMMARY AND RECOMMENDATIONS
●For hemodynamically unstable patients, urgent cardioversion should be

performed.
●Further treatment recommendations regarding the acute management of
tachyarrhythmias are presented throughout this topic.
ACKNOWLEDGMENT The authors and UpToDate would like to thank Dr.
Philip Podrid and Dr. Leonard Ganz, who contributed to earlier versions of this topic
review.
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Link MS. Clinical practice. Evaluation and initial treatment of
supraventricular tachycardia. N Engl J Med 2012; 367:1438.
2. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS Guideline for
the Management of Adult Patients With Supraventricular Tachycardia: A
Report of the American College of Cardiology/American Heart Association
Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J
Am Coll Cardiol 2016; 67:e27.
3. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the
management of patients with supraventricular tachycardiaThe Task Force
for the management of patients with supraventricular tachycardia of the
European Society of Cardiology (ESC). Eur Heart J 2020; 41:655.
4. Kalbfleisch SJ, el-Atassi R, Calkins H, et al. Differentiation of paroxysmal
narrow QRS complex tachycardias using the 12-lead electrocardiogram. J
Am Coll Cardiol 1993; 21:85.
Topic 936 Version 35.0
Close
Lexicomp drug information & Lexi-Interact are subject to the Lexicomp License Agreement.
© 2020 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
 Language
 Subscription and License Agreement

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos







 Wolters Kluwer Health

 Emmi®

 Facts & Comparisons®

 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Patient

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 INTRODUCTION
 DEFINITIONS
 TYPES OF NARROW QRS COMPLEX TACHYCARDIA
o Differential diagnosis of narrow QRS complex tachycardias
o Paroxysmal SVT
 PATHOGENESIS
o Mechanisms of reentry
o Automaticity and triggered activity
 CLINICAL MANIFESTATIONS
 DIAGNOSIS
 EVALUATION
o Assessing the patient for hemodynamic stability
o Assessing the ECG for regularity of the rhythm
o ECG identification of atrial activity
 Methods to aid in identifying P waves
 Valsalva maneuver
 Carotid sinus massage
 Intravenous adenosine
 Administration and side effects
 Possible outcomes following vagal maneuvers or adenosine administration
o ECG characterization of atrial activity
 Atrial rate
 P wave morphology
 Similar to sinus rhythm
 Abnormal P waves
 Retrograde P waves
 RP relationship
 Short RP tachycardias
 Long RP tachycardias
 Undetectable P waves
o Electrophysiologic testing
o Other cardiac testing
 REFERENCES
GRAPHICS view all
 Algorithms
oEvaluation narrow QRS complex tachycardias in unstable patients
 Figures
oSites of reentry in supraventricular tachyarrhythmias
oMechanisms of reentry in cardiac arrhythmias
oTypical atrioventricular nodal reentrant tachycardia
oCommon slow fast AVNRT
oECG generation in common AVNRT
oOrthodromic AVRT
oUncommon fast slow AVNRT
 Tables
oNarrow QRS complex tachycardia classification by anatomy
 Waveforms
oECG atrial fibrillation 1
oECG atrial fibrillation 2
oECG single-lead multifocal atrial tachycardia
oAtrial flutter CS massage
oSingle-lead ECG showing atrial flutter
oAtypical atrial flutter
oECG strip sinus tachycardia
oECG SA nodal reentrant tachycardia
o12 lead WPW
RELATED TOPICS
 Acute myocardial infarction: Role of beta blocker therapy
 Cardiac arrhythmias due to digoxin toxicity
 ECG tutorial: Basic principles of ECG analysis
 Electrocardiographic and electrophysiologic features of atrial flutter
 Invasive diagnostic cardiac electrophysiology studies
 Medical management of symptomatic aortic stenosis
 Overview of catheter ablation of cardiac arrhythmias
 Overview of the acute management of tachyarrhythmias
 Reentry and the development of cardiac arrhythmias
 Second degree atrioventricular block: Mobitz type I (Wenckebach block)
 Supraventricular arrhythmias after myocardial infarction
 The electrocardiogram in atrial fibrillation
 Vagal maneuvers
 Wide QRS complex tachycardias: Approach to management
 Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis
Narrow QRS complex tachycardias: Clinical

manifestations, diagnosis, and evaluation
Author:
Leonard I Ganz, MD, FHRS, FACC
Section Editors:
Bradley P Knight, MD, FACC
Ary L Goldberger, MD
James Hoekstra, MD
Deputy Editor:
INTRODUCTION Tachyarrhythmias, defined as abnormal heart rhythms with
a ventricular rate of 100 or more beats per minute, can result from a variety of
pathologies and are frequently symptomatic. Signs and symptoms related to the
tachyarrhythmia most commonly include palpitations or chest discomfort, but may also
include shock, hypotension, heart failure (HF), shortness of breath, and/or decreased
level of consciousness. Symptoms can sometimes may be more subtle and may include
fatigue, lightheadedness, or exercise intolerance. Some patients are truly asymptomatic;
this may be more common in nonparoxysmal (incessant) tachycardias.
This topic will provide a broad overview of the different causes of narrow QRS complex
tachycardia and an approach to their evaluation and diagnosis. An overview of the acute
management of tachyarrhythmias, along with detailed discussions of specific narrow
complex tachycardias (eg, AVNRT, AVRT, and AT) and a broad discussion of wide
complex tachycardias, are presented separately. (See "Overview of the acute
management of tachyarrhythmias" and "Atrioventricular nodal reentrant
tachycardia" and "Atrioventricular reentrant tachycardia (AVRT) associated with an
accessory pathway" and "Focal atrial tachycardia" and "Wide QRS complex
tachycardias: Approach to the diagnosis" and "Wide QRS complex tachycardias:
Approach to management".)
DEFINITIONS Tachycardias, with a ventricular heart rate exceeding 100 beats
per minute, are broadly categorized based upon the width of the QRS complex on the
electrocardiogram (ECG) [1].
●A narrow QRS complex (<120 milliseconds) reflects rapid activation of the
ventricles via the normal His-Purkinje system, which in turn suggests that the
arrhythmia originates above or within the His bundle (ie, a supraventricular
tachycardia). The site of origin may be in the sinus node, the atria, the
atrioventricular (AV) node, the His bundle, or some combination of these sites.
●A widened QRS (≥120 milliseconds) occurs when ventricular activation is
abnormally slow. The most common reason that a QRS is widened is because
the arrhythmia originates below the His bundle in the bundle branches,
Purkinje fibers, or ventricular myocardium (eg, ventricular tachycardia).
Alternatively, a supraventricular arrhythmia can produce a widened QRS if
there are either pre-existing or rate-related abnormalities within the His-
Purkinje system (eg, supraventricular tachycardia with aberrancy), or if
conduction occurs over an accessory pathway. Thus, wide QRS complex
tachycardias may be either supraventricular or ventricular in origin. (See "Wide
QRS complex tachycardias: Approach to the diagnosis".)
TYPES OF NARROW QRS COMPLEX TACHYCARDIA
Differential diagnosis of narrow QRS complex tachycardias — Narrow QRS

complex tachycardias can be divided into those that require only atrial tissue for their
initiation and maintenance, and those that require the AV junction (table 1) [2].
The narrow QRS complex tachycardias include:
●Sinus tachycardia (ST) (see "Sinus tachycardia: Evaluation and

management")
●AV nodal reentrant tachycardia (AVNRT) (see "Atrioventricular nodal
reentrant tachycardia")
●AV reentrant (or reciprocating) tachycardia (AVRT) (see "Atrioventricular
reentrant tachycardia (AVRT) associated with an accessory pathway")
●Atrial tachycardia (AT) (see "Focal atrial tachycardia")
●Inappropriate ST(see "Sinus tachycardia: Evaluation and management",
section on 'Inappropriate sinus tachycardia')
●Sinoatrial nodal reentrant tachycardia (SANRT) (see "Sinoatrial nodal
reentrant tachycardia (SANRT)")
●Intraatrial reentrant tachycardia (IART) (see "Intraatrial reentrant
tachycardia")
●Atrial fibrillation (see "Overview of atrial fibrillation")
●Atrial flutter (see "Overview of atrial flutter")
●Multifocal AT (MAT) (see "Multifocal atrial tachycardia")
Paroxysmal SVT — The term paroxysmal supraventricular tachycardia (PSVT) is
applied to a subset of narrow QRS complex tachycardias, those intermittent SVTs with
abrupt onset and offset and a regular ventricular response, in contrast to AF, atrial
flutter, and MAT, which have an irregular ventricular response. Because they have
distinct clinical characteristics, these narrow complex tachycardias are usually
considered separately.
The prevalence of PSVT is similar in males and females (although it is slightly higher in
males) and increases progressively with age. Among a prospective cohort of more than
half a million United Kingdom residents, the prevalence of PSVT was approximately 29
per 10,000 persons under age 55 and increased to between 53 (females) and 74
(males) per 10,000 persons ≥65 years of age [3].
PSVTs are often due to reentry, although the sites of reentry vary (figure 1) [1,4]. The
major causes are AVNRT, which accounts for approximately 60 percent of cases; AVRT,
which accounts for approximately 30 percent of cases; and, in about 10 percent of
cases, an AT or SANRT [5]. Junctional ectopic tachycardia and nonparoxysmal
junctional tachycardia are rare in adults but can represent a larger portion of PSVTs in
children.
●AVNRT is characterized by two pathways within the AV node or perinodal
atrial tissue. (See "Atrioventricular nodal reentrant tachycardia".)
●AVRT is characterized by an extranodal accessory pathway connecting the
atrium and ventricle. The ECG shows delta waves during sinus rhythm if there
is antegrade conduction via the accessory pathway, leading to a diagnosis of
Wolff-Parkinson-White syndrome (WPW). The delta waves are lost during an
episode of orthodromic AVRT, the most common tachyarrhythmia in patients
with WPW. (See "Atrioventricular reentrant tachycardia (AVRT) associated
with an accessory pathway" and "Wolff-Parkinson-White syndrome: Anatomy,
epidemiology, clinical manifestations, and diagnosis".)
●SANRT and intraatrial reentrant tachycardia (IART) are the two major types
of paroxysmal reentrant supraventricular tachycardias in which the reentrant
circuit does not involve the AV or accessory pathways. (See "Sinoatrial nodal
reentrant tachycardia (SANRT)" and "Intraatrial reentrant tachycardia".)
●PJRT (permanent form of junctional reciprocating tachycardia) occurs due to
a slowly conducting concealed accessory pathway. (See "Atrioventricular
reentrant tachycardia (AVRT) associated with an accessory pathway", section
on 'Permanent junctional reciprocating tachycardia'.)
●AT can be at times incessant. (See "Focal atrial tachycardia".)
PATHOGENESIS Reentry is the most common cause of narrow QRS
complex tachycardia. Increased automaticity and triggered activity occur less frequently
[6].
Mechanisms of reentry — Reviewed briefly, reentry requires two distinct electrical
conduction pathways or tissues with different electrophysiologic properties that are
linked proximally and distally, forming an anatomic or functional circuit (figure 2) [1,4].
The reentrant circuit may become repetitively activated, producing a sustained reentrant
tachycardia. The type of arrhythmia that ensues with narrow QRS tachycardias is
determined by the characteristics and location of the reentrant circuit (figure 1).
The mechanisms of reentry are discussed in detail elsewhere. (See "Reentry and the
development of cardiac arrhythmias".)
Automaticity and triggered activity — Other mechanisms of narrow QRS complex
tachycardia include:
●Enhanced normal automaticity (as in sinus tachycardia)
●Abnormal automaticity (resulting in an ectopic atrial or junctional tachycardia)
●"Triggered activity," which may underlie some arrhythmias due to digitalis
intoxication (such as atrial tachycardia with or without AV block or arrhythmias
in the setting of acute ischemia or infarction)
These mechanisms are considered in detail in topics dealing with the specific
arrhythmias. (See "Focal atrial tachycardia", section on 'Mechanisms and
etiology' and "Cardiac arrhythmias due to digoxin toxicity".)
CLINICAL MANIFESTATIONS The response to a rapid heart rate can be
quite variable depending on how fast the heart is beating, resultant blood pressure and
tissue perfusion, underlying comorbidities, and the sensitivity of the individual patient to
the symptoms. Patients with a narrow QRS complex tachycardia can present with a
variety of symptoms, including:
●Palpitations
●Syncope or presyncope
●Lightheadedness or dizziness
●Diaphoresis
●Chest pain
●Shortness of breath
Most commonly, patients with a narrow QRS complex tachycardia present with
palpitations, the sensation of a rapid or irregular heart beat felt in the anterior chest or
neck. Usually the symptoms are abrupt in onset, although this may vary depending on
the specific arrhythmia. Palpitations may be associated with diaphoresis,
lightheadedness, or dizziness.
Patients with a narrow QRS complex tachycardia may also report shortness of breath or
chest discomfort. While shortness of breath or chest discomfort can occur in any patient,
those with underlying cardiac comorbidities (eg, coronary heart disease, cardiomyopathy
or valvular heart disease with or without HF) are more likely to present in this fashion,
particularly at higher heart rates (>150 beats per minute).
Syncope is a rare presentation for persons presenting with a narrow QRS complex
tachycardia, since in most instances the heart rate is not so rapid as to impair ventricular
function and cardiac output. However, a narrow QRS complex tachycardia with a very
rapid ventricular rate (>250 beats per minute, as might be seen in persons with atrial
fibrillation or flutter and an accessory pathway) may result in diminished cardiac output
and syncope. (See 'Atrial rate' below.)
The physical examination in a patient with narrow QRS complex tachycardia reveals a
rapid pulse which may be regular or irregular depending on the underlying cardiac
rhythm. Cardiac auscultation also reveals a rapid heartbeat. While other physical
examination findings may be present in situations where the tachycardia has led to or
exacerbated another condition (eg, hypotension following syncope, lung congestion in a
patient with HF), there are no other specific physical examination findings which are
universally seen in patients with a narrow complex tachycardia.
DIAGNOSIS The diagnosis of a narrow QRS complex tachycardia is usually
suspected in a patient with palpitations when a pulse greater than 100 beats per minute
is present on physical examination. The differentiation between narrow and wide QRS
complex tachycardia requires only a surface ECG, which shows a heart rate greater
than 100 beats per minute along with narrow QRS complexes that are less than 120
milliseconds in duration. A variety of arrhythmias result in the ECG appearance of a
narrow QRS complex tachycardia. (See 'Types of narrow QRS complex
tachycardia' above.)
Once a narrow QRS complex tachycardia has been identified, further scrutiny of the
ECG is required to identify the specific arrhythmia in a particular patient, as diagnostic
evaluation and therapy will differ depending on the underlying arrhythmia.
(See 'Evaluation' below.)
Invasive electrophysiology testing is not required to broadly make the diagnosis of a
narrow QRS complex tachycardia, but on rare occasions it is needed to diagnose (and
potentially treat with catheter ablation) the specific arrhythmia. (See 'Electrophysiologic
testing' below.)
EVALUATION Evaluation of a patient with a narrow QRS complex tachycardia
involves two primary components:

●Assessment of the patient for symptoms and signs of hemodynamic stability
(or instability)
●Assessment of the patient's ECG for clues to the type of tachycardia present
Often these steps are performed nearly simultaneously in an acute care setting, as the
provider can be assessing the patient at the same time that the ECG is being obtained.
Assessing the patient for hemodynamic stability — The most important clinical

determination to make when a narrow QRS tachycardia is noted is whether the patient is
experiencing signs and symptoms related to the rapid heart rate. These can include
hypotension, shortness of breath, chest pain suggestive of coronary ischemia, shock,
and/or decreased level of consciousness (algorithm 1 and algorithm 2).
Determining whether a patient's symptoms are related to the tachycardia depends upon
several factors, including age and the presence of underlying cardiac disease. As an
example, PSVT with a heart rate of 200 beats/minute may be tolerated by an otherwise
healthy young adult with no or few symptoms (eg, palpitations). On the other hand, AF
at a rate of 120 beats/minute may precipitate angina in an elderly patient with significant
coronary heart disease.
●Hemodynamically unstable and not sinus rhythm – If a patient has clinically

significant hemodynamic instability potentially due to a narrow QRS complex
tachycardia (algorithm 1), an attempt should be made as quickly as possible to
determine whether the rhythm is sinus tachycardia (ST). If the rhythm is not
sinus tachycardia, or if there is any doubt that the rhythm is sinus
(See 'Similar to sinus rhythm' below and "Overview of the acute management
of tachyarrhythmias" and "Basic principles and technique of external electrical
cardioversion and defibrillation".)
●Hemodynamically unstable and sinus rhythm – If it is certain that the patient's
rhythm is ST and clinically significant cardiac symptoms are present (algorithm
2), management should be focused on the underlying cardiac disorder and on
treating any contributing cause of the rapid heart rate (such as coronary
ischemia, respiratory or cardiac failure, cardiac tamponade, hypovolemia,
anemia, fever, pain, or anxiety). In patients with ST and certain forms of heart
disease, such as coronary disease or aortic stenosis, treatment may need to
be directed at the heart rate itself. In such cases, cautious use of an
intravenous beta blocker is appropriate (eg, metoprolol 5 mg intravenously
every two minutes until the heart rate is controlled, to a total of 15 mg, followed
by an oral regimen). (See "Sinus tachycardia: Evaluation and
management" and "Acute myocardial infarction: Role of beta blocker
therapy" and "Medical management of symptomatic aortic stenosis".)
●Hemodynamically stable – If the patient is not experiencing hemodynamic
instability, a nonemergent approach to the diagnosis of the patient's rhythm
can be undertaken (algorithm 2) [1]. A close examination of the 12-lead ECG
should permit the correct identification of the arrhythmia in 80 percent of cases
[7]. In some patients, increasing the ECG paper speed (from the standard 25
mm/second to 50 mm/second) can improve the likelihood of a correct
diagnosis, or simple vagal blocking maneuvers may slow the ventricular rate to
better elucidate the underlying rhythm [8]. (See 'ECG identification of atrial
activity' below and 'ECG characterization of atrial activity' below.)
Assessing the ECG for regularity of the rhythm — Following the determination of
hemodynamic stability, the next step in the assessment of a narrow QRS complex
tachycardia is to determine if the rhythm appears to be regular or irregular (algorithm 2).
While the majority of narrow QRS complex tachycardias are associated with a regular
ventricular rate (with atrial fibrillation [AF] being the most notable exception), underlying
conduction system disease and certain drug toxicities (ie, digoxin) can lead to irregular
appearing rhythms due to intermittent block of conduction between the atria and the
ventricles.
Examples of regular and irregular rhythms include:
●Regular – sinus tachycardia, AV nodal reentrant tachycardia, AV

reciprocating tachycardia, atrial flutter (usually), atrial tachycardia (AT)
●Irregular – AF, multifocal AT
If the rhythm is irregular, the ECG should be scrutinized for discrete atrial activity and for
any evidence of a pattern to the irregularity. If the rhythm is irregularly irregular (that is,
no pattern can be detected), the arrhythmia will almost always be either:
●AF, where no discernible discrete P waves (waveform 1 and waveform 2) can

be identified (see "The electrocardiogram in atrial fibrillation")
●Multifocal AT, in which discrete P waves of several morphologies (waveform
3) are present (see "Multifocal atrial tachycardia")
If the rhythm is irregular but has some periods of regularity, other arrhythmias (Mobitz I
second degree AV block) and/or drug toxicity (ie, digoxin toxicity) should be considered.
(See "Second degree atrioventricular block: Mobitz type I (Wenckebach
block)" and "Cardiac arrhythmias due to digoxin toxicity".)
ECG identification of atrial activity — Characterization of atrial activity is essential to
the diagnosis of narrow complex tachycardias (algorithm 2). However, the first step in
this process, the identification of P waves, can be difficult.
Methods to aid in identifying P waves — In ideal circumstances, P waves can be
easily seen on the surface ECG. However, due to the rapid rate of the tachycardia, P
waves are often superimposed on other parts of the surface ECG. In cases where P
waves cannot be clearly identified, the Valsalva maneuver, carotid sinus massage, or
the administration of intravenous adenosine may help to clarify the diagnosis [9]. These
maneuvers may also terminate the arrhythmia in some cases (especially if the rhythm is
AVNRT or AVRT). (See 'Possible outcomes following vagal maneuvers or adenosine
administration' below.)
Valsalva maneuver — The Valsalva maneuver induces a temporary slowing of SA
nodal activity and AV nodal conduction by stimulating baroreceptors in the aorta, which
triggers a reflex increase in vagus nerve activity and sympathetic withdrawal. Patients
must be cooperative enough to comply with instructions and must be continually
monitored on a cardiac monitor in order for this maneuver to be successful. The process
of performing and interpreting the hemodynamic responses to the Valsalva maneuver is
discussed in detail elsewhere. (See "Vagal maneuvers", section on 'Valsalva
maneuver'.)
The Valsalva maneuver is generally safe and well-tolerated, though it does require some
effort on the patient's part to perform. While the Valsalva maneuver may not be as
effective as adenosine in slowing the AV nodal conduction rate, it can often be
accomplished while preparing for an adenosine challenge, especially in patients not
eligible for carotid sinus massage. Additionally, the Valsalva maneuver may terminate
some narrow complex tachycardias, although data regarding the effectiveness of the
maneuver are inconclusive. In a 2013 Cochrane Review of three randomized trials (316
patients) that compared the Valsalva maneuver with other vagal maneuvers, there was
insufficient evidence to support or refute the effectiveness of the Valsalva maneuver
[10]. However, given the general safety of the maneuver, its lack of expense, and its
occasional effectiveness, we ask patients to perform the Valsalva maneuver prior to
using other vagal maneuvers or medications.
Carotid sinus massage — Carotid sinus massage induces a temporary slowing of SA
nodal activity and AV nodal conduction. External pressure on the carotid bulb stimulates
baroreceptors in the carotid sinus, which triggers a reflex increase in vagus nerve
activity and sympathetic withdrawal. The process of performing carotid sinus massage is
discussed in detail elsewhere. (See "Vagal maneuvers", section on 'Carotid sinus
massage'.)
Carotid sinus massage is generally safe and well tolerated, but potential complications
include profound hypotension and bradycardia (including transient loss of
consciousness), transient ischemic attack or stroke, and arrhythmias. Due to these
potential complications, carotid sinus massage should be performed with simultaneous
ECG and blood pressure monitoring. (See "Vagal maneuvers", section on
'Complications'.)
Intravenous adenosine — Adenosine interacts with A1 receptors on the surface of
cardiac cells, activating potassium channels and causing an increase in potassium
conductance (IK). Adenosine also indirectly reduces calcium influx (ICa) into cells by
antagonizing catecholamine-stimulated adenylate cyclase. The resulting effects include
a slowing of the sinus rate and an increase in the AV nodal conduction delay, similar to
the effects seen with the Valsalva maneuver and carotid sinus massage [1].
Adenosine is used for the intravenous management of paroxysmal narrow QRS complex
tachycardias in which the AV node is involved. However, like the Valsalva maneuver and
carotid sinus massage, adenosine can have both diagnostic and therapeutic effects,
terminating some AV node dependent arrhythmias and producing transient AV nodal
block that can clarify diagnoses such as atrial flutter or AT. Adenosine is cleared from
the circulation extremely rapidly, with a half-life of less than five seconds, which reduces
the likelihood of serious untoward effects [4].
Administration and side effects — For intravenous adenosine administration, the
patient should be supine and should have ECG and blood pressure monitoring. It is
valuable to perform a 12-lead rhythm strip during administration of adenosine, as there
are often clues at the time of termination as to the mechanism of the PSVT. The drug is
administered by rapid intravenous injection over one to two seconds at a peripheral site,
followed by a normal saline flush. The rapid administration of both the drug and the
saline flush is most easily accomplished through a three-way stopcock. The usual initial
dose is 6 mg, which can be followed by a maximal single dose of 12 mg if not
successful. Repeated dosing beyond the 12 mg bolus is not usually effective. If a central
intravenous access site is used, the initial dose should not exceed 3 mg and may be as
little as 1 mg [4,9].
The effects of adenosine are blocked by methylxanthines such as theophylline and
caffeine and potentiated by dipyridamole. Heart transplant recipients exhibit a
supersensitive response to adenosine [11].
The most common side effects of adenosine are facial flushing (18 percent), shortness
of breath, palpitations, chest pain, and lightheadedness. Patients should be warned
regarding these symptoms before adenosine administration. Transient asystole is a rare
complication.
In patients with an accessory pathway capable of antegrade (atrium to ventricle)
conduction, AF can degenerate into ventricular fibrillation. As a result, caution should be
used when giving adenosine if an accessory pathway with antegrade conduction is a
possible mechanism, and emergency resuscitation equipment should be available.
(See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations,
and diagnosis", section on 'Atrial fibrillation'.)
Possible outcomes following vagal maneuvers or adenosine
administration — Following the Valsalva maneuver, carotid sinus massage, or the
intravenous administration of adenosine to patients with a narrow QRS complex
tachycardia, one of four possible results
may be seen:
●The slowing of SA nodal activity can cause a temporary decrease in the atrial
rate (in patients with sinus tachycardia).
●The slowing of AV nodal conduction can lead to AV nodal block, which may
"unmask" atrial electrical activity (ie, reveal P waves or flutter waves) by
decreasing the number of QRS complexes that obscure the electrical baseline
(waveform 4).
●In some cases, no response is obtained. Usually the lack of any response
would suggest inadequate performance of the vagal maneuver or inadequate
dosing of the adenosine (either insufficient dose or administration which was
too slow such that the adenosine was metabolized prior to arrival in the heart).
●The transient slowing of AV nodal conduction can terminate some narrow
QRS complex arrhythmias by interrupting a reentry circuit that requires AV
nodal conduction (especially AVNRT and AVRT). A continuous ECG tracing
should be recorded during these maneuvers, because the response may aid in
the diagnosis [6]:
•Termination of the tachycardia with a P wave after the last QRS complex
is most common in AVRT or AVNRT and is rarely seen with AT.
•Termination of the tachycardia with a QRS complex can be seen with
AVRT, AVNRT, or AT.
•If the tachycardia continues despite successful induction of at least some
degree of AV nodal blockade, the rhythm is almost certainly AT or atrial
flutter; AVRT is excluded, and AVNRT is very unlikely.
If the use of carotid sinus massage and/or adenosine does not terminate the
tachycardia or permit a diagnosis for the tachycardia that was terminated,
further evaluation begins with characterization of the atrial activity (P waves)
on the ECG. (See 'ECG characterization of atrial activity' below.)
ECG characterization of atrial activity — Identification and characterization of atrial
activity (ie, the P wave) is central to the diagnosis of narrow QRS complex tachycardias
(algorithm 2). The evaluation of atrial activity includes assessment of four features:
●The atrial rate
●The P wave morphology (ie, identical to normal sinus rhythm, retrograde, or
abnormal) (see 'P wave morphology' below)
●The position of the P wave in relation to the preceding and following QRS
complexes (ie, the RP relationship) [7] (see 'RP relationship' below)
●The relationship between atrial and ventricular rates (1:1 or otherwise)
It is uncommon that any one of these features can identify the mechanism of an
arrhythmia. In combination, however, these features (particularly the P wave morphology
and RP relationship) often provide a probable diagnosis.
Atrial rate — There is substantial overlap between the atrial rates of most narrow QRS
complex tachycardias. Thus, this feature in isolation is rarely diagnostic. The exception
is with very fast atrial rates (eg >250 beats/minute), which are generally associated with
one of two diagnoses: atrial flutter or AT.
Atrial flutter has several unique features that often make it easily distinguishable from
other narrow QRS complex tachycardias, including the following:
●The atrial rate is typically 250 to 350 beats per minute. Classically, the atrial
rate is close to 300 beats per minute with 2:1 AV conduction, resulting in a
ventricular rate of 150 beats per minute.
●The P waves typically exhibit a classic "sawtooth" pattern without an
isoelectric baseline; these complexes are referred to as flutter waves or "F"
waves (waveform 5). If this pattern is not evident initially, vagal stimulation and
intravenous adenosine can reduce the ventricular rate and make the "F"
waves more evident (waveform 4).
Atypical reentrant circuits (often seen post-operatively or post-ablation) and the
influence of antiarrhythmic drugs can alter these classic findings, resulting in atypical
flutter waves (waveform 6). The electrocardiographic and electrophysiologic features of
atrial flutter are discussed in detail separately. (See "Electrocardiographic and
electrophysiologic features of atrial flutter".)
P wave morphology — The P wave morphology provides insight into the site of origin
of atrial activity, and therefore the mechanism of the tachycardia. The P wave should be
evaluated in as many leads as possible, ideally all 12 leads of a surface ECG, although
in some situations a single-lead ECG strip may be all that is available for review.
The P wave morphology can be classified into one of three general categories:
●Similarto sinus rhythm

●Retrograde
●Abnormal
Similar to sinus rhythm — The most reliable way to determine if the P wave in a
narrow complex tachycardia is consistent with an origin from the sinus node is to
compare the P wave during the tachycardia to that from the same patient during sinus
rhythm. Although sinus P wave morphology can vary slightly with changes in heart rates,
the P wave during the tachycardia should be nearly identical to that seen on the
baseline ECG in all 12 leads.
If a baseline ECG is not available, characteristics of the P wave can still suggest origin
from the region of the sinus node. A sinus P wave is usually upright in leads I, aVL, and
the inferior leads II, III, and aVF, and negative in lead aVR. These features indicate that
atrial activity is proceeding in a right-to-left and superior-to-inferior direction. (See "ECG
tutorial: Basic principles of ECG analysis", section on 'P wave'.)
At atrial rates greater than approximately 140 beats per minute or in the presence of first
degree AV block, the P wave tends to merge into the preceding T or U wave, making P
wave identification difficult (waveform 7). In such cases, slowing of the ventricular
response using the Valsalva maneuver, carotid sinus massage, or adenosine may allow
for better analysis of the P waves.
If P wave morphology is consistent with origination from the sinus node, the differential
diagnosis of the tachycardia includes:
●ST(see "Sinus tachycardia: Evaluation and management", section on

'Definition and ECG features')
●Inappropriate ST (IST) (see "Sinus tachycardia: Evaluation and
management", section on 'Inappropriate sinus tachycardia')
●Sinoatrial nodal reentrant tachycardia (SANRT) (waveform 8) (see "Sinoatrial
nodal reentrant tachycardia (SANRT)")
●AT, usually originating near the sinus node (see "Focal atrial tachycardia",
section on 'Electrocardiographic features')
P wave morphology alone is not sufficient to distinguish these arrhythmias from one
another. In persons with a P wave morphology that is consistent with origination from the
sinus node, additional ECG features that assist in the diagnosis include:
●Atrial
rate – In ST and IST, the rate typically ranges from 100 to 180 beats
per minute. Faster atrial rates suggest an AT.
●Onset/offset pattern – ST and IST have smooth, gradual changes in rate.
Both SANRT and AT have an abrupt onset and offset, although the rate in AT
can vary significantly with autonomic tone.
●Relationship between atrial and ventricular activity – In ST and IST, there is
usually a 1:1 relationship between atrial and ventricular activity.
●The response to vagal maneuvers or adenosine – With ST or IST, there is a
gradual slowing of the atrial and ventricular rates, followed by a gradual
resumption of the previous rate. In contrast, SNRT can terminate abruptly with
these maneuvers.
Abnormal P waves — Any P wave that does not have the characteristics of a sinus P
wave is considered an abnormal P wave. Abnormal P waves that are due to retrograde
conduction from the ventricle to the atrium are a specific subset of abnormal P waves.
(See 'Retrograde P waves' below.)
Abnormal P waves that are not retrograde are most consistent with AT, although some
patients with AVRT have abnormal P waves.
Retrograde P waves — P waves that are due to retrograde conduction from the
ventricle to the atrium are a specific subset of abnormal P waves. These P waves have
a characteristic morphology and suggest certain diagnoses, specifically:
●AVNRT
●AVRT
The most common retrograde P wave morphology is associated with atrial activation
that originates from the AV node and proceeds in an inferior-to-superior direction. Thus,
the defining trait of a retrograde P wave is that it is negative in the inferior leads II, III,
and aVF. Due to the central location of the AV node, atrial activation proceeds
simultaneously leftward and rightward, so the P wave morphology in leads I, aVL, and
aVR varies among patients, but it is often relatively narrow. In addition, because the AV
node is posteriorly located, the activation is usually posterior-to-anterior, producing a
narrow but positive P wave in lead V1.
Retrograde P waves due to conduction via an accessory pathway can have a variety of
morphologies, depending upon the site of the pathway. However, they are still usually
negative in the inferior leads. (See "Wolff-Parkinson-White syndrome: Anatomy,
epidemiology, clinical manifestations, and diagnosis".)
Because retrograde P waves are often associated with a short RP interval, they can
blend with the terminal portion of the QRS. If a baseline ECG during sinus rhythm is
available for comparison, a pseudo S wave in the inferior leads or a pseudo R' in V1 that
is not present during sinus rhythm is often a retrograde P wave (figure 3) [6,7,12].
(See 'RP relationship' below.)
RP relationship — In patients with a retrograde P wave, the temporal relationship
between the P wave and the R wave divides narrow complex tachycardias into two
categories: short RP and long RP tachycardias. The RP interval is defined as the
interval from the onset of the QRS to the onset of the P wave.
Short RP tachycardias — If the RP interval is less than one-half of the RR interval, the
tachycardia is considered a short RP tachycardia. The differential diagnosis of a short
RP tachycardia is generated by considering the P wave morphology.
●Abnormal P wave – The combination of abnormal P waves and a short RP
interval is most often seen in the setting of an AT with AV nodal conduction
delay. (See 'Abnormal P waves' above.)
●Retrograde P wave – The combination of retrograde P waves and a short RP
interval is typical of the "common" form of AVNRT and of AVRT utilizing an
accessory pathway. (See 'Retrograde P waves' above.)
In the "common" form of AVNRT (which accounts for 90 percent of AVNRT) [13], reentry
occurs in the AV node and perinodal tissues. Antegrade conduction occurs down the
slow pathway and retrograde conduction up the fast pathway (figure 4 and figure 5).
This slow-fast pattern gives rise to retrograde P waves that may be inapparent if
obscured by the QRS complex (figure 3). (See "Atrioventricular nodal reentrant
tachycardia".)
AVRT utilizing an accessory pathway can be either orthodromic or antidromic.
Orthodromic AVRT is more common, and in this form of the arrhythmia, antegrade
conduction occurs through the AV node, producing a narrow QRS complex, and
retrograde conduction to the atrium occurs over an AV bypass tract (figure 6).
(See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory
pathway".)
In contrast, during antidromic AVRT, antegrade conduction occurs through the AV
bypass tract and retrograde conduction occurs through the AV node or a second
accessory pathway. This pattern of activation results in a wide QRS complex (thus,
antidromic AVRT is not a narrow QRS complex tachycardia). (See "Wide QRS complex
tachycardias: Approach to the diagnosis".)
Long RP tachycardias — If the RP interval is more than one-half of the RR interval, the
tachycardia is considered a long RP tachycardia. As with short RP tachycardias, the
differential diagnosis is generated by combining the PR relationship with the P wave
morphology.
●Retrograde P waves – The combination of retrograde P waves and a long RP
interval is usually caused by either "atypical" AVNRT or by AVRT with a slowly
conducting accessory pathway; this combination can also be seen in AT with a
focus that is close to the AV node [6]. P waves are inverted in the inferior
leads as the atria are depolarized from bottom to top. (See 'Retrograde P
waves' above.)
●Abnormal P wave morphology – The combination of abnormal P wave
morphology and a long RP interval usually suggests some form of AT.
However, this pattern can also occur in the atypical or uncommon form of
AVNRT and in AVRT with a slowly conducting accessory pathway (also called
"permanent junctional reciprocating tachycardia" or PJRT) [6]. (See 'Abnormal
P waves' above.)
The atypical form of AVNRT, which accounts for 10 percent of AVNRT [13], is
characterized by antegrade conduction down a fast pathway and retrograde conduction
through a slow pathway. As a result, the P wave occurs very late in the cardiac cycle
(positioning it near to the next QRS complex) (figure 7). (See "Atrioventricular nodal
reentrant tachycardia".)
In AVRT with a slowly conducting accessory pathway (also called "permanent junctional
reciprocating tachycardia" or PJRT), antegrade conduction probably occurs through the
AV node, and retrograde conduction through a slowly conducting accessory pathway
[1,12]. Because of slow conduction through the retrograde limb of the circuit, the
retrograde P wave occurs late in the cardiac cycle. (See "Atrioventricular reentrant
tachycardia (AVRT) associated with an accessory pathway".)
Undetectable P waves — If atrial activity is not evident despite the use of carotid sinus
massage and/or adenosine to "unmask" atrial activity, the most common rhythm is
AVNRT [6]. Other possible rhythms are atrial fibrillation (AF), AVRT, and junctional
tachycardia.
Although AF is typically an irregularly irregular rhythm, when the ventricular rate is very
rapid, it may appear to be more regular. Vagal maneuvers produce a transient decrease
in the ventricular rate with AF, which may make the irregularity more evident.
Junctional tachycardia is an arrhythmia arising from a discrete focus within the AV node
or His bundle. In children, junctional tachycardia, also known as junctional ectopic
tachycardia (JET), is usually associated with significant underlying heart disease. In
adults, this rhythm, generally called nonparoxysmal junctional tachycardia (NPJT), is
seen with acute myocardial infarction, digitalis toxicity, and myocarditis.
(See "Supraventricular arrhythmias after myocardial infarction".)
Atrial activity during junctional tachycardia is variable. Retrograde atrial activation may
occur, with a P wave that either follows each QRS complex or is concealed in the QRS
complex. If retrograde conduction does not occur, independent atrial activity may be
seen, with complete AV dissociation that must be distinguished from AV dissociation due
to complete heart block (in complete heart block, the atrial rate exceeds the ventricular
rate).
Electrophysiologic testing — In some cases, narrow QRS complex tachycardias

cannot be discriminated from each other using noninvasive testing. An
electrophysiologic study (EPS) can provide a definitive diagnosis, but is not necessary
unless it will influence therapy [12]. For some arrhythmias, EPS with ablation can also
be curative. For these reasons, invasive EP testing to define the mechanism of SVT is
rarely carried out as a standalone diagnostic procedure, but rather as a "prelude" to
ablation.
Diagnostic EP may be indicated to determine the mechanism of the arrhythmia in the

following patients with a narrow QRS complex tachycardia:
●Those with severe symptoms such as syncope or presyncope in association

with the arrhythmia, particularly if the resting ECG manifests the pattern of
preexcitation with a delta wave (waveform 9) or a short PR interval without a
delta wave.
●Those with underlying organic heart disease who develop angina or acute HF
during their arrhythmia, even if the rate is relatively slow.
EPS and catheter ablation are discussed in greater detail elsewhere. (See "Invasive
diagnostic cardiac electrophysiology studies" and "Overview of catheter ablation of
cardiac arrhythmias", section on 'Introduction'.)
Other cardiac testing — In addition to close scrutiny of the available ECG data,
patients with narrow QRS complex tachycardia should generally have a baseline
echocardiogram to assess for any evidence of significant underlying structural heart
disease [14]. Additional cardiac testing is variable depending upon the particular
arrhythmia and symptoms but may include one or more of the following tests:
●Ambulatory ECG monitoring (for patients without a definitive ECG-based
diagnosis of their arrhythmia)
●Exercise stress testing (for patients with exercise-associated arrhythmias)
●Stress testing (exercise or pharmacologic) for underlying myocardial ischemia
(for those with symptoms of angina and risk factors for coronary artery
disease)
Arrhythmias in adults" and "Society guideline links: Supraventricular arrhythmias".)
interest.)
●Basicstopic (see "Patient education: Supraventricular tachycardia (SVT)

(The Basics)")
●Tachycardias, defined as abnormal heart rhythms with a ventricular rate of

100 or more beats per minute, can present with either a narrow or wide QRS
complex. A narrow QRS complex (<120 milliseconds) reflects rapid activation
of the ventricles via the normal His-Purkinje system, which in turn suggests
that the arrhythmia originates above or within the His bundle (ie, a
supraventricular tachycardia). The site of origin may be in the sinus node, the
atria, the atrioventricular (AV) node, the His bundle, or some combination of
these sites. (See 'Introduction' above and 'Definitions' above.)
●Most commonly, patients with a narrow QRS complex tachycardia present
with palpitations, usually abrupt in onset. Other presenting symptoms may
include syncope or presyncope, lightheadedness, dizziness, diaphoresis,
chest pain, or shortness of breath. (See 'Clinical manifestations' above.)
●The diagnosis of a narrow QRS complex tachycardia requires only a surface
electrocardiogram (ECG) which shows a heart rate greater than 100 beats per
minute along with narrow QRS complexes that are less than 120 milliseconds
in duration. (See 'Diagnosis' above.)
●The differential diagnosis of narrow QRS complex tachycardias is broad
(table 1), including atrial fibrillation (AF), atrial flutter, sinus tachycardia (ST),
and a variety of paroxysmal supraventricular tachycardias. (See 'Types of
narrow QRS complex tachycardia' above.)
●Evaluation of a patient with a narrow QRS complex tachycardia involves two
primary components (algorithm 1 and algorithm 2): assessment of the patient
for symptoms and signs of hemodynamic stability (or instability), and
assessment of the patient's ECG for clues to the type of tachycardia present.
(See 'Evaluation' above.)
•If a patient has clinically significant hemodynamic instability and the
rhythm is not ST, or if there is any doubt that the rhythm is sinus
•If it is certain that the patient's rhythm is ST and clinically significant
cardiac symptoms are present, management should be focused on the
underlying cardiac disorder and on treating any contributing cause of the
rapid heart rate (such as myocardial ischemia due to coronary heart
disease, respiratory or cardiac failure, hypovolemia, anemia, fever, pain,
or anxiety).
•If the patient is not experiencing hemodynamic instability, a nonemergent
approach to the diagnosis of the patient's rhythm can be undertaken.
●Following the determination of hemodynamic stability, the next step in the
assessment of a narrow QRS complex tachycardia is to determine if the
rhythm appears to be regular or irregular. (See 'Assessing the ECG for
regularity of the rhythm' above.)
●Making a specific diagnosis among the paroxysmal supraventricular
tachycardias is more difficult. Following the determination of the regularity or
irregularity of the rhythm, the most important feature is the identification and
characterization of atrial activity (P waves) (algorithm 2). Utilization of vagal
maneuvers such as the Valsalva maneuver, carotid sinus massage,
or adenosine administration may be required to identify P waves and may at
times ameliorate the abnormal rhythm. (See 'ECG identification of atrial
activity' above.)
●Once P waves are identified, the following characteristics should be
determined: atrial rate, P wave morphology, RP relationship, and AV
relationship. (See 'ECG characterization of atrial activity' above.)
●The overall management of narrow QRS complex tachycardias is discussed
separately. (See "New onset atrial fibrillation" and "Overview of atrial
flutter" and "Overview of the acute management of tachyarrhythmias".)
REFERENCES
1. Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995;
332:162.
2. Katritsis DG, Josephson ME. Differential diagnosis of regular, narrow-QRS
tachycardias. Heart Rhythm 2015; 12:1667.
3. Khurshid S, Choi SH, Weng LC, et al. Frequency of Cardiac Rhythm
Abnormalities in a Half Million Adults. Circ Arrhythm Electrophysiol 2018;
11:e006273.
4. Ferguson JD, DiMarco JP. Contemporary management of paroxysmal
supraventricular tachycardia. Circulation 2003; 107:1096.
5. Trohman RG. Supraventricular tachycardia: implications for the intensivist.
Crit Care Med 2000; 28:N129.
6. Blomström-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC
guidelines for the management of patients with supraventricular
arrhythmias--executive summary: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines
and the European Society of Cardiology Committee for Practice Guidelines
(Writing Committee to Develop Guidelines for the Management of Patients
With Supraventricular Arrhythmias). Circulation 2003; 108:1871.
7. Kalbfleisch SJ, el-Atassi R, Calkins H, et al. Differentiation of paroxysmal
narrow QRS complex tachycardias using the 12-lead electrocardiogram. J
8. Accardi AJ, Miller R, Holmes JF. Enhanced diagnosis of narrow complex
tachycardias with increased electrocardiograph speed. J Emerg Med 2002;
22:123.
9. Link MS. Clinical practice. Evaluation and initial treatment of
supraventricular tachycardia. N Engl J Med 2012; 367:1438.
10. Smith GD, Dyson K, Taylor D, et al. Effectiveness of the Valsalva
Manoeuvre for reversion of supraventricular tachycardia. Cochrane
Database Syst Rev 2013; :CD009502.
11. Ellenbogen KA, Thames MD, DiMarco JP, et al. Electrophysiological effects
of adenosine in the transplanted human heart. Evidence of supersensitivity.
Circulation 1990; 81:821.
12. Chauhan VS, Krahn AD, Klein GJ, et al. Supraventricular tachycardia. Med
Clin North Am 2001; 85:193.
13. Akhtar M, Jazayeri MR, Sra J, et al. Atrioventricular nodal reentry. Clinical,
electrophysiological, and therapeutic considerations. Circulation 1993;
88:282.
Close

 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Patient

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 INTRODUCTION
 EPIDEMIOLOGY
 ANATOMY AND PATHOPHYSIOLOGY
o Anatomy
o Dual AV nodal physiology
 Dual AV nodal pathways during normal sinus rhythm
o Typical AVNRT
o Atypical AVNRT
o Symptoms
o Triggers
o Electrocardiographic characteristics
 DIAGNOSIS
 DIFFERENTIAL DIAGNOSIS
o Sinus tachycardia
o Atrioventricular reentrant tachycardia
o Atrial tachycardia
o Junctional ectopic tachycardia
o Other SVTs
 INITIAL MANAGEMENT
o Electrical cardioversion
o Vagal maneuvers
o Adenosine
o Other AV nodal blocking drugs
 SUBSEQUENT MANAGEMENT
o Acute management of recurrent episodes
o Preventive therapy
 No treatment
 Catheter ablation
 Chronic suppressive therapy
 REFERENCES
GRAPHICS view all
 Algorithms
oAlgorithm AVNRT acute treatment
oAdult tachycardia with a pulse algorithm
 Figures
oAnatomy of Koch's triangle
oLocation of Koch's triangle
oCommon slow fast AVNRT
oECG generation in common AVNRT
oUncommon fast slow AVNRT
oAtypical atrioventricular nodal reentrant tachycardia
oAblation sites for AVNRT
 Tables
oElectrophysiologic characteristics of different types of SVT
oCauses of palpitations
 Waveforms
oEPS tracing AVNRT dual AVN pathways I
oEPS tracing AVNRT dual AVN pathways II
o12 lead ECG uncommon AVNRT
o12 lead ECG common AVNRT
RELATED TOPICS
 Amiodarone: Adverse effects, potential toxicities, and approach to monitoring
 Cardioversion for specific arrhythmias
 Evaluation of palpitations in adults
 Society guideline links: Catheter ablation of arrhythmias
 Syncope in adults: Management
 Vagal maneuvers
Atrioventricular nodal reentrant tachycardia

Author:
Section Editor:
Mark S Link, MD
Deputy Editor:
INTRODUCTION Atrioventricular nodal reentrant tachycardia (AVNRT) is a
regular supraventricular tachycardia (SVT) that results from the formation of a reentry
circuit confined to the AV node and perinodal atrial tissue. Because of its abrupt onset
and termination, AVNRT is categorized as a paroxysmal SVT (PSVT). As with the
majority of SVTs, the QRS complex in AVNRT is usually narrow (ie, ≤120 milliseconds),
reflecting normal ventricular activation through the His-Purkinje system, although
aberrant conduction (eg, underlying bundle branch block) can result in a wide QRS
complex. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis,
and evaluation", section on 'Paroxysmal SVT'.)
This topic will review the mechanisms, clinical manifestations, diagnosis, and the
management of AVNRT. A detailed discussion of the broader approach to narrow QRS
complex tachycardias is presented separately. (See "Narrow QRS complex
tachycardias: Clinical manifestations, diagnosis, and evaluation".)
EPIDEMIOLOGY AVNRT is the most common form of regular, sustained,
paroxysmal supraventricular tachycardia (PSVT), accounting for nearly two-thirds of all

PSVTs, and is more common in women compared with men [1-3]. AVNRT can present
at any age, but as with AV reentrant tachycardia (AVRT) that involves an accessory
pathway, it is more likely to begin in young adults. In a series of 231 patients with
AVNRT, the mean age of symptom onset was 32 years, with two-thirds of cases
beginning after the age of 20 [4].
ANATOMY AND PATHOPHYSIOLOGY The physiologic substrate for
AVNRT involves dual electrical pathways in or near the AV node (table 1) [5,6]. The
arrhythmia usually develops in hearts that are otherwise normal, although it can also
occur in the presence of underlying structural heart disease [7,8]. A more detailed
discussion of the electrophysiology of AVNRT can be found in published reviews
[5,6,9,10]. (See 'Dual AV nodal physiology' below.)
Anatomy — The exact anatomic distribution of these pathways is uncertain. Koch's
triangle is bounded by the tricuspid ring and the tendon of Todoro, which bracket the
coronary sinus at the base of the triangle and are in close proximity forming the apex
near the His bundle at the membranous septum (figure 1 and figure 2) [5,11]. As an
approximation, Koch's triangle can be divided into thirds:
●The anterior third, which contains the AV node and fast pathways
●The middle third
●The posterior third, the usual site of slow pathways
Dual AV nodal physiology — The simplest concept of AV nodal physiology that allows
for reentry involves separate electrical pathways within or proximal to the AV node
(figure 3). This model is supported by clinical observations as well as animal and human
mapping studies [5,12,13]. These pathways may be distinct anatomic structures, or they
may be functionally separate (ie, regions that appear anatomically continuous but have
different electrical properties). It is possible that some cases of AVNRT are acquired
when there is right atrial pressure overload leading to changes in the electrophysiologic
properties of the AV nodal inputs. Rare cases of familial AVNRT have also been
reported [14]. Whether the dual pathways are anatomic or functional, in order for reentry
to occur, they must have different conduction velocities and refractory periods [15]:
●One pathway conducts rapidly and has a relatively long refractory period.
This is called the fast pathway.
●The second pathway conducts relatively slowly and has a shorter refractory
period. This is called the slow pathway.
The origins of the fast and slow pathways are probably in perinodal atrial tissue. These
pathways join and enter a final common pathway in the AV node. While atrial tissue
above the AV node appears to be part of the reentrant circuit, the bundle of His below
the node is not a necessary part of the circuit. This can be illustrated by the following
observations:
●AVNRT is associated with 2:1 AV block in approximately 10 percent of
patients [16]. The AV block in this setting is probably a functional infranodal
block within the bundle of His [16].
●His bundle electrograms indicate that reentry is proximal to the recording site
[17,18].
Not all patients with AVNRT have evidence of dual pathways during electrophysiology
(EP) studies. Conversely, not all patients with dual AV nodal pathways have clinical
AVNRT (waveform 1A-B). The imperfect association between dual AV nodal physiology
and clinical AVNRT was illustrated in a series of 180 patients undergoing EP studies for
a variety of indications [19]. Among the 87 patients with AVNRT, 39 percent did not have
clear evidence of dual AV nodal physiology. In contrast, 30 percent of the 66 patients
with documented dual AV nodal physiology did not have AVNRT. A concealed atrio-
Hisian tract that bypasses the AV node may constitute the retrograde fast pathway in up
to a third of all apparently "typical" AVNRT cases [20]. Thus, the anatomic and
electrophysiologic mechanism of AVNRT may be more complex than the dual AV nodal
physiology model suggests [21,22].
Dual AV nodal pathways during normal sinus rhythm — During normal sinus
rhythm, AV conduction occurs as follows (figure 3):
●The normal sinus beat enters the AV node and the impulse travels down both
the fast and slow pathways.
●The impulse traveling down the fast pathway reaches the His bundle first,
creating a refractory wake.
●The impulse traveling down the slow pathway is extinguished when, in the
area of the final common pathway, it runs into the refractory wake of the
impulse that had traveled down the fast pathway.
Typical AVNRT — Approximately 80 to 90 percent of patients with AVNRT present with
what is called the common form of the arrhythmia. The common form is also called
"typical AVNRT" or "slow-fast" AVNRT.
Typical AVNRT usually initiates as follows (figure 3):
●A premature atrial complex (PAC; also referred to a premature atrial beat,
premature supraventricular complex, or premature supraventricular beat) (or
less commonly, a premature junctional or ventricular beat with retrograde
conduction) arrives at the AV node when the fast pathway is in its refractory
period. Thus, antegrade conduction down the fast pathway is blocked.
●If the premature beat arrives in a specific time window (ie, a "critically timed"
premature beat), the slow pathway, with a shorter refractory period than the
fast pathway, is available for conduction to the ventricle.
●The premature beat conducts via the slow pathway, through the final
common pathway, to the bundle of His. As a result, the PR interval of the
premature beat will be longer than those of normal beats conducted through
the fast pathway.
●If the fast pathway has recovered its excitability by the time the slow pathway
impulse reaches the distal junction of the two pathways, the impulse can
conduct retrograde up the fast pathway. The circuit may then become
repetitive with antegrade conduction back down the slow pathway and
retrograde conduction up the fast pathway resulting in a sustained tachycardia
(figure 3 and figure 4).
This proposed mechanism explains a number of clinical observations in AVNRT:
●A single PAC (or retrograde penetration of the AV node from a junctional or

premature ventricular complex/contraction [PVC; also referred to a premature
ventricular beats or premature ventricular depolarizations]) can initiate the
arrhythmia.
●Penetration of the reentrant circuit by a premature beat can abruptly
terminate the arrhythmia.
Atypical AVNRT — Up to 20 percent of patients with AVNRT have uncommon forms of
the arrhythmia, referred to as "atypical AVNRT." As examples:
●Antegrade conduction can occur down the fast pathway with retrograde
conduction up the slow pathway (figure 5 and figure 6 and waveform 2) [23].
This is referred to as "fast-slow" AVNRT.
●Some patients have multiple slow pathways, resulting in "slow-slow AVNRT"
variants in which both the antegrade and retrograde limbs of the circuit utilize
slow AV nodal pathways.
●Rarely during AVNRT, conduction through the reentrant circuit is so slow that
the heart rate is less than 100 beats per minute, by definition not a
tachycardia. Despite the absence of tachycardia, patients can be symptomatic
and may be treated with a slow pathway ablation. This arrhythmia, sometimes
referred to as AV nodal reentrant arrhythmia (AVNRA), has been mistaken for
a junctional rhythm. (See "Narrow QRS complex tachycardias: Clinical
manifestations, diagnosis, and evaluation", section on 'Undetectable P
waves'.)
Typical and atypical AVNRT have rarely been found to coexist in the same patient
during electrophysiology studies [24].
CLINICAL MANIFESTATIONS
Symptoms — Patients with AVNRT most commonly report palpitations, dizziness or

lightheadedness, and dyspnea. Because of the paroxysmal nature of the arrhythmia, the
onset and termination of the symptoms are usually sudden. Those with significant heart
disease may have additional symptoms such as dyspnea and chest pain. Because atrial
activation occurs coincident with ventricular activation during typical AVNRT, atrial
contraction occurs when the tricuspid valve is closed, causing rhythmic abrupt rises in
venous pressure, and can result in a sensation of neck pounding. Some patients with
AVNRT have a feeling of polyuria and experience a diuresis during or after AVNRT; the
mechanism probably is related to an elevated mean right atrial pressure and plasma
level of atrial natriuretic peptide, which are present during the arrhythmia [25].
In a series of 167 supraventricular tachycardia (SVT) patients referred for
radiofrequency ablation, the 64 patients with AVNRT reported the following symptoms
[26]:
●Palpitations – 98 percent
●Dizziness – 78 percent
●Dyspnea – 47 percent
●Chest pain – 38 percent
●Fatigue – 19 percent
●Syncope – 16 percent
Syncope is an uncommon feature of AVNRT and appears to be more likely with high
heart rates (eg, heart rate ≥170 beats per minute). However, factors other than heart
rate also contribute to syncope. As an example, abnormal vasomotor adaptation during
AVNRT has been reported, suggesting a role for neurally mediated (neurocardiogenic)
responses [27,28].
In very rare cases, AVNRT can result in cardiac arrest [29].
Triggers — Most often there is no apparent precipitating cause for episodes of AVNRT.
However, in some patients, nicotine, alcohol, stimulants, or exercise can initiate
episodes.
Some patients experience the onset of AVNRT during sleep or after sudden bending
forward or squatting, all of which can enhance vagal tone. In contrast to using vagal
maneuvers to terminate AVNRT, increased vagal tone may facilitate the induction of
AVNRT in some circumstances. In one series of 10 patients with AVNRT,
electrophysiologic data were measured before and during continuous enhancement of
vagal tone induced by infusing phenylephrine [30]. Vagal enhancement markedly
prolonged the effective refractory period and functional refractory period of antegrade
conduction in the fast pathway. However, the refractoriness of antegrade conduction in
the slow pathway and retrograde conduction in the fast pathway were unchanged.
Electrocardiographic characteristics — All patients with palpitations should undergo
12-lead electrocardiography (ECG), ideally while symptomatic. There are several ECG
features that are helpful in confirming the diagnosis of AVNRT.
●Ventricular rate – The ventricular rate is generally between 120 and 220
beats per minute.
●Abrupt onset following PAC – If the initiation of the tachycardia is captured on
a tracing, the tachycardia often begins with a PAC with sudden prolongation of
the PR interval (figure 4). (See 'Typical AVNRT' above.)
●Relationship between QRS complexes and P waves – Because of the
relationships between the QRS complex and the following P wave, typical
AVNRT is referred to as a "short RP tachycardia," while atypical AVNRT is a
"long RP tachycardia" [10]. (See "Narrow QRS complex tachycardias: Clinical
manifestations, diagnosis, and evaluation", section on 'RP relationship'.)
•In typical AVNRT, retrograde atrial activation and antegrade ventricular
activation occur almost simultaneously (figure 4). The P wave, therefore,
is usually buried within or fused with the QRS complex.
A component of the P wave is often evident slightly after, or less
commonly before, the QRS (figure 7 and waveform 3). When the P wave
occurs shortly after the QRS complex, the fused waveform can produce a
pseudo-R' (a second R wave) in lead V1 and a pseudo-S wave in the
inferior leads. (See 'Typical AVNRT' above.)
•In atypical AVNRT, retrograde atrial activation occurs long after
ventricular activation, resulting in a P wave so late after the QRS complex
that it appears to be occurring shortly before the next QRS complex
(figure 5 and figure 6 and waveform 2). This pattern resembles that seen
in atrial tachycardias. In such cases, an electrophysiology (EP) study may
be required to define the arrhythmogenic mechanism. (See 'Atypical
AVNRT' above and "Invasive diagnostic cardiac electrophysiology
studies".)
●P wave morphology – The P wave axis, when P waves can be clearly
identified, is abnormal due to retrograde atrial activation. This is usually
manifested on the electrocardiogram as a negative P wave axis with inverted
P waves in leads II, III and aVF [31].
●ST segment depression – Significant ST segment depression during
tachycardia has been observed in 25 to 50 percent of patients with AVNRT,
although it is more commonly seen in those with an AV reentrant tachycardia
associated with an accessory pathway [32-34]. The ST segment depression
does not represent myocardial ischemia in most patients (although it may in
patients with significantly underlying coronary heart disease), but rather
represents abnormalities of repolarization [35].
●T wave inversions following termination – After acute termination of AVNRT
and other paroxysmal SVTs, T wave inversions may be seen in the anterior or
inferior leads in approximately 40 percent of patients [36]. Inverted T waves
may be seen immediately upon termination or may develop within the first six
hours, and can persist for hours to days. The occurrence of negative T waves
is not predicted by clinical parameters, tachycardia rate or duration, or the
presence and extent of ST segment depression during the tachycardia. They
are not the result of coronary artery disease, but are repolarization
abnormalities, likely due to ionic current alterations resulting from the rapid
rate.
DIAGNOSIS The diagnosis of AVNRT should be suspected in a patient with
the abrupt onset and offset of rapid sustained palpitations, often associated with
lightheadedness or dyspnea. The ability for a patient to terminate the symptoms with a
vagal maneuver is also suggestive of AVNRT as a potential etiology of symptoms.
(See 'Symptoms' above and 'Vagal maneuvers' below.)
The diagnosis of AVNRT is typically confirmed following the review of an ECG acquired
during the arrhythmia. When possible, review of the ECG at the onset or termination of
the arrhythmia should be performed as this frequently provides additional information
(ie, initiation following an PAC with sudden prolongation of the PR interval (figure 4)).
When there is sudden termination of a regular paroxysmal supraventricular tachycardia
(PSVT) that has 1:1AV conduction associated with AV block but not due to a PAC (last
beat of the tachycardia is a P wave rather than a QRS complex that occurs at the
expected timing), then an atrial tachycardia is very unlikely.
●In typical AVNRT, the P wave is usually buried within or fused with the QRS
complex, resulting in a pseudo-R' (a second R wave) in lead V1 and a pseudo-
S wave in the inferior leads.
●In atypical AVNRT, the P wave occurs late after the QRS complex, often
appearing shortly before the next QRS complex, resulting in a pattern that
resembles atrial tachycardia.
If the diagnosis cannot be confirmed following review of the surface ECG, invasive
electrophysiology studies can be performed in an effort to confirm the diagnosis.
(See "Invasive diagnostic cardiac electrophysiology studies".)
DIFFERENTIAL DIAGNOSIS The differential diagnosis of palpitations is
extensive (table 2), and the etiology varies depending upon the population studied. The
approach to palpitations is discussed separately. (See "Evaluation of palpitations in
adults".)
Once a tachycardia with a narrow QRS complex has been identified, the differential
diagnosis is generally limited to SVTs, although on rare occasions idiopathic left
ventricular tachycardia (a ventricular tachycardia arising from septum) can present as a
narrow complex tachycardia. (See "Ventricular tachycardia in the absence of apparent
structural heart disease", section on 'Idiopathic left ventricular tachycardia'.)
Sustained narrow QRS complex tachycardias are generally divided according to

whether the QRS complexes occur regularly or irregularly:
●Irregular QRS complexes – Atrial fibrillation, atrial flutter with variable
conduction, multifocal atrial tachycardia
●Regular QRS complexes – Sinus tachycardia, atrial flutter, AVNRT,
atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), and
junctional ectopic tachycardia (JET). The term PSVT generally refers to
AVNRT, AVRT, AT, and JET.
Because AVNRT is a regular tachycardia, the tachycardias with irregular QRS complex
can be excluded immediately. The remainder of the differential diagnosis discussion will
focus on the other regular narrow QRS complex tachycardias.
Sinus tachycardia — Sinus tachycardia is the most common narrow QRS complex

tachycardia. Typically, sinus tachycardia is a response to another condition in which
catecholamine release is physiologically enhanced or, less commonly, the
parasympathetic nervous system withdrawn. In contrast to the abrupt onset and
termination of AVNRT, sinus tachycardia has a gradual onset and offset, which typically
occurs over 30 seconds to several minutes. Additionally, for the vast majority of patients,
sinus tachycardia does not result in symptoms. (See "Sinus tachycardia: Evaluation and
management".)
Atrioventricular reentrant tachycardia — Patients with AVRT can present in a similar
fashion to patients with AVNRT. Both arrhythmias are associated with the abrupt onset
of palpitations, and the surface ECG may appear very similar with regular QRS
complexes and inverted P waves and a short RP interval that is less than one-half of the
RR interval. AVNRT is most easily distinguished from AVRT when evidence of pre-
excitation (short PR interval and delta wave) can be identified on prior ECGs during
normal sinus rhythm (when available) consistent with an accessory pathway and the
potential for AVRT. In the event of concealed pre-excitation, invasive electrophysiology
studies may be required to distinguish AVNRT from AVRT. (See "Atrioventricular
reentrant tachycardia (AVRT) associated with an accessory pathway".)
Atrial tachycardia — As with AVNRT and AVRT, most patients with focal atrial
tachycardia report an abrupt onset of palpitations associated with their episodes of
tachycardia. In contrast to AVNRT, the P wave morphology during atrial tachycardia can
appear normal or abnormal, depending upon the site of origin of the tachycardia, and
the P waves tend to occur prior to the QRS complex, resulting in a long RP tachycardia.
(See "Focal atrial tachycardia".)
Junctional ectopic tachycardia — Junctional ectopic tachycardia (JET) is a focal
ectopic arrhythmia arising from the AV node region itself. It is a rare arrhythmia most
often seen in young children as a congenital arrhythmia or after surgery for congenital
heart disease [37]. JET can be difficult to differentiate from typical AVNRT. However,
JET should be suspected when there is ventriculoatrial block during tachycardia and
when the tachycardia is initiated by a premature junctional beat. Because the substrate
related to JET is near the compact AV node, there is a greater concern for AV block
during catheter ablation of JET compared with AVNRT [38].
Other SVTs — Other than sinus tachycardia, AVRT, and atrial tachycardia, the
remaining SVTs occur far less commonly. Inappropriate sinus tachycardia and sinoatrial
nodal reentrant tachycardia have an identical appearance to sinus tachycardia. In
contrast to sinus tachycardia, sinoatrial nodal reentrant tachycardia can have an abrupt
onset (making it look identical to atrial tachycardia) and requires invasive
electrophysiology studies to diagnose. Inappropriate sinus tachycardia tends to persist
for days to weeks without the typical associations seen with sinus tachycardia (eg, pain,
fever, hypovolemia, etc) and is relatively refractory to rate-slowing medications.
Intraatrial tachycardia is a type of reentrant tachycardia seen almost exclusively in
patients with underlying structural heart disease and prior cardiac procedures resulting
in scar formation (eg, repair of congenital heart disease, catheter ablation for atrial
fibrillation, etc). (See "Sinus tachycardia: Evaluation and management", section on
'Inappropriate sinus tachycardia' and "Sinoatrial nodal reentrant tachycardia
(SANRT)" and "Intraatrial reentrant tachycardia".)
INITIAL MANAGEMENT The initial management of a patient presenting with
a narrow QRS tachycardia and suspected AVNRT is guided by whether or not the
patient is experiencing signs and symptoms of hemodynamic instability (algorithm 1)
related to the rapid heart rate (eg, hypotension, shortness of breath, chest pain
suggestive of coronary ischemia, shock, and/or decreased level of consciousness).
Unstable patients require urgent electrical cardioversion. However, it is very rare that a
patient with paroxysmal supraventricular tachycardia (PSVT) requires electrical
cardioversion.
There are several effective therapies for the acute termination of AVNRT, but few data
regarding the optimal sequence of therapies for the acute termination of AVNRT [39,40].
These treatment options include:
●Vagal maneuvers (see "Vagal maneuvers")
●Intravenous (IV) adenosine
●IV calcium channel blockers or beta blockers
Management recommendations are based upon an understanding of the properties and
risks of the treatment options. Almost all patients, including those who are severely
symptomatic, can be treated first with several attempts at vagal maneuvers or
IV adenosine [39,40]. Our recommendations are in general agreement with published
professional society recommendations [39,40].
Electrical cardioversion — AVNRT almost always terminates with vagal maneuvers or
intravenous antiarrhythmic therapy with adenosine, calcium channel blockers, or beta
blockers. However, if the patient is hemodynamically unstable, or if AVNRT persists in
spite of vagal maneuvers or AV nodal blocking medications, electrical cardioversion
should be considered (algorithm 1). Electrical cardioversion is usually successful but
may require relatively high energy levels, probably due to the deep location of the
reentrant pathway. If sinus rhythm is not restored following an initial 50 to 100 joule
shock, subsequent shocks should be at higher energy levels (algorithm 2). Although
energy requirements with biphasic waveforms have not been reported, they are likely to
be lower than for monophasic waveforms based upon experience with other
arrhythmias. (See "Cardioversion for specific arrhythmias".)
Vagal maneuvers — Vagal maneuvers (eg, Valsalva maneuver or carotid sinus
massage) are safe, easily performed, and effective first-line therapies for patients with
AVNRT (algorithm 1). For patients who are hemodynamically stable and able to
effectively perform the vagal maneuvers, we recommend at least one or two attempts at
a standard Valsalva maneuver, followed by at least one or two attempts using the
modified Valsalva maneuver (if AVNRT persists), as the initial treatment for AVNRT
rather than another vagal maneuver or adenosine.
Vagal maneuvers increase parasympathetic tone, which produces a gradual slowing of
conduction in the antegrade slow pathway. Slowing and eventual block in the antegrade
slow pathway are the usual cause for arrhythmia termination with these interventions
[41], although they can also produce abrupt block in the retrograde fast pathway. In one
systematic review, which included 316 patients with a total of 965 episodes of
supraventricular tachycardia (SVT; which included both AVNRT and atrioventricular
reciprocating tachycardia), the standard Valsalva maneuver (exhaling forcefully against
a closed glottis for 10 to 15 seconds) successfully terminated 45 percent of SVT
episodes and was more successful than carotid sinus massage [42].
To perform a standard Valsalva maneuver, the patient is placed in a supine or semi-
recumbent position and instructed inhale normally and then to exhale forcefully against a
closed glottis for 10 to 15 seconds. A modified Valsalva maneuver (which begins with
the standard Valsalva maneuver and is followed by supine positioning and passive leg
raising) has been proposed as an improvement on the standard Valsalva maneuver. In
the largest randomized trial of vagal maneuvers for the treatment of SVT, 428 patients
with hemodynamically stable SVT were randomly assigned to perform the standard
Valsalva maneuver (strain generating 40 mmHg pressure for 15 seconds while in a
semi-recumbent position) or to perform the standard Valsalva maneuver followed by
supine repositioning (placing the patient supine from the upright or semi-recumbent
position) and passive leg raise for 15 seconds (214 patients per group) [43]. Patients
performing the modified Valsalva maneuver with supine repositioning and passive leg
raise were significantly more likely to have restoration of sinus rhythm at one minute (43
versus 17 percent in the standard Valsalva group; adjusted odds ratio 3.7; 95% CI 2.3-
5.8). When feasible, we recommend the modified Valsalva maneuver given the greater
likelihood of successful restoration of sinus rhythm.
Additional information on the performance and use of vagal maneuvers is presented
separately. (See "Vagal maneuvers".)
Adenosine — If vagal maneuvers cannot be performed or if they fail to terminate the
arrhythmia, IV medical therapy that blocks AV nodal conduction is indicated as the next
step (algorithm 1). For patients with AVNRT that persists following vagal maneuvers (or
in whom vagal maneuvers cannot be adequately performed), we recommend
IV adenosine rather than a calcium channel blocker or a beta blocker.
For IV adenosine administration, the patient should be supine and should have
electrocardiographic and blood pressure monitoring. Whenever possible, a continuous
12-lead ECG rhythm strip should be obtained during administration of adenosine, as
there are often clues at the time of termination as to the mechanism of the SVT.
Adenosine is administered by rapid IV injection over one to two seconds at a peripheral
site, followed by a normal saline flush. The rapid administration of both the drug and the
saline flush is most easily accomplished through a three-way stopcock. The usual initial
dose is 6 mg, which can be followed by a dose of 12 mg if not successful. A dose of 18
mg can be used if 12 mg fails to convert the patient to sinus rhythm. Repeated dosing
beyond the 18 mg bolus is not usually effective. Patients with orthotopic heart
transplants are exquisitely sensitive to adenosine; initial doses should be 1 mg.
The advantages of adenosine over other agents include rapid onset and a short half-life.
Adenosine terminates AVNRT in over 80 percent of cases [44-46]. It is well tolerated in
most patients, with the exception of those with severe bronchospastic asthma or severe
coronary artery disease. Detailed discussions of the use of adenosine for the evaluation
and termination of SVTs are presented separately. (See "Narrow QRS complex
tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Intravenous
adenosine'.)
Other AV nodal blocking drugs — If vagal maneuvers and adenosine have been
ineffective or terminate the tachycardia followed by an immediate recurrence, IV
nondihydropyridine calcium channel blockers (eg, verapamil and diltiazem) or IV beta
blockers (eg, metoprolol, esmolol) can be used (algorithm 1) to terminate AVNRT
[47,48]. A phase 2 trial of an intranasally administered calcium channel blocker,
etripamil, terminated SVT in up to 95 percent of patients [49]. A phase 3 placebo-
controlled trial of etripamil is underway to further assess efficacy, with results expected
in 2020 [50].
The choice between these drugs is usually based on familiarity with and availability of
the particular agents, although a calcium channel blocker would be preferred for a
patient with reactive airway disease and active wheezing. Calcium channel and beta
blockers are generally well tolerated, although potential adverse effects include
hypotension (due to both negative inotropic and vasodilatory effects) and bradycardia
[51-53]. Initial IV dosing options include:
●Verapamil – 5 to 10 mg IV bolus over 2 minutes; if no response, an additional
10 mg IV bolus may be administered 15 to 30 minutes following the initial
dose.
●Diltiazem – 0.25 mg/kg (average dose 20 mg) IV bolus over 2 minutes; if no
response, an additional 0.35 mg/kg (average dose 25 mg) IV bolus may be
administered 15 to 30 minutes following the initial dose.
●Metoprolol – 2.5 to 5 mg IV bolus over 2 to 5 minutes; if no response, an
additional 2.5 to 5 mg IV bolus may be administered every 10 minutes to a
total dose of 15 mg.
●Esmolol – 1 mg/kg IV bolus over 30 seconds, followed by a 150
mcg/kg/minute infusion, if necessary. Infusion rate can be adjusted as needed
to maintain desired heart rate (up to 300 mcg/kg/minute).
Because of their longer half-lives, verapamil, diltiazem, and beta blockers have the
potential to suppress arrhythmia recurrence. Thus, these drugs should be used in
patients who have early arrhythmia recurrence after termination with adenosine.
SUBSEQUENT MANAGEMENT The approach to the management of
subsequent AVNRT episodes is based around acute management of recurrent episodes

and/or preventive therapy to reduce or eliminate recurrences. Because AVNRT is
usually well tolerated in the majority of patients, with a variety of safe and effective
treatment options, and there are no compelling data favoring one therapy over another,
the choice of long-term management strategies is largely influenced by patient
preference. When working with a patient to select a treatment strategy, the following
issues should be considered:
●Frequency of episodes
●Severity of symptoms
●Comorbid conditions
●Medication compliance
●Medication side effects
Patients who have had syncope in the setting of AVNRT may be subject to driving
restrictions, which vary between municipalities. (See "Syncope in adults: Management",
section on 'Driving restrictions'.)
Acute management of recurrent episodes — For the initial management of recurrent
AVNRT, we generally work with the patient to develop a patient-directed treatment
approach using either vagal maneuvers or an oral medication ("pill-in-the-pocket"
approach). For most patients, we suggest a combination of one or more vagal
maneuvers rather than the pill-in-the-pocket approach.
Patients who have experienced prior episodes and who have been educated on the
proper performance of vagal maneuvers are frequently able to terminate subsequent
episodes by performing vagal maneuvers on their own. If one or more vagal maneuvers
successfully terminate the arrhythmia, patients generally do not need to seek urgent
medical attention. Conversely, patients should be instructed to consult with their clinician
or seek medical attention if the arrhythmia persists in spite of several attempts at patient-
directed vagal maneuvers. (See 'Vagal maneuvers' above.)
An alternative patient-directed approach to the management of recurrent AVNRT is the
pill-in-the-pocket approach. For selected patients with infrequent, well-tolerated, and
long-lasting episodes of AVNRT, a single dose of an antiarrhythmic agent that was
previously evaluated under observation can be effective for acute termination of the
arrhythmia [39,54,55]. This strategy can both reduce the need for emergency
department visits and avoid chronic medical therapy or invasive procedures. This
approach has been evaluated with the nondihydropyridine calcium channel blockers,
beta blockers, and the class IC antiarrhythmic drug flecainide [55]. However, based
upon the efficacy of alternative, lower-risk therapies, and the efficacy of catheter
ablation, flecainide is rarely used in the management of AVNRT. The choice of a
particular agent will vary from patient to patient depending on comorbidities and patient
preference.
Preventive therapy — The decision to treat with long-term preventive therapy is based
upon the following factors:
●The frequency of the arrhythmia
●The severity of the symptoms
●Patient tolerance of medications
●Patient preference
Many patients with infrequent episodes of AVNRT, or those with minimal or well-
tolerated symptoms, may prefer a more conservative management approach with either
no specific therapy or pharmacologic suppression. If pharmacologic therapy fails or if the
side effects result from chronic medical therapy, catheter ablation remains an option.
Conversely, for patients with significant symptoms, or for patients who prefer definitive
therapy, even for rare, well-tolerated episodes, catheter ablation may be considered
early in the patient's management [39,40].
No treatment — Patients with infrequent and well-tolerated episodes of AVNRT may
choose no chronic therapy. For these patients, we emphasize the patient-directed
approach to the termination of recurrent episodes using one or more vagal maneuvers,
with the ability to reassess long-term management options at any time should there be a
change in the frequency or severity of recurrences. (See 'Acute management of
recurrent episodes' above and "Vagal maneuvers".)
Catheter ablation — For patients with episodes of AVNRT that are either frequently
occurring, refractory to medical therapy, poorly tolerated (eg, associated with near-
syncope or syncope, angina, or severe dyspnea), or result in admission to the hospital,
we recommend catheter ablation rather than chronic medical therapy as initial long-term
management strategy. In such cases, the risks associated with recurrent arrhythmic
events (eg, syncope with associated trauma) outweigh the procedural risks. In addition,
the potential for definitive therapy makes ablation preferable to medical therapy in this
setting.
Catheter ablation offers the opportunity for definitive cure of AVNRT in greater than 95
percent of patients, with high rates of success in both the typical and atypical forms [56-
58]. However, ablation is associated with a small but non-trivial rate of procedural
complications. The most significant potential complication of radiofrequency ablation for
AVNRT is AV block (approximately 1 percent). Historically, the risk of AV block requiring
permanent pacing following ablation ranged from 1 to 3 percent, but in multiple
contemporary cohorts, the need for permanent pacing following the procedure has
consistently been <1 percent [57,59,60]. Older age and baseline PR interval
prolongation are predictors of an increased risk of post-ablation AV block [61-64].
However, due to its high success rate in curing AVNRT by successful slow pathway
ablation and low complication rate, catheter ablation is increasingly favored among
patients with recurrent AVNRT [39,40]. (See "Overview of catheter ablation of cardiac
arrhythmias", section on 'Complications'.)
The general approach to the catheter ablation of AVNRT is based upon the concept of
dual AV nodal pathways. The most common AVNRT circuit (80 to 90 percent) involves
antegrade conduction down the slow pathway and retrograde conduction up the fast
pathway. The ablation target is the posterior slow pathway (figure 8) since ablation here
carries the lowest risk of AV block, preserves fast pathway function (and a normal PR
interval post-ablation), and is facilitated by reliable anatomic and electrophysiologic
landmarks. The anterior fast pathway can also be ablated, but this approach is now
limited to a few special circumstances since fast pathway ablation results in a long PR
interval during sinus rhythm and is associated with a higher risk of heart block. During
ablation for atypical "fast-slow" AVNRT, the slow pathway is the usual target. The slow
pathway in these patients tends to be posteriorly located near the coronary sinus ostium
as with patients who have typical AVNRT. However, there are reports of rare cases of
atypical AV nodal reentry where the slow retrograde limb of the circuit is located more
superiorly near the compact AV node [65].
The relative efficacy and costs of catheter ablation and medical therapy were compared
in a series of 79 patients with newly documented supraventricular tachycardia (SVT)
who were treated with either ablation or pharmacologic therapy, based upon patient
preference [66]. After a follow-up period of 12 months, both medication and ablation
decreased the frequency of arrhythmia-related symptoms, but ablation was more likely
to result in complete abolition of symptoms (74 versus 33 percent). (See 'Chronic
suppressive therapy' below.)
Chronic suppressive therapy — For patients with poorly tolerated symptomatic
episodes of AVNRT who are not candidates for or who have declined catheter ablation,
chronic medical therapy using beta blockers, nondihydropyridine calcium channel
blockers, or antiarrhythmic drugs can be initiated in an effort to suppress recurrent
arrhythmias.
There are few data comparing the relative efficacy of various agents used for chronic
suppressive therapy of AVNRT. Because they are effective and well tolerated, the
medications that are most commonly used for the chronic suppression of AVNRT are
beta blockers and nondihydropyridine calcium channel blockers
(eg, verapamil and diltiazem). We typically prefer beta blockers rather than calcium
channel blockers unless the patient has reactive airway disease or another
contraindication, although calcium channel blockers may have fewer side effects. The
choice of a starting dose for chronic suppressive medication will vary depending upon
the baseline heart rate and blood pressure.
Among patients who do not respond to diltiazem, verapamil, or beta blockers and who
do not want to pursue ablation, the following antiarrhythmic drugs may be considered:
●Flecainide (class IC)
●Propafenone (class IC)
●Sotalol (class III)
●Dofetilide (class III)
●Amiodarone (class III)
The choice of a particular agent will need to be individualized in each patient based on
other comorbidities. However, due to the potential for significant toxicities, including
proarrhythmia, the use of class I and class III antiarrhythmic drugs for the management
of AVNRT should be reserved for rare cases and should be administered in consultation
with an electrophysiologist. In particular, because of the risk of toxicities with long-term
use, amiodarone is usually avoided in young patients. (See "Amiodarone: Adverse
effects, potential toxicities, and approach to monitoring".)
separately. (See "Society guideline links: Arrhythmias in adults" and "Society guideline
links: Catheter ablation of arrhythmias" and "Society guideline links: Supraventricular
arrhythmias".)
interest.)
●Basicstopic (see "Patient education: Supraventricular tachycardia (SVT)

(The Basics)")
●Atrioventricular nodal reentrant tachycardia (AVNRT), the most common form

of regular, sustained, paroxysmal supraventricular tachycardia (PSVT) which
accounts for nearly two-thirds of all PSVTs, is a regular tachycardia that
results from the formation of a reentry circuit confined to the AV node and
perinodal atrial tissue. The physiologic substrate for AVNRT involves dual
electrical pathways in or near the AV node. (See 'Introduction' above
and 'Epidemiology' above.)
●The simplest concept of AV nodal physiology that allows for reentry involves
separate electrical pathways within or proximal to the AV node (figure 3). The
fast pathway conducts rapidly and has a relatively long refractory period, while
the slow pathway conducts relatively slowly and has a shorter refractory
period. Both typical and atypical forms of AVNRT can result from reentry
involving the fast and slow pathways. Tachycardia is initiated by a premature
beat. (See 'Anatomy and pathophysiology' above.)
●Patients with AVNRT most commonly report palpitations, dizziness or
lightheadedness, and dyspnea. Because of the paroxysmal nature of the
arrhythmia, the onset and termination of the symptoms are usually sudden.
Those with significant heart disease may have additional symptoms such as
dyspnea and chest pain. (See 'Symptoms' above.)
●There are several features seen on an electrocardiogram (ECG) that are
helpful in confirming the diagnosis of AVNRT, including the ventricular rate,
abrupt onset following a PAC, the relationship between QRS complexes and P
waves, and spontaneous termination with AV block in the absence of a PAC.
(See 'Electrocardiographic characteristics' above.)
●The initial management (algorithm 1) of a patient presenting with a narrow
QRS tachycardia and suspected AVNRT is guided by whether or not the
patient is experiencing signs and symptoms of hemodynamic instability related
to the rapid heart rate (eg, hypotension, shortness of breath, chest pain
suggestive of coronary ischemia, shock, and/or decreased level of
consciousness).
•Rare patients who are severely hemodynamically unstable should
undergo urgent cardioversion.
•For patients who are hemodynamically stable and able to effectively
perform the vagal maneuvers, we recommend at least one or two
attempts at a standard Valsalva maneuver, followed by at least one or two
attempts using the modified Valsalva maneuver (if AVNRT persists), as
the initial treatment for AVNRT rather than another vagal maneuver
or adenosine (Grade 1B). (See 'Vagal maneuvers' above.)
•If vagal maneuvers cannot be performed or if they fail to terminate the
arrhythmia, intravenous (IV) medical therapy that blocks AV nodal
conduction is indicated as the next step. For patients with AVNRT that
persists following vagal maneuvers (or in whom vagal maneuvers cannot
be adequately performed), we recommend IV adenosine rather than a
calcium channel blocker or a beta blocker (Grade 1B).
(See 'Adenosine' above.)
•If both vagal maneuvers and adenosine are ineffective, or when these
options are followed by an immediate recurrence of the tachycardia,
IV verapamil, diltiazem, or a beta blocker can be used to terminate or
prevent recurrent AVNRT. (See 'Other AV nodal blocking drugs' above.)
●The approach to the management of subsequent AVNRT episodes is based
around acute management of recurrent episodes and/or preventive therapy to
reduce or eliminate recurrences. Because AVNRT is usually well-tolerated in
the majority of patients, with a variety of safe and effective treatment options,
and there are no compelling data favoring one therapy over another, the
choice of long-term management strategies is largely influenced by patient
preference.
•For the initial management of recurrent AVNRT, we generally work with
the patient to develop a patient-directed treatment approach using either
vagal maneuvers or an oral medication ("pill-in-the-pocket" approach). For
most patients, we suggest a combination of one or more vagal maneuvers
rather than the pill-in-the-pocket approach (Grade 2C). (See 'Acute
management of recurrent episodes' above.)
•Patients with infrequent and well-tolerated episodes of AVNRT may
choose no chronic therapy. For these patients, we emphasize the patient-
directed approach to the termination of recurrent episodes using one or
more vagal maneuvers. (See 'No treatment' above.)
•For patients with episodes of AVNRT that are either frequently occurring
or poorly tolerated (eg, associated with near-syncope or syncope, angina,
or severe dyspnea), we recommend catheter ablation rather than chronic
medical therapy as initial long-term management strategy (Grade 1B). In
such cases, the risks associated with recurrent arrhythmic events (eg,
syncope with associated trauma) outweigh the procedural risks. In
addition, the potential for definitive therapy makes ablation preferable to
medical therapy in this setting. (See 'Catheter ablation' above.)
•For patients with poorly tolerated symptomatic episodes of AVNRT who
are not candidates for or who have declined catheter ablation, chronic
medical therapy using beta blockers, nondihydropyridine calcium channel
blockers, or antiarrhythmic drugs can be initiated in an effort to suppress
recurrent arrhythmias. Our experts typical prefer beta blockers rather than
calcium channel blockers or antiarrhythmic drugs as the initial option for
chronic medical therapy. (See 'Chronic suppressive therapy' above.)
REFERENCES
1. Liuba I, Jönsson A, Säfström K, Walfridsson H. Gender-related differences
in patients with atrioventricular nodal reentry tachycardia. Am J Cardiol
2006; 97:384.
2. Ferguson JD, DiMarco JP. Contemporary management of paroxysmal
3. Ganz LI, Friedman PL. Supraventricular tachycardia. N Engl J Med 1995;
332:162.
4. Goyal R, Zivin A, Souza J, et al. Comparison of the ages of tachycardia
onset in patients with atrioventricular nodal reentrant tachycardia and
accessory pathway-mediated tachycardia. Am Heart J 1996; 132:765.
5. McGuire MA, Bourke JP, Robotin MC, et al. High resolution mapping of
Koch's triangle using sixty electrodes in humans with atrioventricular
junctional (AV nodal) reentrant tachycardia. Circulation 1993; 88:2315.
6. McGuire MA, Janse MJ, Ross DL. "AV nodal" reentry: Part II: AV nodal, AV
junctional, or atrionodal reentry? J Cardiovasc Electrophysiol 1993; 4:573.
7. Meiltz A, Zimmermann M. Atrioventricular nodal reentrant tachycardia in the
elderly: efficacy and safety of radiofrequency catheter ablation. Pacing Clin
Electrophysiol 2007; 30 Suppl 1:S103.
8. Grecu M, Floria M, Georgescu CA. Abnormal atrioventricular node
conduction and atrioventricular nodal reentrant tachycardia in patients older
versus younger than 65 years of age. Pacing Clin Electrophysiol 2009; 32
Suppl 1:S98.
9. Janse MJ, Anderson RH, McGuire MA, Ho SY. "AV nodal" reentry: Part I:
"AV nodal" reentry revisited. J Cardiovasc Electrophysiol 1993; 4:561.
10. Pieper SJ, Stanton MS. Narrow QRS complex tachycardias. Mayo Clin Proc
1995; 70:371.
11. Yamabe H, Shimasaki Y, Honda O, et al. Demonstration of the exact
anatomic tachycardia circuit in the fast-slow form of atrioventricular nodal
reentrant tachycardia. Circulation 2001; 104:1268.
12. Mazgalev TN, Tchou PJ. Surface potentials from the region of the
atrioventricular node and their relation to dual pathway electrophysiology.
13. Sung RJ, Waxman HL, Saksena S, Juma Z. Sequence of retrograde atrial
activation in patients with dual atrioventricular nodal pathways. Circulation
1981; 64:1059.
14. Hayes JJ, Sharma PP, Smith PN, Vidaillet HJ. Familial atrioventricular nodal
reentry tachycardia. Pacing Clin Electrophysiol 2004; 27:73.
15. MOE GK, PRESTON JB, BURLINGTON H. Physiologic evidence for a dual
A-V transmission system. Circ Res 1956; 4:357.
16. Man KC, Brinkman K, Bogun F, et al. 2:1 atrioventricular block during
atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1996;
28:1770.
17. Schmitt C, Miller JM, Josephson ME. Atrioventricular nodal supraventricular
tachycardia with 2:1 block above the bundle of His. Pacing Clin
Electrophysiol 1988; 11:1018.
18. Yeh SJ, Yamamoto T, Lin FC, Wu D. Atrioventricular block in the atypical
form of junctional reciprocating tachycardia: evidence supporting the
atrioventricular node as the site of reentry. J Am Coll Cardiol 1990; 15:385.
19. Bogun F, Daoud E, Goyal R, et al. Comparison of atrial-His intervals in
patients with and without dual atrioventricular nodal physiology and
atrioventricular nodal reentrant tachycardia. Am Heart J 1996; 132:758.
20. Otomo K, Suyama K, Okamura H, et al. Participation of a concealed
atriohisian tract in the reentrant circuit of the slow-fast type of atrioventricular
nodal reentrant tachycardia. Heart Rhythm 2007; 4:703.
21. Wu J, Zipes DP. Mechanisms underlying atrioventricular nodal conduction
and the reentrant circuit of atrioventricular nodal reentrant tachycardia using
optical mapping. J Cardiovasc Electrophysiol 2002; 13:831.
22. Kwaku KF, Josephson ME. Typical AVNRT--an update on mechanisms and
therapy. Card Electrophysiol Rev 2002; 6:414.
23. Otomo K, Nagata Y, Uno K, et al. Atypical atrioventricular nodal reentrant
tachycardia with eccentric coronary sinus activation: electrophysiological
characteristics and essential effects of left-sided ablation inside the coronary
sinus. Heart Rhythm 2007; 4:421.
24. Katritsis DG, Marine JE, Latchamsetty R, et al. Coexistent Types of
Atrioventricular Nodal Re-Entrant Tachycardia: Implications for the
Tachycardia Circuit. Circ Arrhythm Electrophysiol 2015; 8:1189.
25. Abe H, Nagatomo T, Kobayashi H, et al. Neurohumoral and hemodynamic
mechanisms of diuresis during atrioventricular nodal reentrant tachycardia.
Pacing Clin Electrophysiol 1997; 20:2783.
26. Wood KA, Drew BJ, Scheinman MM. Frequency of disabling symptoms in
supraventricular tachycardia. Am J Cardiol 1997; 79:145.
27. Doi A, Miyamoto K, Uno K, et al. Studies on hemodynamic instability in
paroxysmal supraventricular tachycardia: noninvasive evaluations by head-
up tilt testing and power spectrum analysis on electrocardiographic RR
variation. Pacing Clin Electrophysiol 2000; 23:1623.
28. Leitch JW, Klein GJ, Yee R, et al. Syncope associated with supraventricular
tachycardia. An expression of tachycardia rate or vasomotor response?
29. Wang YS, Scheinman MM, Chien WW, et al. Patients with supraventricular
tachycardia presenting with aborted sudden death: incidence, mechanism
and long-term follow-up. J Am Coll Cardiol 1991; 18:1711.
30. Chiou CW, Chen SA, Kung MH, et al. Effects of continuous enhanced vagal
tone on dual atrioventricular node and accessory pathways. Circulation
2003; 107:2583.
31. Ng KS, Lauer MR, Young C, et al. Correlation of P-wave polarity with
underlying electrophysiologic mechanisms of long RP' tachycardia. Am J
Cardiol 1996; 77:1129.
32. Riva SI, Della Bella P, Fassini G, et al. Value of analysis of ST segment
changes during tachycardia in determining type of narrow QRS complex
tachycardia. J Am Coll Cardiol 1996; 27:1480.
33. Güleç S, Ertaş F, Karaoŏuz R, et al. Value of ST-segment depression during
paroxysmal supraventricular tachycardia in the diagnosis of coronary artery
disease. Am J Cardiol 1999; 83:458.
34. Imrie JR, Yee R, Klein GJ, Sharma AD. Incidence and clinical significance of
ST segment depression in supraventricular tachycardia. Can J Cardiol 1990;
6:323.
35. Petsas AA, Anastassiades LC, Antonopoulos AG. Exercise testing for
assessment of the significance of ST segment depression observed during
episodes of paroxysmal supraventricular tachycardia. Eur Heart J 1990;
11:974.
36. Paparella N, Ouyang F, Fucă G, et al. Significance of newly acquired
negative T waves after interruption of paroxysmal reentrant supraventricular
tachycardia with narrow QRS complex. Am J Cardiol 2000; 85:261.
37. Villain E, Vetter VL, Garcia JM, et al. Evolving concepts in the management
of congenital junctional ectopic tachycardia. A multicenter study. Circulation
1990; 81:1544.
38. Fishberger SB, Rossi AF, Messina JJ, Saul JP. Successful radiofrequency
catheter ablation of congenital junctional ectopic tachycardia with
preservation of atrioventricular conduction in a 9-month-old infant. Pacing
Clin Electrophysiol 1998; 21:2132.
Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.
Circulation 2016; 133:e506.
41. Belz MK, Stambler BS, Wood MA, et al. Effects of enhanced
parasympathetic tone on atrioventricular nodal conduction during
atrioventricular nodal reentrant tachycardia. Am J Cardiol 1997; 80:878.
42. Pandya A, Lang E. Valsalva maneuver for termination of supraventricular
tachycardia. Ann Emerg Med 2015; 65:27.
43. Appelboam A, Reuben A, Mann C, et al. Postural modification to the
standard Valsalva manoeuvre for emergency treatment of supraventricular
tachycardias (REVERT): a randomised controlled trial. Lancet 2015;
386:1747.
44. Glatter KA, Cheng J, Dorostkar P, et al. Electrophysiologic effects of
adenosine in patients with supraventricular tachycardia. Circulation 1999;
99:1034.
45. Cairns CB, Niemann JT. Intravenous adenosine in the emergency
department management of paroxysmal supraventricular tachycardia. Ann
Emerg Med 1991; 20:717.
46. Rankin AC, Brooks R, Ruskin JN, McGovern BA. Adenosine and the
treatment of supraventricular tachycardia. Am J Med 1992; 92:655.
47. Waxman HL, Myerburg RJ, Appel R, Sung RJ. Verapamil for control of
ventricular rate in paroxysmal supraventricular tachycardia and atrial
fibrillation or flutter: a double-blind randomized cross-over study. Ann Intern
Med 1981; 94:1.
48. Das G, Tschida V, Gray R, et al. Efficacy of esmolol in the treatment and
transfer of patients with supraventricular tachyarrhythmias to alternate oral
antiarrhythmic agents. J Clin Pharmacol 1988; 28:746.
49. Stambler BS, Dorian P, Sager PT, et al. Etripamil Nasal Spray for
Rapid Conversion of Supraventricular Tachycardia to Sinus Rhythm. J Am
Coll Cardiol 2018; 72:489.
50. https://clinicaltrials.gov/ct2/show/NCT03464019 (Accessed on July 26,
2018).
51. Sung RJ, Elser B, McAllister RG Jr. Intravenous verapamil for termination of
re-entrant supraventricular tachycardias: intracardiac studies correlated with
plasma verapamil concentrations. Ann Intern Med 1980; 93:682.
52. DiMarco JP, Sellers TD, Berne RM, et al. Adenosine: electrophysiologic
effects and therapeutic use for terminating paroxysmal supraventricular
tachycardia. Circulation 1983; 68:1254.
53. Dougherty AH, Jackman WM, Naccarelli GV, et al. Acute conversion of
paroxysmal supraventricular tachycardia with intravenous diltiazem. IV
Diltiazem Study Group. Am J Cardiol 1992; 70:587.
54. Margolis B, DeSilva RA, Lown B. Episodic drug treatment in the
management of paroxysmal arrhythmias. Am J Cardiol 1980; 45:621.
55. Alboni P, Tomasi C, Menozzi C, et al. Efficacy and safety of out-of-hospital
self-administered single-dose oral drug treatment in the management of
infrequent, well-tolerated paroxysmal supraventricular tachycardia. J Am
56. Spector P, Reynolds MR, Calkins H, et al. Meta-analysis of ablation of atrial
flutter and supraventricular tachycardia. Am J Cardiol 2009; 104:671.
57. Chrispin J, Misra S, Marine JE, et al. Current management and clinical
outcomes for catheter ablation of atrioventricular nodal re-entrant
tachycardia. Europace 2018; 20:e51.
58. Katritsis DG, Marine JE, Contreras FM, et al. Catheter Ablation of Atypical
Atrioventricular Nodal Reentrant Tachycardia. Circulation 2016; 134:1655.
59. Hosseini SM, Rozen G, Saleh A, et al. Catheter ablation for cardiac
arrhythmias: utilization and in-hospital complications, 2000 to 2013. J Am
Coll Cardiol EP 2017; 3:1240.
60. Katritsis DG, Zografos T, Siontis KC, et al. Endpoints for Successful Slow
Pathway Catheter Ablation in Typical and Atypical Atrioventricular Nodal Re-
Entrant Tachycardia: A Contemporary, Multicenter Study. J Am Coll Cardiol
EP 2019; 5:113.
61. Boulos M, Hoch D, Schecter S, et al. Age dependence of complete heart
block complicating radiofrequency ablation of the atrioventricular nodal slow
pathway. Am J Cardiol 1998; 82:390.
62. Li YG, Grönefeld G, Bender B, et al. Risk of development of delayed
atrioventricular block after slow pathway modification in patients with
atrioventricular nodal reentrant tachycardia and a pre-existing prolonged PR
interval. Eur Heart J 2001; 22:89.
63. Natale A, Greenfield RA, Geiger MJ, et al. Safety of slow pathway ablation
in patients with long PR interval: further evidence of fast and slow pathway
interaction. Pacing Clin Electrophysiol 1997; 20:1698.
64. Reithmann C, Hoffmann E, Grünewald A, et al. Fast pathway ablation in
patients with common atrioventricular nodal reentrant tachycardia and
prolonged PR interval during sinus rhythm. Eur Heart J 1998; 19:929.
65. Kaneko Y, Naito S, Okishige K, et al. Atypical Fast-Slow Atrioventricular
Nodal Reentrant Tachycardia Incorporating a "Superior" Slow Pathway: A
Distinct Supraventricular Tachyarrhythmia. Circulation 2016; 133:114.
66. Bathina MN, Mickelsen S, Brooks C, et al. Radiofrequency catheter ablation
versus medical therapy for initial treatment of supraventricular tachycardia
and its impact on quality of life and healthcare costs. Am J Cardiol 1998;
82:589.
Close

 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 INTRODUCTION
 NORMAL AV CONDUCTION VERSUS ACCESSORY AV PATHWAY CONDUCTION
 TACHYCARDIAS REQUIRING AN AV ACCESSORY PATHWAY FOR INITIATION AND
MAINTENANCE
o Orthodromic AVRT
 ECG findings in orthodromic AVRT
o Antidromic AVRT
 ECG findings in antidromic AVRT
o Permanent junctional reciprocating tachycardia
 ECG findings in PJRT
 CLINICAL MANIFESTATIONS OF AVRT AND PJRT
 DIAGNOSIS OF AVRT AND PJRT
 TREATMENT OF AVRT AND PJRT
 REFERENCES
GRAPHICS view all
 Algorithms
 Figures
oAnatomy AV accessory pathways
oSites of reentry in supraventricular tachyarrhythmias
oOrthodromic AVRT
oAntidromic AVRT
 Waveforms
oOrthodromic AVRT tutorial
o12 lead ECG orthodromic AVRT
o12-lead ECG antidromic AVRT
oECG Antidromic AVRT
oECG WPW left posterior path
oPermanent junctional tachy
RELATED TOPICS
 Arrhythmia-induced cardiomyopathy
 Atriofascicular ("Mahaim") pathway tachycardia
 Clinical features and diagnosis of supraventricular tachycardia in children
 Left bundle branch block
 Wide QRS complex tachycardias: Causes, epidemiology, and clinical manifestations
Atrioventricular reentrant tachycardia (AVRT)

associated with an accessory pathway
Authors:
Luigi Di Biase, MD, PhD, FHRS, FACC
Edward P Walsh, MD
Section Editors:
Samuel Lévy, MD
Deputy Editor:
Literature review current through: Sep 2020. | This topic last updated: Dec 19, 2019.
INTRODUCTION In 1930, Louis Wolff, Sir John Parkinson, and Paul Dudley
White published a seminal article describing 11 patients who suffered from attacks of
tachycardia associated with a sinus rhythm electrocardiographic (ECG) pattern of bundle
branch block with a short PR interval [1]. This was subsequently termed the Wolff-
Parkinson-White (WPW) syndrome, although earlier isolated case reports describing
similar findings had already been published. In 1943, the ECG features of preexcitation
were correlated with anatomic evidence for the existence of anomalous bundles of
conducting tissue that bypassed all or part of the normal atrioventricular (AV) conduction
system (figure 1).
AV reentrant (or reciprocating) tachycardia (AVRT) is a reentrant tachycardia with an
anatomically defined circuit that consists of two distinct pathways, the normal AV
conduction system and an AV accessory pathway, linked by common proximal (the
atria) and distal (the ventricles) tissues. While other arrhythmias can utilize the
accessory pathway for conduction from the anatomic site of tachycardia origin to other
regions of the heart (eg, atrial fibrillation and atrial flutter) (figure 2), AVRT is a specific
reentrant tachycardia in which the accessory pathway is necessary for initiation and
maintenance of the tachycardia [2].
The different types of AVRT, along with their ECG findings, will be discussed here. The
approach to treatment of arrhythmias associated with an accessory pathway is
presented in detail separately. (See "Treatment of symptomatic arrhythmias associated
with the Wolff-Parkinson-White syndrome".)
NORMAL AV CONDUCTION VERSUS ACCESSORY AV
PATHWAY CONDUCTION Normal AV conduction occurs through the AV
node. However, in the presence of an accessory pathway, conduction from the atria to
the ventricles may occur in a variety of ways (exclusively via the AV node, exclusively
via the accessory pathway, or a combination of both). Normal and accessory AV
conduction are discussed in detail elsewhere. (See "Wolff-Parkinson-White syndrome:
Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Normal AV
conduction versus accessory AV pathway conduction'.)
TACHYCARDIAS REQUIRING AN AV ACCESSORY PATHWAY
FOR INITIATION AND MAINTENANCE AVRT is a reentrant tachycardia
with an anatomically defined circuit that consists of two distinct pathways, the normal AV
conduction system and an AV accessory pathway, linked by common proximal (the
atria) and distal (the ventricles) tissues. If sufficient differences in conduction time and
refractoriness exist between the normal conduction system and the accessory pathway,
a properly timed premature impulse of atrial, junctional, or ventricular origin can initiate
reentry. (See "Reentry and the development of cardiac arrhythmias".)
The two major types of this arrhythmia in persons with an AV accessory pathway are
orthodromic and antidromic AVRT. The width of the QRS complex can usually
distinguish between these paroxysmal arrhythmias:
●Orthodromic AVRT – If the tachycardia has a narrow QRS complex, the

antegrade limb (ie, the pathway that conducts the supraventricular impulse to
the ventricle) is the AV node/His-Purkinje system. In this setting, any
preexcitation (manifest as a delta wave on the surface ECG) seen during sinus
rhythm is lost since antegrade conduction is not occurring via the accessory
pathway (ie, the ventricle is not preexcited) (figure 3 and waveform
1 and waveform 2). (See 'Orthodromic AVRT' below.)
●Antidromic AVRT – If the tachycardia has a wide QRS complex, the
possibilities include AVRT with antegrade conduction over the accessory
pathway (antidromic AVRT) or orthodromic AVRT with aberrant QRS
conduction resulting in a wide QRS complex (figure 4 and waveform
3 and waveform 4). (See 'Antidromic AVRT' below and "Left bundle branch
block", section on 'Functional LBBB' and "Wide QRS complex tachycardias:
Approach to the diagnosis".)
A third type of arrhythmia, permanent junctional reciprocating tachycardia, is a type of
orthodromic AVRT that is typically seen in childhood. (See 'Permanent junctional
reciprocating tachycardia' below.)
Orthodromic AVRT — Orthodromic AVRT comprises 90 to 95 percent of the reentrant
tachycardias associated with the Wolff-Parkinson-White (WPW) syndrome [2,3].
Orthodromic AVRT can be initiated by atrial or ventricular premature beats (APBs or
VPBs) (figure 3) [2].
●APBs initiating orthodromic AVRT are blocked in the accessory pathway but
conduct antegrade to the ventricles over the AV node/His-Purkinje system.
After conduction through the ventricles, the impulse then travels back to the
atria in a retrograde fashion via the AV accessory pathway to complete the
first reentrant loop.
●VPBs initiating orthodromic AVRT are blocked in the AV node/His-Purkinje
system but conduct retrograde to the atria over the accessory pathway. After
conduction through the atria, the impulse then travels back to the ventricles in
an antegrade fashion via the normal AV conduction system to complete the
reentrant circuit [2,4].
ECG findings in orthodromic AVRT — The ECG during orthodromic AVRT (waveform
1 and waveform 2) typically shows the following:
●Ventricular rate ranging from 150 to 250 (or greater) beats per minute and
usually regular
●Narrow QRS complexes (in the absence of underlying conduction system
disease or in the absence of aberrancy)
●Inverted P waves with an RP interval that is usually less than one-half the
tachycardia RR interval (see "Narrow QRS complex tachycardias: Clinical
manifestations, diagnosis, and evaluation", section on 'RP relationship')
●Constant RP interval regardless of the tachycardia cycle length [5]
Beat-to-beat oscillation in QRS amplitude (QRS alternans) sometimes occurs during
orthodromic AVRT and is most commonly seen when the rate is very rapid [6,7]. The
mechanism for QRS alternans is not clear but may in part result from oscillations in the
relative refractory period of the AV node-His-Purkinje system [8,9].
Ischemic-appearing ST segment depression also can occur during orthodromic AVRT,
even in young individuals who are unlikely to have coronary artery disease [10]. Several
factors may contribute to the ST segment depression in these arrhythmias, including
changes in autonomic nervous system tone, intraventricular conduction disturbances, a
longer ventriculoatrial interval, and a retrograde P wave of longer duration that overlaps
into the ST segment [11]. The location of the ST segment changes may vary with the
location of the accessory pathway [12,13].
Antidromic AVRT — Antidromic AVRT is the least common arrhythmia associated with
WPW syndrome, occurring in less than 10 percent of patients [2]. In a retrospective
observational study of 807 patients (age range 5 to 85 years) with preexcitation on a
surface ECG who also underwent invasive electrophysiologic studies (EPS), 63 patients
(8 percent) were found to have inducible antidromic AVRT during EPS (compared with
55 percent rate of inducible orthodromic AVRT in the same population) [14]. In another
retrospective study of 1147 pediatric patients (age less than 21 years) who underwent
invasive EPS, antidromic AVRT was identified in only 30 patients (3 percent), with the
accessory pathways in these patients having rapid anterograde conduction
characteristics [15].
As with orthodromic AVRT, antidromic AVRT can be initiated by atrial or ventricular
premature beats (APBs or VPBs) (figure 4) [2].
●APBs initiating antidromic AVRT are blocked in the AV node/His-Purkinje
system but conduct antegrade to the ventricles over the accessory pathway.
After conduction through the ventricles, the impulse then travels back to the
atria in a retrograde fashion via the AV node/His-Purkinje system to complete
the first reentrant loop.
●VPBs initiating antidromic AVRT are blocked in the accessory pathway but
conduct retrograde to the atria over the AV node/His-Purkinje system. After
conduction through the atria, the impulse then travels back to the ventricles in
an antegrade fashion via the accessory pathway to complete the reentrant
circuit.
An unusual type of antidromic reentry can also occur in patients with an atriofascicular
fiber (sometimes referred to as a Mahaim fiber) that can be difficult to distinguish from
antidromic reentry using a conventional AV accessory pathway reentry in the acute
setting. (See "Atriofascicular ("Mahaim") pathway tachycardia".)
ECG findings in antidromic AVRT — The ECG during antidromic AVRT (figure
4 and waveform 3 and waveform 4) typically shows the following:
●Ventricular rate ranging from 150 to 250 (or greater) beats per minute and
usually regular
●Wide QRS complexes which are fully preexcited
●Inverted P waves with an RP interval that is usually more than one-half the
tachycardia RR interval and a short PR interval (see "Narrow QRS complex
tachycardias: Clinical manifestations, diagnosis, and evaluation", section on
'RP relationship')
●Constant RP interval regardless of the tachycardia cycle length [5]
Susceptibility to antidromic AVRT also appears to be dependent upon a transverse
distance of at least 4 cm between the bypass tract and the normal AV conduction
system. Consequently, most antidromic AVRTs use a left-sided accessory pathway as
the antegrade route for conduction [2,5].
In some patients with antidromic AVRT and a left-sided accessory pathway,
preexcitation may not be apparent in sinus rhythm because the time for the atrial
impulse to reach the atrial insertion of the accessory pathway is longer than the time to
reach the AV node (waveform 5).
A rare variant of antidromic AVRT can occur in patients with multiple accessory
pathways when anterograde conduction occurs over one accessory pathways and
retrograde conduction returns to the atrium via a second accessory pathway. In such
cases, the AV node is not necessary for maintenance of reentry. The ECG during
pathway-pathway tachycardia is indistinguishable from conventional antidromic AVRT,
and confirmation of the precise circuit usually requires mapping at electrophysiology
study. Approximately 10 percent of patients undergoing catheter ablation can be found
to have multiple accessory pathways [16].
Permanent junctional reciprocating tachycardia — Permanent or incessant
junctional reciprocating (or reentrant) tachycardia (PJRT) is a type of orthodromic AVRT
that most often occurs in early childhood, although clinically asymptomatic patients
presenting later in life are not uncommon. In the older patient, PJRT tends to be less
incessant, perhaps due to variable autonomic tone, and has a somewhat slower
ventricular rate, felt to be the result of a prolongation of retrograde conduction through
the accessory pathway [17]. The heart rate is usually between 120 and 200
beats/minute, and the QRS duration is generally normal (waveform 6).
Chronic suppression of PJRT is usually not possible with drugs, and ablation of the
accessory pathway is often necessary to achieve arrhythmia control [3,18-20]. The
incessant nature of PJRT may result in dilated cardiomyopathy and heart failure; these
changes are potentially reversible if the accessory pathway can be successfully ablated
[3,17,18,21]. (See "Clinical features and diagnosis of supraventricular tachycardia in
children", section on 'Permanent junctional reciprocating tachycardia' and "Arrhythmia-
induced cardiomyopathy" and "Treatment of symptomatic arrhythmias associated with
the Wolff-Parkinson-White syndrome", section on 'Catheter ablation'.)
ECG findings in PJRT — PJRT is an orthodromic AVRT mediated by a concealed,
retrogradely conducting AV accessory pathway that has slow and decremental
conduction properties [19,22,23]. Because of this, PJRT has similar ECG findings as
seen in typical orthodromic AVRT. (See 'ECG findings in orthodromic AVRT' above.)
Nevertheless, one major ECG difference is seen between PJRT and typical orthodromic
AVRT. The retrograde conduction properties of the accessory pathway in PJRT are
slower compared with both the anterograde conduction properties of the AV node and
the usual "fast" accessory pathways found in patients with AVRT [17]. Therefore, slow
retrograde conduction over the accessory pathway causes the RP interval during PJRT
to be long, usually more than one-half the tachycardia RR interval.
The accessory pathway in patients with PJRT is most often located within the
posteroseptal region, although other portions of the AV groove may also harbor this
unique pathway [19,20,23,24]. P waves resulting from retrograde conduction are easily
seen on the ECG and are inverted in leads 2, 3, aVF, and V3 to V6.
CLINICAL MANIFESTATIONS OF AVRT AND PJRT The response to
a rapid heart rate can be quite variable depending on how fast the heart is beating,
resultant blood pressure and tissue perfusion, underlying comorbidities, and the
sensitivity of the individual patient to the symptoms. Patients with AV reentrant (or
reciprocating) tachycardia (AVRT) or permanent junctional reciprocating (or reentrant)
tachycardia (PJRT) can present with a variety of symptoms, including:
●Palpitations
●Lightheadedness or dizziness
●Diaphoresis
●Chest pain
Most commonly, patients with AVRT present with palpitations, the sensation of a rapid or
irregular heart beat felt in the anterior chest or neck. Because of the persistent nature
and the rapid ventricular heart rate associated with PJRT, some patients with PJRT may
present with findings of impaired left ventricular function compatible with a tachycardia-
mediated cardiomyopathy. The presenting symptoms of tachycardias and tachycardia-
mediated cardiomyopathy are discussed in greater detail separately. (See "Evaluation of
palpitations in adults" and "Narrow QRS complex tachycardias: Clinical manifestations,
diagnosis, and evaluation", section on 'Clinical manifestations' and "Arrhythmia-induced
cardiomyopathy".)
DIAGNOSIS OF AVRT AND PJRT The diagnosis of AV reentrant (or
reciprocating) tachycardia (AVRT) or permanent junctional reciprocating (or reentrant)

tachycardia (PJRT) typically requires only a surface electrocardiogram (ECG) which
shows a heart rate greater than 100 beats per minute along with regularly occurring
QRS complexes. An old ECG performed when the patient is not having a tachycardia
can be helpful for identifying the presence of a delta wave suggesting preexcitation and
an accessory pathway. Once a QRS complex width has been identified, further scrutiny
of the ECG is required to identify the specific arrhythmia in a particular patient, as
diagnostic evaluation and therapy will differ depending on the underlying arrhythmia
(algorithm 1). (See 'ECG findings in orthodromic AVRT' above and 'ECG findings in
antidromic AVRT' above and 'ECG findings in PJRT' above and "Narrow QRS complex
'Evaluation'.)
Invasive electrophysiology testing is usually not required to broadly make the diagnosis
of AVRT or PJRT, but on rare occasions it is needed to diagnose (and potentially treat
with catheter ablation) the specific arrhythmia. (See "Narrow QRS complex
'Electrophysiologic testing'.)
DIFFERENTIAL DIAGNOSIS The differential diagnosis for patients with
orthodromic AV reentrant (or reciprocating) tachycardia (AVRT) or permanent junctional

reciprocating (or reentrant) tachycardia (PJRT) and a narrow QRS complex (<120 msec
duration) included other supraventricular tachyarrhythmias with regularly occurring,
narrow QRS complexes (algorithm 1). This differential diagnosis is discussed in greater
detail separately. (See "Narrow QRS complex tachycardias: Clinical manifestations,
diagnosis, and evaluation", section on 'Types of narrow QRS complex tachycardia'.)
For patients with a wide QRS complex tachycardia (ie, those with antidromic AVRT; or
those with orthodromic AVRT or PJRT and underlying conduction system disease),
ventricular tachycardia should be a part of the differential diagnosis along with aberrantly
conducted supraventricular tachyarrhythmias (eg, focal atrial tachycardia and AV nodal
reentry tachycardia). This differential diagnosis is discussed in greater detail separately.
(See "Wide QRS complex tachycardias: Causes, epidemiology, and clinical
manifestations", section on 'Differential diagnosis of WCT'.)
TREATMENT OF AVRT AND PJRT The approaches to both acute and
chronic treatment of AV reentrant (or reciprocating) tachycardia or permanent junctional

reciprocating (or reentrant) tachycardia are discussed separately. (See "Treatment of
symptomatic arrhythmias associated with the Wolff-Parkinson-White
syndrome" and "Overview of the acute management of tachyarrhythmias", section on
'Regular narrow QRS complex tachyarrhythmias'.)
links: Catheter ablation of arrhythmias" and "Society guideline links: Supraventricular
arrhythmias".)
●Atrioventricular reentrant (or reciprocating) tachycardia (AVRT) is a reentrant

tachycardia with an anatomically defined circuit that consists of two distinct
pathways, the normal AV conduction system and an AV accessory pathway,
linked by common proximal (the atria) and distal (the ventricles) tissues.
(See 'Introduction' above.)
●The two major types of this arrhythmia in persons with an AV accessory
pathway are orthodromic AVRT (including permanent junctional reciprocating
tachycardia [PJRT]) and antidromic AVRT.
•Orthodromic AVRT comprises 90 to 95 percent of the reentrant
tachycardias associated with the Wolff-Parkinson-White (WPW)
syndrome. The ECG during orthodromic AVRT (waveform
1 and waveform 2) typically shows a regular ventricular rate ranging from
150 to 250 (or greater) beats per minute, narrow QRS complexes,
inverted P waves with an RP interval that is usually less than one-
half the tachycardia RR interval, and a constant RP interval.
(See 'Orthodromic AVRT' above and 'ECG findings in orthodromic
AVRT' above.)
•Antidromic AVRT is the least common arrhythmia associated with WPW
syndrome, occurring in only 5 to 10 percent of patients. The ECG during
antidromic AVRT (figure 4 and waveform 3 and waveform 4) typically
shows a regular ventricular rate ranging from 150 to 250 (or greater)
beats per minute, wide QRS complexes, inverted P waves with an RP
interval that is usually more than one-half the tachycardia RR interval,
and a constant RP interval. (See 'Antidromic AVRT' above and 'ECG
findings in antidromic AVRT' above.)
•PJRT is an orthodromic AVRT most often occurring in early childhood.
PJRT has similar ECG findings as seen in typical orthodromic AVRT with
one major difference; slow retrograde conduction over the accessory
pathway causes the RP interval during PJRT to be long, usually more
than one-half the tachycardia RR interval. (See 'Permanent junctional
reciprocating tachycardia' above and 'ECG findings in PJRT' above.)
●Most commonly, patients with AVRT present with palpitations, the sensation
of a rapid or irregular heart beat felt in the anterior chest or neck. Because of
the persistent nature and the rapid ventricular heart rate associated with
PJRT, some patients with PJRT may present with findings of impaired left
ventricular function compatible with a tachycardia-mediated cardiomyopathy.
(See 'Clinical manifestations of AVRT and PJRT' above.)
●The diagnosis of AVRT or PJRT typically requires only a surface
electrocardiogram (ECG) which shows a heart rate greater than 100 beats per
minute along with regularly occurring QRS complexes. An old ECG performed
when the patient is not having a tachycardia can be helpful for identifying the
presence of a delta wave suggesting preexcitation and an accessory pathway.
Once a narrow QRS complex tachycardia has been identified, further scrutiny
of the ECG is required to identify the specific arrhythmia in a particular patient.
(See 'Diagnosis of AVRT and PJRT' above.)
●The differential diagnosis and approach to treatment for AVRT and PJRT are
discussed in greater detail separately. (See "Treatment of symptomatic
arrhythmias associated with the Wolff-Parkinson-White
syndrome" and "Narrow QRS complex tachycardias: Clinical manifestations,
diagnosis, and evaluation", section on 'Types of narrow QRS complex
tachycardia'.)
REFERENCES
1. Wolff L, Parkinson J, White PD. Bundle-branch block with short P-R interval
in healthy young people prone to paroxysmal tachycardia. 1930. Ann
Noninvasive Electrocardiol 2006; 11:340.
2. Josephson ME. Preexcitation syndromes. In: Clinical Cardiac
Electrophysiology, 4th, Lippincot Williams & Wilkins, Philadelphia 2008.
p.339.
3. Chugh A, Morady F. Atrioventricular reentry and variants. In: Cardiac
electrophysiology from cell to bedside, 5th edition, Zipes DP, Jalife J (Eds),
Saunders/Elsevier, Philadelphia 2009. p.605-614.
4. Akhtar M, Lehmann MH, Denker ST, et al. Electrophysiologic mechanisms
of orthodromic tachycardia initiation during ventricular pacing in the Wolff-
Parkinson-White syndrome. J Am Coll Cardiol 1987; 9:89.
5. Cain ME, Luke RA, Lindsay BD. Diagnosis and localization of accessory
pathways. Pacing Clin Electrophysiol 1992; 15:801.
6. Green M, Heddle B, Dassen W, et al. Value of QRS alteration in determining
the site of origin of narrow QRS supraventricular tachycardia. Circulation
1983; 68:368.
7. Kay GN, Pressley JC, Packer DL, et al. Value of the 12-lead
electrocardiogram in discriminating atrioventricular nodal reciprocating
tachycardia from circus movement atrioventricular tachycardia utilizing a
retrograde accessory pathway. Am J Cardiol 1987; 59:296.
8. Tchou PJ, Lehmann MH, Dongas J, et al. Effect of sudden rate acceleration
on the human His-Purkinje system: adaptation of refractoriness in a
dampened oscillatory pattern. Circulation 1986; 73:920.
9. Gallagher JJ, Sealy WC, Kasell J, Wallace AG. Multiple accessory pathways
in patients with the pre-excitation syndrome. Circulation 1976; 54:571.
10. Man KC, Brinkman K, Bogun F, et al. 2:1 atrioventricular block during
atrioventricular node reentrant tachycardia. J Am Coll Cardiol 1996;
28:1770.
11. Nelson SD, Kou WH, Annesley T, et al. Significance of ST segment
depression during paroxysmal supraventricular tachycardia. J Am Coll
Cardiol 1988; 12:383.
12. Riva SI, Della Bella P, Fassini G, et al. Value of analysis of ST segment
changes during tachycardia in determining type of narrow QRS complex
tachycardia. J Am Coll Cardiol 1996; 27:1480.
13. Scheinman MM, Wang YS, Van Hare GF, Lesh MD. Electrocardiographic
and electrophysiologic characteristics of anterior, midseptal and right
anterior free wall accessory pathways. J Am Coll Cardiol 1992; 20:1220.
14. Brembilla-Perrot B, Pauriah M, Sellal JM, et al. Incidence and prognostic
significance of spontaneous and inducible antidromic tachycardia. Europace
2013; 15:871.
15. Ceresnak SR, Tanel RE, Pass RH, et al. Clinical and electrophysiologic
characteristics of antidromic tachycardia in children with Wolff-Parkinson-
White syndrome. Pacing Clin Electrophysiol 2012; 35:480.
16. Zachariah JP, Walsh EP, Triedman JK, et al. Multiple accessory pathways
in the young: the impact of structural heart disease. Am Heart J 2013;
165:87.
17. Dorostkar PC, Silka MJ, Morady F, Dick M 2nd. Clinical course of persistent
junctional reciprocating tachycardia. J Am Coll Cardiol 1999; 33:366.
18. Aguinaga L, Primo J, Anguera I, et al. Long-term follow-up in patients with
the permanent form of junctional reciprocating tachycardia treated with
radiofrequency ablation. Pacing Clin Electrophysiol 1998; 21:2073.
19. Guarnieri T, Sealy WC, Kasell JH, et al. The nonpharmacologic
management of the permanent form of junctional reciprocating tachycardia.
20. Ticho BS, Saul JP, Hulse JE, et al. Variable location of accessory pathways
associated with the permanent form of junctional reciprocating tachycardia
and confirmation with radiofrequency ablation. Am J Cardiol 1992; 70:1559.
21. Packer DL, Bardy GH, Worley SJ, et al. Tachycardia-induced
cardiomyopathy: a reversible form of left ventricular dysfunction. Am J
Cardiol 1986; 57:563.
22. Brugada P, Vanagt EJ, Bar FW, Wellens HJ. Incessant reciprocating
atrioventricular tachycardia. Factors playing a role in the mechanism of the
arrhythmia. Pacing Clin Electrophysiol 1980; 3:670.
23. Critelli G, Gallagher JJ, Monda V, et al. Anatomic and electrophysiologic
substrate of the permanent form of junctional reciprocating tachycardia. J
24. Okumura K, Henthorn RW, Epstein AE, et al. "Incessant" atrioventricular
(AV) reciprocating tachycardia utilizing left lateral AV bypass pathway with a
long retrograde conduction time. Pacing Clin Electrophysiol 1986; 9:332.
Close

 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 INTRODUCTION
 EPIDEMIOLOGY
o Symptoms
o Physical examination findings
 DIFFERENTIAL DIAGNOSIS OF WCT
o Ventricular tachycardia
o Supraventricular tachycardia
 Aberrant conduction
 Pre-excitation syndrome
 Pacemakers
o Artifact mimicking ventricular tachycardia
 REFERENCES
GRAPHICS view all
 Algorithms
oAlgorithm for tachycardia differential diagnosis after ECG
 Figures
oNormal conduction system
oAccessory AV pathways I
oAccessory AV pathways II
oAccessory AV pathways III
oAntidromic AVRT
oOrthodromic AVRT
 Tables
oCauses of wide QRS tachycardia
 Waveforms
oECG RMVT from LVOT
oECG pre-excited atrial fibrillation
oTremor artifact tutorial
RELATED TOPICS
 Basic approach to delayed intraventricular conduction
 Cardiac excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs
 Cardiac resynchronization therapy in heart failure: Indications
 Congenital long QT syndrome: Epidemiology and clinical manifestations
 ECG tutorial: Preexcitation syndromes
 Examination of the jugular venous pulse
 Modes of cardiac pacing: Nomenclature and selection
 Overview of cardiac pacing in heart failure
 Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy
 Sustained monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and evaluation
 Unexpected rhythms with normally functioning dual-chamber pacing systems
Wide QRS complex tachycardias: Causes,

epidemiology, and clinical manifestations
Author:
Leonard I Ganz, MD, FHRS, FACC
Section Editors:
Peter J Zimetbaum, MD
James Hoekstra, MD
Deputy Editor:
Literature review current through: Sep 2020. | This topic last updated: Apr 10, 2020.
INTRODUCTION Tachycardias are broadly categorized (algorithm 1) based
upon the width of the QRS complex on the electrocardiogram (ECG).

●A narrow QRS complex (<120 milliseconds) reflects rapid activation of the
ventricles via the normal His-Purkinje system (figure 1), which in turn suggests
that the arrhythmia originates above or within the atrioventricular (AV) node
(ie, a supraventricular tachycardia [SVT]).
●A widened QRS complex (≥120 milliseconds) occurs when ventricular
activation is abnormally slow for one of the following reasons (see 'Differential
diagnosis of WCT' below):
•The arrhythmia originates outside of the normal conduction system and
below the AV node (ie, ventricular tachycardia [VT])
•Abnormalities within the His-Purkinje system (ie, SVT with aberrancy)
•Pre-excitation with an SVT conducting antegrade over an accessory
pathway, resulting in direct activation of the ventricular myocardium
A wide QRS complex tachycardia (WCT) represents a unique clinical challenge for three
reasons:
●Diagnosing the arrhythmia is difficult – Although most WCTs are due to VT,
the differential diagnosis includes a variety of SVTs. Diagnostic algorithms to
differentiate these two etiologies are complex and imperfect. (See 'Differential
diagnosis of WCT' below and "Wide QRS complex tachycardias: Approach to
the diagnosis", section on 'Diagnosis'.)
●Urgent therapy is often required – Patients may be unstable at the onset of
the arrhythmia or deteriorate rapidly at any time, particularly if the WCT is VT
or SVT at an extremely rapid rate (eg, >200 beats per minute).
●Misdiagnosis of SVT when the true diagnosis is VT can lead to inappropriate
therapy, which can precipitate hemodynamic collapse and cardiac arrest.
The causes, epidemiology, and clinical manifestations of patients with a WCT will be
discussed here. The initial evaluation, diagnosis, and management of wide QRS
complex tachycardias, as well as discussion of narrow QRS complex tachycardias, are
presented separately. (See "Wide QRS complex tachycardias: Approach to the
diagnosis" and "Wide QRS complex tachycardias: Approach to
management" and "Overview of the acute management of
tachyarrhythmias" and "Secondary prevention of sudden cardiac death in heart failure
and cardiomyopathy" and "Narrow QRS complex tachycardias: Clinical manifestations,
diagnosis, and evaluation".)
EPIDEMIOLOGY Ventricular tachycardia (VT) is the most common cause of
WCT, particularly in patients with a history of cardiac disease. In a series of unselected

patients, VT accounted for up to 80 percent of cases of WCT [1,2]. Among patients with
structural heart disease (eg, those with a prior myocardial infarction), the likelihood of a
WCT being VT exceeds 90 percent [2].
Supraventricular tachycardia (SVT) results in WCT much less frequently than VT.
Among patients with WCT due to SVT, aberrant conduction is the most common reason
for a widened QRS (21 percent of cases in one series) [1]. However, an aberrantly
conducted SVT is still much less common than VT as the cause of WCT. Antidromic AV
reentrant tachycardia (AVRT) is a relatively uncommon cause of WCT (6 percent of
cases in one series) [1].
CLINICAL MANIFESTATIONS
Symptoms — Patients with WCT are rarely asymptomatic, although the type and
intensity of symptoms will vary depending upon the rate of the WCT, the presence or
absence of significant comorbid conditions, and whether the WCT is ventricular
tachycardia (VT) or supraventricular tachycardia (SVT). Patients with WCT typically
present with one or more of the following symptoms:
●Palpitations
●Chest pain
●Sudden cardiac arrest
Physical examination findings — Few physical examination findings in patients with a
WCT are unique to WCT. Common findings may include:
●Tachycardia – By definition, patients will have a pulse exceeding 100 beats
per minute related to the tachycardia.
●Hypotension – Patients may be hypotensive, particularly those with
underlying cardiac disease who are unable to tolerate tachycardia, which may
result in alterations in consciousness.
●Hypoxia and lung crackles – Patients in whom pulmonary congestion and
heart failure result from the WCT may have hypoxia and crackles on lung
examination. Often these patients will have underlying heart disease.
●Evidence of AV dissociation – AV dissociation, which is present in up to 75
percent of patients with VT, is not always easy to detect [3-5]. During AV
dissociation, the normal coordination of atrial and ventricular contraction is
lost, which may produce characteristic physical findings. The presence of AV
dissociation strongly suggests VT, although its absence is less helpful.
Although AV dissociation is typically diagnosed on the ECG, characteristic
physical examination findings include (see "Wide QRS complex tachycardias:
Approach to the diagnosis", section on 'AV dissociation'):
•Marked fluctuations in the blood pressure because of the variability in the
degree of left atrial contribution to left ventricular filling, stroke volume,
and cardiac output.
•Variability in the occurrence and intensity of heart sounds (especially S1;
"cacophony of heart sounds"), which are heard more frequently when the
rate of the tachycardia is slower.
•Cannon "A" waves – Cannon A waves are intermittent and irregular
jugular venous pulsations of greater amplitude than normal waves. They
reflect simultaneous atrial and ventricular activation, resulting in
contraction of the right atrium against a closed tricuspid valve. Prominent
A waves can also be seen during some SVTs, but they are usually
regular, not irregular. Such prominent waves result from simultaneous
atrial and ventricular contraction occurring with every beat. Classically,
this is seen in AV nodal reentrant tachycardia (AVNRT) and has been
called the "frog" sign. (See "Examination of the jugular venous pulse".)
DIFFERENTIAL DIAGNOSIS OF WCT WCTs most often result from
ventricular tachycardia (VT). Other less common causes include supraventricular

tachycardia (SVT) with aberrant conduction, SVT with pre-excitation, SVT with
ventricular pacing, and some types of artifact mimicking WCT (table 1).
Ventricular tachycardia — VT usually originates within the ventricular myocardium,
outside of the normal conduction system, resulting in direct myocardial activation.
Compared with a normally conducted supraventricular beat (which activates the
ventricular myocardium via the normal AV node-His-Purkinje system), ventricular
activation during VT is slower and proceeds in a different sequence. Thus, the QRS
complex is wide and abnormal (waveform 1). As there may be slight changes of the
activation sequence during the VT, reflecting the abnormal pathway of impulse
conduction, there may be subtle changes in QRS complex morphology or in the ST-T
waves.
VT may have one of three typical patterns:
●Monomorphic – Having a uniform and a fairly stable QRS morphology during

an episode
●Polymorphic – Having a continuously varying QRS complex morphology
and/or axis during an episode
●Bidirectional – Every other beat has a different axis as it travels alternately
down different conduction pathways
The features of each form of VT are discussed separately. (See "Sustained
monomorphic ventricular tachycardia: Clinical manifestations, diagnosis, and
evaluation" and "Catecholaminergic polymorphic ventricular
tachycardia" and "Congenital long QT syndrome: Epidemiology and clinical
manifestations".)
Supraventricular tachycardia — When an SVT conducts to the ventricles via the
normal AV node and His-Purkinje system, the activation wavefront spreads quickly
through the ventricles, and the QRS is usually narrow. In addition, the pathway of
conduction to the ventricles is fixed and the same for each impulse, accounting for the
uniformity of the QRS complexes and ST-T waves. However, SVT can also produce a
widened QRS by a number of mechanisms, including aberrant conduction, pre-
excitation, and the activation of ventricular pacing.
Aberrant conduction — The conduction of a supraventricular impulse can be delayed
or blocked in the bundle branches or in the distal Purkinje system, resulting in a wide,
abnormal QRS. This phenomenon is referred to as aberrancy. (See "Basic approach to
delayed intraventricular conduction".)
Aberrant conduction may either be present at baseline or under certain conditions, such
as faster heart rates.
●In patients with a left bundle branch block (LBBB), right bundle branch block,
or a nonspecific intraventricular conduction delay on their baseline ECG, any
SVT will have a widened QRS. Thus, if time allows, review of a baseline ECG
can be helpful in differentiating VT from SVT with aberrancy. The presence of
a conduction abnormality on the baseline ECG does not prove that the
tachycardia is SVT with aberrancy, but the more similar the QRS during the
WCT is to the QRS during sinus rhythm, the more likely it is that the WCT is
an SVT with aberrancy.
In patients with aberrancy at baseline who manifest a WCT in which the QRS
complex is narrower than the baseline QRS, the WCT is likely VT originating
near the ventricular septum, with early engagement of the specialized
conducting system. This scenario is extremely unusual.
●In patients with a narrow QRS complex at baseline which widens at faster
heart rates, conduction is normal during sinus rhythm but aberrant during the
tachycardia. The most common reason for this is rate-related aberration
(functional bundle branch block), in which rapidly generated impulses reach
the conducting fibers before they have fully recovered from the previous
impulse. Such a delay in recovery may also be the result of underlying disease
of the His-Purkinje system, hyperkalemia, or the actions of antiarrhythmic
drugs, particularly the class IC agents (eg, flecainide, propafenone).
The class I antiarrhythmic drugs (table 2) can cause significant slowing of
conduction during SVT and also VT. These drugs, especially class IC agents,
slow conduction and have a property of "use-dependency" (a progressive
decrease in impulse conduction velocity and wider QRS complex duration at
faster heart rates). As a result, these drugs can cause rate-related aberration
and a wide QRS complex during any SVT. However, they can also cause VT
with a very wide, bizarre QRS, which may be incessant [6,7]. (See "Cardiac
excitability, mechanisms of arrhythmia, and action of antiarrhythmic drugs".)
Pre-excitation syndrome — In the pre-excitation syndromes, AV conduction can occur
over the normal conduction system and also via an accessory AV pathway (figure 2A-C).
These two pathways create the anatomic substrate for a reentrant circuit
(macroreentrant circuit), facilitating the development of a circus movement or reentrant
tachycardia known as AV reentrant tachycardia (AVRT). (See "ECG tutorial:
Preexcitation syndromes" and "Atrioventricular reentrant tachycardia (AVRT) associated
with an accessory pathway", section on 'Orthodromic AVRT' and "Atrioventricular
reentrant tachycardia (AVRT) associated with an accessory pathway", section on
'Antidromic AVRT'.)
AVRT, which occurs both in patients with manifest pre-excitation (Wolff-Parkinson-White

[WPW] syndrome) or concealed accessory pathways, can present with a narrow or a
wide QRS complex:
●If antegrade conduction occurs over an accessory pathway and retrograde

conduction occurs over the AV node or a second accessory pathway, the QRS
complex will be wide with an unusual morphology. This is known as
an antidromic AVRT (figure 3 and waveform 2). Antidromic AVRT is difficult
to differentiate from VT because ventricular activation starts outside the
normal intraventricular conduction system in both types of tachycardia (ie,
there is direct myocardial activation). (See "Wide QRS complex tachycardias:
Approach to the diagnosis", section on 'VT versus AVRT'.)
●If antegrade conduction to the ventricles occurs over the AV node and
retrograde conduction is over the accessory pathway, the QRS complex will
be narrow (unless there is aberrant conduction at baseline with a wide QRS
complex). This narrow complex AVRT is known as an orthodromic AVRT
(figure 4 and waveform 3). Orthodromic AVRT can also occur with rate-related
aberrancy, creating a WCT.
In addition, patients with a manifest accessory pathway (ie, WPW syndrome) may
develop a different SVT (eg, atrial tachycardia, atrial fibrillation [AF], or atrial flutter). In
such cases, the atrial impulses may use the accessory pathway to conduct to the
ventricles, and the QRS could be either narrow or wide, depending upon whether
ventricular activation occurs over the normal conduction system, the accessory pathway,
or both (waveform 4). (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology,
clinical manifestations, and diagnosis", section on 'Arrhythmias associated with WPW'.)
Pacemakers — When the ventricles are activated by a pacing device, the QRS complex
is generally wide:
●Most transvenous ventricular pacemakers pace the right ventricle, causing a
wide QRS complex of the LBBB type. Typically, the surface ECG shows a
broad R wave in lead I, indicating conduction from right to left. (See "Overview
of cardiac pacing in heart failure".)
●Pacemakers used in cardiac resynchronization therapy (CRT) usually pace
both ventricles. Although CRT generates a QRS complex that is narrower than
the patient's baseline (a chronically widened QRS is one of the components of
the indication for CRT), it is still usually longer than 120 milliseconds. The
surface ECG usually shows a Q wave or QS complex in lead I, indicating
activation from left to right, and there is usually a RBBB pattern in lead V 1.
(See "Cardiac resynchronization therapy in heart failure: Indications".)
Recognizing that a QRS complex is due to ventricular pacing can be challenging,

particularly during a tachycardia. In addition to characteristic QRS morphology, a pacing
"spike" or stimulus artifact can often be identified. The stimulus artifact is a narrow
electrical signal too rapid to represent myocardial depolarization.
Among patients with a pacemaker or an implantable cardioverter-defibrillator, further
possibilities need to be considered in addition to the usual differential diagnosis of a
WCT. These include:
●In the presence of sinus tachycardia or some SVTs (eg, an atrial tachycardia,
AF, or atrial flutter), the device may "track" the atrial impulse and pace the
ventricle at the rapid rate, resulting in a WCT. (See "Modes of cardiac pacing:
Nomenclature and selection", section on 'Mode switching'.)
●A WCT can result if ventricular paced beats are conducted retrograde
(backward) through the AV node to the atrium, resulting in an atrial signal,
which the pacemaker senses and tracks with another ventricular stimulus. This
ventricular paced beat is also conducted retrograde, and the cycle repeats
indefinitely, a process termed pacemaker-mediated tachycardia (PMT) or
endless loop tachycardia. PMT usually occurs at the upper rate limit. A
different mechanism of pacemaker-associated tachycardia, non-reentrant
repetitive ventriculoatrial synchrony, also creates a wide complex rhythm, but
usually at the lower rate limit or sensor-mediated rate rather than at the upper
rate limit.
These and other arrhythmias associated with pacemakers are discussed in detail
separately. (See "Unexpected rhythms with normally functioning dual-chamber pacing
systems", section on 'Pacemaker-mediated tachycardia'.)
Artifact mimicking ventricular tachycardia — ECG artifact, particularly when
observed on a single-lead rhythm strip, may be misdiagnosed as VT (waveform 5) [8].
The presence of narrow-complex beats that can be seen to "march" through the
supposed WCT at a fixed rate strongly supports the diagnosis of artifact.
links: Ventricular arrhythmias" and "Society guideline links: Supraventricular
arrhythmias".)
●A wide QRS complex tachycardia (WCT) represents a unique clinical

challenge for two reasons: Diagnosis of the arrhythmia is frequently difficult,
and urgent therapy is often required. (See 'Introduction' above.)
●Ventricular tachycardia (VT) is the most common cause of WCT, particularly
in patients with a history of cardiac disease, while supraventricular tachycardia
(SVT) results in WCT (due to aberrant conduction, pre-excitation, or
ventricular pacing) much less frequently. WCT is identified as VT in up to 80
percent of unselected patients and more than 90 percent of patients with
known structural heart disease. (See 'Epidemiology' above and 'Differential
diagnosis of WCT' above.)
●Patients with WCT are rarely asymptomatic, although the type and intensity
of symptoms will vary depending upon the rate of the WCT, the presence or
absence of significant comorbid conditions, and whether the WCT is VT or
SVT. Patients with WCT typically present with one or more of the following:
palpitations, chest pain, shortness of breath, syncope/presyncope, or sudden
cardiac arrest. (See 'Clinical manifestations' above.)
●The differential diagnosis of WCTs includes (see 'Differential diagnosis of
WCT' above):
•VT, including monomorphic VT, polymorphic VT, and bidirectional VT
•SVT with aberrant conduction
•SVT with conduction over an accessory pathway
•Paced ventricular rhythms
•ECG artifact
REFERENCES
1. Miller JM, Das MK. Differential diagnosis of narrow and wide complex
tachycardias. In: Cardiac Electrophysiology From Cell to Bedside, 7th, Zipes
DP, Jalife J, Stevenson WG (Eds), W.B. Saunders, Philadelphia 2018.
2. Vereckei A. Current algorithms for the diagnosis of wide QRS complex
tachycardias. Curr Cardiol Rev 2014; 10:262.
3. Gupta AK, Thakur RK. Wide QRS complex tachycardias. Med Clin North
Am 2001; 85:245.
4. Tchou P, Young P, Mahmud R, et al. Useful clinical criteria for the diagnosis
of ventricular tachycardia. Am J Med 1988; 84:53.
5. Wellens HJ, Bär FW, Lie KI. The value of the electrocardiogram in the
differential diagnosis of a tachycardia with a widened QRS complex. Am J
Med 1978; 64:27.
6. Ranger S, Talajic M, Lemery R, et al. Kinetics of use-dependent ventricular
conduction slowing by antiarrhythmic drugs in humans. Circulation 1991;
83:1987.
7. Ranger S, Talajic M, Lemery R, et al. Amplification of flecainide-induced
ventricular conduction slowing by exercise. A potentially significant clinical
consequence of use-dependent sodium channel blockade. Circulation 1989;
79:1000.
8. Knight BP, Pelosi F, Michaud GF, et al. Physician interpretation of
electrocardiographic artifact that mimics ventricular tachycardia. Am J Med
2001; 110:335.
Close

 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Patient

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 INTRODUCTION
 EXTERNAL CARDIOVERSION/DEFIBRILLATION
o Preparation and personnel
o Supplemental oxygen
o Paddle/pad placement
o Energy selection for defibrillation
o Efficacy
 Atrial fibrillation
 Atrial flutter
 Supraventricular tachycardia
 Ventricular tachycardia
 Ventricular fibrillation
o Special populations
 Cardioversion during pregnancy
 Cardioversion in patients with permanent pacemakers/ICDs
 Cardioversion in patients with digitalis toxicity
o Complications
 ST segment and T wave changes
 Arrhythmia and conduction abnormalities
 Thromboembolism
 Myocardial necrosis
 Myocardial dysfunction
 Pulmonary edema
 Transient hypotension
 Cutaneous burns
 INTERNAL CARDIOVERSION/DEFIBRILLATION
o Technique and efficacy
o Internal cardioversion complications
o Implantable cardioverter-defibrillators
 ACKNOWLEDGMENT
 REFERENCES
GRAPHICS view all
 Algorithms
oAdult tachycardia with a pulse algorithm
oAdult cardiac arrest algorithm 2018 update
 Figures
oDefibrillation waveforms in ICDs
oHands-free pacemaker/defibrillator pad positioning
oFlutter circuit right atrium
 Tables
oDirect Current CV for AF protocol
oAntiarrhythmics and energy
oACC AHA skills internal CV I
oACC AHA skills internal CV II
 Waveforms
o12 lead ECG atrial flutter
RELATED TOPICS
 Advanced cardiac life support (ACLS) in adults
 Amiodarone: Clinical uses
 Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism
 Atrial fibrillation: Cardioversion
 Automated external defibrillators
 Clinical uses of sotalol
 Digitalis (cardiac glycoside) poisoning
 Embolic risk and the role of anticoagulation in atrial flutter
 Implantable cardioverter-defibrillators: Overview of indications, components, and functions
 Nonstress test and contraction stress test
 Patient education: Cardioversion (Beyond the Basics)
 Patient education: Heart failure and atrial fibrillation (The Basics)
 Patient education: Implantable cardioverter-defibrillators (Beyond the Basics)
 Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation
 Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with
reduced LVEF
 Procedural sedation in adults outside the operating room
 Restoration of sinus rhythm in atrial flutter
 Rhythm control versus rate control in atrial fibrillation
 Role of echocardiography in atrial fibrillation
 Supportive data for advanced cardiac life support in adults with sudden cardiac arrest
 Sustained monomorphic ventricular tachycardia in patients with structural heart disease:
Treatment and prognosis
 Temporary cardiac pacing
 Troponin testing: Clinical use
Cardioversion for specific arrhythmias

Author:
Section Editor:
Richard L Page, MD
Deputy Editor:
Susan B Yeon, MD, JD, FACC
Literature review current through: Sep 2020. | This topic last updated: May 01, 2019.
INTRODUCTION Electrical cardioversion and defibrillation have become
routine procedures in the management of patients with cardiac arrhythmias.

Cardioversion is the delivery of energy that is synchronized to the QRS complex, while
defibrillation is asynchronous delivery of a shock randomly during the cardiac cycle.
Early defibrillators delivered energy in a monophasic waveform, meaning that electrons
flowed in a single direction. The newer defibrillators deliver a biphasic waveform,
meaning that during the shock, polarity and electron flow reverse. In addition to
reversing polarity, biphasic defibrillators also deliver a more consistent magnitude of
current (figure 1). In general, biphasic defibrillators successfully terminate arrhythmias at
lower energies than monophasic defibrillators. The relative efficacy of biphasic and
monophasic defibrillators has been compared in a number of settings and is discussed
in detail separately. (See "Basic principles and technique of external electrical
cardioversion and defibrillation", section on 'Monophasic versus biphasic waveforms'.)
This topic will review the clinical settings in which electrical cardioversion and
defibrillation are used, along with a brief discussion of the complications that can occur
independent of the arrhythmia that is being treated. The basic principles and technique
of electrical cardioversion and defibrillation, the specific indications for external
cardioversion and defibrillation, and the use of the automated external defibrillator are
presented separately. (See "Basic principles and technique of external electrical
cardioversion and defibrillation" and "Automated external defibrillators".)
EXTERNAL CARDIOVERSION/DEFIBRILLATION
Preparation and personnel — Nonemergency electrical cardioversion should ideally be

performed in a controlled environment with monitoring capabilities and the nearby
availability of emergency equipment should complications arise. The following are
considered part of the routine preparation and monitoring involved in electrical
cardioversion:
●Standard cardiorespiratory monitoring, including blood pressure, pulse,
oxygen saturation, end-tidal CO2 monitoring, and cardiac telemetry.
●Intravenous access for administration of sedation and for management of any
rhythm-related complications (ie, ventricular fibrillation, sinus bradycardia, etc).
●Available supplemental oxygen, suction device, and intubation equipment for
management of respiratory complications (though supplemental oxygen
should be removed prior to delivery of the electrical shock) (see 'Supplemental
oxygen' below).
●Available code cart with medications used in advanced cardiac life support in
the event of life-threatening arrhythmias (see "Advanced cardiac life support
(ACLS) in adults").
●There is considerable activation of thoracic skeletal muscles during a
transthoracic shock that causes patients and their arms to move during a
shock. For this reason, and because these patients are anticoagulated,
padding or cushioning should be placed between the patient's extremities and
any hard bed railings to avoid injury during cardioversion.
While many cardiologists are trained in the administration of moderate sedation,
sedation may also be administered by an anesthesiologist who can immediately assist in
the management of respiratory complications should any develop. An advantage of
having an anesthesiologist routinely administer sedation for elective cardioversions is
that at many hospitals, the use of ultra-short acting sedatives such as propofol is
restricted to anesthesiologists. The tradeoff for such involvement is often added costs
and scheduling complexity. (See "Procedural sedation in adults outside the operating
room", section on 'Complications'.)
Elective cardioversions for atrial fibrillation and flutter can also be safely performed
autonomously by a midlevel provider. With appropriate clinical training, a protocol that
includes a guideline-directed procedural checklist (table 1), physician supervision, and
sedation administered by an anesthesiologist, an advanced practice nurse can safely
perform cardioversions autonomously with excellent patient satisfaction and outcomes
[1].
Supplemental oxygen — Supplemental oxygen is a fire hazard in the event of electrical
arcing during external cardioversion or defibrillation. Because of this, supplemental
oxygen flow should be stopped, or the oxygen delivery device (eg, nasal cannula, face
mask, etc) removed from the patient, prior to the delivery of an external shock. Oxygen
flow can be restarted after the shock has been delivered.
Paddle/pad placement — For electrical cardioversion of atrial tachyarrhythmias,
particularly atrial fibrillation, an anterior-posterior pad position is preferred to anterior-
lateral placement (figure 2) based on evidence from several randomized trials that have
shown higher success rates and lower energy requirements for successful cardioversion
with the anterior-posterior configuration [2,3]. The historical rationale for the superiority
of the anterior-posterior position is a more favorable shock vector through the atria as
well as reduced transthoracic impedance. Moreover, there is some evidence that
applying external force to self-adhesive electrodes may decrease transthoracic
impedance further [4]. However, pad placement may not significantly affect outcomes of
cardioversion with contemporary defibrillator devices that employ impedance
compensated biphasic waveforms [5]. For urgent cardioversion/defibrillation of unstable
rhythms, an anterior-lateral pad configuration may be preferred for ease of application,
and device manufacturer recommendations should be followed in all cases. (See "Basic
principles and technique of external electrical cardioversion and defibrillation", section
on 'Electrodes'.)
Energy selection for defibrillation — The amount of energy selected for initial
attempts of defibrillation has been controversial. The energy selected should be
sufficient to accomplish prompt defibrillation because repeated failures expose the heart
to damage from prolonged ischemia and multiple shocks. On the other hand, excessive
energy should be avoided, since myocardial damage from high-energy shocks has been
demonstrated in experimental studies, although the frequency with which this occurs in
humans is not known [6,7].
In 2010, the American Heart Association issued guidelines for cardiopulmonary
resuscitation and emergency cardiovascular care that discussed detailed starting energy
levels for treatment of various types of arrhythmias [8]. In the 2014 AHA/ACC/HRS
guidelines on the management of atrial fibrillation, no specific energy levels for
cardioversion or defibrillation are discussed, but some broad concepts are presented.
We agree with the suggested initial energy selection for specific arrhythmias as
addressed in the society guidelines, with the following suggested initial energy
requirements for monophasic and biphasic waveforms [8]:
●When available, a biphasic defibrillator is preferred due to greater efficacy.
●For atrial fibrillation, 120 to 200 joules for biphasic devices and 200 joules for
monophasic devices (algorithm 1).
●For atrial flutter, 50 to 100 joules for biphasic devices and 100 joules for
monophasic devices.
●For ventricular tachycardia with a pulse, 100 joules for biphasic devices and
200 joules for monophasic devices.
●For ventricular fibrillation or pulseless ventricular tachycardia, 120 to 200
joules for biphasic devices and 360 joules for monophasic devices (algorithm
2).
●To increase the likelihood of initial shock success and reduce the duration of
sedation, a higher initial energy may be considered, particularly in obese
patients or in patients known to be difficult to cardiovert.
When an external defibrillator is being prepared to deliver a rescue shock in the event
that an implantable defibrillator fails to convert a patient during defibrillation threshold
testing, the energy should be set to the maximum output and in the asynchronous mode.
Cardioversion with higher energy levels may be effective when prior cardioversion
attempts using a maximal energy of 360 joules have failed to restore sinus rhythm. In
one study, 55 patients who did not have sinus rhythm restored after at least two
attempts of external cardioversion with 360 joules underwent cardioversion with 720
joules, which was performed by using two external cardioverters, each connected to its
own pair of patches [9]. Sinus rhythm was restored in 84 percent of these patients with
no major complications, hemodynamic compromise, or strokes occurring after the
procedure.
As another option besides high-energy cardioversion, pretreatment with an
antiarrhythmic drug can facilitate cardioversion at lower energy levels. Pretreatment
with ibutilide prior to electrical cardioversion has been shown to significantly improve the
rate of successful cardioversion to sinus rhythm and was also associated with the use of
significantly lower energy levels to achieve cardioversion
[10]. Amiodarone, sotalol, quinidine, and procainamide have also been shown to
increase the likelihood of successful cardioversion or lower the energy threshold
required for cardioversion [11]. When an antiarrhythmic drug is chosen, however, the
potential side effects must be carefully considered. (See "Amiodarone: Adverse effects,
potential toxicities, and approach to monitoring" and "Clinical uses of sotalol".)
Efficacy — External cardioversion and defibrillation have been used in the treatment of
a variety of arrhythmias, with variable results depending on the chronicity of the
arrhythmia, triggers for the arrhythmia, and the patient’s overall clinical condition. For
example, electrical cardioversion success rates approach 100 percent in patients with
atrial flutter or atrial fibrillation of short duration and no structural heart disease, while the
success rates are much lower in patients with chronic atrial fibrillation and concomitant
mitral valve disease. The term "failed cardioversion" can indicate failure to restore sinus
rhythm at all, or an immediate recurrence of the arrhythmia. It is important to differentiate
these two failure mechanisms because different approaches can be used to address
each type of failure.
While antiarrhythmic medications can sometimes result in restoration of sinus rhythm
without electrical cardioversion, they are primarily used in an effort to maintain sinus
rhythm following successful electrical cardioversion. However, many antiarrhythmic
drugs can alter the defibrillation threshold, ie, the minimal amount of energy necessary
for reversion of an arrhythmia (table 2). Amiodarone, quinidine, flecainide,
and phenytoin may cause a significant rise in defibrillation thresholds [12-15].
(See "Amiodarone: Clinical uses" and "Amiodarone: Adverse effects, potential toxicities,
and approach to monitoring".)
Atrial fibrillation — Atrial fibrillation (AF) is the most frequent arrhythmia treated with
electrical cardioversion. Cardioversion is part of the overall treatment approach to AF,
which also includes rate control and anticoagulation. To reduce the risk of
thromboembolism following cardioversion, therapeutic anticoagulation is generally
recommended for at least three to four weeks before and after cardioversion.
Alternatively, the presence of existing intracardiac thrombus should be excluded using
transesophageal echocardiography prior to cardioversion if therapeutic anticoagulation
has not been achieved for an adequate duration. However, a negative TEE does not
preclude the need for anticoagulation at the time of the cardioversion or afterwards.
Detailed discussions regarding the decision to perform cardioversion versus rate control,
as well as the optimal approach to anticoagulation, are provided elsewhere. (See "Atrial
fibrillation: Cardioversion" and "Rhythm control versus rate control in atrial
fibrillation" and "Prevention of embolization prior to and after restoration of sinus rhythm
in atrial fibrillation" and "Atrial fibrillation: Anticoagulant therapy to prevent
thromboembolism" and "Role of echocardiography in atrial fibrillation", section on
'Transesophageal echocardiography'.)
The energy requirement for successful cardioversion of AF varies according to the type
of electrical waveform and chronicity of AF (algorithm 1) [8]. (See "Basic principles and
technique of external electrical cardioversion and defibrillation", section on 'Energy
selection for cardioversion and defibrillation'.)
●When monophasic waveforms are used, 100 to 200 joules (watt-seconds) is
often adequate to restore sinus rhythm, although >200 joules may be required,
particularly for AF of long duration. The overall success rate (at any level of
energy) of electrical cardioversion for AF is 75 to 95 percent and is related
inversely both to the duration of AF and to left atrial size [16,17].
●Most modern defibrillators deliver biphasic waveforms. When biphasic
waveforms are used, the energy requirements are less (generally 50 percent
of that required with monophasic waveforms) and efficacy is higher [18,19]. In
a study of 912 patients with AF or atrial flutter, restoration of sinus rhythm was
higher with the use of biphasic waveforms (94 versus 84 percent for
monophasic waveforms) and the cumulative energy was lower (199 J versus
554 J) [18]. The use of biphasic waveforms may be of particular benefit in
patients who fail to revert with the use of monophasic waveforms [20].
Although it had been hoped that cardioversion to and maintenance of sinus rhythm
would improve the prognosis of and reduce embolic risk in patients with AF, this concept
was not confirmed in the two largest randomized trials comparing rate control plus
anticoagulation versus rhythm control for AF (the AFFIRM and RACE trials) [21,22].
Both studies showed a trend toward a lower incidence of the primary endpoint with rate
control and anticoagulation (hazard ratio 0.87 for mortality in AFFIRM and 0.73 for a
composite endpoint in RACE). In addition, embolization occurred with equal frequency
regardless of whether a rhythm control or a rate control strategy was adopted. In both
groups, embolization primarily occurred after warfarin had been stopped or when the
INR was subtherapeutic. (See "Rhythm control versus rate control in atrial fibrillation".)
Atrial flutter — Electrical cardioversion is highly successful in the treatment of typical
(type I) atrial flutter, which arises from a single reentrant circuit in the right atrium
(waveform 1 and figure 3). The energy requirement for successful cardioversion of
typical (type I) atrial flutter is usually lower than that required for atrial fibrillation
(algorithm 1) [8]. Many patients with type I atrial flutter can be cardioverted with 50 to
100 joules or less, particularly with biphasic defibrillators [23-26]. In a review including
985 cardioversions in 840 patients with atrial flutter, the median energy level for
successful cardioversion was 50 joules with a biphasic defibrillatory and 200 joules with
a monophasic defibrillator [24]. (See "Restoration of sinus rhythm in atrial
flutter" and "Electrocardiographic and electrophysiologic features of atrial
flutter" and "Basic principles and technique of external electrical cardioversion and
defibrillation", section on 'Energy selection for cardioversion and defibrillation'.)
In contrast to typical (type I) atrial flutter, atypical (type II) atrial flutter may result from
reentrant circuits in various locations and tends to require higher energy levels for
cardioversion, but in most cases sinus rhythm can be successfully restored. While
starting at 50 to 100 joules may be effective for cardioversion of atypical (type II) atrial
flutter, particularly with biphasic defibrillators, this approach has the potential adverse
effect of requiring additional shocks [23]. (See "Electrocardiographic and
electrophysiologic features of atrial flutter".)
The role of anticoagulation during and after cardioversion is similar to that with atrial
fibrillation and is discussed in detail elsewhere. (See "Embolic risk and the role of
anticoagulation in atrial flutter".)
Supraventricular tachycardia — The most common mechanisms for supraventricular
tachycardia are atrioventricular (AV) nodal reentry, AV reentrant tachycardia, and atrial
tachycardia. These arrhythmias often terminate with vagal maneuvers or intravenous
antiarrhythmic therapy with adenosine or verapamil when they are AV nodal dependent;
as such, electrical cardioversion is usually not required. However, if these arrhythmias
persist and electrical cardioversion is attempted, cardioversion is usually successful but
may require relatively high energy levels, probably due to the deep location of the
reentrant pathway. If sinus rhythm is not restored following an initial 50 to 100 joule
shock, subsequent shocks should be at higher energy levels (algorithm 1). Although
energy requirements with biphasic waveforms have not been reported, they are likely to
be lower than for monophasic waveforms based upon experience with other
arrhythmias. (See "Atrioventricular nodal reentrant tachycardia".)
Ventricular tachycardia — Electrical cardioversion is usually successful in the acute
treatment of ventricular tachycardia (VT), which typically arises from a reentrant circuit in
the ventricle. If a distinct QRS and T wave are identified, allowing the delivery of energy
to be synchronized to the QRS complex, monomorphic VT can often be terminated with
a low-energy shock. Despite the potential for terminating VT with very low-energy
shocks, one must consider the seriousness of the arrhythmia and the desire to avoid
repeated shocks. As a result, the initial synchronized shock in these circumstances is
recommended to be 100 joules with either a biphasic or monophasic waveform
(algorithm 1) [8]. (See "Sustained monomorphic ventricular tachycardia in patients with
structural heart disease: Treatment and prognosis" and "Basic principles and technique
of external electrical cardioversion and defibrillation", section on 'Energy selection for
cardioversion and defibrillation'.)
In contrast, synchronized cardioversion may be impossible or hazardous if the VT is
rapid and distinct QRS complexes are not identified, if the QRS complexes are wide and
bizarre, or if the VT is polymorphic. In these settings, there is a potential for delivery of a
discharge on the T wave, possibly provoking ventricular fibrillation. Under these
circumstances, nonsynchronized defibrillation should be performed starting with 120 to
200 joules for a biphasic device or 360 joules for a monophasic device.
(See "Catecholaminergic polymorphic ventricular tachycardia".)
Ventricular fibrillation — The only definitive treatment for ventricular fibrillation (VF) is
defibrillation. When defibrillation is performed promptly, the success rate for terminating
ventricular fibrillation can be as high as 95 percent [27-30]. However, the success rate
falls substantially as the duration of ventricular fibrillation increases, probably due to
myocardial ischemia, acidosis, and other metabolic changes. These cellular changes
are associated with an electrophysiologic deterioration of ventricular fibrillation, leading
to an increase in fibrillation cycle length and prolonged diastolic duration between
fibrillation action potentials [31].
For these reasons, defibrillation as soon as possible has been considered to be the
standard of care for VF (algorithm 2). Some studies suggest that when VF has been
present for longer than four to five minutes, outcomes are better if cardiopulmonary
resuscitation is performed prior to defibrillation [32,33]. The recommended starting
energy to effectively defibrillate VF is 360 joules when monophasic waveforms are used
and 120 to 200 joules with biphasic waveforms (algorithm 1) [8]. There is no reported
benefit to using more than 360 joules, and there may be harm since high-energy shocks
may be associated with myocardial damage and the risk for developing new
arrhythmias. (See "Supportive data for advanced cardiac life support in adults with
sudden cardiac arrest", section on 'Defibrillation' and "Advanced cardiac life support
(ACLS) in adults", section on 'Ventricular fibrillation and pulseless ventricular
tachycardia' and "Basic principles and technique of external electrical cardioversion and
defibrillation", section on 'Energy selection for cardioversion and
defibrillation' and 'Complications' below.)
Special populations
Cardioversion during pregnancy — Cardioversion can be performed during
pregnancy without affecting the rhythm of the fetus [34,35]. It is recommended, however,
that the fetal heart rate be monitored during the procedure using standard fetal
monitoring techniques. (See "Nonstress test and contraction stress test".)
Cardioversion in patients with permanent pacemakers/ICDs — Several precautions
are necessary when attempting external electrical cardioversion or defibrillation in a
patient with a permanent pacemaker or an implantable cardioverter defibrillator (ICD).
Defibrillation in these patients can damage the pulse generator, the lead system, or the
myocardial tissue, resulting in device dysfunction [36]. The electrode paddle (or patch)
should be at least 12 cm from the pulse generator and an anteroposterior paddle
position is recommended [37,38]. Elective cardioversion should be initiated with the
lowest indicated energy (which will vary depending on the arrhythmia) in order to avoid
damage to the device circuitry and the electrode-myocardial interface. After
cardioversion, the pacemaker should be interrogated and evaluated to ensure normal
pacemaker function. When these precautions have been used, cardioversion with either
monophasic or biphasic shocks is safe and effective in patients with an implantable
device [39].
Alternatively, in patients with an ICD, internal cardioversion can be attempted by an
electrophysiologist using the device programmer to deliver the shock. (See 'Internal
cardioversion/defibrillation' below.)
Cardioversion in patients with digitalis toxicity — Patients with digitalis overdose or
intoxication can present with almost any type of arrhythmia, including tachyarrhythmias
and bradyarrhythmias. In particular, ventricular arrhythmias (including VF) are more
likely to occur in patients who have digitalis toxicity, especially if the patient is also
hypokalemic. There is a relative contraindication to cardioversion in the setting of
digitalis toxicity since digitalis sensitizes the heart to the electrical stimulus and, hence,
cardioversion could trigger additional arrhythmias, most importantly ventricular
fibrillation.
●Supraventricular arrhythmias – Cardioversion should be deferred until
digitalis levels have returned to a normal range and clinical toxicity has
resolved. If urgent restoration of sinus rhythm is necessary for a
hemodynamically unstable supraventricular arrhythmia, the lowest energy that
is likely to be successful should be used. In addition, rapid atrial pacing may
be successful for certain arrhythmias (eg, atrial flutter) and is probably the
safest method. (See "Atrial fibrillation: Cardioversion", section on 'Electrical
cardioversion' and "Restoration of sinus rhythm in atrial flutter", section on
'Atrial pacing'.)
●Ventricular arrhythmias – If cardioversion must be performed for a life-
threatening ventricular arrhythmia, prophylactic lidocaine (1 mg/kg up to a
maximum dose of 100 mg IV push) should be given and the lowest indicated
energy levels used.
When time permits, hypokalemia should be corrected prior to cardioversion.
(See "Digitalis (cardiac glycoside) poisoning".)
Complications — While electrical cardioversion and defibrillation are generally well
tolerated, complications may occur. Most complications are self-limiting (eg, changes in
the electrocardiogram, hypotension related to sedation and/or vasodilation) or relatively
benign (eg, skin irritation). However, providers should be aware of potential life-
threatening complications such as postcardioversion arrhythmias and the possibility of
thromboembolism.
ST segment and T wave changes — Electrocardiographic (ECG) changes can occur
immediately after cardioversion, usually consisting of ST segment and T wave changes
[40-44]. ECG changes, including ST segment elevation, are nonspecific findings and
should not be used as the sole criteria for identifying an acute ischemic event as the
cause for the ventricular tachyarrhythmia [44].
In one study of 56 patients with ventricular arrhythmias treated with monophasic shocks,
ST segment and T wave changes were common immediately after cardioversion but
usually resolved within five minutes [40]. The ECG changes included ST segment
elevation in 15 percent, ST segment depression in 35 percent, or an increase in T wave
amplitude.
Transient ST elevation has also been reported in a series of patients undergoing
cardioversion with monophasic waveforms for atrial arrhythmias [41]. These changes
were noted primarily in the precordial leads, and normalized within 1.5 minutes. The
occurrence of ST segment elevation was associated with a lower conversion rate and
lower rate of long-term maintenance of sinus rhythm.
The pathogenesis of ST elevation is uncertain, since elevations in cardiac enzymes (ie,
CK-MB and troponin) are uncommon and, when they occur, are usually minimal [45-47].
However, both the incidence and the extent of ST segment changes appear to be lower
with the use of biphasic waveforms [48,49].
Arrhythmia and conduction abnormalities — Arrhythmias are frequently observed
after cardioversion [16,40,50-52]. In many cases these arrhythmias are benign (eg,
sinus tachycardia, nonsustained ventricular tachycardia [VT]), but in other cases the
arrhythmias can be clinically and/or hemodynamically significant (eg, ventricular
fibrillation [VF], sustained VT).
●Ventricular arrhythmias – Runs of nonsustained ventricular tachycardia (VT)
are seen in up to five percent of patients, and can occur in patients with or
without structural heart disease [40]. On the other hand, a sustained
ventricular arrhythmia generally occurs only in patients with clinically
documented VT or long-lasting VF [16,40]. Cardioversion can also induce VF,
usually but not always after the administration of an asynchronous shock [16].
The occurrence of ventricular arrhythmias does not appear to be related to the
number of shocks and cannot be prevented by antiarrhythmic therapy.
Conversely, antiarrhythmic drugs may contribute to the development of new
arrhythmias [53].
●Atrial arrhythmias – Atrial arrhythmias can also occur following cardioversion.
Approximately 30 percent of patients have a supraventricular tachycardia,
primarily sinus tachycardia. However, AV nodal reentrant tachycardia and
atrial flutter have been observed following cardioversion attempts for chronic
atrial fibrillation (AF) [51].
●Bradyarrhythmias and conduction abnormalities – Bradyarrhythmias following
electrical cardioversion are relatively rare. In a retrospective multicenter cohort
study of 6906 electrical cardioversions in 2868 patients with atrial fibrillation
and less than 48 hours of symptoms, bradyarrhythmias were identified
following 63 cardioversions (0.9 percent) in 54 patients [54]. Pre-procedure
use of digoxin, beta blocker, or antiarrhythmic drug did not impact the
development of bradyarrhythmias post-cardioversion. Nevertheless, it is
reasonable to anticipate clinically significant bradycardia in patients
undergoing cardioversion who have been in AF for over a year, have very slow
ventricular rates during AF, or in whom amiodarone loading was recently
administered.
A transient left bundle branch block is occasionally seen after cardioversion, but high-
degree atrioventricular block is more common. In one study of 75 patients who
underwent 112 shocks, sinus bradycardia occurred in 18 patients and high-degree AV
block in 11 [50]. Temporary pacing was necessary in 10 patients. The likelihood of
requiring either external or transvenous cardiac pacing immediately after a cardioversion
is much lower in clinical practice than this study suggests. The incidence appears to be
less than 1 percent. Patients receiving antiarrhythmic drugs are more prone to develop
bradycardia and asystole and an external pacemaker should be readily available in such
patients [16,50]. (See "Temporary cardiac pacing".)
Thromboembolism — Cardioversion may be associated with pulmonary or systemic
thromboembolism. Thromboembolism after the return of synchronous atrial contraction
can occur because of dislodgement of left atrial thrombi present at the time of
cardioversion or a thrombus that forms after cardioversion due to transient post
conversion left atrial mechanical dysfunction. This complication is more likely to occur in
patients with atrial fibrillation (AF) who have not been anticoagulated prior to
cardioversion. Patients with a previous embolism do not have an increased risk of
embolization if anticoagulation of adequate intensity and length are administered [55].
The estimated incidence of thromboembolism varies, but in a large nonrandomized
series that included 437 patients, thromboembolism occurred in 5.3 percent of patients
who were not anticoagulated compared with 0.8 percent of those who were receiving
anticoagulation [56]. For patients with AF of at least 48 hours duration, the current
recommendation is to anticoagulate patients for several weeks prior to and following
cardioversion. (See "Prevention of embolization prior to and after restoration of sinus
rhythm in atrial fibrillation".)
Myocardial necrosis — Minimal myocardial necrosis, particularly of the epicardium,
may occur as a result of high-energy shocks. This is typically asymptomatic and is
manifested by small rises in serum CK-MB and troponin levels. In contrast, substantial
elevations of either CK-MB or troponin following electrical cardioversion, or the
development of chest pain suggestive of angina, suggests the presence of myocardial
injury from causes unrelated to the procedure. As such, we do not routinely monitor
cardiac enzymes following electrical cardioversion in asymptomatic patients.
Although the cause is unknown, it has been suggested that myocardial necrosis may be
due to the sustained depolarization of a critical mass of myocardial cells [42]. The risk of
myocardial necrosis appears related to the amount of energy delivered with each shock
rather than to the number of shocks, although many repeated shocks may lead to
myocardial damage and scarring.
●In one study of 30 patients who underwent cardioversion, an increase in
serum CK-MB was seen in only two patients, despite substantial release of CK
from skeletal muscle [57]. Furthermore, the small release of CK-MB in this
report cannot be considered diagnostic for myocardial damage since the total
CK from skeletal muscle includes approximately 1 percent CK-MB [58].
(See "Troponin testing: Clinical use".)
●The desire for improved specificity in the diagnosis of myocardial injury has
led to measurement of the serum troponin levels. Among 38 patients
undergoing elective cardioversion, only three patients had minimal elevations
of troponin I (0.8 to 1.5 mcg/L), suggesting subtle myocardial injury [46]. Two
other studies, however, reported no elevations in troponin T following
cardioversion [47,59].
Myocardial dysfunction — Global left ventricular dysfunction due to myocardial
stunning may be seen in patients with cardiac arrest who have undergone successful
cardiopulmonary resuscitation. This is related in part to defibrillation, but is also a result
of the arrhythmia itself and due to the absence of cardiac output and coronary blood flow
during the period of arrest with resultant ischemia. Myocardial dysfunction due to
stunning may reverse within the first 24 to 48 hours after cardiac arrest. It is routine to
image the heart and evaluate ventricular function shortly after a patient suffers a cardiac
arrest to determine if there is evidence of structural heart disease. This evaluation
should not be delayed. However, it is important to recognize that ventricular dysfunction
may be transient and that imaging should be repeated within a few days if ventricular
dysfunction is present immediately after the arrest [60].
In animals, the severity of postresuscitation myocardial dysfunction is related, in part, to
the energy used for defibrillation [61]. Further support for this observation comes from
another animal study comparing biphasic and monophasic waveforms for reversion of
ventricular fibrillation [62]. Although lower-energy biphasic waveforms were as effective
as higher-energy monophasic waveforms for restoration of sinus rhythm, there was less
myocardial dysfunction after defibrillation with the use of biphasic waveforms.
The process of electrical cardioversion may transiently injure or "stun" the atria as well
[63,64].
Pulmonary edema — Pulmonary edema is a rare complication of cardioversion, which
is probably due to transient left atrial standstill or left ventricular dysfunction. It is
unrelated to the amount of energy used. Pulmonary edema may be more common in
patients with AF associated with valvular heart disease or left ventricular dysfunction. In
this setting, the return of atrial systole after cardioversion can result in a significant
elevation in left atrial pressure and pulmonary edema [65].
Transient hypotension — Transient hypotension can occur for several hours after
cardioversion. Most patients require no therapy; if necessary, the fall in blood pressure
usually responds to fluid replacement [66]. Although the mechanism is not certain, the
hypotension may be related to vasodilation or the use of sedation during the procedure.
Cutaneous burns — Following cardioversion or defibrillation, skin burns occur in 20 to
25 percent of patients and are more likely with improper technique and placement of
electrodes [67]. The risk of burns is less with the use of biphasic waveforms and the use
of gel-based pads [68]. The use of steroid cream, silver sulfadiazine cream, or
topical ibuprofen reduces the pain and inflammation [69,70].
INTERNAL CARDIOVERSION/DEFIBRILLATION
Technique and efficacy — Internal or intracardiac cardioversion is an effective

technique for patients in whom external cardioversion has failed to restore sinus rhythm.
However, the need for internal cardioversion has been greatly diminished due to the
efficacy of biphasic waveform defibrillators and the availability of ibutilide in restoring
sinus rhythm. In addition, given the invasive nature of the procedure, specialized training
is required to perform internal cardioversion. An ACC/AHA task force on clinical
competency has published recommendations for technical and cognitive skills needed to
perform internal direct current cardioversion (table 3A-B) [71].
Internal cardioversion can be performed in various ways:
●Using a preexisting implantable cardioverter defibrillator (ICD) to deliver a

clinician-directed shock.
●Using epicardial wires placed during surgery or internal paddles applied
directly to the epicardium in a patient with a sternotomy [72].
●Two defibrillation electrodes are placed in the right atrium and coronary sinus
or in the right atrium and left pulmonary artery, respectively, and then
intracardiac shocks are delivered by an external defibrillator.
Internal cardioversion appears more effective for the restoration of sinus rhythm in
patients with atrial fibrillation (AF) who have failed conventional external cardioversion
[73-76]. As an example, one prospective study evaluated internal cardioversion in 141
patients with AF who had either failed external cardioversion or had had AF induced
during an electrophysiology study [73]. AF was successfully terminated in 92 percent of
patients with paroxysmal AF (≤7 days duration), 89 percent of patients with AF of
intermediate duration (8 to 30 days), and 70 percent of patients with chronic AF (>30
days duration). No ventricular arrhythmias were induced during 1779 R wave
synchronized shocks.
Another prospective cohort study compared external and internal cardioversion in 187
patients with a mean duration of AF of 10 months [77]. Internal cardioversion was
significantly more effective than external cardioversion in restoring sinus rhythm (93
versus 79 percent). In addition, internal cardioversion was successfully in restoring sinus
rhythm in 88 percent of patients in whom external cardioversion had failed.
As with external cardioversion, the likelihood of restoration of sinus rhythm with internal
cardioversion decreases with the duration of atrial fibrillation and increasing left atrial
size [73]. The recurrence rate is similar after both types of cardioversion. (See "Atrial
fibrillation: Cardioversion".)
Internal cardioversion complications — Although internal cardioversion is an effective
approach for restoring sinus rhythms in patients with atrial fibrillation refractory to
pharmacologic or external electrical cardioversion, one study reported that complications
occurred in 19 percent of patients, including low cardiac output from ventricular
stunning, pericardial effusion, and a brief period of ventricular asystole requiring
ventricular pacing [78]. Another report of 25 patients found that 36 percent developed
transient bradycardia, related to sinus and atrioventricular nodal depression, requiring
temporary ventricular pacing [79]. Shocks of up to 20 joules did not affect the function of
permanent pacemakers.
Implantable cardioverter-defibrillators — Implantable cardioverter-defibrillators (ICDs)
are in widespread use in patients with a history of sustained ventricular tachycardia or
ventricular fibrillation and also for primary prevention in selected patients. In patients
with an ICD, internal cardioversion can be attempted by a cardiologist using the device
programmer to deliver the shock. The advantage of using the ICD is that it avoids the
risk of a skin irritation from an external shock and the small chance of damage to the
ICD system from the shock. The disadvantage of using the ICD is that it consumes
some of the battery in the device and does not always work for cardioversion of atrial
arrhythmias. Indications for and efficacy of ICDs are discussed in detail elsewhere.
(See "Implantable cardioverter-defibrillators: Overview of indications, components, and
functions" and "Primary prevention of sudden cardiac death in patients with
cardiomyopathy and heart failure with reduced LVEF".)
Arrhythmias in adults" and "Society guideline links: Ventricular arrhythmias" and "Society
guideline links: Supraventricular arrhythmias".)
interest.)
●Basics topics (see "Patient education: Heart failure and atrial fibrillation (The
Basics)")
●Beyond the Basics topics (see "Patient education: Cardioversion (Beyond the
Basics)" and "Patient education: Implantable cardioverter-defibrillators
(Beyond the Basics)")
●Electrical cardioversion and defibrillation have become routine procedures in

the management of patients with cardiac arrhythmias. Cardioversion is the
delivery of energy that is synchronized to the QRS complex, while defibrillation
is asynchronous delivery of a shock randomly during the cardiac cycle.
●Electrical cardioversion success rates approach 100 percent in patients with
atrial flutter or atrial fibrillation of short duration and no structural heart
disease, while the success rates are much lower in patients with chronic atrial
fibrillation and concomitant mitral valve disease. The term "failed
cardioversion" can indicate failure to restore sinus rhythm at all, or an
immediate recurrence of the arrhythmia. It is important to differentiate these
two failure mechanisms because different approaches can be used to address
each type of failure. (See 'Efficacy' above and 'Atrial fibrillation' above
and 'Atrial flutter' above.)
●Electrical cardioversion is usually successful in the acute treatment of
ventricular tachycardia. If a distinct QRS and T wave are identified,
synchronized cardioversion can be attempted. In contrast, synchronized
cardioversion may be impossible or hazardous if distinct QRS complexes are
not identified. As such, under these circumstances, asynchronous defibrillation
should be used. (See 'Ventricular tachycardia' above.)
●Defibrillation is the only definitive treatment for ventricular fibrillation (VF),
with high success rates when performed promptly. However, the success rate
falls substantially as the duration of ventricular fibrillation increases, probably
due to myocardial ischemia, acidosis, and other metabolic changes. For these
reasons, defibrillation as soon as possible has been considered to be the
standard of care for VF (algorithm 2). (See 'Ventricular fibrillation' above.)
●Once an arrhythmia has been identified, the most important factor in the
likelihood of a successful cardioversion or defibrillation is the choice of the
initial energy level to be delivered to the patient. The following are suggested
initial energy requirements for monophasic and biphasic waveforms
(see "Basic principles and technique of external electrical cardioversion and
defibrillation", section on 'Energy selection for cardioversion and defibrillation'):
•When available, a biphasic defibrillator is preferred due to greater
efficacy.
•For atrial fibrillation, 120 to 200 joules for biphasic devices and 200
joules for monophasic devices.
•For atrial flutter, 50 to 100 joules for biphasic devices and 100 joules for
monophasic devices.
•For ventricular tachycardia with a pulse, 100 joules for both biphasic and
monophasic devices.
•For ventricular fibrillation or pulseless ventricular tachycardia, 120 to 200
joules for biphasic devices and 360 joules for monophasic devices.
•To increase the likelihood of initial shock success and reduce the
duration of sedation, a higher initial energy may be considered.
●While electrical cardioversion and defibrillation are generally well tolerated,
complications may occur. Most complications are self-limited (eg, changes in
the electrocardiogram, hypotension related to sedation and/or vasodilation) or
relatively benign (eg, skin irritation). However, providers should be aware of
potential life-threatening complications such as post-cardioversion arrhythmias
and thromboembolism. (See 'Complications' above.)
●Internal or intracardiac cardioversion is an effective technique for patients in
whom external cardioversion has failed to restore sinus rhythm. The need for
internal cardioversion has been greatly diminished due to the efficacy of
biphasic waveform defibrillators in restoring sinus rhythm. Given the invasive
nature of the procedure, specialized training is required to perform internal
cardioversion. (See 'Internal cardioversion/defibrillation' above.)
ACKNOWLEDGMENT The editors of UpToDate would like to acknowledge
Ramsey Wehbe, MD, who contributed to earlier versions of this topic review.
REFERENCES
1. Strzelczyk TA, Kaplan RM, Medler M, Knight BP. Outcomes Associated
With Electrical Cardioversion for Atrial Fibrillation When Performed
Autonomously by an Advanced Practice Provider. JACC Clin Electrophysiol
2017; 3:1447.
2. Kirchhof P, Eckardt L, Loh P, et al. Anterior-posterior versus anterior-lateral
electrode positions for external cardioversion of atrial fibrillation: a
randomised trial. Lancet 2002; 360:1275.
3. Botto GL, Politi A, Bonini W, et al. External cardioversion of atrial fibrillation:
role of paddle position on technical efficacy and energy requirements. Heart
1999; 82:726.
4. Ramirez FD, Fiset SL, Cleland MJ, et al. Effect of Applying Force to Self-
Adhesive Electrodes on Transthoracic Impedance: Implications for Electrical
Cardioversion. Pacing Clin Electrophysiol 2016; 39:1141.
5. Walsh SJ, McCarty D, McClelland AJ, et al. Impedance compensated
biphasic waveforms for transthoracic cardioversion of atrial fibrillation: a
multi-centre comparison of antero-apical and antero-posterior pad positions.
Eur Heart J 2005; 26:1298.
6. Dahl CF, Ewy GA, Warner ED, Thomas ED. Myocardial necrosis from direct
current countershock. Effect of paddle electrode size and time interval
between discharges. Circulation 1974; 50:956.
7. Warner ED, Dahl C, Ewy GA. Myocardial injury from transthoracic
defibrillator countershock. Arch Pathol 1975; 99:55.
8. Link MS, Atkins DL, Passman RS, et al. Part 6: electrical therapies:
automated external defibrillators, defibrillation, cardioversion, and pacing:
2010 American Heart Association Guidelines for Cardiopulmonary
Resuscitation and Emergency Cardiovascular Care. Circulation 2010;
122:S706.
9. Saliba W, Juratli N, Chung MK, et al. Higher energy synchronized external
direct current cardioversion for refractory atrial fibrillation. J Am Coll Cardiol
1999; 34:2031.
10. Oral H, Souza JJ, Michaud GF, et al. Facilitating transthoracic cardioversion
of atrial fibrillation with ibutilide pretreatment. N Engl J Med 1999; 340:1849.
11. Sung RJ. Facilitating electrical cardioversion of persistant atrial fibrillation by
antiarrhythmic drugs: update on clinical trial results. Card Electrophysiol Rev
2003; 7:300.
12. Babbs CF, Yim GK, Whistler SJ, et al. Elevation of ventricular defibrillation
threshold in dogs by antiarrhythmic drugs. Am Heart J 1979; 98:345.
13. Troup PJ, Chapman PD, Olinger GN, Kleinman LH. The implanted
defibrillator: relation of defibrillating lead configuration and clinical variables
to defibrillation threshold. J Am Coll Cardiol 1985; 6:1315.
14. Tacker WA Jr, Niebauer MJ, Babbs CF, et al. The effect of newer
antiarrhythmic drugs on defibrillation threshold. Crit Care Med 1980; 8:177.
15. Van Gelder IC, Crijns HJ, Van Gilst WH, et al. Effects of flecainide on the
atrial defibrillation threshold. Am J Cardiol 1989; 63:112.
16. DeSilva RA, Graboys TB, Podrid PJ, Lown B. Cardioversion and
defibrillation. Am Heart J 1980; 100:881.
17. Lown B. Electrical reversion of cardiac arrhythmias. Br Heart J 1967;
29:469.
18. Gurevitz OT, Ammash NM, Malouf JF, et al. Comparative efficacy of
monophasic and biphasic waveforms for transthoracic cardioversion of atrial
fibrillation and atrial flutter. Am Heart J 2005; 149:316.
19. Page RL, Kerber RE, Russell JK, et al. Biphasic versus monophasic shock
waveform for conversion of atrial fibrillation: the results of an international
randomized, double-blind multicenter trial. J Am Coll Cardiol 2002; 39:1956.
20. Khaykin Y, Newman D, Kowalewski M, et al. Biphasic versus monophasic
cardioversion in shock-resistant atrial fibrillation:. J Cardiovasc
21. Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and
rhythm control in patients with atrial fibrillation. N Engl J Med 2002;
347:1825.
22. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control
and rhythm control in patients with recurrent persistent atrial fibrillation. N
Engl J Med 2002; 347:1834.
23. Fuster V, Rydén LE, Cannom DS, et al. ACC/AHA/ESC 2006 Guidelines for
the Management of Patients with Atrial Fibrillation: a report of the American
College of Cardiology/American Heart Association Task Force on Practice
Guidelines and the European Society of Cardiology Committee for Practice
Guidelines (Writing Committee to Revise the 2001 Guidelines for the
Management of Patients With Atrial Fibrillation): developed in collaboration
with the European Heart Rhythm Association and the Heart Rhythm Society.
24. Niebauer MJ, Brewer JE, Chung MK, Tchou PJ. Comparison of the
rectilinear biphasic waveform with the monophasic damped sine waveform
for external cardioversion of atrial fibrillation and flutter. Am J Cardiol 2004;
93:1495.
25. Gallagher MM, Guo XH, Poloniecki JD, et al. Initial energy setting, outcome
and efficiency in direct current cardioversion of atrial fibrillation and flutter. J
26. Mortensen K, Risius T, Schwemer TF, et al. Biphasic versus monophasic
shock for external cardioversion of atrial flutter: a prospective, randomized
trial. Cardiology 2008; 111:57.
27. Faddy SC, Powell J, Craig JC. Biphasic and monophasic shocks for
transthoracic defibrillation: a meta analysis of randomised controlled trials.
Resuscitation 2003; 58:9.
28. Morrison LJ, Dorian P, Long J, et al. Out-of-hospital cardiac arrest rectilinear
biphasic to monophasic damped sine defibrillation waveforms with
advanced life support intervention trial (ORBIT). Resuscitation 2005; 66:149.
29. Martens PR, Russell JK, Wolcke B, et al. Optimal Response to Cardiac
Arrest study: defibrillation waveform effects. Resuscitation 2001; 49:233.
30. Stothert JC, Hatcher TS, Gupton CL, et al. Rectilinear biphasic waveform
defibrillation of out-of-hospital cardiac arrest. Prehosp Emerg Care 2004;
8:388.
31. Tovar OH, Jones JL. Electrophysiological deterioration during long-duration
ventricular fibrillation. Circulation 2000; 102:2886.
32. Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influence of cardiopulmonary
resuscitation prior to defibrillation in patients with out-of-hospital ventricular
fibrillation. JAMA 1999; 281:1182.
33. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic
cardiopulmonary resuscitation to patients with out-of-hospital ventricular
fibrillation: a randomized trial. JAMA 2003; 289:1389.
34. VOGEL JH, PRYOR R, BLOUNT SG Jr. DIRECT-CURRENT
DEFIBRILLATION DURING PREGNANCY. JAMA 1965; 193:970.
35. Schroeder JS, Harrison DC. Repeated cardioversion during pregnancy.
Treatment of refractory paroxysmal atrial tachycardia during 3 successive
pregnancies. Am J Cardiol 1971; 27:445.
36. Waller C, Callies F, Langenfeld H. Adverse effects of direct current
cardioversion on cardiac pacemakers and electrodes Is external
cardioversion contraindicated in patients with permanent pacing systems?
Europace 2004; 6:165.
37. Gould L, Patel S, Gomes GI, Chokshi AB. Pacemaker failure following
external defibrillation. Pacing Clin Electrophysiol 1981; 4:575.
38. Levine PA, Barold SS, Fletcher RD, Talbot P. Adverse acute and chronic
effects of electrical defibrillation and cardioversion on implanted unipolar
cardiac pacing systems. J Am Coll Cardiol 1983; 1:1413.
39. Manegold JC, Israel CW, Ehrlich JR, et al. External cardioversion of atrial
fibrillation in patients with implanted pacemaker or cardioverter-defibrillator
systems: a randomized comparison of monophasic and biphasic shock
energy application. Eur Heart J 2007; 28:1731.
40. Eysmann SB, Marchlinski FE, Buxton AE, Josephson ME.
Electrocardiographic changes after cardioversion of ventricular arrhythmias.
41. Van Gelder IC, Crijns HJ, Van der Laarse A, et al. Incidence and clinical
significance of ST segment elevation after electrical cardioversion of atrial
fibrillation and atrial flutter. Am Heart J 1991; 121:51.
42. Chun PK, Davia JE, Donohue DJ. ST-segment elevation with elective DC
cardioversion. Circulation 1981; 63:220.
43. Zelinger AB, Falk RH, Hood WB Jr. Electrical-induced sustained myocardial
depolarization as a possible cause for transient ST elevation post-DC
elective cardioversion. Am Heart J 1982; 103:1073.
44. Kok LC, Mitchell MA, Haines DE, et al. Transient ST elevation after
transthoracic cardioversion in patients with hemodynamically unstable
ventricular tachyarrhythmia. Am J Cardiol 2000; 85:878.
45. Reiffel JA, Gambino SR, McCarthy DM, Leahey EB Jr. Direct current
cardioversion. Effect on creatine kinase, lactic dehydrogenase and
myocardial isoenzymes. JAMA 1978; 239:122.
46. Allan JJ, Feld RD, Russell AA, et al. Cardiac troponin I levels are normal or
minimally elevated after transthoracic cardioversion. J Am Coll Cardiol 1997;
30:1052.
47. Neumayr G, Hagn C, Gänzer H, et al. Plasma levels of troponin T after
electrical cardioversion of atrial fibrillation and flutter. Am J Cardiol 1997;
80:1367.
48. Reddy RK, Gleva MJ, Gliner BE, et al. Biphasic transthoracic defibrillation
causes fewer ECG ST-segment changes after shock. Ann Emerg Med
1997; 30:127.
49. Ambler JJ, Deakin CD. A randomized controlled trial of efficacy and ST
change following use of the Welch-Allyn MRL PIC biphasic waveform versus
damped sine monophasic waveform for external DC cardioversion.
Resuscitation 2006; 71:146.
50. Waldecker B, Brugada P, Zehender M, et al. Dysrhythmias after direct-
current cardioversion. Am J Cardiol 1986; 57:120.
51. LEMBERG L, CASTELLANOS A Jr, SWENSON J, GOSSELIN A.
ARRHYTHMIAS RELATED TO CARDIOVERSION. Circulation 1964;
30:163.
52. PELESKA B. CARDIAC ARRHYTHMIAS FOLLOWING CONDENSER
DISCHARGES AND THEIR DEPENDENCE UPON STRENGTH OF
CURRENT AND PHASE OF CARDIAC CYCLE. Circ Res 1963; 13:21.
53. Cohen TJ, Scheinman MM, Pullen BT, et al. Emergency intracardiac
defibrillation for refractory ventricular fibrillation during routine
electrophysiologic study. J Am Coll Cardiol 1991; 18:1280.
54. Grönberg T, Nuotio I, Nikkinen M, et al. Arrhythmic complications after
electrical cardioversion of acute atrial fibrillation: the FinCV study. Europace
2013; 15:1432.
55. Elhendy A, Gentile F, Khandheria BK, et al. Safety of electrical
cardioversion in patients with previous embolic events. Mayo Clin Proc
2001; 76:364.
56. Bjerkelund CJ, Orning OM. The efficacy of anticoagulant therapy in
preventing embolism related to D.C. electrical conversion of atrial fibrillation.
Am J Cardiol 1969; 23:208.
57. Ehsani A, Ewy GA, Sobel BE. Effects of electrical countershock on serum
creatine phosphokinase (CPK) isoenzyme activity. Am J Cardiol 1976;
37:12.
58. Lindberg K, Lundin A, Nordlander R, et al. Detection of acute myocardial
infarction by a new, sensitive and rapid method for determination of creatine
kinase B-subunit activity. Eur Heart J 1980; 1:327.
59. Goktekin O, Melek M, Gorenek B, et al. Cardiac troponin T and cardiac
enzymes after external transthoracic cardioversion of ventricular
arrhythmias in patients with coronary artery disease. Chest 2002; 122:2050.
60. Kern KB, Hilwig RW, Rhee KH, Berg RA. Myocardial dysfunction after
resuscitation from cardiac arrest: an example of global myocardial stunning.
J Am Coll Cardiol 1996; 28:232.
61. Xie J, Weil MH, Sun S, et al. High-energy defibrillation increases the
severity of postresuscitation myocardial dysfunction. Circulation 1997;
96:683.
62. Sun S, Klouche K, Tang W, Weil MH. The effects of biphasic and
conventional monophasic defibrillation on postresuscitation myocardial
function. J Am Coll Cardiol 2001; 37:1753.
63. Grimm RA, Stewart WJ, Maloney JD, et al. Impact of electrical cardioversion
for atrial fibrillation on left atrial appendage function and spontaneous echo
contrast: characterization by simultaneous transesophageal
echocardiography. J Am Coll Cardiol 1993; 22:1359.
64. Omran H, Jung W, Rabahieh R, et al. Left atrial chamber and appendage
function after internal atrial defibrillation: a prospective and serial
transesophageal echocardiographic study. J Am Coll Cardiol 1997; 29:131.
65. Gowda RM, Misra D, Khan IA, Schweitzer P. Acute pulmonary edema after
cardioversion of cardiac arrhythmias. Int J Cardiol 2003; 92:271.
66. Resnekov L. High-energy electrical current and myocardial damage. Med
Instrum 1978; 12:24.
67. Ambler JJ, Sado DM, Zideman DA, Deakin CD. The incidence and severity
of cutaneous burns following external DC cardioversion. Resuscitation 2004;
61:281.
68. Ambler JJ, Deakin CD. A randomised controlled trial of the effect of biphasic
or monophasic waveform on the incidence and severity of cutaneous burns
following external direct current cardioversion. Resuscitation 2006; 71:293.
69. Ambler JJ, Zideman DA, Deakin CD. The effect of prophylactic topical
steroid cream on the incidence and severity of cutaneous burns following
external DC cardioversion. Resuscitation 2005; 65:179.
70. Ambler JJ, Zideman DA, Deakin CD. The effect of topical non-steroidal anti-
inflammatory cream on the incidence and severity of cutaneous burns
following external DC cardioversion. Resuscitation 2005; 65:173.
71. Tracy CM, Akhtar M, DiMarco JP, et al. American College of
Cardiology/American Heart Association Clinical Competence Statement on
invasive electrophysiology studies, catheter ablation, and cardioversion: A
report of the American College of Cardiology/American Heart
Association/American College of Physicians-American Society of Internal
Medicine Task Force on Clinical Competence. Circulation 2000; 102:2309.
72. Liebold A, Wahba A, Birnbaum DE. Low-energy cardioversion with
epicardial wire electrodes: new treatment of atrial fibrillation after open heart
surgery. Circulation 1998; 98:883.
73. Lévy S, Ricard P, Lau CP, et al. Multicenter low energy transvenous atrial
defibrillation (XAD) trial results in different subsets of atrial fibrillation. J Am
74. Lévy S, Lauribe P, Dolla E, et al. A randomized comparison of external and
internal cardioversion of chronic atrial fibrillation. Circulation 1992; 86:1415.
75. Lévy S. Internal defibrillation: where we have been and where we should be
going? J Interv Card Electrophysiol 2005; 13 Suppl 1:61.
76. Schmitt C, Alt E, Plewan A, et al. Low energy intracardiac cardioversion
after failed conventional external cardioversion of atrial fibrillation. J Am Coll
Cardiol 1996; 28:994.
77. Alt E, Ammer R, Schmitt C, et al. A comparison of treatment of atrial
fibrillation with low-energy intracardiac cardioversion and conventional
external cardioversion. Eur Heart J 1997; 18:1796.
78. Mansourati J, Larlet JM, Salaun G, et al. Safety of high energy internal
cardioversion for atrial fibrillation. Pacing Clin Electrophysiol 1997; 20:1919.
79. Prakash A, Saksena S, Mathew P, Krol RB. Internal atrial defibrillation:
effect on sinus and atrioventricular nodal function and implanted cardiac
pacemakers. Pacing Clin Electrophysiol 1997; 20:2434.
Close

 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Patient

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 INTRODUCTION
 ACUTE TREATMENT OF SYMPTOMATIC ARRHYTHMIAS
o Initial assessment of hemodynamic stability
o Acute termination of orthodromic AVRT
 Permanent junctional reciprocating tachycardia
o Acute termination of antidromic AVRT
o Acute treatment of atrial fibrillation with preexcitation
 Avoidance of AV nodal blockers
 TREATMENT TO PREVENT RECURRENT ARRHYTHMIAS
o Catheter ablation
 Indications for ablation
 Symptomatic patients
 Asymptomatic patients
 Localizing the accessory pathway
 Efficacy
 Arrhythmia recurrence
 Complications
o Surgical ablation
o Medical therapy for arrhythmia prevention
 Prevention of recurrent orthodromic AVRT
 Prevention of recurrent antidromic AVRT
 Prevention of recurrent preexcited atrial fibrillation
 REFERENCES
GRAPHICS view all
 Tables
oDrug Rx arrhythmias WPW
 Waveforms
o12 lead WPW
oEP study tracings preablation mapping WPW
oWPW radiofrequency ablation
oEP study tracings post RF ablation WPW
RELATED TOPICS
 Amiodarone: Clinical uses
 Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Recommendations
 Calcium channel blockers in the treatment of cardiac arrhythmias
 Cardioversion for specific arrhythmias
 Patient education: Wolff-Parkinson-White syndrome (Beyond the Basics)
 Patient education: Wolff-Parkinson-White syndrome (The Basics)
 Therapeutic use of ibutilide
 Vagal maneuvers
Treatment of symptomatic arrhythmias associated

with the Wolff-Parkinson-White syndrome
Authors:
Luigi Di Biase, MD, PhD, FHRS, FACC
Edward P Walsh, MD
Section Editors:
Samuel Lévy, MD
Deputy Editor:
Literature review current through: Sep 2020. | This topic last updated: Sep 02, 2020.
INTRODUCTION Conduction from the atria to the ventricles normally occurs
via the atrioventricular node (AV)-His-Purkinje system. Patients with a preexcitation

syndrome have an additional pathway, known as an accessory pathway, which directly
connects the atria and ventricles, bypassing the AV node. Normal conduction through
the AV node is slower than conduction over the accessory pathway. Thus, when there is
conduction over an accessory pathway, the ventricles are activated earlier than if the
impulse had traveled through the AV node. This early activation, referred to
as preexcitation, is responsible for the classic electrocardiographic (ECG) findings of a
shortened PR interval and, in most patients, a delta wave (waveform 1).
Symptoms, ranging from mild palpitations to syncope and, rarely, even sudden cardiac
death, are the result of tachycardia, usually due to a macroreentrant circuit involving the
AV node, the ventricles, the accessory pathway, and the atria. This classic
supraventricular tachycardia associated with WPW syndrome is called AV reentrant or
reciprocating tachycardia (AVRT). However, preexcited atrial fibrillation or atrial flutter
with a rapid ventricular response may also result in symptoms. Fortunately, the
incidence of sudden death in patients with the WPW syndrome is quite low, ranging from
0 to 0.39 percent annually in several large case series, with the lowest risk seen in
asymptomatic patients.
Patients with the WPW syndrome are usually treated because of symptomatic
arrhythmias. Treatment may sometimes be extended to asymptomatic patients with a
WPW pattern if certain "high-risk" features are present. However, most asymptomatic
patients with the WPW electrocardiographic pattern are not treated. Treatment options
for persons with arrhythmias and the WPW syndrome include nonpharmacologic
therapies (ie, catheter ablation of the accessory pathway) as well as pharmacologic
therapy (to slow ventricular heart rates or to prevent arrhythmias). The choice of the
optimal therapy depends on the acuity of the arrhythmia(s) and the risk of sudden
cardiac death, with pharmacologic agents being the treatment of choice for most acute
arrhythmias, while catheter ablation is nearly always preferred for the long-term
prevention of recurrent arrhythmias involving the accessory pathway.
This topic will review the available therapeutic options for the treatment of arrhythmias in
the WPW syndrome. The clinical manifestations, approach to diagnosis, and the types of
arrhythmias which can occur in persons with an accessory pathway and the WPW
pattern are discussed separately. (See "Wolff-Parkinson-White syndrome: Anatomy,
epidemiology, clinical manifestations, and diagnosis" and "Atrioventricular reentrant
tachycardia (AVRT) associated with an accessory pathway".)
ACUTE TREATMENT OF SYMPTOMATIC ARRHYTHMIAS While
the preferred long-term treatment approach for patients with an accessory pathway,
preexcitation, and symptomatic arrhythmias is catheter-based radiofrequency ablation,
patients who present with an acute arrhythmia often require initial pharmacologic
therapy for ventricular rate control or restoration of sinus rhythm. However, because of
the electrophysiologic differences between AV nodal tissue and tissue comprising an
accessory pathway, standard therapy for heart rate control may actually worsen
symptoms and lead to clinical deterioration in patients with a tachycardia involving an
accessory pathway. Knowledge of the presence of an accessory pathway is critical in
choosing the correct initial pharmacologic therapy. (See 'Treatment to prevent recurrent
arrhythmias' below and "Overview of the acute management of tachyarrhythmias".)
Initial assessment of hemodynamic stability — As with any patient presenting with a
symptomatic tachyarrhythmia, patients with a tachycardia suspected to involve an
accessory pathway should undergo an initial assessment of hemodynamic status.
Patients who are hemodynamically stable can be evaluated and treated according to the
type of suspected arrhythmia. However, patients with hemodynamic instability or
compromise related to an ongoing tachycardia should undergo urgent electrical
cardioversion [1,2]. The technique for urgent electrical cardioversion is discussed
elsewhere. (See "Cardioversion for specific arrhythmias".)
Acute termination of orthodromic AVRT — In patients with orthodromic
atrioventricular reciprocating tachycardia (AVRT), antegrade conduction occurs via the
AV node with retrograde conduction via an accessory pathway. In such patients,
antegrade conduction across the AV node is typically the "weak link" of the reentrant
circuit. Thus, the approach to patients with orthodromic AVRT is similar to patients with
other types of paroxysmal supraventricular tachycardia, where relatively specific
therapies that lengthen AV nodal refractoriness and depress its conduction can block
the impulse within the AV node and terminate and prevent the tachycardia.
(See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory
pathway", section on 'Orthodromic AVRT' and "Overview of the acute management of
tachyarrhythmias", section on 'Regular narrow QRS complex tachyarrhythmias'.)
We employ a step-wise approach to termination of orthodromic AVRT (table 1). We
recommend initial treatment of acute symptomatic orthodromic AVRT with one or more
vagal maneuvers (such as the Valsalva maneuver and carotid sinus massage) [1,2].
These may be sufficient to cause AV node block and tachycardia termination in many
patients [3]. (See "Vagal maneuvers".)
If vagal maneuvers are ineffective, pharmacologic therapy with an AV nodal blocking
agent (ie, adenosine, verapamil, beta blockers) should be instituted. We suggest
intravenous adenosine rather than intravenous verapamil as the initial choice based on
its efficacy and short half-life. If adenosine is ineffective, we proceed with intravenous
verapamil as the second line agent.
●Intravenous adenosine is usually given as an initial dose of 6 mg for a full-
grown patient (0.1 mg/kg in a child to a maximum dose of 6 mg), which can be
followed by a dose of 12 mg (0.2 mg/kg in a child to a maximum dose of 12
mg) if the initial dose is unsuccessful. A dose of 18 mg can be used if 12 mg
fails to convert the patient to sinus rhythm. Repeated dosing beyond the 18
mg bolus is not usually effective.
The drug is administered by rapid intravenous injection over one to two
seconds at a peripheral site, followed by a 10 cc normal saline flush. The
patient should be supine and should be advised in advance of the possibility of
feeling lightheaded, dizzy, or near syncopal during the injection. (See "Narrow
QRS complex tachycardias: Clinical manifestations, diagnosis, and
evaluation", section on 'Intravenous adenosine'.)
Intravenous adenosine is effective for acute termination of orthodromic AVRT
in 80 to 90 percent of patients [4-6]. Its ultrashort duration of action makes it a
preferred agent before resorting to emergent DC cardioversion in the patient
whose hemodynamic state is more tenuous. On rare occasions, adenosine
has been reported to transiently increase atrial vulnerability to atrial fibrillation
(AF), a potentially serious proarrhythmic effect, and cause atrial ectopy that
can reinitiate orthodromic AVRT after acute tachycardia termination [4,7-9].
●Intravenous verapamil, given as 5 mg boluses in a full-grown patient (0.1
mg/kg in children to a maximum dose of 5 mg; contraindicated in children less
than 12 months of age) every two to three minutes (up to a cumulative initial
dose of up to 15 mg), is as effective as adenosine for acutely terminating
orthodromic AVRT, provided that the patient is not profoundly hypotensive or
suffering from heart failure associated with severely depressed ventricular
systolic function rather than the rapid heart rate (table 1) [10,11].
(See "Calcium channel blockers in the treatment of cardiac arrhythmias".)
If vagal maneuvers, adenosine, and verapamil are all ineffective in terminating
orthodromic AVRT, second line therapy choices include intravenous procainamide and
beta blockers approved for intravenous administration (propranolol, metoprolol,
and esmolol) (table 1) [12-14].
●Procainamide (20 to 50 mg/minute given intravenously while monitoring the
blood pressure closely every 5 to 10 minutes until the arrhythmia terminates,
hypotension ensues, the QRS is prolonged by more than 50 percent, or a total
of 17 mg/kg [1.2 g for a 70 kg patient] has been given) slows conduction and
prolongs refractoriness in atrial and ventricular myocardium, accessory
pathways, and the His-Purkinje system, while having no effect or causing
slight shortening of AV nodal refractory period [15,16]. For young children, the
dose for procainamide is a bolus given over 15 to 30 minutes (7 to 10 mg/kg
bolus for infants <12 months of age compared with 10 to 15 mg/kg bolus for
children older than 12 months), followed by an infusion of 20 to 50
micrograms/kg/minute. Procainamide is the preferred drug if the orthodromic
AVRT presents as a wide QRS complex tachycardia due to functional or
preexisting chronic bundle branch block or if the diagnosis of orthodromic
AVRT is in doubt. (See "Wide QRS complex tachycardias: Approach to
management".)
●Metoprolol – 2.5 to 5 mg IV bolus over two to five minutes; if no response, an
additional 2.5 to 5 mg IV bolus may be administered every 10 minutes to a
total dose of 15 mg.
Permanent junctional reciprocating tachycardia — Permanent junctional
reciprocating tachycardia (PJRT) is a persistent tachycardia (with a long RP interval on
the surface electrocardiogram) that most often occurs in early childhood and is usually
caused by a rare type of orthodromic AVRT involving a slowly conducting concealed
accessory pathway, which is usually posteroseptal in location. As implied by the name,
PJRT is incessant. (See "Atrioventricular reentrant tachycardia (AVRT) associated with
an accessory pathway", section on 'Permanent junctional reciprocating tachycardia'.)
Ablation of the accessory pathway is the preferred treatment for PJRT caused by a
slowly conducting accessory pathway since this arrhythmia is often refractory to medical
therapy. In a cohort of 194 patients (median age at diagnosis 3.2 months, 57 percent
less than one year of age) from 11 institutions treated for PJRT between 2000 and 2010,
initial medical management (attempted in 76 percent of patients) led to complete control
of the arrhythmia in only 23 percent of patients [17]. An additional 47 percent of patients
had clinical improvement with slower and/or less sustained tachycardia, but perfect
pharmacologic control is less common.
However, in patients presenting with acute symptomatic PJRT, the choice of initial
medical therapy is similar to conventional orthodromic AVRT
[18]. Adenosine and verapamil can be tried but usually only interrupt PJRT for a few
beats. Intravenous procainamide will occasionally result in a longer-lasting interruption
of PJRT, but it rarely results in perfect control. As a temporizing measure prior to
ablation, effective medical control of PJRT can often be achieved with oral flecainide.
(See 'Acute termination of orthodromic AVRT' above and 'Catheter ablation' below.)
Acute termination of antidromic AVRT — In patients with antidromic atrioventricular
reciprocating tachycardia (AVRT), antegrade conduction occurs via the accessory
pathway with retrograde conduction usually via the AV node (or sometimes via a second
accessory pathway if multiple pathways are present). Even though retrograde AV node
conduction may be a "weak link" during antidromic AVRT, intravenously administered
AV node-specific blocking drugs such as adenosine, verapamil, and beta blockers
should be avoided unless the tachycardia is definitely known to be antidromic AVRT.
Practically speaking, verification of this is difficult outside the electrophysiology
laboratory, so the intravenous drug of choice for acute treatment to terminate known or
suspected antidromic AVRT is procainamide [2]. Procainamide is typically infused
intravenously at 20 to 50 mg/minute given while monitoring the blood pressure closely
every 5 to 10 minutes until the arrhythmia terminates, hypotension ensues, the QRS is
prolonged by more than 50 percent, or a total of 17 mg/kg (1.2 g for a 70 kg patient) has
been given. Even if it does not result in tachycardia termination, intravenous
procainamide will usually slow the tachycardia rate and improve the hemodynamic state
(table 1).
If the diagnosis is not certain, the patient should be considered to have an undiagnosed
wide QRS tachycardia; of particular concern is ventricular tachycardia, which can
become hemodynamically unstable or even degenerate into ventricular fibrillation
following administration of one of these drugs. If uncertainty ever exists about the exact
tachycardia mechanism, a presumptive diagnosis of ventricular tachycardia should be
made, and the patient treated accordingly. (See "Atrioventricular reentrant tachycardia
(AVRT) associated with an accessory pathway", section on 'Antidromic
AVRT' and "Wide QRS complex tachycardias: Approach to the diagnosis" and "Wide
QRS complex tachycardias: Approach to management".)
Acute treatment of atrial fibrillation with preexcitation — In patients with an
accessory pathway capable of antegrade conduction who develop atrial fibrillation (AF),
conduction to the ventricle often occurs through a combination of the normal conduction
pathway (via the AV node) and the accessory pathway. However, because most
accessory pathways have a shorter refractory period than the AV node, the ventricular
rate can be more rapid if AV conduction occurs preferentially via the accessory pathway.
As such, AV nodal blocking drugs (adenosine, verapamil, beta blockers, and digoxin)
should be avoided in patients with preexcited atrial fibrillation since blocking the AV
node will promote conduction down the accessory pathway and may sometimes directly
enhance the rate of conduction over the accessory pathway. (See 'Avoidance of AV
nodal blockers' below.)
The goals of acute drug therapy for preexcited AF are prompt control of the ventricular
response and, ideally, termination of atrial fibrillation. If the patient is unstable because
of a rapid ventricular response, electrical cardioversion should be performed. For more
stable patients, trials of intravenous medications can be performed cautiously.
Treatment of preexcited AF requires a parenteral drug with rapid onset of action that
lengthens antegrade refractoriness and slows conduction in both the AV node/His-
Purkinje system and the accessory pathway.
The following is our approach to the acute treatment of patients with preexcited AF,
which is consistent with published professional society guidelines [1,2,19]:
●For patients who are hemodynamically unstable, we recommend urgent
electrical cardioversion [1,2,19]. (See "Cardioversion for specific arrhythmias",
section on 'External cardioversion/defibrillation'.)
●For patients who are hemodynamically stable, we suggest initial medical
therapy for rhythm control versus rate control. This is based on the greater
ease of controlling the ventricular rate in sinus rhythm. While there is no clear
first-line medication for rhythm control, options
include procainamide and ibutilide [1,2].
•Intravenous procainamide is effective for acute therapy of preexcited AF
because of its effects on atrial and ventricular myocardium without any AV
nodal blocking effect. Because of its effect on atrial myocardium,
procainamide may terminate AF; however, if AF persists, the ventricular
rate usually slows due to effects on refractoriness and conduction in the
accessory pathway. The pediatric experience with ibutilide is very limited,
so procainamide is usually the preferred intravenous drug option for
preexcited atrial fibrillation in the younger population.
Procainamide is typically infused intravenously at 20 to 50 mg/minute
given while monitoring the blood pressure closely every 5 to 10 minutes
until the arrhythmia terminates, hypotension ensues, the QRS is
prolonged by more than 50 percent, or a total of 17 mg/kg (1.2 g for a 70
kg patient) has been given. Even if it does not result in tachycardia
termination, intravenous procainamide will usually slow the tachycardia
rate and improve the hemodynamic state (table 1). This is often followed
by an infusion of 1 to 4 mg/minute.
For young children, the dose for procainamide is a bolus given over 15 to
30 minutes (7 to 10 mg/kg bolus for infants <12 months of age compared
with 10 to 15 mg/kg bolus for children older than 12 months), followed by
an infusion of 20 to 50 micrograms/kg/minute.
•Ibutilide, a class III antiarrhythmic drug that prolongs the refractoriness of
the AV node, His-Purkinje system, and accessory pathway, is useful for
acute termination of AF and atrial flutter. In one series of 22 patients with
WPW and AF during an electrophysiologic study, ibutilide prolonged the
shortest preexcited RR interval and terminated the arrhythmia in 95
percent [20]. (See "Therapeutic use of ibutilide".)
●For all patients with preexcited AF, we recommend not using standard AV
nodal blocking medications (ie, beta blockers, non-dihydropyridine calcium
channel blockers [verapamil and diltiazem], digoxin, adenosine,
and amiodarone). Blocking the AV node may result in increased conduction of
atrial impulses to the ventricle by way of the accessory pathway, increasing
the ventricular rate and potentially resulting in hemodynamic instability.
(See 'Avoidance of AV nodal blockers' below.)
The class IC antiarrhythmic drugs flecainide and propafenone and the class III
agent dofetilide are effective when used in this setting, but the parenteral formulations of
these drugs are not approved for use in some countries, including the United States [21-
24].
Avoidance of AV nodal blockers — AV node-specific antiarrhythmic drugs that are
normally used to control the ventricular rate during atrial fibrillation (AF)
are contraindicated (table 1) for patients with preexcited AF:
●Verapamil is perhaps the most dangerous AV nodal blocker to administer to
patients with preexcited AF [25-27]. Intravenous verapamil lengthens AV node
refractoriness, decreases concealed conduction into the accessory pathway,
and has no direct effect on the accessory pathway. Myocardial contractility
and systemic vascular resistance are also reduced; these effects may cause a
reflex increase in already elevated sympathetic tone that further shortens
accessory pathway refractoriness. Precipitation of cardiac arrest by
degeneration of preexcited AF to ventricular fibrillation has been reported after
intravenous verapamil administration [27].
●Adenosine causes an effect similar to verapamil and also can precipitate
ventricular fibrillation. Adenosine will not convert AF and has only a transient
effect on the AV node. Its use is contraindicated in AF.
●Beta blockers, when used alone, do not increase accessory pathway
refractoriness. Additionally, inhibition of AV node conduction may enhance the
preexcited ventricular rate response by decreasing the degree of concealed
retrograde conduction into the accessory pathway. An accessory pathway with
a short intrinsic antegrade refractory period that was initially competing with
the AV node could then become the dominant route for rapid, antegrade
conduction.
●Amiodarone, which may slow conduction in an accessory pathway during
chronic oral administration, is not known to slow accessory pathway
conduction with acute IV administration [28,29]. Because amiodarone also has
beta blocking properties, it may increase conduction via the accessory
pathway, leading to a faster ventricular rate and the potential for ventricular
fibrillation [19]. Amiodarone should generally not be used in patients with AF
and accessory pathway.
●Digoxin is also contraindicated because of blockade of AV nodal conduction
and its unpredictable effect on accessory pathway refractoriness [30]. The
vagomimetic action of digoxin lengthens AV node refractoriness and reduces
concealed retrograde conduction into the accessory pathway.
TREATMENT TO PREVENT RECURRENT ARRHYTHMIAS Once
patients with the Wolff-Parkinson-White syndrome have been stabilized following an

acute episode of symptomatic tachyarrhythmia, patients should be evaluated for
additional therapy aimed at preventing recurrent symptomatic arrhythmias. The
preferred long-term treatment approach for nearly all patients with an accessory
pathway, preexcitation, and a symptomatic arrhythmia is catheter ablation of the
accessory pathway. However, for patients who are not candidates for ablation
procedures, or for very select patients with rare, well-tolerated arrhythmias,
antiarrhythmic therapy is an alternative. When antiarrhythmic drugs are used, the choice
of agent is determined by the etiology of the arrhythmia and its electrophysiologic
properties (table 1).
Catheter ablation — For patients with an accessory pathway and symptomatic
arrhythmias including orthodromic AVRT, antidromic AVRT, and preexcited atrial
fibrillation (AF) or atrial flutter, we recommend catheter ablation [1]. Initial case-series
demonstrated both the safety and efficacy of this approach, data which have been
replicated in numerous studies [31-37]. The standard energy source used to ablate
accessory pathways is radiofrequency current, although cryoenergy can be used as an
alternative to radiofrequency energy to ablate accessory pathways that are in close
proximity to the AV node or bundle of His [38].
Indications for ablation — Patients with an accessory pathway are candidates for
ablation in the following settings:
●Symptomatic tachyarrhythmias
●Occupations in which the development of symptoms would put themselves or
others at risk (eg, truck drivers or airline pilots, some athletes)
●Selected asymptomatic patients (see 'Asymptomatic patients' below)
Symptomatic patients — Symptom control is the most common indication for ablation.
The 2015 ACC/AHA/HRS guidelines on the management of supraventricular
arrhythmias recommended catheter ablation as a first-line therapy for patients who have
had symptomatic AVRT or preexcited AF [1].
Asymptomatic patients — The optimal approach is controversial in asymptomatic
patients who are coincidentally found to have evidence of an accessory pathway on an
ECG (ie, WPW pattern) [39-41]. The risk of sudden cardiac death (SCD) is low, and the
risk of developing symptoms also appears to be low, although a wide range of
incidences have been reported [42,43]. Among those with a WPW ECG pattern, the
likelihood of developing symptoms varies with age. Children are at the highest risk, while
those who remain asymptomatic over age 35 years are unlikely to develop symptoms
[40]. In a prospective study of 550 asymptomatic patients with WPW ECG pattern who
were followed for a median of 22 months, 13 patients (2.4 percent) developed
ventricular fibrillation (VF) [44], most of whom (11 of 13) were children. Fortunately, all of
the patients developed warning symptoms (usually presyncope or dizziness) and sought
medical attention, and none died from the VF episode.
The 2015 ACC/AHA/HRS guidelines state that observation of patients with WPW pattern
alone is reasonable; however, the guidelines also state that catheter ablation is
reasonable in asymptomatic patients [1]. Additionally, in a 2012 consensus statement on
the management of asymptomatic young patients with the WPW pattern, ablation is
recommended for patients felt to be at higher risk of SCD based on the results of
electrophysiologic testing [45]. (See "Wolff-Parkinson-White syndrome: Anatomy,
epidemiology, clinical manifestations, and diagnosis", section on 'Electrophysiology
studies (EPS)'.)
For most asymptomatic patients with preexcitation, particularly those over age 35 to 40
years, we suggest observation. However, in some asymptomatic patients, particularly
children, who are felt to be at higher risk of an arrhythmia or SCD, we encourage
consultation with an electrophysiologist to discuss catheter ablation as a therapeutic
option.
Localizing the accessory pathway — The location of most accessory pathways can

be estimated using the preexcitation pattern on the surface electrocardiogram. However,
more precise localization of the accessory pathway during catheter-based mapping prior
to catheter ablation utilizes several parameters [34].
●To determine the atrial insertion site, the earliest site of retrograde atrial
activation during orthodromic atrioventricular (AV) reciprocating tachycardia
(AVRT) or ventricular pacing must be identified [46,47]. The assumption is that
the local retrograde ventriculoatrial (VA) interval on the recording electrode will
be shortest at the atrial insertion site. Compared with pacing at sites more
remote from the accessory pathway, atrial pacing near the atrial insertion of
the accessory pathway will create a greater degree of preexcitation with a
shorter delay between the stimulus and the onset of the delta wave [48].
●More precise localization of the ventricular insertion site is obtained by
mapping along the AV groove in sinus rhythm to determine the site of earliest
ventricular activation during preexcited beats. Local ventricular activation at
the ventricular insertion site frequently precedes the onset of the delta wave
on the surface ECG by 10 to 40 milliseconds (waveform 2) [49,50]. If
preexcitation is minimal in sinus rhythm, then atrial pacing can be performed to
facilitate ventricular preexcitation by delaying AV nodal conduction.
Efficacy — The acute success rate with catheter-based ablation is approximately 85 to
95 percent but can approach 100 percent depending upon the location of the accessory
pathway and the precision of pathway localization [34-37,44]. Success rates are lower
(84 to 89 percent) for septal accessory pathways (waveform 3 and waveform 4)
[31,32,35,36,51-55]. Additionally, long-term success rates may be closer to 80 percent
at five years post-ablation [56].
As examples of the efficacy of ablation:
●In a meta-analysis that included data from 64 studies, including 3495 patients
undergoing radiofrequency catheter ablation (RFA) and 749 patients
undergoing cryoablation of septal accessory pathways, acute procedural
success was similar with either approach (89 versus 86 percent with RFA
versus cryoablation, respectively) [55]. Long-term success rates were higher
with RFA (88 versus 76 percent with cryoablation), although cryoablation
resulted in lower risk of persistent AV block (0 versus 3 percent with RFA).
●In a study of 519 patients from a single, large volume center who underwent
EP study and radiofrequency ablation of accessory pathways in the late 1990s
and were followed for an average of 22 months, accessory pathway
conduction was abolished in 92 percent of patients, although one or two
additional ablation procedures were required in 6 percent [54].
●In a single-center, prospective observational study of 1168 patients who
underwent RFA between May 2005 and May 2010 and were followed for a
median of eight years, there were no episodes of ventricular fibrillation or
sudden cardiac death [44].
In addition to location (ie, septal, lateral, etc) of the accessory pathway, the efficacy of
catheter ablation can be affected by the presence of multiple accessory pathways and
the depth of the accessory pathway within the myocardial (ie, epicardial versus
endocardial).
●Multiple accessory pathways – Multiple accessory pathways are found in as

many as 13 percent of patients with WPW syndrome. Ablation of multiple
accessory pathways is possible, but it requires a longer procedure time and is
associated with a higher rate of recurrence [35,57,58]. As an example, in one
study of 858 patients undergoing EP study and ablation for WPW syndrome in
which multiple accessory pathways were identified in 8.5 percent of patients,
procedural success was similar for single and multiple pathways, but the rate
of recurrent arrhythmias over a mean follow-up of 43 months was significantly
higher in persons with multiple accessory pathways (9.5 versus 2.5 percent)
[58].
●Epicardial accessory pathway location – One reason that catheter ablation
may fail is with an accessory pathway that is located closer to the epicardial
surface. In such patients, the usual ablation procedure via transvenous
catheters at the endocardial surface may not affect the critical tissue. Although
not widely done, percutaneous epicardial ablation is possible via subxiphoid
access of the pericardial space. The feasibility of this approach was
demonstrated in a report of 48 patients with a variety of arrhythmias (10 with
WPW syndrome) who had failed endocardial ablation [59]. Via subxiphoid
instrumentation, 5 of the 10 patients had accessory pathways localized to the
epicardial surface, and three were successfully ablated.
Catheter ablation is also effective in the treatment of PJRT. From a cohort of 194
patients (median age at diagnosis 3.2 months, 57 percent less than one year of age)
from 11 institutions treated for PJRT between 2000 and 2010, 140 patients underwent a
total of 175 catheter ablation procedures [17]. PJRT was successfully eliminated in 90
percent of patients, with minor complications reported in only 9 percent of patients, and
no major complications.
Arrhythmia recurrence — Recurrent arrhythmias involving an accessory pathway,
manifested by return of delta waves on the electrocardiogram or spontaneous
paroxysmal supraventricular tachycardia, have been reported in 5 to 12 percent of
patients [36,51,52,58,60]. The recurrence rate is higher with ablation of multiple
pathways or right free wall or septal accessory pathways [53,58,60]. Approximately one-
half of recurrences occur in the first 12 hours after the procedure [60]. Repeat ablation
usually leads to permanent cure in patients who experience a recurrence [60].
To unmask any residual conduction via an accessory pathway prior to ending the
ablation procedure, intravenous adenosine can be administered to transiently block the
AV node. We primarily use adenosine when there is difficulty determining if the pathway
has been successfully ablated.
Atrial fibrillation (AF) can recur following accessory pathway ablation; however, the
ability for atrial fibrillation to be preexcited with conduction via an accessory pathway
should be reduced or eliminated following ablation. In a series of 91 patients with
documented paroxysmal AF prior to successful ablation of an accessory pathways, 18
(20 percent) had recurrent episodes of AF at two-year follow-up, although advancing
age was the only independent predictor of recurrent AF on multivariate analysis [61].
Complications — Data on complication rates come from both case series and a
voluntary national registry. The reported incidence of nonfatal complications is on the
order of 2 to 4 percent, which is similar to rates seen with ablation procedures for other
arrhythmias [35,36,45]. (See "Overview of catheter ablation of cardiac arrhythmias",
section on 'Complications'.)
The incidence and nature of complications in general clinical practice was illustrated in a
report from a voluntary national registry in the United States of 3357 patients undergoing
EP study and ablation for a variety of indications [36]. Among the 654 patients treated
for WPW syndrome, major procedural complications occurred in 2 percent, most
commonly cardiac tamponade.
Specific complications may occur that are related to the anatomic site of ablation,
including complete AV block resulting from ablation of a septal accessory pathway near
the AV node, acute interatrial shunting related to transseptal catheterization for ablation
of left-sided accessory pathways (although there are usually no adverse long-term
sequelae), and inappropriate sinus tachycardia may be present following ablation of a
posteroseptal accessory pathway, suggesting disruption of the parasympathetic and/or
sympathetic innervation of the sinus and AV nodes [62-68].
Surgical ablation — Prior to the advent of catheter-mediated radiofrequency ablation,
surgical ablation of accessory pathways was the standard technique in patients with
drug-refractory WPW syndrome. The long-term success rate for WPW surgery is now
almost 100 percent with an operative mortality rate of less than 1 percent [69-71].
Despite these excellent outcomes, catheter-mediated radiofrequency ablation has
emerged as the preferred therapy for treatment of accessory pathways. However,
surgical ablation remains an effective treatment strategy in patients suffering from highly
symptomatic and hemodynamically unstable, drug-refractory arrhythmias in whom
radiofrequency energy catheter ablation has failed, when performed at centers with a
proven track record of success in performing the procedure [72].
Medical therapy for arrhythmia prevention — For patients with an accessory pathway
and symptomatic arrhythmias (including orthodromic AVRT, antidromic AVRT, and
preexcited atrial fibrillation or atrial flutter) who are not candidates for or who refuse
ablation of the accessory pathway, we suggest pharmacologic therapy aimed at
preventing further arrhythmias and/or slowing the ventricular response rate [1].
Chronic therapy with verapamil or digoxin should be avoided in all patients with WPW
syndrome.
Prevention of recurrent orthodromic AVRT — The efficacy of an antiarrhythmic drug
in preventing orthodromic atrioventricular reciprocating tachycardia (AVRT) is related to
its ability to alter the electrophysiologic properties of the circuit, rendering it incapable of
sustaining reentry. Antiectopic activity to decrease the number of arrhythmia triggers
(eg, premature atrial complex [PACs; also referred to a premature atrial beat, premature
supraventricular complex, or premature supraventricular beat] and ventricular premature
beats) is another desirable effect.
●The class IC antiarrhythmic drugs flecainide and propafenone (table 2)
possess the most favorable benefit/risk ratio and are the drugs of choice for
prevention of recurrent orthodromic AVRT [73-76]. An important exception is
the presence of known coronary disease, a setting in which class IC drugs can
increase mortality due to proarrhythmia [77]. Both flecainide and propafenone
have been approved for prevention of paroxysmal supraventricular
tachyarrhythmias, including orthodromic AVRT. Propafenone has a potential
advantage since it also has mild beta blocking activity [75,76].
●Beta blockers are still occasionally used as second-line therapy for chronic
suppression of orthodromic AVRT in patients with "low-risk" WPW accessory
pathways (eg, only intermittently manifest or know to have a long effective
refractory period), but they are not advised for patients who have developed or
may develop preexcited atrial fibrillation. Chronic therapy
with verapamil or digoxin should be avoided in all patients with WPW
syndrome.
●The class IA antiarrhythmic drugs (table 2) lengthen antegrade and
retrograde refractoriness and slow conduction in the accessory pathway.
However, these drugs are less potent than the class IC drugs, they only
minimally lengthen AV node refractoriness, and they have a substantial risk of
intolerable noncardiac adverse effects.
●Amiodarone has multiple electrophysiologic effects that make it effective in
suppressing orthodromic AVRT, including beta blocking activity, class III
effects to prolong action potential repolarization, blockade of the fast sodium
and slow calcium inward currents, and suppression of ectopic beats [78-80]
(see "Amiodarone: Clinical uses"). These effects result in slowing of impulse
conduction and lengthening of refractoriness in both the bypass tract and the
AV node/His-Purkinje system. However, it has a number of common adverse
effects, including pulmonary, thyroid, and hepatic toxicity, which is a concern
for patients with WPW who are often young and may require many years of
therapy. (See "Amiodarone: Adverse effects, potential toxicities, and approach
to monitoring".)
Prevention of recurrent antidromic AVRT — Ablation of the accessory pathway is the
preferred therapy for chronic prevention of antidromic AVRT. An important concern
about long-term medical therapy of this arrhythmia is the potential for very rapid
ventricular rates should atrial fibrillation (AF) develop, given that the accessory pathway
is capable of antegrade preexcited conduction during AF. We suggest drug therapy for
the prevention of recurrent antidromic AVRT only in patients who are not candidates for
or who refuse ablation of the accessory pathway. (See 'Catheter ablation' above.)
The selection of an effective antiarrhythmic drug should be based upon the effect of the
drug on the electrophysiologic properties of the various parts of the reentrant circuit and
on the ability to suppress the arrhythmia. The AV nodal blocking agents (beta blockers,
calcium channel blockers, and digoxin) are contraindicated because of the possible
occurrence of atrial fibrillation with accelerated conduction down the accessory pathway.
(See 'Avoidance of AV nodal blockers' above.)
The class IC drugs flecainide and propafenone (table 2) are the agents of choice in the
absence of other contraindications such as underlying structural heart disease or
myocardial ischemia (table 1). These drugs may increase mortality in patients with
known coronary disease due to proarrhythmia [77]. Class IA drugs and amiodarone are
also effective but are less desirable because of side effects.
Prevention of recurrent preexcited atrial fibrillation — Ablation of the accessory
pathway is the preferred therapy for the prevention of recurrent preexcited atrial
fibrillation (AF). While ablation of the accessory pathway will not directly impact the
development of AF, it should prevent the possibility of very rapid ventricular rates due to
antegrade conduction via the accessory pathway. We suggest medical therapy for the
prevention of recurrent preexcited AF only in patients who are not candidates for, or
refuse, ablation of the accessory pathway. (See 'Catheter ablation' above.)
The drug selected for prevention of intermittent AF in the WPW syndrome should
possess antifibrillatory activity on the atrial myocardium, antiectopic activity to suppress
both PACs and ventricular premature beats that can induce AF, and should prevent
AVRT since the latter can subsequently degenerate into AF. The drug must also
lengthen refractoriness in both the accessory pathway and the AV node and His-
Purkinje system to provide adequate background protection against a rapid ventricular
response should AF intermittently occur. (See "Antiarrhythmic drugs to maintain sinus
rhythm in patients with atrial fibrillation: Recommendations" and "Atrial fibrillation:
Anticoagulant therapy to prevent thromboembolism".)
The class IC drugs flecainide and propafenone (table 2) possess the best
electrophysiologic profile for achieving these goals if no cardiac contraindications exist
[81,82]. Class IA drugs are less potent and have more noncardiac adverse effects as
previously noted. Amiodarone may be useful for the prevention of recurrent AF when
class IC and IA drugs are ineffective and/or not tolerated and when ablation therapy is
inappropriate or has failed [83,84]. Amiodarone should not be used in the acute
management of AF. (See 'Avoidance of AV nodal blockers' above.)
Arrhythmias in adults" and "Society guideline links: Catheter ablation of
arrhythmias" and "Society guideline links: Supraventricular arrhythmias".)
interest.)
●Basics topic (see "Patient education: Wolff-Parkinson-White syndrome (The

Basics)")
●Beyond the Basics topic (see "Patient education: Wolff-Parkinson-White
syndrome (Beyond the Basics)")
●Patients with the Wolff-Parkinson-White (WPW) syndrome are generally

treated because of symptomatic arrhythmia or the risk of a life-threatening
arrhythmia. Most asymptomatic adults with the WPW pattern are usually not
treated. However, certain asymptomatic subgroups (pediatric patients, those
with congenital heart defects, those with cardiomyopathies of any sort) usually
undergo risk-stratification testing and may be considered for treatment
depending upon the findings. Treatment options for persons include
nonpharmacologic therapies (ie, catheter ablation of the accessory pathway)
as well as pharmacologic therapy (to slow ventricular heart rates or to prevent
arrhythmias). The choice of the optimal therapy depends on the acuity of the
arrhythmia(s) and the risk of sudden cardiac death. (See 'Introduction' above.)
●All patients with any arrhythmia (ie, orthodromic AVRT, antidromic AVRT,
atrial fibrillation/flutter) involving an accessory pathway should have a prompt
initial assessment of hemodynamic status.
Patients who are felt to be hemodynamically unstable related to their
arrhythmia should undergo urgent electrical cardioversion. (See 'Initial
assessment of hemodynamic stability' above and "Cardioversion for specific
arrhythmias".)
●For patients with acute symptomatic orthodromic AVRT who are
hemodynamically stable, our approach is as follows (table 1) (see 'Acute
termination of orthodromic AVRT' above):
•We recommend initial treatment with one or more vagal maneuvers
rather than pharmacologic therapy (Grade 1B).
•If vagal maneuvers are ineffective, pharmacologic therapy with an AV
nodal blocking agent (ie, adenosine, verapamil, beta blockers) should be
instituted. We suggest intravenous adenosine rather than intravenous
verapamil as the initial choice based on its efficacy and short half-life
(Grade 2B).
•If adenosine is ineffective, we proceed with intravenous verapamil as the
second line agent. If orthodromic AVRT persists,
intravenous procainamide and beta blockers approved for intravenous
administration (eg, propranolol, metoprolol, and esmolol) are additional
therapeutic options.
●For patients with acute symptomatic antidromic AVRT who are
hemodynamically stable, we treat with intravenous procainamide in an effort to
terminate the tachycardia or, if the tachycardia persists, slow the ventricular
response. (See 'Acute termination of antidromic AVRT' above.)
●For patients with acute symptomatic preexcited atrial fibrillation (AF) who are
hemodynamically stable, our approach is as follows (see 'Acute treatment of
atrial fibrillation with preexcitation' above):
•We suggest initial medical therapy for rhythm control versus rate control
(Grade 2C). This is based on the greater ease of controlling the
ventricular rate in sinus rhythm. While there is no clear first-line
medication for rhythm control, options include procainamide and ibutilide.
•For all patients with preexcited AF, we recommend NOT using standard
AV nodal blocking medications (ie, beta blockers, non-dihydropyridine
calcium channel blockers [verapamil and diltiazem], digoxin, adenosine,
and amiodarone) (Grade 1A). Blocking the AV node may result in
increased conduction of atrial impulses to the ventricle by way of the
accessory pathway, increasing the ventricular rate and potentially
resulting in hemodynamic instability. (See 'Avoidance of AV nodal
blockers' above.)
●For patients with an accessory pathway and symptomatic arrhythmias
including orthodromic AVRT, antidromic AVRT, and preexcited atrial fibrillation
or atrial flutter, we recommend catheter ablation (Grade 1A). (See 'Catheter
ablation' above.)
●For patients with an accessory pathway and symptomatic arrhythmias
(including orthodromic AVRT, antidromic AVRT, and preexcited atrial
fibrillation or atrial flutter) who are not candidates for, or refuse, ablation of the
accessory pathway, we suggest pharmacologic therapy (Grade 2C).
(See 'Medical therapy for arrhythmia prevention' above.)
•For prevention of recurrent orthodromic AVRT in the absence of
underlying structural heart disease, class IC antiarrhythmic drugs
(eg, flecainide, propafenone) are the drugs of choice, although beta
blockers, class IA antiarrhythmic drugs, and amiodarone may also be
considered.
•For prevention of recurrent antidromic AVRT and preexcited atrial
fibrillation in the absence of underlying structural heart disease, class IC
antiarrhythmic drugs (eg, flecainide, propafenone) are also the drugs of
choice. However, the AV nodal blocking agents (beta blockers, calcium
channel blockers, and digoxin) are contraindicated in these patients, so
class IA antiarrhythmic drugs and amiodarone should be considered in
patients with concurrent structural heart disease.
●For patients with preexcitation and symptomatic arrhythmias or AF or atrial
flutter who have failed catheter ablation of the accessory pathway, we typically
perform a repeat attempt at catheter ablation or consider proceeding with
surgical ablation. (See 'Catheter ablation' above and 'Surgical ablation' above.)
●For most asymptomatic patients with preexcitation, particularly those over
age 35 to 40, we suggest observation rather than ablation or
pharmacotherapy. (Grade 2C). However, in some asymptomatic patients,
particularly children, who are felt to be at higher risk of an arrhythmia or SCD,
we encourage consultation with an electrophysiologist to discuss catheter
ablation as a therapeutic option. (See 'Asymptomatic patients' above.)
REFERENCES
Task Force on Clinical Practice Guidelines and the Heart Rhythm Society.
3. Walker S, Cutting P. Impact of a modified Valsalva manoeuvre in the
termination of paroxysmal supraventricular tachycardia. Emerg Med J 2010;
27:287.
4. Belardinelli L, Linden J, Berne RM. The cardiac effects of adenosine. Prog
Cardiovasc Dis 1989; 32:73.
5. diMarco JP, Sellers TD, Lerman BB, et al. Diagnostic and therapeutic use of
adenosine in patients with supraventricular tachyarrhythmias. J Am Coll
Cardiol 1985; 6:417.
6. DiMarco JP, Sellers TD, Berne RM, et al. Adenosine: electrophysiologic
effects and therapeutic use for terminating paroxysmal supraventricular
tachycardia. Circulation 1983; 68:1254.
7. Exner DV, Muzyka T, Gillis AM. Proarrhythmia in patients with the Wolff-
Parkinson-White syndrome after standard doses of intravenous adenosine.
Ann Intern Med 1995; 122:351.
8. Dougherty AH, Gilman JK, Wiggins S, et al. Provocation of atrioventricular
reentry tachycardia: a paradoxical effect of adenosine. Pacing Clin
9. DiMarco JP, Miles W, Akhtar M, et al. Adenosine for paroxysmal
supraventricular tachycardia: dose ranging and comparison with verapamil.
Assessment in placebo-controlled, multicenter trials. The Adenosine for
PSVT Study Group. Ann Intern Med 1990; 113:104.
10. Rinkenberger RL, Prystowsky EN, Heger JJ, et al. Effects of intravenous
and chronic oral verapamil administration in patients with supraventricular
tachyarrhythmias. Circulation 1980; 62:996.
11. Sung RJ, Elser B, McAllister RG Jr. Intravenous verapamil for termination of
re-entrant supraventricular tachycardias: intracardiac studies correlated with
plasma verapamil concentrations. Ann Intern Med 1980; 93:682.
12. Jackman WM, Friday KJ, Fitzgerald DM, et al. Use of intracardiac
recordings to determine the site of drug action in paroxysmal
supraventricular tachycardia. Am J Cardiol 1988; 62:8L.
13. Kowey PR, Friehling TD, Marinchak RA. Electrophysiology of beta blockers
in supraventricular arrhythmias. Am J Cardiol 1987; 60:32D.
14. Anderson S, Blanski L, Byrd RC, et al. Comparison of the efficacy and
safety of esmolol, a short-acting beta blocker, with placebo in the treatment
of supraventricular tachyarrhythmias. The Esmolol vs Placebo Multicenter
Study Group. Am Heart J 1986; 111:42.
15. Mandel WJ, Laks MM, Obayashi K, et al. The Wolff-Parkinson-White
syndrome: pharmacologic effects of procaine amide. Am Heart J 1975;
90:744.
16. Wellens HJ. The wide QRS tachycardia. Ann Intern Med 1986; 104:879.
17. Kang KT, Potts JE, Radbill AE, et al. Permanent junctional reciprocating
tachycardia in children: a multicenter experience. Heart Rhythm 2014;
11:1426.
18. Dorostkar PC, Silka MJ, Morady F, Dick M 2nd. Clinical course of persistent
junctional reciprocating tachycardia. J Am Coll Cardiol 1999; 33:366.
19. January CT, Wann LS, Alpert JS, et al. 2014 AHA/ACC/HRS guideline for
the management of patients with atrial fibrillation: executive summary: a
report of the American College of Cardiology/American Heart Association
Task Force on practice guidelines and the Heart Rhythm Society.
20. Glatter KA, Dorostkar PC, Yang Y, et al. Electrophysiological effects of
ibutilide in patients with accessory pathways. Circulation 2001; 104:1933.
21. Bianconi L, Boccadamo R, Pappalardo A, et al. Effectiveness of intravenous
propafenone for conversion of atrial fibrillation and flutter of recent onset.
Am J Cardiol 1989; 64:335.
22. Suttorp MJ, Kingma JH, Jessurun ER, et al. The value of class IC
antiarrhythmic drugs for acute conversion of paroxysmal atrial fibrillation or
flutter to sinus rhythm. J Am Coll Cardiol 1990; 16:1722.
23. Suttorp MJ, Kingma JH, Lie-A-Huen L, Mast EG. Intravenous flecainide
versus verapamil for acute conversion of paroxysmal atrial fibrillation or
flutter to sinus rhythm. Am J Cardiol 1989; 63:693.
24. Krahn AD, Klein GJ, Yee R. A randomized, double-blind, placebo-controlled
evaluation of the efficacy and safety of intravenously administered dofetilide
in patients with Wolff-Parkinson-White syndrome. Pacing Clin Electrophysiol
2001; 24:1258.
25. Garratt C, Antoniou A, Ward D, Camm AJ. Misuse of verapamil in pre-
excited atrial fibrillation. Lancet 1989; 1:367.
26. Gulamhusein S, Ko P, Carruthers SG, Klein GJ. Acceleration of the
ventricular response during atrial fibrillation in the Wolff-Parkinson-White
syndrome after verapamil. Circulation 1982; 65:348.
27. McGovern B, Garan H, Ruskin JN. Precipitation of cardiac arrest by
verapamil in patients with Wolff-Parkinson-White syndrome. Ann Intern Med
1986; 104:791.
28. Boriani G, Biffi M, Frabetti L, et al. Ventricular fibrillation after intravenous
amiodarone in Wolff-Parkinson-White syndrome with atrial fibrillation. Am
Heart J 1996; 131:1214.
29. Simonian SM, Lotfipour S, Wall C, Langdorf MI. Challenging the superiority
of amiodarone for rate control in Wolff-Parkinson-White and atrial fibrillation.
Intern Emerg Med 2010; 5:421.
30. Sellers TD Jr, Bashore TM, Gallagher JJ. Digitalis in the pre-excitation
syndrome. Analysis during atrial fibrillation. Circulation 1977; 56:260.
31. Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory
atrioventricular pathways (Wolff-Parkinson-White syndrome) by
radiofrequency current. N Engl J Med 1991; 324:1605.
32. Kuck KH, Schlüter M, Geiger M, et al. Radiofrequency current catheter
ablation of accessory atrioventricular pathways. Lancet 1991; 337:1557.
33. Calkins H, Sousa J, el-Atassi R, et al. Diagnosis and cure of the Wolff-
Parkinson-White syndrome or paroxysmal supraventricular tachycardias
during a single electrophysiologic test. N Engl J Med 1991; 324:1612.
34. Chen SA, Tai CT. Ablation of atrioventricular accessory pathways: current
technique-state of the art. Pacing Clin Electrophysiol 2001; 24:1795.
35. Calkins H, Langberg J, Sousa J, et al. Radiofrequency catheter ablation of
accessory atrioventricular connections in 250 patients. Abbreviated
therapeutic approach to Wolff-Parkinson-White syndrome. Circulation 1992;
85:1337.
36. Scheinman MM, Huang S. The 1998 NASPE prospective catheter ablation
registry. Pacing Clin Electrophysiol 2000; 23:1020.
38. Rodriguez LM, Geller JC, Tse HF, et al. Acute results of transvenous
cryoablation of supraventricular tachycardia (atrial fibrillation, atrial flutter,
Wolff-Parkinson-White syndrome, atrioventricular nodal reentry
tachycardia). J Cardiovasc Electrophysiol 2002; 13:1082.
39. Wellens HJ. Should catheter ablation be performed in asymptomatic
patients with Wolff-Parkinson-White syndrome? When to perform catheter
ablation in asymptomatic patients with a Wolff-Parkinson-White
electrocardiogram. Circulation 2005; 112:2201.
40. Pappone C, Santinelli V. Should catheter ablation be performed in
asymptomatic patients with Wolff-Parkinson-White syndrome? Catheter
ablation should be performed in asymptomatic patients with Wolff-
Parkinson-White syndrome. Circulation 2005; 112:2207.
41. Chevalier P, Cadi F, Scridon A, et al. Prophylactic radiofrequency ablation in
asymptomatic patients with Wolff-Parkinson-White is not yet a good
strategy: a decision analysis. Circ Arrhythm Electrophysiol 2013; 6:185.
42. Todd DM, Klein GJ, Krahn AD, et al. Asymptomatic Wolff-Parkinson-White
syndrome: is it time to revisit guidelines? J Am Coll Cardiol 2003; 41:245.
43. Etheridge SP, Escudero CA, Blaufox AD, et al. Life-threatening event risk in
children with Wolff-Parkinson-White syndrome: a multicenter international
study. J Am Coll Cardiol EP 2018; 4:433.
44. Pappone C, Vicedomini G, Manguso F, et al. Wolff-Parkinson-White
syndrome in the era of catheter ablation: insights from a registry study of
2169 patients. Circulation 2014; 130:811.
45. Pediatric and Congenital Electrophysiology Society (PACES), Heart Rhythm
Society (HRS), American College of Cardiology Foundation (ACCF), et al.
PACES/HRS expert consensus statement on the management of the
asymptomatic young patient with a Wolff-Parkinson-White (WPW,
ventricular preexcitation) electrocardiographic pattern: developed in
partnership between the Pediatric and Congenital Electrophysiology Society
(PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing
bodies of PACES, HRS, the American College of Cardiology Foundation
(ACCF), the American Heart Association (AHA), the American Academy of
Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS). Heart
Rhythm 2012; 9:1006.
46. Crossen KJ, Lindsay BD, Cain ME. Reliability of retrograde atrial activation
patterns during ventricular pacing for localizing accessory pathways. J Am
47. Jackman WM, Friday KJ, Yeung-Lai-Wah JA, et al. New catheter technique
for recording left free-wall accessory atrioventricular pathway activation.
Identification of pathway fiber orientation. Circulation 1988; 78:598.
48. Denes P, Wyndham CR, Amat-y-Leon F, et al. Atrial pacing at multiple sites
in the Wolff-Parkinson-White syndrome. Br Heart J 1977; 39:506.
49. Mitchell LB, Mason JW, Scheinman MM, et al. Recordings of basal
ventricular preexcitation from electrode catheters in patients with accessory
atrioventricular connections. Circulation 1984; 69:233.
50. Chen X, Borggrefe M, Shenasa M, et al. Characteristics of local electrogram
predicting successful transcatheter radiofrequency ablation of left-sided
accessory pathways. J Am Coll Cardiol 1992; 20:656.
51. Scheinman MM. Catheter ablation for cardiac arrhythmias, personnel, and
facilities. North American Society of Pacing and Electrophysiology Ad Hoc
Committee on Catheter Ablation. Pacing Clin Electrophysiol 1992; 15:715.
52. Kay GN, Epstein AE, Dailey SM, Plumb VJ. Role of radiofrequency ablation
in the management of supraventricular arrhythmias: experience in 760
consecutive patients. J Cardiovasc Electrophysiol 1993; 4:371.
53. Calkins H, Yong P, Miller JM, et al. Catheter ablation of accessory
pathways, atrioventricular nodal reentrant tachycardia, and the
atrioventricular junction: final results of a prospective, multicenter clinical
trial. The Atakr Multicenter Investigators Group. Circulation 1999; 99:262.
54. Dagres N, Clague JR, Kottkamp H, et al. Radiofrequency catheter ablation
of accessory pathways. Outcome and use of antiarrhythmic drugs during
follow-up. Eur Heart J 1999; 20:1826.
55. Bravo L, Atienza F, Eidelman G, et al. Safety and efficacy of cryoablation vs.
radiofrequency ablation of septal accessory pathways: systematic review of
the literature and meta-analyses. Europace 2018; 20:1334.
56. Backhoff D, Klehs S, Muller MJ, et al. Long-term follow-up after
radiofrequency catheter ablation of accessory atrioventricular pathways in
children. J Am Coll Cardiol EP 2018; 4:448.
57. Chen SA, Hsia CP, Chiang CE, et al. Reappraisal of radiofrequency ablation
of multiple accessory pathways. Am Heart J 1993; 125:760.
58. Huang JL, Chen SA, Tai CT, et al. Long-term results of radiofrequency
catheter ablation in patients with multiple accessory pathways. Am J Cardiol
1996; 78:1375.
59. Schweikert RA, Saliba WI, Tomassoni G, et al. Percutaneous pericardial
instrumentation for endo-epicardial mapping of previously failed ablations.
60. Langberg JJ, Calkins H, Kim YN, et al. Recurrence of conduction in
accessory atrioventricular connections after initially successful
radiofrequency catheter ablation. J Am Coll Cardiol 1992; 19:1588.
61. Dagres N, Clague JR, Lottkamp H, et al. Impact of radiofrequency catheter
ablation of accessory pathways on the frequency of atrial fibrillation during
long-term follow-up; high recurrence rate of atrial fibrillation in patients older
than 50 years of age. Eur Heart J 2001; 22:423.
62. Liu J, Dole LR. Late complete atrioventricular block complicating
radiofrequency catheter ablation of a left posteroseptal accessory pathway.
63. Seidl K, Hauer B, Zahn R, Senges J. Unexpected complete AV block
following transcatheter ablation of a left posteroseptal accessory pathway.
64. Kessler DJ, Pirwitz MJ, Horton RP, et al. Intracardiac shunts resulting from
transseptal catheterization for ablation of accessory pathways in otherwise
normal hearts. Am J Cardiol 1998; 82:391.
65. Fitchet A, Turkie W, Fitzpatrick AP. Transeptal approach to ablation of left-
sided arrhythmias does not lead to persisting interatrial shunt: a
transesophageal echocardiographic study. Pacing Clin Electrophysiol 1998;
21:2070.
66. Kocovic DZ, Harada T, Shea JB, et al. Alterations of heart rate and of heart
rate variability after radiofrequency catheter ablation of supraventricular
tachycardia. Delineation of parasympathetic pathways in the human heart.
67. Psychari SN, Theodorakis GN, Koutelou M, et al. Cardiac denervation after
radiofrequency ablation of supraventricular tachycardias. Am J Cardiol
1998; 81:725.
68. Hamdan MH, Page RL, Wasmund SL, et al. Selective parasympathetic
denervation following posteroseptal ablation for either atrioventricular nodal
reentrant tachycardia or accessory pathways. Am J Cardiol 2000; 85:875.
69. Cox JL, Gallagher JJ, Cain ME. Experience with 118 consecutive patients
undergoing operation for the Wolff-Parkinson-White syndrome. J Thorac
Cardiovasc Surg 1985; 90:490.
70. Lawrie GM, Lin HT, Wyndham CR, DeBakey ME. Surgical treatment of
supraventricular arrhythmias. Results in 67 patients. Ann Surg 1987;
205:700.
71. Johnson DC, Nunn GR, Richards DA, et al. Surgical therapy for
supraventricular tachycardia, a potentially curable disorder. J Thorac
72. Holman WL, Kay GN, Plumb VJ, Epstein AE. Operative results after
unsuccessful radiofrequency ablation for Wolff-Parkinson-White syndrome.
Am J Cardiol 1992; 70:1490.
73. Kim SS, Lal R, Ruffy R. Treatment of paroxysmal reentrant supraventricular
tachycardia with flecainide acetate. Am J Cardiol 1986; 58:80.
74. Ward DE, Jones S, Shinebourne EA. Use of flecainide acetate for refractory
junctional tachycardias in children with the Wolff-Parkinson-White
syndrome. Am J Cardiol 1986; 57:787.
75. Ludmer PL, McGowan NE, Antman EM, Friedman PL. Efficacy of
propafenone in Wolff-Parkinson-White syndrome: electrophysiologic findings
and long-term follow-up. J Am Coll Cardiol 1987; 9:1357.
76. Musto B, D'Onofrio A, Cavallaro C, Musto A. Electrophysiological effects
and clinical efficacy of propafenone in children with recurrent paroxysmal
77. Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients
receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia
Suppression Trial. N Engl J Med 1991; 324:781.
78. Rosenbaum MB, Chiale PA, Ryba D, Elizari MV. Control of
tachyarrhythmias associated with Wolff-Parkinson-White syndrome by
amiodarone hydrochloride. Am J Cardiol 1974; 34:215.
79. Wellens HJ, Lie KI, Bär FW, et al. Effect of amiodarone in the Wolff-
Parkinson-White syndrome. Am J Cardiol 1976; 38:189.
80. Feld GK, Nademanee K, Weiss J, et al. Electrophysiologic basis for the
suppression by amiodarone of orthodromic supraventricular tachycardias
complicating pre-excitation syndromes. J Am Coll Cardiol 1984; 3:1298.
81. Chouty F, Coumel P. Oral flecainide for prophylaxis of paroxysmal atrial
fibrillation. Am J Cardiol 1988; 62:35D.
82. Antman EM, Beamer AD, Cantillon C, et al. Long-term oral propafenone
therapy for suppression of refractory symptomatic atrial fibrillation and atrial
flutter. J Am Coll Cardiol 1988; 12:1005.
83. Kappenberger LJ, Fromer MA, Steinbrunn W, Shenasa M. Efficacy of
amiodarone in the Wolff-Parkinson-White syndrome with rapid ventricular
response via accessory pathway during atrial fibrillation. Am J Cardiol 1984;
54:330.
84. Feld GK, Nademanee K, Stevenson W, et al. Clinical and electrophysiologic
effects of amiodarone in patients with atrial fibrillation complicating the
Wolff-Parkinson-White syndrome. Am Heart J 1988; 115:102.
Close
 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 SUMMARY
 INTRODUCTION
 CLASSIFICATION
 ELECTROPHYSIOLOGIC FEATURES
o Typical flutters
o Atypical right atrial flutters
 Lesion macroreentrant tachycardia
 Nonatriotomy-related right atrial flutter
 Upper loop reentry
o Atypical left atrial flutters
 Post-Maze or atrial fibrillation ablation left atrial flutters
 Left atrial macroreentry
o Atrioventricular node and the ventricular response
 ELECTROCARDIOGRAPHIC FEATURES
o Morphology of the QRS complex
o Pitfalls
 MANAGEMENT
 SUMMARY
 REFERENCES
GRAPHICS view all
 Figures
 Tables
 Waveforms
oECG atrial flutter preexcitation
oTypical atrial flutter
oReverse typical atrial flutter
oECG in lower loop reentry flutter
oECG atriotomy-related right atrial flutter after mitral repair
oECG atypical left AFL through scar anterior septum prior AF
oECG atypical roof dependent left AFL after AF ablation
oECG of a patient with clockwise mitral annular flutter
oAtrial flutter RA recording
RELATED TOPICS
 Atrial fibrillation and flutter after cardiac surgery
 Atrial flutter: Maintenance of sinus rhythm
 Control of ventricular rate in atrial flutter
 Management of complications in patients with Fontan circulation
 Surgical ablation to prevent recurrent atrial fibrillation
Electrocardiographic and electrophysiologic features

of atrial flutter
Author:
Section Editors:
Deputy Editor:
Literature review current through: Sep 2020. | This topic last updated: Mar 28, 2019.
INTRODUCTION Atrial flutter (AFL) is an abnormal cardiac rhythm
characterized by rapid, regular atrial depolarizations at a typical atrial rate of 250 to 350
beats per minute. There is frequently 2:1 conduction across the atrioventricular (AV)
node, meaning that every other atrial depolarization reaches the ventricles. As a result,
the ventricular rate is usually one-half the AFL rate in the absence of AV node
dysfunction. AFL is classified as typical or atypical based on whether the flutter circuit
traverses the cavotricuspid isthmus in the right atrium [1].
Other topic reviews discuss the clinical aspects of AFL. (See "Overview of atrial
flutter" and "Restoration of sinus rhythm in atrial flutter" and "Control of ventricular rate in
atrial flutter" and "Atrial flutter: Maintenance of sinus rhythm" and "Embolic risk and the
role of anticoagulation in atrial flutter" and "Atrial fibrillation and flutter after cardiac
surgery".)
CLASSIFICATION The first classification scheme in 1970 defined atrial flutter
(AFL) as "common" or "atypical," depending on whether the flutter wave had a negative
sawtooth pattern in the inferior leads [2]. A few years later, the terms types I and II were
created to describe flutter [1]. Type I AFL was classified as a macroreentrant atrial
tachycardia while type II AFL was considered unclassified because the mechanisms
were not fully understood.
A 2001 working group from Europe and North America tried to reconcile new data from
electrophysiology studies and activation mapping [3]. Flutter was defined as a regular
tachycardia ≥240 beats/min with no isoelectric baseline between atrial deflections.
Typical and reversal typical flutter were characterized, as described below, and all other
flutters were atypical.
An American College of Cardiology, American Heart Association, and Heart Rhythm
Society guideline on the management of supraventricular tachycardia reaffirmed the
classification of AFL into cavo-tricuspid-isthmus (CTI)-dependent ("typical") versus non-
CTI dependent ("atypical") [4] and this is the methodology currently used.
Typical AFL is a macroreentrant atrial tachycardia, with the inferior border of the circuit
traversing the isthmus of tissue between the inferior vena cava and tricuspid annulus as
a necessary component. AFL involving this cavotricuspid isthmus is referred to as
"typical" or "isthmus-dependent" flutter.
In the most common form of CTI-dependent flutter, the reentrant circuit rotates around
the tricuspid annulus in a counterclockwise direction when the heart is viewed in a left
anterior oblique projection, traversing up the septum and down the lateral wall. This is
the arrhythmia associated with the classic electrocardiogram finding of sawtooth flutter
waves in the inferior leads. (See 'Electrocardiographic features' below.)
Less often, the reentrant circuit rotates in the opposite direction. This arrhythmia is
called "clockwise" or "reverse" typical flutter.
Atypical AFL is an intraatrial reentrant tachycardia or AFL that does not involve the CTI.
It may be a lesion macroreentrant tachycardia, lower or upper loop flutter, intra-isthmus
reentry, non-atriotomy-related right atrial flutter, left atrial macroreentry, post-Maze or
atrial fibrillation ablation left atrial flutters, or mitral annular flutter [5]. It is frequently seen
in those who have had prior cardiac surgery, prior intracardiac ablation, congenital heart
disease, or cardiomyopathy but may also be idiopathic. Atypical flutter may be in the
right or left atrium and usually revolves around a prior incisional or idiopathic scar,
ablation lesion set, or other fixed anatomic barriers. If there has been an incomplete
ablation line from a prior procedure, this can increase the chances of an atypical flutter.
Many patients with congenital heart disease, especially with more complex disease or
surgical repairs, will present with atypical flutter [6]. Some patients with idiopathic atrial
fibrosis will also present with scar-based atypical flutters.
ELECTROPHYSIOLOGIC FEATURES Electrophysiologic studies, using
entrainment mapping and electroanatomic mapping, have been used to define the atrial
flutter (AFL) circuit in the electrophysiology laboratory and at surgery [7-11].
The principal electrophysiologic features of AFL are:
●Reentry
●Excitable gap
●Transient entrainment and termination by rapid atrial pacing
Electrophysiologically, AFL is a reentrant arrhythmia in that it excites an area of the
atrium and then travels sufficiently slowly in a pathway that is long enough such that the
initially excited area recovers its excitability and is reactivated [7-9,12-15]. Either a single
premature extrastimulus or rapid atrial pacing can initiate AFL and, because there is an
excitable gap, terminate the arrhythmia [13-15]. The excitable gap is the portion of a
reentrant circuit that has recovered its excitability and can again be depolarized,
allowing for entrainment with overdrive pacing during AFL [13,14,16]. (See "Reentry and
the development of cardiac arrhythmias", section on 'Definition and characteristics'.)
Typical AFL commonly starts after a transitional rhythm of variable duration, usually
atrial fibrillation [17,18]. It has been postulated that a fundamental feature that
determines whether an atrial arrhythmia becomes sustained typical AFL or atrial
fibrillation is the development of a line of functional refractoriness or block between the
vena cavae [18]. In spontaneous typical AFL, the critical line of functional block between
the vena cavae may be created by transient atrial fibrillation. This line of block results in
unidirectional block and stable AFL follows. According to this theory, if the line of
functional block is not created, atrial fibrillation persists or the rhythm reverts back to
sinus.
Another view, based in part on a small electrophysiologic study of 10 patients,
emphasizes the anatomic barriers as well as the properties of conduction and
refractoriness during atrial fibrillation to explain the usual pattern observed with typical
AFL [19]. In the electrophysiology laboratory, premature electrical stimulation may
function in a manner similar to the transitional atrial fibrillation in forming the critical
functional line of block between the vena cavae [18].
An additional determinant of whether the transitional atrial tachyarrhythmia becomes
AFL or atrial fibrillation may be the cycle length of the flutter [18]. If the cycle length is
critically short, it will create fibrillatory conduction and atrial fibrillation.
Lastly, the electrical properties of the isthmus may also be a factor in the tendency for
AFL to disorganize into atrial fibrillation in some patients [20].
Similar to what has been reported in atrial fibrillation, AFL results in electrical remodeling
of the atrial myocardium, perhaps accounting for the observation that untreated AFL can
eventually lead to atrial fibrillation [21]. In contrast to the normal situation in which the
atrial refractory period shortens with an increase in rate and prolongs when the rate
decreases, the refractory period fails to lengthen appropriately at slow rates (eg, with
return to sinus rhythm) in patients with AFL present for a mean of 8.5 months (range 1 to
32 months) [22]. This abnormality persists for at least 30 minutes after cardioversion to
sinus rhythm; the duration of AFL has no significant impact upon the magnitude of these
electrophysiologic changes. Those with a history of AFL, but not fibrillation, have
significant changes in the electrophysiologic properties of the right atrium, even when
they are in normal sinus rhythm. The right atrium is more likely to be enlarged, have
lower voltage suggesting scar, longer P wave duration, and slowed conduction velocity
most prominent in the lower right atrium, and sinus node dysfunction [23].
The duration of AFL does impact the time course of electrical remodeling recovery after
arrhythmia termination. As an example, one study of 25 patients with paroxysmal or
chronic flutter (average duration 17 months) found that, in those with paroxysmal AFL,
the refractory period shortened after a 5- to 10-minute period of flutter and reversed
within five minutes of restoration of sinus rhythm; atrial fibrillation developed in some
patients when the refractory period was at its nadir [24]. In patients with chronic AFL, the
atrial refractory period increased during the first three weeks after resumption of sinus
rhythm.
Typical flutters — A large macroreentrant circuit in the right atrium is involved in typical
AFL.
If one begins the cycle at the end of the negative deflection of the F wave in lead II, the
impulse at that point exists in the low right atrial septum between the inferior vena cava
(IVC) and the tricuspid valve.
In counterclockwise typical flutter, the impulse then travels anteriorly through the region
of the low septum, ascends superiorly and anteriorly up the septal and posterior walls of
the right atrium, and returns or descends over the anterior and lateral free wall (figure 1)
[25]. This circuit is then completed through the region between the tricuspid valve and
IVC (counterclockwise reentry). A reverse direction of rotation (clockwise reentry,
ascending the anterior wall, and descending the posterior and septal walls) is seen in
reverse typical AFL [3,25].
The crista terminalis (and its continuation as the eustachian ridge) and IVC commonly
form the posterior barrier, while the tricuspid annulus constitutes the anterior barrier of
the circuit (figure 1) [11,26]. This has potential clinical implications, since this region can
be a target for ablation therapy in patients with refractory AFL [26,27]. (See "Atrial flutter:
Maintenance of sinus rhythm", section on 'RF catheter ablation'.)
The presence of slow conduction in the cavotricuspid isthmus has been confirmed by
noncontact mapping [28]. The cavotricuspid isthmus is a part of the circuit most
vulnerable to interval-dependent conduction delay [16] and termination of AFL
with ibutilide, propafenone, or amiodarone is due in part to failure of impulse conduction
through this tissue [22]. (See "Overview of catheter ablation of cardiac arrhythmias",
section on 'Noncontact mapping'.)
The typical AFL circuit has been thought to run anterior to the superior vena cava (SVC)
in most patients [29]. However, a study of 15 patients with typical flutter using
noncontact and entrainment mapping showed that the posterior wall was a part of the
circuit in seven patients [30]. In a study of 50 patients using entrainment mapping,
between one-quarter to one-third did not use the atrial roof anterior to the SVC as part of
the circuit [31]. These studies imply that the crista terminalis is not always a fixed barrier
to conduction and the circuit can be posterior to the SVC.
Partial isthmus atrial flutter is a type of typical flutter where a wavefront goes between
the IVC and coronary sinus ostium after conducting through the posterior cavo-tricuspid-
isthmus (CTI). This wavefront then conducts around the CS ostium and up the septum,
but also goes retrograde back into the anterior CTI. For this circuit to occur, there must
either be a pectinate muscle that breaks the CTI into an anterior and posterior portion
[32] or rapid conduction through the eustachian ridge [26].
Intra-isthmus reentry is usually seen in those with prior CTI ablation [33]. The circuit is
contained entirely within the CTI and may be in the septal, medial, or anterior portions,
with areas of long fractionated potentials the best target for ablation [33].
The circuit for lower loop reentry circles around the IVC, on the septal side usually
between the IVC and coronary sinus ostium [34]. It exits out on the low lateral wall, with
wavefront one conducting up the lateral wall and wavefront two going through the CTI,
anterior to the coronary sinus ostium, and up the septal wall in a manner similar to
counterclockwise typical flutter. The two wave fronts collide somewhere in the lateral
right atrium or septum, but the dominant circuit still encircles the IVC. Lower loop reentry
frequently morphs into counterclockwise AFL and may be associated with an atrial
myopathy [5].
Atypical right atrial flutters
Lesion macroreentrant tachycardia — An atriotomy scar or suture line can act as an
obstacle to conduction and create reentry. There may also be atrial septal defect
patches that can lead to an atypical flutter circuit. In addition, scar from congenital heart
disease lesions such as after an atrial level switch surgery (Mustard or Senning repairs)
for transposition of the great arteries or after a Fontan repair may lead to atypical
flutters. (See "Management of complications in patients with Fontan circulation", section
on 'Arrhythmias'.)
Atriotomy scar-related atypical flutters are the most common of this type, where the scar
is vertical along the lateral right atrium. The anterior right atrial wall may have ascending
or descending activation depending on whether the circuit is clockwise or
counterclockwise, while the septum may have more variable conduction [3]. The circuit
wraps around the incision, with the upper turnaround point between the scar and SVC
and the lower turnaround point between the scar and IVC. Alternatively, one of the
turnaround points may be through an area of conduction within the scar. As is true for all
flutters, entrainment and activation mapping are helpful for defining the circuit. The
atriotomy region will have double potentials and low voltage to denote its location.
During flutter, the double potentials are more widely spaced in the center of the scar and
usually become one single fractionated electrogram at the turnaround points.
Typical flutter may be seen after ablation of this atypical flutter, if a prior cavotricuspid
isthmus ablation has not previously been completed.
Nonatriotomy-related right atrial flutter — For unexplained reasons, some patients

will have areas of low voltage in the right atrium. This may lead to a scar similar to an
atriotomy lesion, even though there has been no cardiac incision. This leads to a flutter
wrapping around the scar, though may also be a figure-8 reentry if there is conduction
through the low voltage area [32]. Ablation from the lower border of the scar to the IVC
frequently terminates the arrhythmia.
Upper loop reentry — This circuit crosses through a conduction gap in the crista
terminalis in the upper right atrium, which is where the successful site of ablation can be
[35]. It can be clockwise or counterclockwise, with activation going up or down the
anterior right atrial free wall. At least one patient also demonstrated successful ablation
in the region between the fossa ovalis and IVC [32], indicating that this tachycardia
circuit may not be as clearly defined as previously thought.
Atypical left atrial flutters
Post-Maze or atrial fibrillation ablation left atrial flutters — These tachycardias are
most frequently due to incomplete ablation lines from either a transvenous catheter
ablation or a surgical Maze procedure. They may also be related to left atrial fibrosis
seen in those with a history of atrial arrhythmias. They are usually seen in the anterior
wall, through the roof, or on the septum. Mapping can often be difficult due to low
voltages. (See "Surgical ablation to prevent recurrent atrial fibrillation", section on 'Maze
procedure'.)
Mitral annular flutter wraps around the mitral valve clockwise or counterclockwise
[36,37]. Entrainment from a catheter in the coronary sinus will frequently demonstrate
concealed entrainment on all poles for mitral annular flutter, but not for other left atrial
flutters. It can be difficult to terminate and often needs ablation within the coronary sinus
to achieve a line of block [38]. Even in the presence of apparent complete block, there
may still be recurrence of mitral flutter as there may only be significant conduction
slowing rather than block [39].
Left atrial macroreentry — Less commonly, atypical flutters can occur in those with no
prior ablation or surgery in the left atrium. They may be located on the anterior or
posterior wall and are bounded by an anatomic obstacle like the mitral annulus [40].
They may be a single circuit or double loop and are associated with low voltage signals
with areas of fractionated signals [41].
Atrioventricular node and the ventricular response — The electrophysiologic events
in AFL can be viewed as an input (the F waves) and an output (QRS complexes) that is
processed through a regulator or black box (the atrioventricular [AV] node). The
electrophysiologic characteristics of the AV node, which is a "slow response" tissue in
comparison to the atria, primarily determine the ventricular response. (See "The
electrocardiogram in atrial fibrillation".)
As noted below (see 'Electrophysiologic features' above), the ventricular response in
AFL is generally one-half the atrial input, resulting in a ventricular rate of about 150
beats/min. 3:1 and 4:1 input/output ratios are also relatively common, leading to
ventricular rates of about 100 and 75 beats/min, respectively. Thus, AFL should be
considered whenever the electrocardiogram shows a heart rate of 150, 100, and 75
beats/min.
Rarely, the input/output ratio is 1:1, resulting in a ventricular response of nearly 300
beats/min. This may occur in states characterized by marked catecholamine excess and
in the presence of AV bypass tracts with preexcitation (waveform 1). A 1:1 response is
more commonly seen when the atrial rate is slowed and AV nodal conduction is
enhanced, leading to ventricular rates of 220 to 250 beats/min. This combination can be
induced by class IA or IC antiarrhythmic drugs (table 1) due to:
●Slowing of the conduction velocity in the reentrant circuit and therefore the
flutter rate by inhibition of sodium channels.
●Increasing AV nodal conduction by their vagolytic effects.
These characteristics have implications for management. (See "Control of ventricular
rate in atrial flutter".)
Partial or complete block in the AV node or in the specialized infranodal conduction

system (His bundle, bundle branches and fascicles, and terminal Purkinje fibers) may
lead to escape or accelerated rhythms from within the AV node or below to assume
control of the ventricles. The ventricular rate in this setting may be normal, faster, or
slower than is normal for these lower pacemakers.
The diagnosis of complete heart block may be missed if F waves are not carefully
matched with R waves or when the lower escape rate approaches an arithmetic divisor
of the flutter rate. As is true for atrial fibrillation, there may be a Wenckebach type of exit
block around such an escape site, resulting in group beating. (See "The
electrocardiogram in atrial fibrillation", section on 'Effect of high degrees of
atrioventricular nodal block and exit block on ventricular response'.)
ELECTROCARDIOGRAPHIC FEATURES The electrocardiographic
features of typical atrial flutter (AFL) in the presence of normal atrioventricular (AV)

nodal conduction are (waveform 2):
●P waves are absent.
●For counterclockwise typical AFL, biphasic "sawtooth" flutter waves (F
waves) are present at a rate of about 300 beats/min, with the range being 240
to 340 beats/min [1].
●The F waves are fairly regular on the surface electrocardiogram with constant
amplitude, duration, morphology, and reproducibility throughout the cardiac
cycles. There can be very subtle variability, however, as spectral analysis has
detected an underlying periodic pattern modulated by an interplay between the
autonomic nervous system, respiratory system, and ventricular rate [42].
●The F waves usually do not have an isoelectric interval between them (ie, the
F waves blend into one another) unless the rate of the AFL is slow.
●In counterclockwise typical AFL, the F waves have an axis of around 90º
and are prominently negative in the inferior leads (II, III, aVF). The F waves
often have an initial slowly downsloping segment followed by a sharp negative
deflection, then a sharp positive deflection that may have a positive overshoot
leading into the next downward deflection (waveform 2). With 2:1 flutter, there
is commonly a negative deflection superimposed on the ST segment, giving
the appearance of ST depression related to myocardial ischemia.
●In clockwise typical AFL (reverse typical AFL), the F waves are usually
positive in the inferior leads due to an opposite direction of atrial activation, but
there is significant heterogeneity in the F wave morphology [3]. The F wave
may even have a sine wave pattern. The deflection in V1 is often broad and
negative (waveform 3) (panel B).
●The ventricular response (R-R intervals) is usually one-half the rate of the
atrial input (ie, 2:1 AV nodal conduction with a ventricular response of about
150 beats/min). This finding is sufficiently common and the diagnosis of AFL
should be considered whenever the ventricular rate is about 150 beats/min.
AV block greater than 2:1 in the absence of drugs that slow the ventricular
response suggests AV nodal disease and the possibility of associated sinus
node disease, which may be part of the tachy-brady syndrome.
A 1:1 AV response suggests accessory bypass tracts, sympathetic excess,
parasympathetic withdrawal, or class IC antiarrhythmic agents. Even ratios of
input to output (eg, 2:1, 4:1) are more common than odd numbers (eg, 3:1,
5:1). Odd ratios and shifting ratios (eg, alteration of 2:1 with 4:1) probably
reflect bilevel block in the AV node.
●The QRS complex is narrow unless there is functional aberration, preexisting
bundle branch or fascicular block, preexcitation, or ventricular pacing.
The electrocardiographic features of atypical AFL are:
●F waves are regular, but in contrast to typical AFL, there may be an
isoelectric appearance between F waves if there is an area of significantly
slowed conduction.
●There is no clear F wave morphology to identify the location consistently, as
atypical flutters are often associated with atrial scar that can alter conduction
velocity and direction. That said, some patterns described below may be seen.
●Lower loop reentry typically has negative F waves in the inferior leads
(waveform 4). Upper loop reentry has positive F waves in the inferior leads
and negative, flat, or barely positive F waves in lead I [43].
●Intra-isthmus reentry will appear like typical counterclockwise AFL.
●If there is a negative F wave in V1, the flutter is usually in the right atrium
(waveform 5).
●Left atrial flutters have variable morphologies, but may have a positive F
wave in V1 or may be isoelectric (waveform 6) [5]. It is often positive in the
inferior leads, but not always (waveform 7).
●Counterclockwise mitral annular flutter is positive in V1-6 and the inferior
leads and negative in aVL [44]. Clockwise mitral annular flutter is positive in
the right precordial leads but usually negative and then positive in the lateral
precordial leads (waveform 8). It is negative in the inferior leads and positive in
I and aVL.
Morphology of the QRS complex — Activation through the AV node and infranodal
conduction system is normal in AFL, so the QRS complex is narrow unless:
●A preexisting conduction defect is present.
●Functional block occurs in a portion of the infranodal conduction system,
leading to a bundle branch or fascicular block. The refractory period of the
bundle branches and fascicles is determined by the preceding cycle length. A
long preceding cycle lengthens the refractory period in these structures, so a
premature beat is more likely to be functionally blocked after a long cycle,
known as Ashman's phenomenon.
●Preexcitation through an AV bypass tract is present.
●Ventricular pacing is present.
Pitfalls — The electrocardiographic criteria listed above are usually sufficient to make
the proper diagnosis; there are, however, potential pitfalls:
●One of the F waves may be obscured by the QRS complex or the ST-T wave
(waveform 9) in patients with 2:1 AV nodal conduction. In this setting, AFL
may be misdiagnosed as a sinus tachycardia or a paroxysmal supraventricular
tachycardia with downsloping ST depression.
●In clockwise, typical flutter, the F waves may be positive, and if every other F
wave is obscured, it may be mistaken for a long RP tachycardia such as sinus
tachycardia, ectopic atrial tachycardia, atypical AV nodal reentrant
tachycardia, or AV reciprocating tachycardia.
●The atrial electrical potential may be small and the F waves may be difficult to
see in the standard leads. Sometimes it may be necessary to increase the
gain of the electrocardiogram to see the F waves more clearly (ie, 20 mm/mV).
●Atrial fibrillation, especially with coarse fibrillatory waves in lead V1, is often
misdiagnosed as AFL [45]. Examination of a rhythm strip will often show that
the atrial fibrillatory rate and morphology change over a period of time. We
discourage using the term AFL-fibrillation, since the rhythm more closely
resembles atrial fibrillation in its response to drugs that slow AV nodal
conduction and in the higher energy requirement for direct current
cardioversion.
●Sometimes the negative F wave merges with the beginning or end of the
QRS complex, suggesting a pathologic Q wave in the first case and a
conduction delay in the second. Likewise, the F wave may appear to cause
pathologic ST-segment depression.
●The F wave morphology may appear atypical in those with congenital heart
disease, atrial fibrosis, following cardiac surgery, or after left atrial ablation for
atrial fibrillation even though the rhythm is typical flutter [46,47]. Prior
extensive ablation in the left atrium may alter the morphology of F waves in
typical AFL, due to reductions in left atrial potentials and changes in the atrial
activation sequence. This was illustrated in a series of 15 patients who had
undergone circumferential left atrial ablation for the treatment of atrial
fibrillation and later developed typical AFL (12 counterclockwise, 3 clockwise)
[47]. In 9 of 15 cases, the F waves were upright in the inferior leads, including
7 of 12 of typical counterclockwise flutter.
●Electrocardiography and telemetry artifacts caused by tremor [48] or
electromagnetic interference [49,50] may suggest the occurrence of AFL, but
this “pseudo-atrial flutter” will be revealed when the tremor or interference
ceases.
DIFFERENTIAL DIAGNOSIS The differential diagnosis of atrial flutter
(AFL) includes a number of supraventricular tachyarrhythmias. (See "Focal atrial

tachycardia" and "Intraatrial reentrant tachycardia" and "Sinoatrial nodal reentrant
tachycardia (SANRT)" and "Cardiac arrhythmias due to digoxin toxicity" and "Multifocal
atrial tachycardia" and "Atrioventricular nodal reentrant tachycardia" and "Narrow QRS
complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on
'Types of narrow QRS complex tachycardia'.)
As noted above, obscured atrial activity or F waves that resemble normal or inverted P
waves may suggest sinus tachycardia, paroxysmal supraventricular tachycardia, or atrial
fibrillation.
There are four major ways to help establish the correct diagnosis:
●An earlier electrocardiogram, if available, may allow comparison of the F or

presumed P wave with the previous P wave morphology.
●Scrutiny of the ST-segment and T waves may show a bump or irregularity
caused by a second flutter wave.
●Decreasing atrioventricular (AV) nodal conduction physiologically with a
vagotonic maneuver (such as the Valsalva maneuver or carotid sinus
massage) or with a rapidly acting drug (such as adenosine, verapamil,
or esmolol) will increase the AV nodal block and reveal the atrial F waves
(waveform 9).
●Recording from an atrial catheter, atrial pacing wire, or an esophageal
electrode will also demonstrate the regular atrial activity (waveform 10).
Even with these maneuvers, ectopic atrial tachycardia and other supraventricular
tachycardias with 2:1 block may remain in the differential diagnosis. Furthermore, two
types of arrhythmia can occur in the same patient, as a supraventricular tachycardia can
initiate AFL or atrial fibrillation.
An example of this difficulty occurs when AFL has a slow ventricular response that
overlaps with the rate seen in other supraventricular tachycardias. If, for example, the
patient is taking digitalis for flutter, then an atrial tachycardia with a 2:1 AV response that
reflects a high degree of digitalis toxicity must be excluded. Treatment of these two
disorders is clearly different, and atrial morphology may be of little help in identifying the
underlying arrhythmia. In this setting, establishment of the correct diagnosis may
depend upon the clinical history, plasma digoxin levels, and the response following
cessation of digoxin therapy.
As noted above, complete heart block may be difficult to recognize in the presence of
AFL. The presence of F waves and a regular rate of the lower pacemaker may lead to
the appearance of an uncomplicated AFL.
MANAGEMENT The control of ventricular rate and the approach to
anticoagulant therapy for patient with atrial flutter is discussed elsewhere.

(See "Overview of atrial flutter" and "Embolic risk and the role of anticoagulation in atrial
flutter".)
Cardioversion in patients with atrial flutter is discussed separately. (See "Restoration of
sinus rhythm in atrial flutter".)
The approach to the maintenance of sinus rhythm and the impact of electrophysiologic
type is discussed separately. (See "Atrial flutter: Maintenance of sinus
rhythm" and "Atrial flutter: Maintenance of sinus rhythm", section on 'RF catheter
ablation'.)
SUMMARY Atrial flutter (AFL) is a supraventricular tachycardia with regular
flutter waves and usually an absent isoelectric interval. The rhythm is due to
macroreentry, has an excitable gap, and can be transiently entrained and terminated by
rapid atrial pacing. Electrocardiographic characteristics include:
●Biphasic, sawtooth F waves, best seen in the inferior electrocardiogram leads
(II, III, aVF), at about 300 beats/min are the classic finding for typical,
counterclockwise AFL.
●The ventricular response is a multiple of the atrial rate, though most
frequently is 2:1 with a ventricular rate of 150 beats/min.
●Flutter waves may sometimes be obscured in the QRS complex in 2:1
conduction.
●Typical AFL most frequently rotates counterclockwise posterior to the
tricuspid valve and uses the critical region of the cavotricuspid isthmus within
the circuit. Clockwise, typical AFL uses the same circuit, but rotates in the
opposite direction.
●Atypical AFL is any flutter that does not involve the cavotricuspid isthmus.
The flutter wave morphology does not have a characteristic pattern to localize
the flutter circuit.
REFERENCES
1. Wells JL Jr, MacLean WA, James TN, Waldo AL. Characterization of atrial
flutter. Studies in man after open heart surgery using fixed atrial electrodes.
2. Puech P, Latour H, Grolleau R. [Flutter and his limits]. Arch Mal Coeur Vaiss
1970; 63:116.
3. Saoudi N, Cosío F, Waldo A, et al. A classification of atrial flutter and regular
atrial tachycardia according to electrophysiological mechanisms and
anatomical bases; a Statement from a Joint Expert Group from The Working
Group of Arrhythmias of the European Society of Cardiology and the North
American Society of Pacing and Electrophysiology. Eur Heart J 2001;
22:1162.
5. Bun SS, Latcu DG, Marchlinski F, Saoudi N. Atrial flutter: more than just one
of a kind. Eur Heart J 2015; 36:2356.
6. Khairy P, Aboulhosn J, Gurvitz MZ, et al. Arrhythmia burden in adults with
surgically repaired tetralogy of Fallot: a multi-institutional study. Circulation
2010; 122:868.
7. Peuch P, Gallay P, Grolleau R. Mechanism of atrial flutter in humans. In:
Atrial Arrhythmias: Current Concepts and Management, Tourboul P, Waldo
AL (Eds), Mosby Year Book, St Louis 1990. p.190.
8. Klein GJ, Guiraudon GM, Sharma AD, Milstein S. Demonstration of
macroreentry and feasibility of operative therapy in the common type of
atrial flutter. Am J Cardiol 1986; 57:587.
9. Cosio FG, Arribas F, Barbero JM, et al. Validation of double-spike
electrograms as markers of conduction delay or block in atrial flutter. Am J
Cardiol 1988; 61:775.
10. Tai CT, Chen SA, Chiang CE, et al. Characterization of low right atrial
isthmus as the slow conduction zone and pharmacological target in typical
atrial flutter. Circulation 1997; 96:2601.
11. Kalman JM, Olgin JE, Saxon LA, et al. Activation and entrainment mapping
defines the tricuspid annulus as the anterior barrier in typical atrial flutter.
12. Disertori M, Inama G, Vergara G, et al. Evidence of a reentry circuit in the
common type of atrial flutter in man. Circulation 1983; 67:434.
13. Waldo AL, MacLean WA, Karp RB, et al. Entrainment and interruption of
atrial flutter with atrial pacing: studies in man following open heart surgery.
14. Watson RM, Josephson ME. Atrial flutter. I. Electrophysiologic substrates
and modes of initiation and termination. Am J Cardiol 1980; 45:732.
15. Inoue H, Matsuo H, Takayanagi K, Murao S. Clinical and experimental
studies of the effects of atrial extrastimulation and rapid pacing on atrial
flutter cycle. Evidence of macro-reentry with an excitable gap. Am J Cardiol
1981; 48:623.
16. Callans DJ, Schwartzman D, Gottlieb CD, et al. Characterization of the
excitable gap in human type I atrial flutter. J Am Coll Cardiol 1997; 30:1793.
17. Waldo AL, Cooper TB. Spontaneous onset of type I atrial flutter in patients.
18. Waldo AL. Mechanisms of atrial flutter and atrial fibrillation: distinct entities
or two sides of a coin? Cardiovasc Res 2002; 54:217.
19. Roithinger FX, Karch MR, Steiner PR, et al. Relationship between atrial
fibrillation and typical atrial flutter in humans: activation sequence changes
during spontaneous conversion. Circulation 1997; 96:3484.
20. Narayan SM, Bode F, Karasik PL, Franz MR. Alternans of atrial action
potentials during atrial flutter as a precursor to atrial fibrillation. Circulation
2002; 106:1968.
21. Morton JB, Byrne MJ, Power JM, et al. Electrical remodeling of the atrium in
an anatomic model of atrial flutter: relationship between substrate and
triggers for conversion to atrial fibrillation. Circulation 2002; 105:258.
22. Franz MR, Karasik PL, Li C, et al. Electrical remodeling of the human
atrium: similar effects in patients with chronic atrial fibrillation and atrial
23. Stiles MK, Wong CX, John B, et al. Characterization of atrial remodeling
studied remote from episodes of typical atrial flutter. Am J Cardiol 2010;
106:528.
24. Sparks PB, Jayaprakash S, Vohra JK, Kalman JM. Electrical remodeling of
the atria associated with paroxysmal and chronic atrial flutter. Circulation
2000; 102:1807.
25. Kalman JM, Olgin JE, Saxon LA, et al. Electrocardiographic and
electrophysiologic characterization of atypical atrial flutter in man: use of
activation and entrainment mapping and implications for catheter ablation. J
Cardiovasc Electrophysiol 1997; 8:121.
26. Nakagawa H, Lazzara R, Khastgir T, et al. Role of the tricuspid annulus and
the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of
the septal isthmus and a new technique for rapid identification of ablation
success. Circulation 1996; 94:407.
27. Cosio FG, López-Gil M, Goicolea A, et al. Radiofrequency ablation of the
inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J
Cardiol 1993; 71:705.
28. Schilling RJ, Peters NS, Goldberger J, et al. Characterization of the
anatomy and conduction velocities of the human right atrial flutter circuit
determined by noncontact mapping. J Am Coll Cardiol 2001; 38:385.
29. Shah DC, Jaïs P, Haïssaguerre M, et al. Three-dimensional mapping of the
common atrial flutter circuit in the right atrium. Circulation 1997; 96:3904.
30. Dixit S, Lavi N, Robinson M, et al. Noncontact electroanatomic mapping to
characterize typical atrial flutter: participation of right atrial posterior wall in
the reentrant circuit. J Cardiovasc Electrophysiol 2011; 22:422.
31. Maury P, Duparc A, Hebrard A, et al. Prevalence of typical atrial flutter with
reentry circuit posterior to the superior vena cava: use of entrainment at the
atrial roof. Europace 2008; 10:190.
32. Yang Y, Cheng J, Bochoeyer A, et al. Atypical right atrial flutter patterns.
33. Yang Y, Varma N, Badhwar N, et al. Prospective observations in the clinical
and electrophysiological characteristics of intra-isthmus reentry. J
34. Cheng J, Cabeen WR Jr, Scheinman MM. Right atrial flutter due to lower
loop reentry: mechanism and anatomic substrates. Circulation 1999;
99:1700.
35. Tai CT, Huang JL, Lin YK, et al. Noncontact three-dimensional mapping and
ablation of upper loop re-entry originating in the right atrium. J Am Coll
Cardiol 2002; 40:746.
36. Wasmer K, Mönnig G, Bittner A, et al. Incidence, characteristics, and
outcome of left atrial tachycardias after circumferential antral ablation of
atrial fibrillation. Heart Rhythm 2012; 9:1660.
37. Chae S, Oral H, Good E, et al. Atrial tachycardia after circumferential
pulmonary vein ablation of atrial fibrillation: mechanistic insights, results of
catheter ablation, and risk factors for recurrence. J Am Coll Cardiol 2007;
50:1781.
38. Bai R, Di Biase L, Mohanty P, et al. Ablation of perimitral flutter following
catheter ablation of atrial fibrillation: impact on outcomes from a randomized
study (PROPOSE). J Cardiovasc Electrophysiol 2012; 23:137.
39. Miyazaki S, Shah AJ, Hocini M, et al. Recurrent spontaneous clinical
perimitral atrial tachycardia in the context of atrial fibrillation ablation. Heart
Rhythm 2015; 12:104.
40. Zhang J, Tang C, Zhang Y, et al. Electroanatomic characterization and
ablation outcome of nonlesion related left atrial macroreentrant tachycardia
in patients without obvious structural heart disease. J Cardiovasc
41. Fukamizu S, Sakurada H, Hayashi T, et al. Macroreentrant atrial tachycardia
in patients without previous atrial surgery or catheter ablation: clinical and
electrophysiological characteristics of scar-related left atrial anterior wall
reentry. J Cardiovasc Electrophysiol 2013; 24:404.
42. Stambler BS, Ellenbogen KA. Elucidating the mechanisms of atrial flutter
cycle length variability using power spectral analysis techniques. Circulation
1996; 94:2515.
43. Yuniadi Y, Tai CT, Lee KT, et al. A new electrocardiographic algorithm to
differentiate upper loop re-entry from reverse typical atrial flutter. J Am Coll
Cardiol 2005; 46:524.
44. Gerstenfeld EP, Dixit S, Bala R, et al. Surface electrocardiogram
characteristics of atrial tachycardias occurring after pulmonary vein isolation.
Heart Rhythm 2007; 4:1136.
45. Knight BP, Michaud GF, Strickberger SA, Morady F. Electrocardiographic
differentiation of atrial flutter from atrial fibrillation by physicians. J
Electrocardiol 1999; 32:315.
46. Khairy P, Stevenson WG. Catheter ablation in tetralogy of Fallot. Heart
Rhythm 2009; 6:1069.
47. Chugh A, Latchamsetty R, Oral H, et al. Characteristics of cavotricuspid
isthmus-dependent atrial flutter after left atrial ablation of atrial fibrillation.
48. Baranchuk A, Kang J. Pseudo-atrial flutter: Parkinson tremor. Cardiol J
2009; 16:373.
49. Chakravarthy M, Mattur K, Raghavan R, et al. Artifactual 'atrial flutter'
caused by a continuous passive motion device after total knee replacement.
Anaesth Intensive Care 2009; 37:1038.
50. Hoffmayer KS, Goldschlager N. Pseudoatrial flutter. J Electrocardiol 2008;
41:201.
Close
 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 SUMMARY
 INTRODUCTION
 CLASSIFICATION
 ELECTROPHYSIOLOGIC FEATURES
o Typical flutters
o Atypical right atrial flutters
 Lesion macroreentrant tachycardia
 Nonatriotomy-related right atrial flutter
 Upper loop reentry
o Atypical left atrial flutters
 Post-Maze or atrial fibrillation ablation left atrial flutters
 Left atrial macroreentry
o Atrioventricular node and the ventricular response
 ELECTROCARDIOGRAPHIC FEATURES
o Morphology of the QRS complex
o Pitfalls
 MANAGEMENT
 SUMMARY
 REFERENCES
GRAPHICS view all
 Figures
 Tables
 Waveforms
oECG atrial flutter preexcitation
oTypical atrial flutter
oReverse typical atrial flutter
oECG in lower loop reentry flutter
oECG atriotomy-related right atrial flutter after mitral repair
oECG atypical left AFL through scar anterior septum prior AF
oECG atypical roof dependent left AFL after AF ablation
oECG of a patient with clockwise mitral annular flutter
oAtrial flutter RA recording
RELATED TOPICS
 Atrial fibrillation and flutter after cardiac surgery
 Atrial flutter: Maintenance of sinus rhythm
 Control of ventricular rate in atrial flutter
 Management of complications in patients with Fontan circulation
Electrocardiographic and electrophysiologic features

of atrial flutter
Author:
Section Editors:
Deputy Editor:
Literature review current through: Sep 2020. | This topic last updated: Mar 28, 2019.
INTRODUCTION Atrial flutter (AFL) is an abnormal cardiac rhythm
characterized by rapid, regular atrial depolarizations at a typical atrial rate of 250 to 350
beats per minute. There is frequently 2:1 conduction across the atrioventricular (AV)
node, meaning that every other atrial depolarization reaches the ventricles. As a result,
the ventricular rate is usually one-half the AFL rate in the absence of AV node
dysfunction. AFL is classified as typical or atypical based on whether the flutter circuit
traverses the cavotricuspid isthmus in the right atrium [1].
Other topic reviews discuss the clinical aspects of AFL. (See "Overview of atrial
flutter" and "Restoration of sinus rhythm in atrial flutter" and "Control of ventricular rate in
atrial flutter" and "Atrial flutter: Maintenance of sinus rhythm" and "Embolic risk and the
role of anticoagulation in atrial flutter" and "Atrial fibrillation and flutter after cardiac
surgery".)
CLASSIFICATION The first classification scheme in 1970 defined atrial flutter
(AFL) as "common" or "atypical," depending on whether the flutter wave had a negative
sawtooth pattern in the inferior leads [2]. A few years later, the terms types I and II were
created to describe flutter [1]. Type I AFL was classified as a macroreentrant atrial
tachycardia while type II AFL was considered unclassified because the mechanisms
were not fully understood.
A 2001 working group from Europe and North America tried to reconcile new data from
electrophysiology studies and activation mapping [3]. Flutter was defined as a regular
tachycardia ≥240 beats/min with no isoelectric baseline between atrial deflections.
Typical and reversal typical flutter were characterized, as described below, and all other
flutters were atypical.
An American College of Cardiology, American Heart Association, and Heart Rhythm
Society guideline on the management of supraventricular tachycardia reaffirmed the
classification of AFL into cavo-tricuspid-isthmus (CTI)-dependent ("typical") versus non-
CTI dependent ("atypical") [4] and this is the methodology currently used.
Typical AFL is a macroreentrant atrial tachycardia, with the inferior border of the circuit
traversing the isthmus of tissue between the inferior vena cava and tricuspid annulus as
a necessary component. AFL involving this cavotricuspid isthmus is referred to as
"typical" or "isthmus-dependent" flutter.
In the most common form of CTI-dependent flutter, the reentrant circuit rotates around
the tricuspid annulus in a counterclockwise direction when the heart is viewed in a left
anterior oblique projection, traversing up the septum and down the lateral wall. This is
the arrhythmia associated with the classic electrocardiogram finding of sawtooth flutter
waves in the inferior leads. (See 'Electrocardiographic features' below.)
Less often, the reentrant circuit rotates in the opposite direction. This arrhythmia is
called "clockwise" or "reverse" typical flutter.
Atypical AFL is an intraatrial reentrant tachycardia or AFL that does not involve the CTI.
It may be a lesion macroreentrant tachycardia, lower or upper loop flutter, intra-isthmus
reentry, non-atriotomy-related right atrial flutter, left atrial macroreentry, post-Maze or
atrial fibrillation ablation left atrial flutters, or mitral annular flutter [5]. It is frequently seen
in those who have had prior cardiac surgery, prior intracardiac ablation, congenital heart
disease, or cardiomyopathy but may also be idiopathic. Atypical flutter may be in the
right or left atrium and usually revolves around a prior incisional or idiopathic scar,
ablation lesion set, or other fixed anatomic barriers. If there has been an incomplete
ablation line from a prior procedure, this can increase the chances of an atypical flutter.
Many patients with congenital heart disease, especially with more complex disease or
surgical repairs, will present with atypical flutter [6]. Some patients with idiopathic atrial
fibrosis will also present with scar-based atypical flutters.
ELECTROPHYSIOLOGIC FEATURES Electrophysiologic studies, using
entrainment mapping and electroanatomic mapping, have been used to define the atrial
flutter (AFL) circuit in the electrophysiology laboratory and at surgery [7-11].
The principal electrophysiologic features of AFL are:
●Reentry
●Excitable gap
●Transient entrainment and termination by rapid atrial pacing
Electrophysiologically, AFL is a reentrant arrhythmia in that it excites an area of the
atrium and then travels sufficiently slowly in a pathway that is long enough such that the
initially excited area recovers its excitability and is reactivated [7-9,12-15]. Either a single
premature extrastimulus or rapid atrial pacing can initiate AFL and, because there is an
excitable gap, terminate the arrhythmia [13-15]. The excitable gap is the portion of a
reentrant circuit that has recovered its excitability and can again be depolarized,
allowing for entrainment with overdrive pacing during AFL [13,14,16]. (See "Reentry and
the development of cardiac arrhythmias", section on 'Definition and characteristics'.)
Typical AFL commonly starts after a transitional rhythm of variable duration, usually
atrial fibrillation [17,18]. It has been postulated that a fundamental feature that
determines whether an atrial arrhythmia becomes sustained typical AFL or atrial
fibrillation is the development of a line of functional refractoriness or block between the
vena cavae [18]. In spontaneous typical AFL, the critical line of functional block between
the vena cavae may be created by transient atrial fibrillation. This line of block results in
unidirectional block and stable AFL follows. According to this theory, if the line of
functional block is not created, atrial fibrillation persists or the rhythm reverts back to
sinus.
Another view, based in part on a small electrophysiologic study of 10 patients,
emphasizes the anatomic barriers as well as the properties of conduction and
refractoriness during atrial fibrillation to explain the usual pattern observed with typical
AFL [19]. In the electrophysiology laboratory, premature electrical stimulation may
function in a manner similar to the transitional atrial fibrillation in forming the critical
functional line of block between the vena cavae [18].
An additional determinant of whether the transitional atrial tachyarrhythmia becomes
AFL or atrial fibrillation may be the cycle length of the flutter [18]. If the cycle length is
critically short, it will create fibrillatory conduction and atrial fibrillation.
Lastly, the electrical properties of the isthmus may also be a factor in the tendency for
AFL to disorganize into atrial fibrillation in some patients [20].
Similar to what has been reported in atrial fibrillation, AFL results in electrical remodeling
of the atrial myocardium, perhaps accounting for the observation that untreated AFL can
eventually lead to atrial fibrillation [21]. In contrast to the normal situation in which the
atrial refractory period shortens with an increase in rate and prolongs when the rate
decreases, the refractory period fails to lengthen appropriately at slow rates (eg, with
return to sinus rhythm) in patients with AFL present for a mean of 8.5 months (range 1 to
32 months) [22]. This abnormality persists for at least 30 minutes after cardioversion to
sinus rhythm; the duration of AFL has no significant impact upon the magnitude of these
electrophysiologic changes. Those with a history of AFL, but not fibrillation, have
significant changes in the electrophysiologic properties of the right atrium, even when
they are in normal sinus rhythm. The right atrium is more likely to be enlarged, have
lower voltage suggesting scar, longer P wave duration, and slowed conduction velocity
most prominent in the lower right atrium, and sinus node dysfunction [23].
The duration of AFL does impact the time course of electrical remodeling recovery after
arrhythmia termination. As an example, one study of 25 patients with paroxysmal or
chronic flutter (average duration 17 months) found that, in those with paroxysmal AFL,
the refractory period shortened after a 5- to 10-minute period of flutter and reversed
within five minutes of restoration of sinus rhythm; atrial fibrillation developed in some
patients when the refractory period was at its nadir [24]. In patients with chronic AFL, the
atrial refractory period increased during the first three weeks after resumption of sinus
rhythm.
Typical flutters — A large macroreentrant circuit in the right atrium is involved in typical
AFL.
If one begins the cycle at the end of the negative deflection of the F wave in lead II, the
impulse at that point exists in the low right atrial septum between the inferior vena cava
(IVC) and the tricuspid valve.
In counterclockwise typical flutter, the impulse then travels anteriorly through the region
of the low septum, ascends superiorly and anteriorly up the septal and posterior walls of
the right atrium, and returns or descends over the anterior and lateral free wall (figure 1)
[25]. This circuit is then completed through the region between the tricuspid valve and
IVC (counterclockwise reentry). A reverse direction of rotation (clockwise reentry,
ascending the anterior wall, and descending the posterior and septal walls) is seen in
reverse typical AFL [3,25].
The crista terminalis (and its continuation as the eustachian ridge) and IVC commonly
form the posterior barrier, while the tricuspid annulus constitutes the anterior barrier of
the circuit (figure 1) [11,26]. This has potential clinical implications, since this region can
be a target for ablation therapy in patients with refractory AFL [26,27]. (See "Atrial flutter:
Maintenance of sinus rhythm", section on 'RF catheter ablation'.)
The presence of slow conduction in the cavotricuspid isthmus has been confirmed by
noncontact mapping [28]. The cavotricuspid isthmus is a part of the circuit most
vulnerable to interval-dependent conduction delay [16] and termination of AFL
with ibutilide, propafenone, or amiodarone is due in part to failure of impulse conduction
through this tissue [22]. (See "Overview of catheter ablation of cardiac arrhythmias",
section on 'Noncontact mapping'.)
The typical AFL circuit has been thought to run anterior to the superior vena cava (SVC)
in most patients [29]. However, a study of 15 patients with typical flutter using
noncontact and entrainment mapping showed that the posterior wall was a part of the
circuit in seven patients [30]. In a study of 50 patients using entrainment mapping,
between one-quarter to one-third did not use the atrial roof anterior to the SVC as part of
the circuit [31]. These studies imply that the crista terminalis is not always a fixed barrier
to conduction and the circuit can be posterior to the SVC.
Partial isthmus atrial flutter is a type of typical flutter where a wavefront goes between
the IVC and coronary sinus ostium after conducting through the posterior cavo-tricuspid-
isthmus (CTI). This wavefront then conducts around the CS ostium and up the septum,
but also goes retrograde back into the anterior CTI. For this circuit to occur, there must
either be a pectinate muscle that breaks the CTI into an anterior and posterior portion
[32] or rapid conduction through the eustachian ridge [26].
Intra-isthmus reentry is usually seen in those with prior CTI ablation [33]. The circuit is
contained entirely within the CTI and may be in the septal, medial, or anterior portions,
with areas of long fractionated potentials the best target for ablation [33].
The circuit for lower loop reentry circles around the IVC, on the septal side usually
between the IVC and coronary sinus ostium [34]. It exits out on the low lateral wall, with
wavefront one conducting up the lateral wall and wavefront two going through the CTI,
anterior to the coronary sinus ostium, and up the septal wall in a manner similar to
counterclockwise typical flutter. The two wave fronts collide somewhere in the lateral
right atrium or septum, but the dominant circuit still encircles the IVC. Lower loop reentry
frequently morphs into counterclockwise AFL and may be associated with an atrial
myopathy [5].
Atypical right atrial flutters
Lesion macroreentrant tachycardia — An atriotomy scar or suture line can act as an
obstacle to conduction and create reentry. There may also be atrial septal defect
patches that can lead to an atypical flutter circuit. In addition, scar from congenital heart
disease lesions such as after an atrial level switch surgery (Mustard or Senning repairs)
for transposition of the great arteries or after a Fontan repair may lead to atypical
flutters. (See "Management of complications in patients with Fontan circulation", section
on 'Arrhythmias'.)
Atriotomy scar-related atypical flutters are the most common of this type, where the scar
is vertical along the lateral right atrium. The anterior right atrial wall may have ascending
or descending activation depending on whether the circuit is clockwise or
counterclockwise, while the septum may have more variable conduction [3]. The circuit
wraps around the incision, with the upper turnaround point between the scar and SVC
and the lower turnaround point between the scar and IVC. Alternatively, one of the
turnaround points may be through an area of conduction within the scar. As is true for all
flutters, entrainment and activation mapping are helpful for defining the circuit. The
atriotomy region will have double potentials and low voltage to denote its location.
During flutter, the double potentials are more widely spaced in the center of the scar and
usually become one single fractionated electrogram at the turnaround points.
Typical flutter may be seen after ablation of this atypical flutter, if a prior cavotricuspid
isthmus ablation has not previously been completed.
Nonatriotomy-related right atrial flutter — For unexplained reasons, some patients

will have areas of low voltage in the right atrium. This may lead to a scar similar to an
atriotomy lesion, even though there has been no cardiac incision. This leads to a flutter
wrapping around the scar, though may also be a figure-8 reentry if there is conduction
through the low voltage area [32]. Ablation from the lower border of the scar to the IVC
frequently terminates the arrhythmia.
Upper loop reentry — This circuit crosses through a conduction gap in the crista
terminalis in the upper right atrium, which is where the successful site of ablation can be
[35]. It can be clockwise or counterclockwise, with activation going up or down the
anterior right atrial free wall. At least one patient also demonstrated successful ablation
in the region between the fossa ovalis and IVC [32], indicating that this tachycardia
circuit may not be as clearly defined as previously thought.
Atypical left atrial flutters
Post-Maze or atrial fibrillation ablation left atrial flutters — These tachycardias are
most frequently due to incomplete ablation lines from either a transvenous catheter
ablation or a surgical Maze procedure. They may also be related to left atrial fibrosis
seen in those with a history of atrial arrhythmias. They are usually seen in the anterior
wall, through the roof, or on the septum. Mapping can often be difficult due to low
voltages. (See "Surgical ablation to prevent recurrent atrial fibrillation", section on 'Maze
procedure'.)
Mitral annular flutter wraps around the mitral valve clockwise or counterclockwise
[36,37]. Entrainment from a catheter in the coronary sinus will frequently demonstrate
concealed entrainment on all poles for mitral annular flutter, but not for other left atrial
flutters. It can be difficult to terminate and often needs ablation within the coronary sinus
to achieve a line of block [38]. Even in the presence of apparent complete block, there
may still be recurrence of mitral flutter as there may only be significant conduction
slowing rather than block [39].
Left atrial macroreentry — Less commonly, atypical flutters can occur in those with no
prior ablation or surgery in the left atrium. They may be located on the anterior or
posterior wall and are bounded by an anatomic obstacle like the mitral annulus [40].
They may be a single circuit or double loop and are associated with low voltage signals
with areas of fractionated signals [41].
Atrioventricular node and the ventricular response — The electrophysiologic events
in AFL can be viewed as an input (the F waves) and an output (QRS complexes) that is
processed through a regulator or black box (the atrioventricular [AV] node). The
electrophysiologic characteristics of the AV node, which is a "slow response" tissue in
comparison to the atria, primarily determine the ventricular response. (See "The
electrocardiogram in atrial fibrillation".)
As noted below (see 'Electrophysiologic features' above), the ventricular response in
AFL is generally one-half the atrial input, resulting in a ventricular rate of about 150
beats/min. 3:1 and 4:1 input/output ratios are also relatively common, leading to
ventricular rates of about 100 and 75 beats/min, respectively. Thus, AFL should be
considered whenever the electrocardiogram shows a heart rate of 150, 100, and 75
beats/min.
Rarely, the input/output ratio is 1:1, resulting in a ventricular response of nearly 300
beats/min. This may occur in states characterized by marked catecholamine excess and
in the presence of AV bypass tracts with preexcitation (waveform 1). A 1:1 response is
more commonly seen when the atrial rate is slowed and AV nodal conduction is
enhanced, leading to ventricular rates of 220 to 250 beats/min. This combination can be
induced by class IA or IC antiarrhythmic drugs (table 1) due to:
●Slowing of the conduction velocity in the reentrant circuit and therefore the
flutter rate by inhibition of sodium channels.
●Increasing AV nodal conduction by their vagolytic effects.
These characteristics have implications for management. (See "Control of ventricular
rate in atrial flutter".)
Partial or complete block in the AV node or in the specialized infranodal conduction

system (His bundle, bundle branches and fascicles, and terminal Purkinje fibers) may
lead to escape or accelerated rhythms from within the AV node or below to assume
control of the ventricles. The ventricular rate in this setting may be normal, faster, or
slower than is normal for these lower pacemakers.
The diagnosis of complete heart block may be missed if F waves are not carefully
matched with R waves or when the lower escape rate approaches an arithmetic divisor
of the flutter rate. As is true for atrial fibrillation, there may be a Wenckebach type of exit
block around such an escape site, resulting in group beating. (See "The
electrocardiogram in atrial fibrillation", section on 'Effect of high degrees of
atrioventricular nodal block and exit block on ventricular response'.)
ELECTROCARDIOGRAPHIC FEATURES The electrocardiographic
features of typical atrial flutter (AFL) in the presence of normal atrioventricular (AV)

nodal conduction are (waveform 2):
●For counterclockwise typical AFL, biphasic "sawtooth" flutter waves (F
waves) are present at a rate of about 300 beats/min, with the range being 240
to 340 beats/min [1].
●The F waves are fairly regular on the surface electrocardiogram with constant
amplitude, duration, morphology, and reproducibility throughout the cardiac
cycles. There can be very subtle variability, however, as spectral analysis has
detected an underlying periodic pattern modulated by an interplay between the
autonomic nervous system, respiratory system, and ventricular rate [42].
●The F waves usually do not have an isoelectric interval between them (ie, the
F waves blend into one another) unless the rate of the AFL is slow.
●In counterclockwise typical AFL, the F waves have an axis of around 90º
and are prominently negative in the inferior leads (II, III, aVF). The F waves
often have an initial slowly downsloping segment followed by a sharp negative
deflection, then a sharp positive deflection that may have a positive overshoot
leading into the next downward deflection (waveform 2). With 2:1 flutter, there
is commonly a negative deflection superimposed on the ST segment, giving
the appearance of ST depression related to myocardial ischemia.
●In clockwise typical AFL (reverse typical AFL), the F waves are usually
positive in the inferior leads due to an opposite direction of atrial activation, but
there is significant heterogeneity in the F wave morphology [3]. The F wave
may even have a sine wave pattern. The deflection in V1 is often broad and
negative (waveform 3) (panel B).
●The ventricular response (R-R intervals) is usually one-half the rate of the
atrial input (ie, 2:1 AV nodal conduction with a ventricular response of about
150 beats/min). This finding is sufficiently common and the diagnosis of AFL
should be considered whenever the ventricular rate is about 150 beats/min.
AV block greater than 2:1 in the absence of drugs that slow the ventricular
response suggests AV nodal disease and the possibility of associated sinus
node disease, which may be part of the tachy-brady syndrome.
A 1:1 AV response suggests accessory bypass tracts, sympathetic excess,
parasympathetic withdrawal, or class IC antiarrhythmic agents. Even ratios of
input to output (eg, 2:1, 4:1) are more common than odd numbers (eg, 3:1,
5:1). Odd ratios and shifting ratios (eg, alteration of 2:1 with 4:1) probably
reflect bilevel block in the AV node.
●The QRS complex is narrow unless there is functional aberration, preexisting
bundle branch or fascicular block, preexcitation, or ventricular pacing.
The electrocardiographic features of atypical AFL are:
●F waves are regular, but in contrast to typical AFL, there may be an
isoelectric appearance between F waves if there is an area of significantly
slowed conduction.
●There is no clear F wave morphology to identify the location consistently, as
atypical flutters are often associated with atrial scar that can alter conduction
velocity and direction. That said, some patterns described below may be seen.
●Lower loop reentry typically has negative F waves in the inferior leads
(waveform 4). Upper loop reentry has positive F waves in the inferior leads
and negative, flat, or barely positive F waves in lead I [43].
●Intra-isthmus reentry will appear like typical counterclockwise AFL.
●If there is a negative F wave in V1, the flutter is usually in the right atrium
(waveform 5).
●Left atrial flutters have variable morphologies, but may have a positive F
wave in V1 or may be isoelectric (waveform 6) [5]. It is often positive in the
inferior leads, but not always (waveform 7).
●Counterclockwise mitral annular flutter is positive in V1-6 and the inferior
leads and negative in aVL [44]. Clockwise mitral annular flutter is positive in
the right precordial leads but usually negative and then positive in the lateral
precordial leads (waveform 8). It is negative in the inferior leads and positive in
I and aVL.
Morphology of the QRS complex — Activation through the AV node and infranodal
conduction system is normal in AFL, so the QRS complex is narrow unless:
●A preexisting conduction defect is present.
●Functional block occurs in a portion of the infranodal conduction system,
leading to a bundle branch or fascicular block. The refractory period of the
bundle branches and fascicles is determined by the preceding cycle length. A
long preceding cycle lengthens the refractory period in these structures, so a
premature beat is more likely to be functionally blocked after a long cycle,
known as Ashman's phenomenon.
●Preexcitation through an AV bypass tract is present.
●Ventricular pacing is present.
Pitfalls — The electrocardiographic criteria listed above are usually sufficient to make
the proper diagnosis; there are, however, potential pitfalls:
●One of the F waves may be obscured by the QRS complex or the ST-T wave
(waveform 9) in patients with 2:1 AV nodal conduction. In this setting, AFL
may be misdiagnosed as a sinus tachycardia or a paroxysmal supraventricular
tachycardia with downsloping ST depression.
●In clockwise, typical flutter, the F waves may be positive, and if every other F
wave is obscured, it may be mistaken for a long RP tachycardia such as sinus
tachycardia, ectopic atrial tachycardia, atypical AV nodal reentrant
tachycardia, or AV reciprocating tachycardia.
●The atrial electrical potential may be small and the F waves may be difficult to
see in the standard leads. Sometimes it may be necessary to increase the
gain of the electrocardiogram to see the F waves more clearly (ie, 20 mm/mV).
●Atrial fibrillation, especially with coarse fibrillatory waves in lead V1, is often
misdiagnosed as AFL [45]. Examination of a rhythm strip will often show that
the atrial fibrillatory rate and morphology change over a period of time. We
discourage using the term AFL-fibrillation, since the rhythm more closely
resembles atrial fibrillation in its response to drugs that slow AV nodal
conduction and in the higher energy requirement for direct current
cardioversion.
●Sometimes the negative F wave merges with the beginning or end of the
QRS complex, suggesting a pathologic Q wave in the first case and a
conduction delay in the second. Likewise, the F wave may appear to cause
pathologic ST-segment depression.
●The F wave morphology may appear atypical in those with congenital heart
disease, atrial fibrosis, following cardiac surgery, or after left atrial ablation for
atrial fibrillation even though the rhythm is typical flutter [46,47]. Prior
extensive ablation in the left atrium may alter the morphology of F waves in
typical AFL, due to reductions in left atrial potentials and changes in the atrial
activation sequence. This was illustrated in a series of 15 patients who had
undergone circumferential left atrial ablation for the treatment of atrial
fibrillation and later developed typical AFL (12 counterclockwise, 3 clockwise)
[47]. In 9 of 15 cases, the F waves were upright in the inferior leads, including
7 of 12 of typical counterclockwise flutter.
●Electrocardiography and telemetry artifacts caused by tremor [48] or
electromagnetic interference [49,50] may suggest the occurrence of AFL, but
this “pseudo-atrial flutter” will be revealed when the tremor or interference
ceases.
DIFFERENTIAL DIAGNOSIS The differential diagnosis of atrial flutter
(AFL) includes a number of supraventricular tachyarrhythmias. (See "Focal atrial

tachycardia" and "Intraatrial reentrant tachycardia" and "Sinoatrial nodal reentrant
tachycardia (SANRT)" and "Cardiac arrhythmias due to digoxin toxicity" and "Multifocal
atrial tachycardia" and "Atrioventricular nodal reentrant tachycardia" and "Narrow QRS
complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on
'Types of narrow QRS complex tachycardia'.)
As noted above, obscured atrial activity or F waves that resemble normal or inverted P
waves may suggest sinus tachycardia, paroxysmal supraventricular tachycardia, or atrial
fibrillation.
There are four major ways to help establish the correct diagnosis:
●An earlier electrocardiogram, if available, may allow comparison of the F or

presumed P wave with the previous P wave morphology.
●Scrutiny of the ST-segment and T waves may show a bump or irregularity
caused by a second flutter wave.
●Decreasing atrioventricular (AV) nodal conduction physiologically with a
vagotonic maneuver (such as the Valsalva maneuver or carotid sinus
massage) or with a rapidly acting drug (such as adenosine, verapamil,
or esmolol) will increase the AV nodal block and reveal the atrial F waves
(waveform 9).
●Recording from an atrial catheter, atrial pacing wire, or an esophageal
electrode will also demonstrate the regular atrial activity (waveform 10).
Even with these maneuvers, ectopic atrial tachycardia and other supraventricular
tachycardias with 2:1 block may remain in the differential diagnosis. Furthermore, two
types of arrhythmia can occur in the same patient, as a supraventricular tachycardia can
initiate AFL or atrial fibrillation.
An example of this difficulty occurs when AFL has a slow ventricular response that
overlaps with the rate seen in other supraventricular tachycardias. If, for example, the
patient is taking digitalis for flutter, then an atrial tachycardia with a 2:1 AV response that
reflects a high degree of digitalis toxicity must be excluded. Treatment of these two
disorders is clearly different, and atrial morphology may be of little help in identifying the
underlying arrhythmia. In this setting, establishment of the correct diagnosis may
depend upon the clinical history, plasma digoxin levels, and the response following
cessation of digoxin therapy.
As noted above, complete heart block may be difficult to recognize in the presence of
AFL. The presence of F waves and a regular rate of the lower pacemaker may lead to
the appearance of an uncomplicated AFL.
MANAGEMENT The control of ventricular rate and the approach to
anticoagulant therapy for patient with atrial flutter is discussed elsewhere.

(See "Overview of atrial flutter" and "Embolic risk and the role of anticoagulation in atrial
flutter".)
Cardioversion in patients with atrial flutter is discussed separately. (See "Restoration of
sinus rhythm in atrial flutter".)
The approach to the maintenance of sinus rhythm and the impact of electrophysiologic
type is discussed separately. (See "Atrial flutter: Maintenance of sinus
rhythm" and "Atrial flutter: Maintenance of sinus rhythm", section on 'RF catheter
ablation'.)
SUMMARY Atrial flutter (AFL) is a supraventricular tachycardia with regular
flutter waves and usually an absent isoelectric interval. The rhythm is due to
macroreentry, has an excitable gap, and can be transiently entrained and terminated by
rapid atrial pacing. Electrocardiographic characteristics include:
●Biphasic, sawtooth F waves, best seen in the inferior electrocardiogram leads
(II, III, aVF), at about 300 beats/min are the classic finding for typical,
counterclockwise AFL.
●The ventricular response is a multiple of the atrial rate, though most
frequently is 2:1 with a ventricular rate of 150 beats/min.
●Flutter waves may sometimes be obscured in the QRS complex in 2:1
conduction.
●Typical AFL most frequently rotates counterclockwise posterior to the
tricuspid valve and uses the critical region of the cavotricuspid isthmus within
the circuit. Clockwise, typical AFL uses the same circuit, but rotates in the
opposite direction.
●Atypical AFL is any flutter that does not involve the cavotricuspid isthmus.
The flutter wave morphology does not have a characteristic pattern to localize
the flutter circuit.
REFERENCES
1. Wells JL Jr, MacLean WA, James TN, Waldo AL. Characterization of atrial
flutter. Studies in man after open heart surgery using fixed atrial electrodes.
2. Puech P, Latour H, Grolleau R. [Flutter and his limits]. Arch Mal Coeur Vaiss
1970; 63:116.
3. Saoudi N, Cosío F, Waldo A, et al. A classification of atrial flutter and regular
atrial tachycardia according to electrophysiological mechanisms and
anatomical bases; a Statement from a Joint Expert Group from The Working
Group of Arrhythmias of the European Society of Cardiology and the North
American Society of Pacing and Electrophysiology. Eur Heart J 2001;
22:1162.
5. Bun SS, Latcu DG, Marchlinski F, Saoudi N. Atrial flutter: more than just one
of a kind. Eur Heart J 2015; 36:2356.
6. Khairy P, Aboulhosn J, Gurvitz MZ, et al. Arrhythmia burden in adults with
surgically repaired tetralogy of Fallot: a multi-institutional study. Circulation
2010; 122:868.
7. Peuch P, Gallay P, Grolleau R. Mechanism of atrial flutter in humans. In:
Atrial Arrhythmias: Current Concepts and Management, Tourboul P, Waldo
AL (Eds), Mosby Year Book, St Louis 1990. p.190.
8. Klein GJ, Guiraudon GM, Sharma AD, Milstein S. Demonstration of
macroreentry and feasibility of operative therapy in the common type of
atrial flutter. Am J Cardiol 1986; 57:587.
9. Cosio FG, Arribas F, Barbero JM, et al. Validation of double-spike
electrograms as markers of conduction delay or block in atrial flutter. Am J
Cardiol 1988; 61:775.
10. Tai CT, Chen SA, Chiang CE, et al. Characterization of low right atrial
isthmus as the slow conduction zone and pharmacological target in typical
atrial flutter. Circulation 1997; 96:2601.
11. Kalman JM, Olgin JE, Saxon LA, et al. Activation and entrainment mapping
defines the tricuspid annulus as the anterior barrier in typical atrial flutter.
12. Disertori M, Inama G, Vergara G, et al. Evidence of a reentry circuit in the
common type of atrial flutter in man. Circulation 1983; 67:434.
13. Waldo AL, MacLean WA, Karp RB, et al. Entrainment and interruption of
atrial flutter with atrial pacing: studies in man following open heart surgery.
14. Watson RM, Josephson ME. Atrial flutter. I. Electrophysiologic substrates
and modes of initiation and termination. Am J Cardiol 1980; 45:732.
15. Inoue H, Matsuo H, Takayanagi K, Murao S. Clinical and experimental
studies of the effects of atrial extrastimulation and rapid pacing on atrial
flutter cycle. Evidence of macro-reentry with an excitable gap. Am J Cardiol
1981; 48:623.
16. Callans DJ, Schwartzman D, Gottlieb CD, et al. Characterization of the
excitable gap in human type I atrial flutter. J Am Coll Cardiol 1997; 30:1793.
17. Waldo AL, Cooper TB. Spontaneous onset of type I atrial flutter in patients.
18. Waldo AL. Mechanisms of atrial flutter and atrial fibrillation: distinct entities
or two sides of a coin? Cardiovasc Res 2002; 54:217.
19. Roithinger FX, Karch MR, Steiner PR, et al. Relationship between atrial
fibrillation and typical atrial flutter in humans: activation sequence changes
during spontaneous conversion. Circulation 1997; 96:3484.
20. Narayan SM, Bode F, Karasik PL, Franz MR. Alternans of atrial action
potentials during atrial flutter as a precursor to atrial fibrillation. Circulation
2002; 106:1968.
21. Morton JB, Byrne MJ, Power JM, et al. Electrical remodeling of the atrium in
an anatomic model of atrial flutter: relationship between substrate and
triggers for conversion to atrial fibrillation. Circulation 2002; 105:258.
22. Franz MR, Karasik PL, Li C, et al. Electrical remodeling of the human
atrium: similar effects in patients with chronic atrial fibrillation and atrial
23. Stiles MK, Wong CX, John B, et al. Characterization of atrial remodeling
studied remote from episodes of typical atrial flutter. Am J Cardiol 2010;
106:528.
24. Sparks PB, Jayaprakash S, Vohra JK, Kalman JM. Electrical remodeling of
the atria associated with paroxysmal and chronic atrial flutter. Circulation
2000; 102:1807.
25. Kalman JM, Olgin JE, Saxon LA, et al. Electrocardiographic and
electrophysiologic characterization of atypical atrial flutter in man: use of
activation and entrainment mapping and implications for catheter ablation. J
26. Nakagawa H, Lazzara R, Khastgir T, et al. Role of the tricuspid annulus and
the eustachian valve/ridge on atrial flutter. Relevance to catheter ablation of
the septal isthmus and a new technique for rapid identification of ablation
success. Circulation 1996; 94:407.
27. Cosio FG, López-Gil M, Goicolea A, et al. Radiofrequency ablation of the
inferior vena cava-tricuspid valve isthmus in common atrial flutter. Am J
Cardiol 1993; 71:705.
28. Schilling RJ, Peters NS, Goldberger J, et al. Characterization of the
anatomy and conduction velocities of the human right atrial flutter circuit
determined by noncontact mapping. J Am Coll Cardiol 2001; 38:385.
29. Shah DC, Jaïs P, Haïssaguerre M, et al. Three-dimensional mapping of the
common atrial flutter circuit in the right atrium. Circulation 1997; 96:3904.
30. Dixit S, Lavi N, Robinson M, et al. Noncontact electroanatomic mapping to
characterize typical atrial flutter: participation of right atrial posterior wall in
the reentrant circuit. J Cardiovasc Electrophysiol 2011; 22:422.
31. Maury P, Duparc A, Hebrard A, et al. Prevalence of typical atrial flutter with
reentry circuit posterior to the superior vena cava: use of entrainment at the
atrial roof. Europace 2008; 10:190.
32. Yang Y, Cheng J, Bochoeyer A, et al. Atypical right atrial flutter patterns.
33. Yang Y, Varma N, Badhwar N, et al. Prospective observations in the clinical
and electrophysiological characteristics of intra-isthmus reentry. J
34. Cheng J, Cabeen WR Jr, Scheinman MM. Right atrial flutter due to lower
loop reentry: mechanism and anatomic substrates. Circulation 1999;
99:1700.
35. Tai CT, Huang JL, Lin YK, et al. Noncontact three-dimensional mapping and
ablation of upper loop re-entry originating in the right atrium. J Am Coll
Cardiol 2002; 40:746.
36. Wasmer K, Mönnig G, Bittner A, et al. Incidence, characteristics, and
outcome of left atrial tachycardias after circumferential antral ablation of
atrial fibrillation. Heart Rhythm 2012; 9:1660.
37. Chae S, Oral H, Good E, et al. Atrial tachycardia after circumferential
pulmonary vein ablation of atrial fibrillation: mechanistic insights, results of
catheter ablation, and risk factors for recurrence. J Am Coll Cardiol 2007;
50:1781.
38. Bai R, Di Biase L, Mohanty P, et al. Ablation of perimitral flutter following
catheter ablation of atrial fibrillation: impact on outcomes from a randomized
study (PROPOSE). J Cardiovasc Electrophysiol 2012; 23:137.
39. Miyazaki S, Shah AJ, Hocini M, et al. Recurrent spontaneous clinical
perimitral atrial tachycardia in the context of atrial fibrillation ablation. Heart
Rhythm 2015; 12:104.
40. Zhang J, Tang C, Zhang Y, et al. Electroanatomic characterization and
ablation outcome of nonlesion related left atrial macroreentrant tachycardia
in patients without obvious structural heart disease. J Cardiovasc
41. Fukamizu S, Sakurada H, Hayashi T, et al. Macroreentrant atrial tachycardia
in patients without previous atrial surgery or catheter ablation: clinical and
electrophysiological characteristics of scar-related left atrial anterior wall
reentry. J Cardiovasc Electrophysiol 2013; 24:404.
42. Stambler BS, Ellenbogen KA. Elucidating the mechanisms of atrial flutter
cycle length variability using power spectral analysis techniques. Circulation
1996; 94:2515.
43. Yuniadi Y, Tai CT, Lee KT, et al. A new electrocardiographic algorithm to
differentiate upper loop re-entry from reverse typical atrial flutter. J Am Coll
Cardiol 2005; 46:524.
44. Gerstenfeld EP, Dixit S, Bala R, et al. Surface electrocardiogram
characteristics of atrial tachycardias occurring after pulmonary vein isolation.
45. Knight BP, Michaud GF, Strickberger SA, Morady F. Electrocardiographic
differentiation of atrial flutter from atrial fibrillation by physicians. J
Electrocardiol 1999; 32:315.
46. Khairy P, Stevenson WG. Catheter ablation in tetralogy of Fallot. Heart
Rhythm 2009; 6:1069.
47. Chugh A, Latchamsetty R, Oral H, et al. Characteristics of cavotricuspid
isthmus-dependent atrial flutter after left atrial ablation of atrial fibrillation.
48. Baranchuk A, Kang J. Pseudo-atrial flutter: Parkinson tremor. Cardiol J
2009; 16:373.
49. Chakravarthy M, Mattur K, Raghavan R, et al. Artifactual 'atrial flutter'
caused by a continuous passive motion device after total knee replacement.
Anaesth Intensive Care 2009; 37:1038.
50. Hoffmayer KS, Goldschlager N. Pseudoatrial flutter. J Electrocardiol 2008;
41:201.
Close
 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®
 CME5.0
 Log Out

 Contents
 Calculators


Find

 Patient

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 INTRODUCTION
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 ARRHYTHMIAS ASSOCIATED WITH ARRHYTHMIA-INDUCED CARDIOMYOPATHY
o Supraventricular arrhythmias
 Atrial fibrillation and atrial flutter
 Atrial tachycardia
 Reentrant supraventricular tachycardias
o Ventricular arrhythmias
o Frequent ectopic beats
 Frequent ventricular ectopy
 Frequent atrial ectopy
 CLINICAL PRESENTATION
o Signs and symptoms
o ECG findings
 APPROACH TO THE DIAGNOSIS
 DIAGNOSTIC TESTING
o Cardiac monitoring
o Assessment of cardiac structure and function
o Excluding other causes of cardiomyopathy
 TREATMENT
o Patients with atrial fibrillation or flutter
o Patients with another SVT
o Patients with frequent ectopy
o Patients with refractory tachyarrhythmias
 FOLLOW-UP
 PROGNOSIS
 REFERENCES
GRAPHICS view all
 Tables
oTachy mediated CM treatment
RELATED TOPICS
 Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and clinical manifestations
 Atrial tachyarrhythmias in children
 Cardiac resynchronization therapy in atrial fibrillation
 Cardiac resynchronization therapy in heart failure: Indications
 Causes of dilated cardiomyopathy
 Definition and classification of the cardiomyopathies
 Determining the etiology and severity of heart failure or cardiomyopathy
 Evaluation of the patient with suspected heart failure
 Hemodynamic consequences of atrial fibrillation and cardioversion to sinus rhythm
 Hypertrophic cardiomyopathy: Prevalence, pathophysiology, and management of concurrent atrial
arrhythmias
 Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac death
 Nutritional antioxidants in atherosclerotic cardiovascular disease
 Overview of the management of heart failure with reduced ejection fraction in adults
 Patient education: Atrial fibrillation (Beyond the Basics)
 Patient education: Catheter ablation for abnormal heartbeats (Beyond the Basics)
 Premature ventricular complexes: Treatment and prognosis
 Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with
reduced LVEF
 Society guideline links: Cardiac implantable electronic devices
 Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy
Arrhythmia-induced cardiomyopathy
Author:
Cynthia M Tracy, MD
Section Editor:
William J McKenna, MD
Deputy Editor:
Susan B Yeon, MD, JD, FACC
INTRODUCTION Cardiomyopathies are diseases of the heart muscle,
inclusive of a variety of myocardial disorders that manifest with various structural and
functional phenotypes and are frequently genetic. Although some have defined
cardiomyopathy to include myocardial disease caused by known cardiovascular causes
(such as hypertension, ischemic heart disease, or valvular disease), current major
society definitions of cardiomyopathy exclude heart disease secondary to such
cardiovascular disorders [1,2]. (See "Definition and classification of the
cardiomyopathies" and "Causes of dilated cardiomyopathy".)
The prognosis in patients with dilated cardiomyopathy is variable and dependent on the
cause; importantly, there are some etiologies that may improve or resolve following
treatment. One such cause is an arrhythmia-induced cardiomyopathy (also known as
tachycardia-induced cardiomyopathy, tachycardia-mediated cardiomyopathy, and
tachymyopathy), a relatively rare though well-recognized entity caused by long-standing
tachycardia, which in most instances is readily treatable with a good prognosis [3].
Arrhythmia-induced cardiomyopathy has been reported with nearly all types of
tachyarrhythmias and frequent ectopy, both supraventricular and ventricular [4].
A common clinical problem is determining whether the tachycardia is the primary cause
of the patient's cardiomyopathy, or if the tachycardia is secondary to a cardiomyopathy
of different etiology. This topic will discuss arrhythmia-induced cardiomyopathy as a
primary cause of cardiomyopathy. Arrhythmias occurring in the setting of a specific
cardiomyopathy are discussed separately. (See "Hypertrophic cardiomyopathy:
Prevalence, pathophysiology, and management of concurrent atrial
arrhythmias" and "Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac
death" and "Arrhythmogenic right ventricular cardiomyopathy: Anatomy, histology, and
clinical manifestations", section on 'Ventricular arrhythmias'.)
EPIDEMIOLOGY While the exact incidence of arrhythmia-induced
cardiomyopathy remains unclear, an association between tachycardia and

cardiomyopathy has been recognized for some time [5-8]. Virtually every form of
supraventricular tachyarrhythmia, including ectopic atrial tachycardia, nonparoxysmal
junctional tachycardia, and atrial fibrillation (AF), has been associated with reversible left
ventricular dysfunction or "cardiomyopathy." The development of a cardiomyopathy has
also been documented with ventricular tachyarrhythmias and frequent ectopic beats [9-
11]. (See "Hemodynamic consequences of atrial fibrillation and cardioversion to sinus
rhythm" and 'Frequent ectopic beats' below.)
Some insight into the prevalence of arrhythmia-induced cardiomyopathy can be derived

from cohort studies of patients undergoing catheter ablation for symptomatic
arrhythmias. As examples:
●Among a cohort of 331 patients who were referred for catheter ablation of
incessant atrial tachycardia (AT), myocardial dysfunction was present in 9
percent of patients [12]. Patients with an arrhythmia-induced cardiomyopathy
were younger (mean age 39 versus 51 years), more frequently male (60
versus 38 percent), and had incessant or very frequent paroxysmal
tachycardia (100 versus 20 percent).
●Among a cohort of 625 patients undergoing catheter ablation for a variety of
tachyarrhythmias, a tachycardia-induced cardiomyopathy was present in 2.7
percent (17 of 625 patients) [13].
●Among a cohort of 1269 patients undergoing ablation for atrial flutter, 184 had
reduced ejection fractions (<40 percent) at baseline [14].
PATHOPHYSIOLOGY Chronic tachycardia ultimately produces significant
cardiac structural changes, including left ventricular dilatation and cellular morphologic
changes [15-19]. However, the exact mechanism by which tachycardia produces these
changes is not well defined.
Animal models, initially developed in the general investigation of heart failure (HF), have
been studied extensively in the evaluation of arrhythmia-induced cardiomyopathy. Rapid
pacing produces changes in animals that are similar to those observed in humans,
including a marked depression of left ventricular ejection fraction (LVEF), elevated filling
pressures, depressed cardiac output, and increased systemic vascular resistance [16-
18,20-24]. These changes are generally reversible with cessation of the tachycardia,
although in some cases LVEF may not return to baseline [24,25]. Similar findings have
been reported in an animal model following the delivery of ventricular premature beats in
a bigeminal pattern for 12 weeks, which resulted in left ventricular dilatation and
reduction in LVEF [26].
The morphologic and biochemical changes that result from an arrhythmia-induced
cardiomyopathy also may produce electrophysiologic abnormalities. In a canine model,
chronic tachycardia was associated with ventricular arrhythmias (including polymorphic
ventricular tachycardia and sudden death) that result from a prolongation in
repolarization [27].
Many alterations in neurohumoral and cellular activation have been described, and
several factors probably contribute to the development of rate-related myocardial
dysfunction. Although data supporting certain potential mechanisms are compelling, it
remains unclear whether they play an etiologic role or if they arise as a consequence of
tachycardia.
●Depletion of myocardial energy stores and myocardial ischemia –

Studies in animal models have shown that persistent tachycardia depletes
high-energy stores as evidenced by reduced myocardial levels of creatine,
phosphocreatine, and adenosine triphosphate (ATP), and diminished activity
of the Na-K-ATPase pump [28-30]. These changes are probably due to
alterations in cellular metabolism with mitochondrial injury and increased
activity of Krebs cycle oxidative enzymes [15,20].
Myocardial ischemia may play a role in the development of arrhythmia-induced
cardiomyopathy. Similar depletions in high-energy stores are seen in ischemic
models following vessel occlusion, situations where high-energy stores are
rapidly depleted and left ventricular dysfunction occurs [31,32]. High-energy
stores return to normal within days after the ischemic insults. Tachycardia-
induced depletion of high-energy stores, which may be mediated in part by
ischemia, is reversible and may explain the reversibility of this
cardiomyopathy.
Abnormalities in subendocardial to subepicardial flow ratios and impaired
coronary flow have been found in arrhythmia-induced cardiomyopathy [33-36].
The impaired coronary blood flow occurs in association with elevation in
cardiac filling pressures and impaired left ventricular diastolic function
[25,37,38].
●Abnormal calcium handling and beta adrenergic responsiveness –
Abnormalities in both calcium channel activity and sarcoplasmic reticulum
calcium transport may contribute to the myocardial dysfunction in arrhythmia-
induced cardiomyopathy [20,35]. Diminished beta-adrenergic responsiveness
has also been described and may be due to reduced myocyte beta-1 receptor
density (downregulation) [37,39,40]. The reduction in beta receptor density
and responsiveness is independent of hemodynamic and neurohumoral
factors [41].
●Oxidative stress and injury – In patients with atrial fibrillation and atrial
dysfunction, there is histologic evidence of oxidative stress and injury in the
atrial myocardium [42]. This results in peroxynitrite formation, which modifies
myofibrillar proteins, contributes to loss of fibrillar protein function, and alters
myofibrillar energetics.
Support for the role of oxidative stress comes from one animal study which
found that the administration of the antioxidant vitamins E, C, and beta-
carotene attenuated the cardiac dysfunction and prevented beta receptor
downregulation produced by rapid cardiac pacing [43]. (See "Nutritional
antioxidants in atherosclerotic cardiovascular disease".)
●Genetic basis and ACE gene polymorphism – An association has been
reported between a gene polymorphism and arrhythmia-induced
cardiomyopathy. Levels of angiotensin converting enzyme (ACE) are
associated with a 287 base pair insertion (I)/deletion (D) polymorphism in
intron 16 of the ACE gene. The DD genotype is associated with increased
serum ACE levels and a higher incidence of both ischemic and idiopathic
dilated cardiomyopathy. In a study comparing 20 patients with arrhythmia-
induced cardiomyopathy, 20 controls with persistent tachycardia but normal
LV function, and 24 normal volunteers, the DD genotype was significantly
more common in the patients with arrhythmia-induced cardiomyopathy [44].
●Histopathologic and immunologic findings – Among a cohort of 189
patients with new onset HF and reduced ejection fractions not related to
valvular or ischemic heart disease, 19 patients met criteria for tachycardia-
induced cardiomyopathy. Endomyocardial biopsies in the tachycardia-induced
cardiomyopathy patients showed a stronger myocardial expression of major
histocompatibility complex class II molecule and enhanced infiltration of
CD68+ macrophages compared with patients with idiopathic dilated
cardiomyopathy. Compared to patients with ischemic cardiomyopathy, those
with tachycardia induced cardiomyopathy had fewer T cells and macrophages.
Fibrosis was also less prominent in the tachycardia induced cardiomyopathy
patients. However, electron microscopy in these patients showed abnormal
mitochondrial distribution and enhanced myocyte size. RNA expression
analysis showed alterations in metabolic pathways [45].
ARRHYTHMIAS ASSOCIATED WITH ARRHYTHMIA-INDUCED
CARDIOMYOPATHY A number of tachyarrhythmias have been associated
with arrhythmia-induced cardiomyopathy, including atrial fibrillation, atrial flutter, atrial

tachycardia, reentrant supraventricular tachycardias, and ventricular tachycardia [11,46-
60]. In addition, very frequent ectopic beats, both atrial and ventricular, have been
associated with arrhythmia-induced cardiomyopathy. Regardless of the arrhythmia,
therapy to restore normal sinus rhythm or to slow the ventricular rate (or eliminate
ectopy) appears to result in an improvement in left ventricular function (table 1).
However, most descriptive series include only a small number of patients.
Supraventricular arrhythmias
Atrial fibrillation and atrial flutter — Epidemiologic studies have shown that patients
with atrial fibrillation (AF) are at increased risk for HF [61]. In some patients, restoration
of sinus rhythm or control of the rapid ventricular rate markedly improves or even
normalizes the left ventricular ejection fraction (LVEF), indicating that the left ventricular
dysfunction was primarily due to the rapid AF rather than another etiology. Improvement
in left ventricular function is seen with both rhythm and rate control, although it may be
more likely with rhythm control. (See "Hemodynamic consequences of atrial fibrillation
and cardioversion to sinus rhythm".)
There is an association between HF and atrial fibrillation, and it is often not possible to
determine which is causative. Nevertheless, an estimated 25 to 50 percent of patients
with LV dysfunction and AF have some component of arrhythmia-induced
cardiomyopathy [4,62-64].
There are less data on the frequency and predictors of arrhythmia-induced
cardiomyopathy in patients with atrial flutter. In one study of patients undergoing ablation
for atrial flutter, 25 percent had evidence for cardiomyopathy prior to ablation [65]. Of
these, 57 percent had significant improvement in their ejection fraction post ablation.
The only predictor of reversibility of cardiomyopathy in this study was average heart rate.
Similarly, in a cohort of 1269 patients undergoing ablation for atrial flutter, 184 had
reduced LVEF (<40 percent) at baseline. Of these patients with reduced LVEF, 103
patients (56 percent) had marked improvement in LVEF at six months. Those who
experienced improvement in the LVEF had similar survival to patients who did not have
baseline depressed LVEF. Those whose LVEF failed to improve had a three-fold higher
mortality [14].
Atrial tachycardia — Incessant atrial tachycardia (AT), an infrequent cause of
symptomatic supraventricular tachyarrhythmia, can cause myocardial dysfunction in
approximately 10 percent of patients [12]. Children are more likely than adults to present
with arrhythmia-induced cardiomyopathy due to incessant AT. When AT is seen in
adults, it is more commonly associated with another cardiac problem, and distinguishing
the effect of tachycardia from that of the underlying cardiac disease may be difficult.
(See "Focal atrial tachycardia", section on 'Incessant AT resulting in
cardiomyopathy' and "Atrial tachyarrhythmias in children", section on 'Focal atrial
tachycardia and atrial ectopic tachycardia'.)
Incessant AT and ectopic AT have been associated with the development of
cardiomyopathy that can be reversed with restoration of sinus rhythm [46-52]. Improved
techniques for catheter ablation frequently permit definitive therapy for AT, which can
lead to the resolution of myocardial dysfunction with a high degree of success
[12,46,52]. (See "Focal atrial tachycardia", section on 'Treatment of incessant AT'.)
Reentrant supraventricular tachycardias — Reentrant supraventricular tachycardias,
including atrioventricular nodal reentrant tachycardia (AVNRT) and atrioventricular
reciprocating tachycardia (AVRT), are more commonly paroxysmal but can cause a
persistent tachycardia. Cases of arrhythmia-induced cardiomyopathy have been
described with persistent junctional reciprocating tachycardia, accessory pathway
mediated tachycardia (ie, AVRT) and AVNRT [50,54-57]. In the absence of other factors,
the cardiomyopathy related to an incessant reentrant supraventricular tachycardia is
reversible following catheter ablation [55]. (See "Atrioventricular reentrant tachycardia
(AVRT) associated with an accessory pathway" and "Atrioventricular nodal reentrant
tachycardia".)
Ventricular arrhythmias — Only rare reports have described reversible
cardiomyopathy related to ventricular tachycardia (VT) since this arrhythmia is usually
associated with some form of underlying structural heart disease. However, idiopathic
left ventricular tachycardia or right ventricular outflow tract VT can arise in structurally
normal hearts [9,10,54]. In rare cases, these arrhythmias are persistent or repetitive
enough to result in a cardiomyopathy. In one study of patients with repetitive
monomorphic VT and/or ventricular premature beats (PVCs), an arrhythmia-induced
cardiomyopathy was seen in 9 percent, all of which improved with treatment [66]. Similar
to supraventricular arrhythmias, the myopathy usually reverses following ablation of the
arrhythmia [58]. (See "Ventricular tachycardia in the absence of apparent structural
heart disease".)
Unlike monomorphic VT, which can be present and hemodynamically stable for
extended periods of time, polymorphic VT, which is generally an unstable rhythm, and
ventricular fibrillation, a non-perfusing rhythm, are not associated with arrhythmia-
induced cardiomyopathy.
Frequent ectopic beats

Frequent ventricular ectopy — Very frequent ventricular ectopy in the form of PVCs
has been associated with a reversible cardiomyopathy, even in the absence of
sustained ventricular arrhythmias [11,59,66-74]. While most earlier studies defined
"frequent" as greater than 10 percent of overall heartbeats, in contemporary practice a
cutoff of >15 percent of all heartbeats is more commonly used. Although some patients
with similarly high PVC burdens can maintain normal cardiac function, PVC-induced
cardiomyopathy has also been reported in patients with PVC burdens as low as 4 to 5
percent.
●In a prospective observational cohort study of 80 patients (59 percent male,
mean age 53 years) with frequent PVCs (mean PVC burden 22 percent) and
reduced left ventricular ejection fraction (LVEF ≤50 percent) who underwent
catheter ablation, 53 patients (66 percent) had successful long-term
elimination of PVCs, with significant improvement in LVEF and New York
Heart Association (NYHA) functional class [70].
●In a 2014 systematic review and meta-analysis of radiofrequency ablation for
the treatment of idiopathic PVCs originating from the right ventricular outflow
tract, catheter ablation was associated with a significant improvement in LVEF,
though the meta-analysis was limited by significant heterogeneity among the
studies [75]. (See "Premature ventricular complexes: Treatment and
prognosis", section on 'Treatment'.)
In addition to the overall frequency of PVCs, QRS duration, epicardial site of origin of
PVCs, and resulting dyssynchrony all appear to play a role in the development of
cardiomyopathy and are associated with outcomes following catheter ablation. Greater
dyssynchrony increases the risk of cardiomyopathy, wider QRS complexes appear more
likely to result in cardiomyopathy with a lower overall burden of PVCs while also being
associated with longer times to normalization of LV systolic function following ablation,
and epicardial PVC origin also appears to predict delayed LV function recovery [74,76-
80].
Frequent atrial ectopy — Premature atrial complex (PAC; also referred to a premature
atrial beat, premature supraventricular complex, or premature supraventricular beat)
are usually benign, but a high burden of PACs has been associated with a reversible
cardiomyopathy [81,82].
CLINICAL PRESENTATION The clinical presentation of arrhythmia-
induced cardiomyopathy is variable but usually involves signs and/or symptoms related
to the tachyarrhythmia (eg, palpitations, dyspnea, chest discomfort, etc), HF (eg,
dyspnea, edema, weight gain, orthopnea, etc), or both. In our experience, HF symptoms
are more common since patients with symptomatic tachyarrhythmias will frequently seek
medical attention earlier in the course of their care and prior to the development of a
cardiomyopathy. The approach to the patient with suspected arrhythmia-induced
cardiomyopathy includes a thorough history and physical examination, with
appropriately selected tests to establish the diagnosis, assess acuity, severity and
etiology. Several professional societies have issued recommendations for the evaluation
of patients with suspected HF or cardiomyopathy [83-86]. (See "Evaluation of the patient
with suspected heart failure", section on 'Clinical presentation'.)
Signs and symptoms — The clinical presentation of arrhythmia-induced
cardiomyopathy is variable but usually involves symptoms of palpitations or HF. Patients
may present with palpitations or other symptom (eg, dyspnea, chest discomfort) related
to the rapidity or irregularity of their arrhythmia. However, those with more rapid heart
rates typically present with symptoms related to the inappropriate heart rate before
enough time has elapsed to result in a cardiomyopathy. In contrast, patients with
tachycardia but a relatively slower heart rate and no obvious symptoms may have little
or no awareness of the arrhythmia. While such patients without palpitations are
occasionally discovered during a routine medical exam for other reasons, typically they
present with fatigue, decreased exercise tolerance, or symptomatic HF.
(See "Evaluation of the patient with suspected heart failure", section on 'Clinical
presentation'.)
Given that patients with more rapid heart rates often present earlier with symptoms
related to the tachycardia, some investigators have hypothesized that patients with atrial
arrhythmias who subsequently develop arrhythmia-induced cardiomyopathy have slower
overall heart rates than patients who do not develop arrhythmia-induced
cardiomyopathy. Published reports in both adult and pediatric populations support this
hypothesis:
●In a retrospective cohort study of 331 patients who had undergone ablation
for atrial tachycardia (AT), among whom 9 percent presented with evidence of
arrhythmia-induced cardiomyopathy, those with arrhythmia-induced
cardiomyopathy had slower ventricular heart rates during tachycardia
compared with patients who did not have arrhythmia-induced cardiomyopathy
(120 versus 149 beats per minute) [12]. (See "Focal atrial tachycardia",
section on 'Incessant AT resulting in cardiomyopathy'.)
●In a retrospective cohort study of 16 pediatric patients with focal AT, those
with AT arising from the atrial appendages were more likely to be
asymptomatic at presentation, more likely to have a ventricular heart rate less
than 120 beats per minute, and more commonly presented with arrhythmia-
induced cardiomyopathy [87].
ECG findings — All patients should have an electrocardiogram (ECG) to document the
cardiac rhythm and ventricular heart rate. Whenever possible, obtaining prior ECGs can
be extremely helpful to determine whether ambiguous P wave morphologies are related
to the sinus node (as seen on prior tracings) versus an ectopic atrial focus. There are no
specific ECG findings that distinguish patients with and without arrhythmia-induced
cardiomyopathy, and the ECG findings will vary depending upon the underlying
tachyarrhythmia. However, by definition, all patients with an arrhythmia-induced
cardiomyopathy should have a heart rate greater than 100 beats per minute.
APPROACH TO THE DIAGNOSIS Arrhythmia-induced cardiomyopathy is
defined by the presence of a sustained tachycardia (or frequent episodes of tachycardia

or very frequent ectopy) which results in left ventricular (LV) systolic dysfunction.
Determining which of the pathologies (the arrhythmia or the cardiomyopathy) is the
primary pathologic process is key to establishing the diagnosis. Usually the diagnosis of
arrhythmia-induced cardiomyopathy can only be made following a successful trial of
therapy to slow the ventricular rate or to restore sinus rhythm along with the exclusion of
other potential causes of cardiomyopathy.
Patients in whom arrhythmia-induced cardiomyopathy is suspected should undergo

continuous cardiac monitoring for 24 to 48 hours and have non-invasive imaging to
assess cardiac structure and function. For most patients, a transthoracic
echocardiogram is the preferred test for assessing cardiac structure and function due to
its widespread availability and ease of performance; however, cardiac magnetic
resonance (CMR) imaging is a reasonable alternative approach in centers with expertise
in this modality.
DIAGNOSTIC TESTING Once arrhythmia-induced cardiomyopathy is
suspected, appropriately selected tests can help to establish the diagnosis. All of the
following are performed as part of the initial evaluation.
Cardiac monitoring — Heart rate over time should be continuously measured for 24 to
48 hours using inpatient telemetry or ambulatory (Holter) monitoring to document the
average heart rate and, in some cases, provide additional information on the underlying
rhythm [88]. A sustained heart rate greater than 100 beats per minute, and particularly
greater than 120 beats per minutes, is consistent with arrhythmia-induced
cardiomyopathy. Because of the potential reversible nature of arrhythmia-induced
cardiomyopathy, if uncertainty persists regarding the cardiac rhythm, full invasive
electrophysiologic studies may be necessary to establish the underlying cardiac rhythm
and guide the optimal therapy. (See 'Treatment' below and "Invasive diagnostic cardiac
electrophysiology studies".)
Assessment of cardiac structure and function — All patients with suspected
arrhythmia-induced cardiomyopathy should undergo an assessment of cardiac structure
and function to document left ventricular size and function, in particular left ventricular
ejection fraction. Transthoracic echocardiography is the most common and widespread
test for documenting cardiac structure and function, but cardiac magnetic resonance
(CMR) imaging is an alternative approach. While there are no absolute
echocardiographic parameters that can distinguish arrhythmia-induced cardiomyopathy
from other forms of dilated cardiomyopathy, in general, the LV end-diastolic dimension
tends to be smaller in patients with arrhythmia-induced cardiomyopathy [4,89].
CMR may be useful in following patients who have experienced improved ejection
fraction (EF) after treatment of the arrhythmia. CMR demonstration of late gadolinium
enhancement indicating the presence of fibrosis and scar suggests incomplete
resolution [90]. Alternatively, in assessing the underlying cause of arrhythmia-induced
cardiomyopathy, patients in one study with frequent ventricular premature beats who
failed to improve EF after treatment were found to have late gadolinium enhancement
on CMR, and likely the cause of the cardiomyopathy was not purely tachycardia
mediated [91].
Studies have suggested the use of two-dimensional strain echocardiography as a tool to
predict recovery from arrhythmia induced cardiomyopathy [92]. In a study of 71 patients
with presumed tachycardia-induced cardiomyopathy, a lower LVEF at baseline and
higher relative apical longitudinal strain ratio (RALSR) were associated with no recovery
in LVEF during follow-up. However, by multivariate analysis the RALSR was found to be
a significant predictor of functional recovery after the arrhythmia was treated.
Excluding other causes of cardiomyopathy — Patients with newly diagnosed HF
and/or cardiomyopathy require an assessment for genetic and other causes of left
ventricular dysfunction and exclusion of significant underlying coronary heart disease
(CHD). Decisions on the initial use of stress testing or coronary angiography should be
made based on the presence or absence of symptoms suggestive of CHD and the
individual patient's likelihood of CHD. The differential diagnosis of dilated
cardiomyopathy, and the approach to excluding CHD, are discussed in greater detail
separately. While patients with HF and cardiomyopathies of other etiologies may exhibit
rapid heart rates (eg, persistent sinus tachycardia), this can usually be distinguished
from an arrhythmia-induced cardiomyopathy by comparison of ECG findings over time
(eg, sinus P wave morphology) and response to treatment. (See "Causes of dilated
cardiomyopathy" and "Determining the etiology and severity of heart failure or
cardiomyopathy", section on 'Detection of coronary artery disease'.)
TREATMENT The initial treatments for a patient with HF and suspected
arrhythmia-induced cardiomyopathy are the same as those used in most other patients
with HF with reduced ejection fraction (eg, angiotensin converting enzyme [ACE]
inhibitors or angiotensin receptor blockers [ARBs], beta blockers, diuretics) and
tachyarrhythmias (eg, rate-control medications, consideration of antiarrhythmic drugs
and/or cardioversion). However, because of the potential reversible nature of
arrhythmia-induced cardiomyopathy, aggressive efforts should be made to achieve
excellent ventricular heart rate control or to restore sinus rhythm [4]. Additionally, given
the potentially reversible nature of this condition, an adequate trial of therapy is required
prior to assessment of the need for cardiac resynchronization therapy or an implantable
cardioverter-defibrillator. (See "Cardiac resynchronization therapy in heart failure:
Indications" and "Primary prevention of sudden cardiac death in patients with
cardiomyopathy and heart failure with reduced LVEF" and "Overview of the
management of heart failure with reduced ejection fraction in adults", section on
'Pharmacologic therapy'.)
Patients with atrial fibrillation or flutter — For patients with newly recognized atrial
fibrillation (AF) or atrial flutter with a rapid ventricular response, initial therapy is to
promptly achieve rate control through appropriate AV nodal blocking agents and
appropriate anticoagulation. Beyond this step, controversy still exists as to whether rate
control or rhythm control is the optimal therapy:
●For minimally symptomatic patients with AF in whom adequate rate control is
achieved, we continue medical therapy.
●For patients with AF who remain significantly symptomatic or patients in
whom adequate rate control is not achieved with medical therapy alone, we
pursue a rhythm control strategy.
●For patients with atrial flutter, rapid ventricular rates, and newly recognized
depressed ejection fraction (EF), rate control may be difficult to achieve with
medication. Because of this, we perform early electrical cardioversion in these
patients.
Management of AF and/or atrial flutter is geared towards avoidance of thromboembolic
events, reduction of symptoms, and avoidance of arrhythmia-induced cardiomyopathy.
Control of heart rate can be met through either a rate control strategy with
atrioventricular (AV) nodal blocking agents (or ablation and pacer implant in cases of
multiple drug failures) or through maintenance of sinus rhythm (rhythm control strategy).
In patients with AF or atrial flutter resulting in cardiomyopathy that is suspected to be
arrhythmia-induced, heart rate control through either means (rate control or rhythm
control) can be very effective at improving cardiac function [93-95]. Strategies for rate
control versus rhythm control are discussed elsewhere, and choices of agents are
dictated by cardiac structure, underlying pathology, and function. (See "Overview of
atrial fibrillation" and "Restoration of sinus rhythm in atrial flutter", section on
'Indications' and "Rhythm control versus rate control in atrial fibrillation".)
Studies of minimally symptomatic patients with persistent atrial fibrillation have
suggested that a rhythm control strategy does not provide a significant outcomes benefit
compared with a rate control alone, and a rhythm control strategy potentially exposes
the patient to risks of antiarrhythmic therapy [96,97]. Subsequent studies have affirmed
these findings and also demonstrated the challenge in maintaining sinus rhythm in some
patients when using the rhythm control strategy [98-100]. Studies of patients with HF
and AF have also failed to show benefit of a rhythm over a rate control strategy
[101,102]. However, all of these studies were performed in large populations of all
patients with AF and did not distinguish patients with and without arrhythmia-induced
cardiomyopathy.
At initial presentation of the patient with rapid ventricular rates and newly recognized
depressed EF, the concern exists that at least some component is related to arrhythmia-
induced cardiomyopathy. This is particularly suspected in younger patients with severe
symptoms from the AF. A trial of early cardioversion is warranted in these patients with
subsequent monitoring for improvement in cardiac function [103].
Patients with another SVT — For supraventricular tachyarrhythmias (SVTs) other than
AF or atrial flutter that result in arrhythmia-induced cardiomyopathy, restoration of sinus
rhythm is the usual goal. Options for the restoration of sinus rhythm include electrical
cardioversion, antiarrhythmic drugs, and catheter ablation of the arrhythmia. The initial
choice of modality will vary depending upon the underlying SVT as well as the local
expertise and availability of options (ie, some centers do not perform catheter ablation)
but should be made in conjunction with an electrophysiologist experienced in the
treatment of sustained tachyarrhythmias.
Certain SVTs are more amenable to electrical cardioversion (eg, atrioventricular nodal
reentrant tachycardia), while others are often refractory or recurrent following
cardioversion (eg, atrial tachycardia). Often, atrial arrhythmias can be refractory to
antiarrhythmics, and AV nodal blocking agents may be required in high doses to achieve
appropriate heart rates. In patients with depressed left ventricular ejection fraction
(LVEF), it is important to avoid agents that have a higher likelihood of proarrhythmia
(eg, flecainide) or that could further depress LVEF (eg, disopyramide). If an ablation is
performed, close follow-up is required even after successful ablation because of the
tendency for cardiomyopathy to recur if tachycardia recurs. (See "Focal atrial
tachycardia", section on 'Catheter ablation' and "Treatment of symptomatic arrhythmias
associated with the Wolff-Parkinson-White syndrome", section on 'Catheter
ablation' and "Atrial tachyarrhythmias in children", section on
'Management' and "Atrioventricular nodal reentrant tachycardia", section on 'Catheter
ablation'.)
Patients with frequent ectopy — For patients presenting with a high burden of
premature ventricular complex/contraction (PVC; also referred to a premature ventricular
beats or premature ventricular depolarizations) and newly recognized cardiomyopathy,
initial management is to look for underlying causes (such as coronary artery disease
[CAD], valvular heart disease, arrhythmogenic right ventricular dysplasia [ARVD], etc)
and initiation of guideline-based optimal medical therapy for HF [104]. Correction of
electrolytes and initiation of beta blockers are typical first therapies. (See "Overview of
the management of heart failure with reduced ejection fraction in adults".)
Given the possibility of arrhythmia-induced cardiomyopathy in patients with a high PVC
burden (eg, >15 to 20 percent of total beats on a 24-hour ambulatory monitor) and
associated with left ventricular dysfunction, we generally pursue radiofrequency catheter
ablation [104-106]. Catheter ablation of high-frequency PVCs has emerged as a safe
and effective therapy and may be considered if medical management is ineffective or
poorly tolerated and depending on patient preference [59,74,107-109]. While it is not
possible to specify an exact percentage (PVC burden) for which a patient might benefit
from ablation of frequent PVCs as studies have had a wide range in their inclusion
criteria, consideration may be given with a burden of above 10 percent, but our
approach is typically to offer ablation at a higher burden (eg, >15 to 20 percent PVCs).
The approach to catheter ablation in patients with a high PVC burden is discussed in
greater detail separately. (See "Ventricular arrhythmias: Overview in patients with heart
failure and cardiomyopathy" and "Premature ventricular complexes: Treatment and
prognosis", section on 'Catheter ablation'.)
Patients with refractory tachyarrhythmias — On rare occasions when all efforts at
ventricular rate control, restoration of sinus rhythm, and catheter ablation of the
arrhythmia have been unsuccessful, ablation of the AV node with insertion of a
permanent pacemaker may be considered. All other therapeutic options should be
exhausted before considering this approach. For these patients, implantation of a
biventricular pacing unit should also be considered [110]. (See "Cardiac
resynchronization therapy in atrial fibrillation" and "Cardiac resynchronization therapy in
heart failure: Indications".)
FOLLOW-UP Whereas the initial cardiomyopathy may have taken months to
develop, recurrent tachycardia can lead to an abrupt decline in left ventricular ejection
fraction (LVEF). Diastolic dysfunction can persist even after systolic function has
normalized and can lead to decreased coronary flow reserve. In patients who develop a
recurrence of the arrhythmia, the increased myocardial oxygen demand in the face of
the decreased reserve can lead to redevelopment of cardiomyopathy [111,112]. As
such, close ongoing monitoring with clinic visits, ambulatory (Holter) monitoring, and
echocardiography are essential. Although there are minimal data and no society
guidelines regarding the frequency of monitoring in these patients, we follow up with
patients using a combination of clinic visits, echocardiography, and ambulatory
monitoring every three to six months for one to two years following the initial clinical
improvement.
The following is a typical follow-up schedule:
●4 to 6 weeks after initial presentation – Clinical follow-up, electrocardiogram

(ECG)
●3 months after initial presentation – Clinical follow-up, ECG, echocardiogram,
outpatient ambulatory monitor
●6 months after initial presentation – Clinical follow-up, ECG
●12 months after initial presentation – Clinical follow-up, ECG,
echocardiogram, ECG, outpatient ambulatory monitor if symptoms suggest
recurrence
●18 to 24 months after initial presentation – Clinical follow-up, ECG
If complete recovery of EF is noted and angiotensin converting enzyme (ACE) inhibitors
and beta blockers are tapered off, additional monitoring is required to be sure that EF
remains normal [4].
PROGNOSIS Following the restoration of sinus rhythm or ventricular rate
control of the presenting tachycardia, most patients will have significant improvement
and/or normalization of left ventricular ejection fraction (LVEF) over a period of months.
As such, patients who have not experienced sudden cardiac arrest or a sustained
ventricular arrhythmia, and whose LVEF has improved to 40 percent or greater, usually
do not require implantation of an implantable cardioverter-defibrillator (ICD).
(See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and
heart failure with reduced LVEF".)
In some patients whose LVEF has normalized, the LV chamber may remain somewhat
enlarged. Despite the apparent normalization of cardiac function when a tachycardia has
been terminated or rate controlled, ultrastructural abnormalities of the myocardium may
persist [60]. Additional evidence for persistent myocardial abnormality despite
normalization of systolic function was seen in a study of successfully ablated patients
with atrial tachycardia (AT). These patients demonstrated LV structure and function
changes including diffuse fibrosis on contrast-enhanced cardiac magnetic resonance
imaging (MRI) long after successful ablation (64±36 months) [90]. As noted previously,
late-gadolinium enhancement on cardiac magnetic resonance suggests the presence of
fibrosis and identifies irreversible structural changes that may predict incomplete
recovery of LV function. For any patient whose ejection fraction fails to normalize with
correction of the tachyarrhythmia, other underlying pathology should be considered
including permanent structural changes [90,113]. If arrhythmia-induced cardiomyopathy
recurs, these patients are at substantial risk for sudden death, and ICD implantation
should be contemplated [111].
links: Ventricular arrhythmias" and "Society guideline links: Cardiac implantable
electronic devices" and "Society guideline links: Supraventricular arrhythmias".)
interest.)
●Beyond the Basics topics (see "Patient education: Atrial fibrillation (Beyond

the Basics)" and "Patient education: Catheter ablation for abnormal heartbeats
(Beyond the Basics)")
●Arrhythmia-induced cardiomyopathy is a relatively rare cause of a dilated

cardiomyopathy resulting from prolonged periods of rapid ventricular heart
rates. Arrhythmia-induced cardiomyopathy often improves or resolves
following treatment and is associated with a good prognosis in most patients.
●Chronic tachycardia ultimately produces significant structural changes in the
heart, with impressive left ventricular dilatation and cellular morphologic
changes leading to a cardiomyopathy. The precise mechanism(s) by which a
chronic tachycardia produces these changes remain incompletely described.
(See 'Pathophysiology' above.)
●Virtually all tachyarrhythmias have been reported to cause arrhythmia-
induced cardiomyopathy, and frequent ectopic beats have also been
associated with this condition. In most cases, the myocardial dysfunction
improves or normalizes following therapy to control the ventricular heart rate or
to restore normal sinus rhythm. (See 'Arrhythmias associated with arrhythmia-
induced cardiomyopathy' above.)
●The clinical presentation of arrhythmia-induced cardiomyopathy is variable
but usually involves signs and/or symptoms related to the tachyarrhythmia (eg,
palpitations, dyspnea, chest discomfort, etc), heart failure (HF; eg, dyspnea,
edema, weight gain, orthopnea, etc), or both. In our experience, HF symptoms
are more common since patients with symptomatic tachyarrhythmias will
frequently seek medical attention earlier in the course of their care and prior to
the development of a cardiomyopathy. (See 'Clinical presentation' above.)
●All patients should have an electrocardiogram (ECG) to document the cardiac
rhythm and ventricular heart rate, with comparison to prior ECGs when
available. There are no specific ECG findings that distinguish patients with and
without arrhythmia-induced cardiomyopathy, and the ECG findings will vary
depending upon the underlying tachyarrhythmia. (See 'ECG findings' above.)
●Arrhythmia-induced cardiomyopathy is defined by the presence of a
sustained tachycardia (or frequent episodes of tachycardia or very frequent
ectopy) that results in with left ventricular (LV) systolic dysfunction. Usually the
diagnosis of arrhythmia-induced cardiomyopathy can only be made following a
successful trial of therapy to slow the ventricular rate or to restore sinus
rhythm along with the exclusion of other potential causes of cardiomyopathy.
Patients in whom arrhythmia-induced cardiomyopathy is suspected should
undergo continuous cardiac monitoring for 24 to 48 hours and have non-
invasive imaging to assess cardiac structure and function. For most patients, a
transthoracic echocardiogram is the preferred test for assessing cardiac
structure and function, although cardiac magnetic resonance (CMR) imaging is
a reasonable alternative. (See 'Approach to the diagnosis' above
and 'Diagnostic testing' above.)
●The initial treatments for a patient with HF and suspected arrhythmia-induced
cardiomyopathy are the same as those used in most other patients with HF
(eg, angiotensin converting enzyme [ACE] inhibitors or angiotensin receptor
blockers [ARBs], beta blockers, diuretics) and tachyarrhythmias (eg, rate-
control medications, consideration of antiarrhythmic drugs and/or
cardioversion). However, because of the potential reversible nature of
arrhythmia-induced cardiomyopathy, aggressive efforts should be made to
achieve excellent ventricular heart rate control or to restore sinus rhythm.
(See 'Treatment' above.)
•For minimally symptomatic patients with atrial fibrillation (AF) in whom
adequate rate control is achieved, we continue medical therapy.
•For patients with AF who remain significantly symptomatic, or patients in
whom adequate rate control is not achieved with medical therapy alone,
we pursue a rhythm control strategy. (See "Rhythm control versus rate
control in atrial fibrillation" and "Atrial fibrillation: Cardioversion".)
•For patients with atrial flutter, rapid ventricular rates, and newly
recognized depressed EF, rate control may be difficult to achieve with
medication. Because of this, we perform early electrical cardioversion in
these patients. (See "Restoration of sinus rhythm in atrial flutter".)
•For supraventricular tachyarrhythmias (SVTs) other than AF or atrial
flutter that result in arrhythmia-induced cardiomyopathy, restoration of
sinus rhythm is the usual goal. The initial choice of modality (ie, electrical
cardioversion, antiarrhythmic drugs, or catheter ablation of the arrhythmia)
will vary depending upon the underlying SVT as well as the local expertise
and availability of options.
•For patients presenting with a high burden of ventricular premature beats
(PVCs) and associated with left ventricular dysfunction, we generally
pursue radiofrequency catheter ablation.
•On rare occasions when all efforts at ventricular rate control, restoration
of sinus rhythm, and catheter ablation of the arrhythmia have been
unsuccessful for the treatment of SVTs, ablation of the AV node with
insertion of a permanent pacemaker may be considered.
●Close ongoing monitoring with clinic visits, ambulatory (Holter) monitoring,
and echocardiography is essential to assess for any recurrence. We follow up
with patients using a combination of clinic visits, echocardiography, and
ambulatory monitoring every three to six months for one to two years following
the initial clinical improvement. (See 'Follow-up' above.)
REFERENCES
1. Westphal JG, Rigopoulos AG, Bakogiannis C, et al. The MOGE(S)
classification for cardiomyopathies: current status and future outlook. Heart
Fail Rev 2017; 22:743.
2. Yancy CW, Jessup M, Bozkurt B, et al. 2017 ACC/AHA/HFSA Focused
Update of the 2013 ACCF/AHA Guideline for the Management of Heart
Failure: A Report of the American College of Cardiology/American Heart
Association Task Force on Clinical Practice Guidelines and the Heart
Failure Society of America. J Card Fail 2017; 23:628.
3. Shinbane JS, Wood MA, Jensen DN, et al. Tachycardia-induced
cardiomyopathy: a review of animal models and clinical studies. J Am Coll
Cardiol 1997; 29:709.
4. Gopinathannair R, Etheridge SP, Marchlinski FE, et al. Arrhythmia-Induced
Cardiomyopathies: Mechanisms, Recognition, and Management. J Am Coll
Cardiol 2015; 66:1714.
5. Kasper EK, Agema WR, Hutchins GM, et al. The causes of dilated
cardiomyopathy: a clinicopathologic review of 673 consecutive patients. J
6. SHACHNOW N, SPELLMAN S, RUBIN I. Persistent supraventricular
tachycardia; case report with review of literature. Circulation 1954; 10:232.
7. Engel TR, Bush CA, Schaal SF. Tachycardia-aggravated heart disease. Ann
Intern Med 1974; 80:384.
8. Coleman HN 3rd, Taylor RR, Pool PE, et al. Congestive heart failure
following chronic tachycardia. Am Heart J 1971; 81:790.
9. Vijgen J, Hill P, Biblo LA, Carlson MD. Tachycardia-induced cardiomyopathy
secondary to right ventricular outflow tract ventricular tachycardia:
improvement of left ventricular systolic function after radiofrequency catheter
ablation of the arrhythmia. J Cardiovasc Electrophysiol 1997; 8:445.
10. Singh B, Kaul U, Talwar KK, Wasir HS. Reversibility of "tachycardia induced
cardiomyopathy" following the cure of idiopathic left ventricular tachycardia
using radiofrequency energy. Pacing Clin Electrophysiol 1996; 19:1391.
11. Baman TS, Lange DC, Ilg KJ, et al. Relationship between burden of
premature ventricular complexes and left ventricular function. Heart Rhythm
2010; 7:865.
12. Medi C, Kalman JM, Haqqani H, et al. Tachycardia-mediated
cardiomyopathy secondary to focal atrial tachycardia: long-term outcome
after catheter ablation. J Am Coll Cardiol 2009; 53:1791.
13. Donghua Z, Jian P, Zhongbo X, et al. Reversal of cardiomyopathy in
patients with congestive heart failure secondary to tachycardia. J Interv
Card Electrophysiol 2013; 36:27.
14. Brembilla-Perrot B, Ferreira JP, Manenti V, et al. Predictors and prognostic
significance of tachycardiomyopathy: insights from a cohort of 1269 patients
undergoing atrial flutter ablation. Eur J Heart Fail 2016; 18:394.
15. Spinale FG, Hendrick DA, Crawford FA, et al. Chronic supraventricular
tachycardia causes ventricular dysfunction and subendocardial injury in
swine. Am J Physiol 1990; 259:H218.
16. Howard RJ, Stopps TP, Moe GW, et al. Recovery from heart failure:
structural and functional analysis in a canine model. Can J Physiol
Pharmacol 1988; 66:1505.
17. Morgan DE, Tomlinson CW, Qayumi AK, et al. Evaluation of ventricular
contractility indexes in the dog with left ventricular dysfunction induced by
rapid atrial pacing. J Am Coll Cardiol 1989; 14:489.
18. Spinale FG, Tomita M, Zellner JL, et al. Collagen remodeling and changes
in LV function during development and recovery from supraventricular
tachycardia. Am J Physiol 1991; 261:H308.
19. Kajstura J, Zhang X, Liu Y, et al. The cellular basis of pacing-induced dilated
cardiomyopathy. Myocyte cell loss and myocyte cellular reactive
hypertrophy. Circulation 1995; 92:2306.
20. O'Brien PJ, Ianuzzo CD, Moe GW, et al. Rapid ventricular pacing of dogs to
heart failure: biochemical and physiological studies. Can J Physiol
Pharmacol 1990; 68:34.
21. Ohno M, Cheng CP, Little WC. Mechanism of altered patterns of left
ventricular filling during the development of congestive heart failure.
22. Armstrong PW, Stopps TP, Ford SE, de Bold AJ. Rapid ventricular pacing in
the dog: pathophysiologic studies of heart failure. Circulation 1986; 74:1075.
23. Wilson JR, Douglas P, Hickey WF, et al. Experimental congestive heart
failure produced by rapid ventricular pacing in the dog: cardiac effects.
24. Damiano RJ Jr, Tripp HF Jr, Asano T, et al. Left ventricular dysfunction and
dilatation resulting from chronic supraventricular tachycardia. J Thorac
25. Yamamoto K, Burnett JC Jr, Meyer LM, et al. Ventricular remodeling during
development and recovery from modified tachycardia-induced
cardiomyopathy model. Am J Physiol 1996; 271:R1529.
26. Huizar JF, Kaszala K, Potfay J, et al. Left ventricular systolic dysfunction
induced by ventricular ectopy: a novel model for premature ventricular
contraction-induced cardiomyopathy. Circ Arrhythm Electrophysiol 2011;
4:543.
27. Pak PH, Nuss HB, Tunin RS, et al. Repolarization abnormalities, arrhythmia
and sudden death in canine tachycardia-induced cardiomyopathy. J Am Coll
Cardiol 1997; 30:576.
28. Moe GW, Montgomery C, Howard RJ, et al. Left ventricular myocardial
blood flow, metabolism, and effects of treatment with enalapril: further
insights into the mechanisms of canine experimental pacing-induced heart
failure. J Lab Clin Med 1993; 121:294.
29. Spinale FG, Holzgrefe HH, Mukherjee R, et al. LV and myocyte structure
and function after early recovery from tachycardia-induced cardiomyopathy.
Am J Physiol 1995; 268:H836.
30. Spinale FG, Clayton C, Tanaka R, et al. Myocardial Na+,K(+)-ATPase in
tachycardia induced cardiomyopathy. J Mol Cell Cardiol 1992; 24:277.
31. Kloner RA, DeBoer LW, Darsee JR, et al. Recovery from prolonged
abnormalities of canine myocardium salvaged from ischemic necrosis by
coronary reperfusion. Proc Natl Acad Sci U S A 1981; 78:7152.
32. Reimer KA, Hill ML, Jennings RB. Prolonged depletion of ATP and of the
adenine nucleotide pool due to delayed resynthesis of adenine nucleotides
following reversible myocardial ischemic injury in dogs. J Mol Cell Cardiol
1981; 13:229.
33. Spinale FG, Tanaka R, Crawford FA, Zile MR. Changes in myocardial blood
flow during development of and recovery from tachycardia-induced
cardiomyopathy. Circulation 1992; 85:717.
34. Shannon RP, Komamura K, Shen YT, et al. Impaired regional
subendocardial coronary flow reserve in conscious dogs with pacing-
induced heart failure. Am J Physiol 1993; 265:H801.
35. Perreault CL, Shannon RP, Komamura K, et al. Abnormalities in intracellular
calcium regulation and contractile function in myocardium from dogs with
pacing-induced heart failure. J Clin Invest 1992; 89:932.
36. Tanaka R, Fulbright BM, Mukherjee R, et al. The cellular basis for the
blunted response to beta-adrenergic stimulation in supraventricular
tachycardia-induced cardiomyopathy. J Mol Cell Cardiol 1993; 25:1215.
37. Sasayama S, Asanoi H, Ishizaka S. Continuous measurement of the
pressure-volume relationship in experimental heart failure produced by rapid
ventricular pacing in conscious dogs. Eur Heart J 1992; 13 Suppl E:47.
38. Selby DE, Palmer BM, LeWinter MM, Meyer M. Tachycardia-induced
diastolic dysfunction and resting tone in myocardium from patients with a
normal ejection fraction. J Am Coll Cardiol 2011; 58:147.
39. Marzo KP, Frey MJ, Wilson JR, et al. Beta-adrenergic receptor-G protein-
adenylate cyclase complex in experimental canine congestive heart failure
produced by rapid ventricular pacing. Circ Res 1991; 69:1546.
40. Wakili R, Yeh YH, Yan Qi X, et al. Multiple potential molecular contributors
to atrial hypocontractility caused by atrial tachycardia remodeling in dogs.
Circ Arrhythm Electrophysiol 2010; 3:530.
41. Yonemochi H, Yasunaga S, Teshima Y, et al. Rapid electrical stimulation of
contraction reduces the density of beta-adrenergic receptors and
responsiveness of cultured neonatal rat cardiomyocytes. Possible
involvement of microtubule disassembly secondary to mechanical stress.
42. Mihm MJ, Yu F, Carnes CA, et al. Impaired myofibrillar energetics and
oxidative injury during human atrial fibrillation. Circulation 2001; 104:174.
43. Shite J, Qin F, Mao W, et al. Antioxidant vitamins attenuate oxidative stress
and cardiac dysfunction in tachycardia-induced cardiomyopathy. J Am Coll
Cardiol 2001; 38:1734.
44. Deshmukh PM, Krishnamani R, Romanyshyn M, et al. Association of
angiotensin converting enzyme gene polymorphism with tachycardia
cardiomyopathy. Int J Mol Med 2004; 13:455.
45. Mueller KAL, Heinzmann D, Klingel K, et al. Reply: Histopathological and
Immunological Characteristics of Tachycardia-Induced Cardiomyopathy. J
46. Chiladakis JA, Vassilikos VP, Maounis TN, et al. Successful radiofrequency
catheter ablation of automatic atrial tachycardia with regression of the
cardiomyopathy picture. Pacing Clin Electrophysiol 1997; 20:953.
47. Gillette PC, Smith RT, Garson A Jr, et al. Chronic supraventricular
tachycardia. A curable cause of congestive cardiomyopathy. JAMA 1985;
253:391.
48. Gallagher JJ. Tachycardia and cardiomyopathy: the chicken-egg dilemma
revisited. J Am Coll Cardiol 1985; 6:1172.
49. Bertil Olsson S, Blomström P, Sabel KG, William-Olsson G. Incessant
ectopic atrial tachycardia: successful surgical treatment with regression of
dilated cardiomyopathy picture. Am J Cardiol 1984; 53:1465.
50. Packer DL, Bardy GH, Worley SJ, et al. Tachycardia-induced
cardiomyopathy: a reversible form of left ventricular dysfunction. Am J
Cardiol 1986; 57:563.
51. Rao PS, Najjar HN. Congestive cardiomyopathy due to chronic tachycardia:
resolution of cardiomyopathy with antiarrhythmic drugs. Int J Cardiol 1987;
17:216.
52. Gillette PC, Wampler DG, Garson A Jr, et al. Treatment of atrial automatic
tachycardia by ablation procedures. J Am Coll Cardiol 1985; 6:405.
53. Sanders P, Morton JB, Kistler PM, et al. Reversal of atrial mechanical
dysfunction after cardioversion of atrial fibrillation: implications for the
mechanisms of tachycardia-mediated atrial cardiomyopathy. Circulation
2003; 108:1976.
54. Fishberger SB, Colan SD, Saul JP, et al. Myocardial mechanics before and
after ablation of chronic tachycardia. Pacing Clin Electrophysiol 1996; 19:42.
56. Leman RB, Gillette PC, Zinner AJ. Resolution of congestive cardiomyopathy
caused by supraventricular tachycardia using amiodarone. Am Heart J
1986; 112:622.
57. Corey WA, Markel ML, Hoit BD, Walsh RA. Regression of a dilated
cardiomyopathy after radiofrequency ablation of incessant supraventricular
tachycardia. Am Heart J 1993; 126:1469.
58. Grimm W, Menz V, Hoffmann J, Maisch B. Reversal of tachycardia induced
cardiomyopathy following ablation of repetitive monomorphic right
ventricular outflow tract tachycardia. Pacing Clin Electrophysiol 2001;
24:166.
59. Yarlagadda RK, Iwai S, Stein KM, et al. Reversal of cardiomyopathy in
patients with repetitive monomorphic ventricular ectopy originating from the
right ventricular outflow tract. Circulation 2005; 112:1092.
60. Nerheim P, Birger-Botkin S, Piracha L, Olshansky B. Heart failure and
sudden death in patients with tachycardia-induced cardiomyopathy and
recurrent tachycardia. Circulation 2004; 110:247.
61. Stewart S, Hart CL, Hole DJ, McMurray JJ. A population-based study of the
long-term risks associated with atrial fibrillation: 20-year follow-up of the
Renfrew/Paisley study. Am J Med 2002; 113:359.
62. Luchsinger JA, Steinberg JS. Resolution of cardiomyopathy after ablation of
atrial flutter. J Am Coll Cardiol 1998; 32:205.
63. Redfield MM, Kay GN, Jenkins LS, et al. Tachycardia-related
cardiomyopathy: a common cause of ventricular dysfunction in patients with
atrial fibrillation referred for atrioventricular ablation. Mayo Clin Proc 2000;
75:790.
64. Edner M, Caidahl K, Bergfeldt L, et al. Prospective study of left ventricular
function after radiofrequency ablation of atrioventricular junction in patients
with atrial fibrillation. Br Heart J 1995; 74:261.
65. Pizzale S, Lemery R, Green MS, et al. Frequency and predictors of
tachycardia-induced cardiomyopathy in patients with persistent atrial flutter.
Can J Cardiol 2009; 25:469.
66. Hasdemir C, Ulucan C, Yavuzgil O, et al. Tachycardia-induced
cardiomyopathy in patients with idiopathic ventricular arrhythmias: the
incidence, clinical and electrophysiologic characteristics, and the predictors.
J Cardiovasc Electrophysiol 2011; 22:663.
67. Bogun F, Crawford T, Reich S, et al. Radiofrequency ablation of frequent,
idiopathic premature ventricular complexes: comparison with a control group
without intervention. Heart Rhythm 2007; 4:863.
68. Yokokawa M, Kim HM, Good E, et al. Relation of symptoms and symptom
duration to premature ventricular complex-induced cardiomyopathy. Heart
Rhythm 2012; 9:92.
69. Mountantonakis SE, Frankel DS, Gerstenfeld EP, et al. Reversal of outflow
tract ventricular premature depolarization-induced cardiomyopathy with
ablation: effect of residual arrhythmia burden and preexisting
cardiomyopathy on outcome. Heart Rhythm 2011; 8:1608.
70. Penela D, Van Huls Van Taxis C, Aguinaga L, et al. Neurohormonal,
structural, and functional recovery pattern after premature ventricular
complex ablation is independent of structural heart disease status in
patients with depressed left ventricular ejection fraction: a prospective
multicenter study. J Am Coll Cardiol 2013; 62:1195.
71. El Kadri M, Yokokawa M, Labounty T, et al. Effect of ablation of frequent
premature ventricular complexes on left ventricular function in patients with
nonischemic cardiomyopathy. Heart Rhythm 2015; 12:706.
72. Baser K, Bas HD, LaBounty T, et al. Recurrence of PVCs in patients with
PVC-induced cardiomyopathy. Heart Rhythm 2015; 12:1519.
73. Penela D, Acosta J, Aguinaga L, et al. Ablation of frequent PVC in patients
meeting criteria for primary prevention ICD implant: Safety of withholding the
implant. Heart Rhythm 2015; 12:2434.
74. Laplante L, Benzaquen BS. A Review of the Potential Pathogenicity and
Management of Frequent Premature Ventricular Contractions. Pacing Clin
75. Lamba J, Redfearn DP, Michael KA, et al. Radiofrequency catheter ablation
for the treatment of idiopathic premature ventricular contractions originating
from the right ventricular outflow tract: a systematic review and meta-
analysis. Pacing Clin Electrophysiol 2014; 37:73.
76. Yokokawa M, Kim HM, Good E, et al. Impact of QRS duration of frequent
premature ventricular complexes on the development of cardiomyopathy.
77. Carballeira Pol L, Deyell MW, Frankel DS, et al. Ventricular premature
depolarization QRS duration as a new marker of risk for the development of
ventricular premature depolarization-induced cardiomyopathy. Heart
Rhythm 2014; 11:299.
78. Deyell MW, Park KM, Han Y, et al. Predictors of recovery of left ventricular
dysfunction after ablation of frequent ventricular premature depolarizations.
79. Yokokawa M, Good E, Crawford T, et al. Recovery from left ventricular
dysfunction after ablation of frequent premature ventricular complexes.
80. Walters TE, Rahmutula D, Szilagyi J, et al. Left Ventricular Dyssynchrony
Predicts the Cardiomyopathy Associated With Premature Ventricular
Contractions. J Am Coll Cardiol 2018; 72:2870.
81. Pacchia CF, Akoum NW, Wasmund S, Hamdan MH. Atrial bigeminy results
in decreased left ventricular function: an insight into the mechanism of PVC-
induced cardiomyopathy. Pacing Clin Electrophysiol 2012; 35:1232.
82. Hasdemir C, Simsek E, Yuksel A. Premature atrial contraction-induced
cardiomyopathy. Europace 2013; 15:1790.
83. Dickstein K, Cohen-Solal A, Filippatos G, et al. ESC Guidelines for the
diagnosis and treatment of acute and chronic heart failure 2008: the Task
Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure
2008 of the European Society of Cardiology. Developed in collaboration with
the Heart Failure Association of the ESC (HFA) and endorsed by the
European Society of Intensive Care Medicine (ESICM). Eur Heart J 2008;
29:2388.
84. Heart Failure Society Of America . Evaluation of patients for ventricular
dysfunction and heart failure. J Card Fail 2006; 12:e16.
85. Arnold JM, Liu P, Demers C, et al. Canadian Cardiovascular Society
consensus conference recommendations on heart failure 2006: diagnosis
and management. Can J Cardiol 2006; 22:23.
86. Yancy CW, Jessup M, Bozkurt B, et al. 2013 ACCF/AHA guideline for the
management of heart failure: a report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines.
J Am Coll Cardiol 2013; 62:e147.
87. Sakaguchi H, Miyazaki A, Yamamoto M, et al. Clinical characteristics of
focal atrial tachycardias arising from the atrial appendages during childhood.
89. Jeong YH, Choi KJ, Song JM, et al. Diagnostic approach and treatment
strategy in tachycardia-induced cardiomyopathy. Clin Cardiol 2008; 31:172.
90. Ling LH, Kalman JM, Ellims AH, et al. Diffuse ventricular fibrosis is a late
outcome of tachycardia-mediated cardiomyopathy after successful ablation.
Circ Arrhythm Electrophysiol 2013; 6:697.
91. Hasdemir C, Yuksel A, Camli D, et al. Late gadolinium enhancement CMR
in patients with tachycardia-induced cardiomyopathy caused by idiopathic
ventricular arrhythmias. Pacing Clin Electrophysiol 2012; 35:465.
92. Kusunose K, Torii Y, Yamada H, et al. Clinical Utility of Longitudinal Strain
to Predict Functional Recovery in Patients With Tachyarrhythmia and
Reduced LVEF. JACC Cardiovasc Imaging 2017; 10:118.
93. Grogan M, Smith HC, Gersh BJ, Wood DL. Left ventricular dysfunction due
to atrial fibrillation in patients initially believed to have idiopathic dilated
cardiomyopathy. Am J Cardiol 1992; 69:1570.
94. Gentlesk PJ, Sauer WH, Gerstenfeld EP, et al. Reversal of left ventricular
dysfunction following ablation of atrial fibrillation. J Cardiovasc
95. Manolis AG, Katsivas AG, Lazaris EE, et al. Ventricular performance and
quality of life in patients who underwent radiofrequency AV junction ablation
and permanent pacemaker implantation due to medically refractory atrial
tachyarrhythmias. J Interv Card Electrophysiol 1998; 2:71.
96. Wyse DG, Waldo AL, DiMarco JP, et al. A comparison of rate control and
rhythm control in patients with atrial fibrillation. N Engl J Med 2002;
347:1825.
97. Van Gelder IC, Hagens VE, Bosker HA, et al. A comparison of rate control
and rhythm control in patients with recurrent persistent atrial fibrillation. N
Engl J Med 2002; 347:1834.
98. Corley SD, Epstein AE, DiMarco JP, et al. Relationships between sinus
rhythm, treatment, and survival in the Atrial Fibrillation Follow-Up
Investigation of Rhythm Management (AFFIRM) Study. Circulation 2004;
109:1509.
99. Opolski G, Torbicki A, Kosior DA, et al. Rate control vs rhythm control in
patients with nonvalvular persistent atrial fibrillation: the results of the Polish
How to Treat Chronic Atrial Fibrillation (HOT CAFE) Study. Chest 2004;
126:476.
100. Carlsson J, Miketic S, Windeler J, et al. Randomized trial of rate-control
versus rhythm-control in persistent atrial fibrillation: the Strategies of
Treatment of Atrial Fibrillation (STAF) study. J Am Coll Cardiol 2003;
41:1690.
101. Al-Khatib SM, Shaw LK, Lee KL, et al. Is rhythm control superior to rate
control in patients with atrial fibrillation and congestive heart failure? Am J
Cardiol 2004; 94:797.
102. Roy D, Talajic M, Nattel S, et al. Rhythm control versus rate control for
atrial fibrillation and heart failure. N Engl J Med 2008; 358:2667.
103. Anter E, Jessup M, Callans DJ. Atrial fibrillation and heart failure: treatment
considerations for a dual epidemic. Circulation 2009; 119:2516.
104. Latchamsetty R, Bogun F. Premature Ventricular Complex-Induced
Cardiomyopathy. JACC Clin Electrophysiol 2019; 5:537.
105. Eugenio PL. Frequent Premature Ventricular Contractions: An Electrical
Link to Cardiomyopathy. Cardiol Rev 2015; 23:168.
106. Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS
Guideline for Management of Patients With Ventricular Arrhythmias and the
Prevention of Sudden Cardiac Death: A Report of the American College of
Cardiology/American Heart Association Task Force on Clinical Practice
Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2018; 72:e91.
107. Takemoto M, Yoshimura H, Ohba Y, et al. Radiofrequency catheter
ablation of premature ventricular complexes from right ventricular outflow
tract improves left ventricular dilation and clinical status in patients without
structural heart disease. J Am Coll Cardiol 2005; 45:1259.
108. Zhong L, Lee YH, Huang XM, et al. Relative efficacy of catheter ablation vs
antiarrhythmic drugs in treating premature ventricular contractions: a single-
center retrospective study. Heart Rhythm 2014; 11:187.
109. Berruezo A, Penela D, Jáuregui B, et al. Mortality and morbidity reduction
after frequent premature ventricular complexes ablation in patients with left
ventricular systolic dysfunction. Europace 2019; 21:1079.
110. Leon AR, Greenberg JM, Kanuru N, et al. Cardiac resynchronization in
patients with congestive heart failure and chronic atrial fibrillation: effect of
upgrading to biventricular pacing after chronic right ventricular pacing. J Am
111. Dandamudi G, Rampurwala AY, Mahenthiran J, et al. Persistent left
ventricular dilatation in tachycardia-induced cardiomyopathy patients after
appropriate treatment and normalization of ejection fraction. Heart Rhythm
2008; 5:1111.
112. Moe GW, Armstrong P. Pacing-induced heart failure: a model to study the
mechanism of disease progression and novel therapy in heart failure.
Cardiovasc Res 1999; 42:591.
113. Ling LH, Taylor AJ, Ellims AH, et al. Sinus rhythm restores ventricular
function in patients with cardiomyopathy and no late gadolinium
enhancement on cardiac magnetic resonance imaging who undergo
catheter ablation for atrial fibrillation. Heart Rhythm 2013; 10:1334.
Close
 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®
Skip to OutlineSkip to TopicSkip to Help

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 SUMMARY
 INTRODUCTION
 ESCAPE ATRIAL BEATS
 ECTOPIC ATRIAL RHYTHM
 ATRIAL TACHYCARDIA
o Atrial tachycardia with atrioventricular block
 WANDERING ATRIAL PACEMAKER
 MULTIFOCAL ATRIAL TACHYCARDIA
 PREMATURE ATRIAL COMPLEX
 ATRIAL FIBRILLATION AND ATRIAL FLUTTER
 ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA
 ATRIOVENTRICULAR REENTRANT TACHYCARDIA
 ATRIOFASCICULAR AND MAHAIM FIBER TACHYCARDIAS
 JUNCTIONAL ECTOPIC RHYTHM
 JUNCTIONAL PREMATURE BEATS
 JUNCTIONAL ESCAPE BEATS
 SUMMARY
GRAPHICS view all
 Figures
oAtypical atrioventricular nodal reentrant tachycardia
oOrthodromic AVRT
oAntidromic AVRT
oJunctional ectopic rhythm
 Waveforms
oEscape atrial beats tutorial
oEctopic atrial rhythm tutorial
oAtrial tachycardia tutorial
oAtrial tach with block tutorial
oWandering atrial pacer tutorial
oMultifocal atrial tach tutorial
oAtrial premature beat tutorial
oBlocked APB tutorial
oAPB with aberration tutorial
oAVN reentrant tach tutorial
oOrthodromic AVRT tutorial
oJunctional premature tutorial
oJunctional escape tutorial
RELATED TOPICS
 Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome
 Atriofascicular ("Mahaim") pathway tachycardia
 ECG tutorial: Intraventricular block
 General principles of asynchronous activation and preexcitation
 Sinoatrial nodal pause, arrest, and exit block
 Supraventricular premature beats
ECG tutorial: Atrial and atrioventricular nodal

(supraventricular) arrhythmias
Author:
Section Editor:
Deputy Editor:
INTRODUCTION Supraventricular rhythms appear on an electrocardiogram
as narrow complex rhythms, which may be regular or irregular. They may have a normal
rate, be tachycardic, or be bradycardic depending on the underlying arrhythmia
mechanism and presence of atrioventricular nodal block. Bundle branch blocks may be
present either at baseline or due to rate-related aberrancy, which can make the QRS
complex wide, though these rhythms are more commonly narrow complex. When
evaluating the rhythm, the most important steps are to evaluate for the presence of P
waves and determine if the morphology, axis, and duration match the normal sinus
rhythm P wave.
ESCAPE ATRIAL BEATS Escape atrial beats may occur after a long sinus
pause, usually resulting from sinus node exit block or sinus node arrest (waveform 1).
(See "Sinoatrial nodal pause, arrest, and exit block".) If the pause is long enough, there
will be an escape atrial rhythm at a rate correlating with the intrinsic automaticity of the
atrial focus. This may be a single atrial beat, multiple atrial complexes, or a sustained
ectopic atrial rhythm due to an ectopic site. (See 'Ectopic atrial rhythm' below.)
The rate of the escape atrial beats is slower than that of the sinus node (since it is an
escape rhythm) and the P wave morphology differs from that of the sinus P wave,
depending upon the location of the ectopic atrial focus. (See 'Ectopic atrial
rhythm' below.)
ECTOPIC ATRIAL RHYTHM Ectopic atrial rhythm occurs when the
dominant pacemaker is an ectopic focus in the atrium and not the sinus node (waveform
2). This may result from sinus node failure and the development of an escape atrial
rhythm (generally at a rate of 30 to 60 beats per minute) or the acceleration of an
ectopic atrial focus faster than the rate of the sinus node. In such cases, sinus node
impulse generation is suppressed.
The direction of atrial activation may be altered when an atrial rhythm is present since
the pacemaker focus is outside the sinus node. The P wave morphology, axis, and
duration vary based on the site of origin within the atrium. The QRS complexes of an
ectopic atrial rhythm resemble those seen during sinus rhythm since myocardial
activation is still via the His Purkinje system. However, since atrial activation is abnormal
and no longer via the normal intra-atrial pathways, right and left atrial abnormalities
(hypertrophy or conduction abnormality) cannot be reliably diagnosed.
ATRIAL TACHYCARDIA When the ectopic atrial rhythm is at a rate >100
beats per minute, it is termed “atrial tachycardia.” (See "Focal atrial tachycardia".)

Atrial tachycardia with 1:1 conduction is a supraventricular tachyarrhythmia that typically
has a rate of 140 to 220 beats per minute (waveform 3). The QRS complexes occur at
regular intervals (there is constant RR cycle length), and there is a P wave with a
uniform morphology and the same PR interval. The baseline between successive P
waves (if AV block is present) is flat and isoelectric on the electrocardiogram. The QRS
complexes are similar to those seen during sinus rhythm since activation of the
ventricular myocardium is unaltered and is via the His-Purkinje system. Commonly,
there is a warm-up phase at the onset of the tachycardia, during which gradual rate
acceleration or progressive shortening of the PP cycle length between the first several
beats occurs. There may also be a cool-down phase at the end of the tachycardia,
during which the rate gradually decelerates, with progressive lengthening of the PP
cycle length.
Although all of the P waves are the same, they have a different morphology than the
sinus P wave, depending on the site of origin. The best lead for determining whether the
location is from the left or right atrium is V1. A negative or biphasic positive/negative P
wave in V1 was 100 percent specific in one study for predicting a right atrial location.
(See "Focal atrial tachycardia", section on 'Localization of AT focus'.) Similarly, a
positive or biphasic negative/positive P wave in V1 was 100 percent sensitive for a left
atrial location.
In general, there is prolongation of the PR interval as a result of decremental conduction

through the atrioventricular (AV) node. In other words, there is a progressive slowing of
the rate of impulse conduction through the AV node as the atrial rate increases.
Therefore, the PR interval is usually longer than in sinus rhythm. On occasion, the PR
interval may be shorter than that seen during sinus rhythm if the ectopic atrial focus is
close to the AV node and bypasses intra-atrial conduction, or if there is significant
sympathetic tone.
Since the ectopic focus is within the atrial myocardium and not affected by the vagus
nerve, activation of the parasympathetic nervous system (as produced by carotid sinus
pressure) does not alter the atrial rate of the tachycardia. However, increased
parasympathetic nervous activity (or adenosine) may block the AV node and result in
slowing of the ventricular rate, unmasking the atrial activity (waveform 4). In this
situation, sequential, discrete, non-conducted P waves are seen, and there is an
isoelectric baseline between the P waves. An increase in circulating catecholamines
may increase the atrial rate by directly enhancing the automaticity of the ectopic atrial
focus.
Atrial tachycardia with atrioventricular block — If the atrial rate is faster than the
capability of the AV node to conduct each impulse, some of the impulses do not traverse
through the node, resulting in a form of AV block (waveform 4). The ventricular rate may
be variable or occur in a repeating pattern, such as 2:1, 3:1, 4:1, or Wenckebach. AV
nodal block may occur because of:
●Normal AV nodal decremental properties
●Increased vagal tone to the AV node (such as with digitalis or carotid sinus
pressure)
●Intrinsic AV nodal disease
●Drugs that depress nodal function (such as calcium channel blockers and
beta-blockers)
WANDERING ATRIAL PACEMAKER A wandering atrial pacemaker
(also termed "multifocal atrial rhythm") is present when there are three or more ectopic
foci within the atrial myocardium that serve as the dominant pacemaker (waveform 5).
Since they discharge in random fashion, the site of atrial origin is continuously shifting
and may be located anywhere in the atrial myocardium. As a result, there is a changing
vector of atrial activation that causes a changing P wave morphology and PR interval
duration. A dominant P wave (sinus or atrial) cannot be identified. The rate is less than
100 beats per minute.
The QRS intervals have variable cycle lengths since the ectopic foci exhibit differences
in automaticity and rates of impulse generation. The rhythm is therefore irregularly
irregular, and it can be confused with atrial fibrillation. However, in contrast to atrial
fibrillation, distinct P waves of multiple morphologies are present. Sinus arrhythmia may
also be irregularly irregular; however, one P wave morphology is seen in this situation.
This arrhythmia may also be confused with sinus rhythm with multifocal premature atrial
complexes, although in this situation, a dominant sinus P wave can be identified and
there are periods of RR interval regularity.
MULTIFOCAL ATRIAL TACHYCARDIA Multifocal atrial tachycardia is
similar to a wandering atrial pacemaker in that there are three or more independent
ectopic foci, except that the heart rate is greater than 100 beats per minute (waveform
6). (See "Multifocal atrial tachycardia".)
This arrhythmia usually occurs when there is damage to or distension of the atrial
myocardium. Within such a myocardium, there is the potential for multiple independent
ectopic foci that generate impulses at variable rates. If there is sympathetic nervous
system activation, there can be an increase in the heart rate.
Since these foci are located in multiple areas of the atrial myocardium, there is great
variability of the P wave morphology and axis, the PR intervals, and the cycle lengths of
the QRS complexes. The QRS morphology is unchanged and is similar to sinus rhythm
since ventricular activation is normal.
Since the rhythm is rapid and irregularly irregular, it is often confused with atrial
fibrillation. However, with atrial fibrillation, there are no distinct or organized atrial
waveforms (P waves) seen.
PREMATURE ATRIAL COMPLEX Premature atrial complex (PAC; also
referred to a premature atrial beat, premature supraventricular complex, or premature

supraventricular beat)
occurs when there is premature or early activation of the atrial myocardium as a result of
an impulse generated by an ectopic focus within the atrial myocardium rather than the
sinus node (waveform 7). The interval between the last sinus beat and the ectopic beat
is shorter than the interval between two sinus beats (ie, it is premature).
(See "Supraventricular premature beats".)
PACs can be unifocal or multifocal. The P waves of the premature complexes exhibit
identical morphology in unifocal PACs and variable morphology in multifocal PACs.
Atrial bigeminy and trigeminy refer to rhythms in which every other beat (bigeminy) or
every third beat (trigeminy) is a PAC. Apart from the repeating pattern, there is no
clinical significance to this finding.
The P wave morphology differs from that of sinus rhythm and its axis and morphology
depend upon the atrial location of the ectopic focus. The PR interval is often longer than
that of the sinus beat, a result of decremental conduction, though this finding may be
subtle. However, the PR interval may be shorter if the ectopic focus is near the
atrioventricular (AV) node and does not occur too prematurely. Since activation of the
ventricular myocardium occurs in a normal fashion, the QRS complex is unchanged from
that of sinus rhythm.
Premature activation of the atrial myocardium by an ectopic focus results in a transient

and variable effect on sinus nodal function and impulse generation. These findings can
be reproduced in the electrophysiology lab during testing of the sinoatrial conduction
time (see "Invasive diagnostic cardiac electrophysiology studies", section on
'Electrocardiographic and electrophysiologic recordings'):
●If the sinus node is depressed and reset, it activates the atrium after an
interval identical to the usual sinus cycle length. In this setting, there is less
than a full compensatory pause. In other words, the cycle length measured
between the last P wave before and the first P wave after the premature beat
is less than twice the cycle length of two sinus P waves.
●If the premature beat collides with the sinus node impulse in the sinoatrial
junction, the sinus node activity is not suppressed and there is a true
compensatory pause seen. The cycle length between the sinus beat just prior
to and the first beat after the ectopic beat is twice the cycle length of two
successive sinus beats.
●If the PAC is appropriately timed such that it only results in a slowing of
impulse conduction through the sinoatrial junction, as opposed to block, there
is a delay in atrial activation of the next sinus beat, and the compensatory
pause will have a cycle length greater than two sinus beat cycle lengths.
●If there is sinus node dysfunction present, the PAC may depress the sinus
node and there may be a long delay before sinus node automaticity recovers.
In this situation, the pause is much longer than a full compensatory pause.
●The PAC is said to be interpolated when it does not affect the sinus node and
sinus rhythm is not altered.
Nonconducted or blocked PACs occur when there is premature activation of the atrial
myocardium from an ectopic atrial focus at a time when the AV node is still refractory
due to the previous sinus beat (waveform 8). Since the block is in the AV node, there is
an isolated P wave with no QRS. The P wave may be difficult to see if it is located within
the ST segment or T wave of the prior beat.
Aberrant conduction of a PAC generally occurs when there is conduction delay or block
within the right or left bundle branches, although abnormal conduction along an
accessory pathway can also be a cause (waveform 9). The PAC is conducted through
the AV junction but reaches one of the bundles or its fascicles at a time when it has not
yet recovered and is still relatively refractory. Impulse conduction via this pathway is
therefore blocked, although conduction will occur normally through the other parts of the
His-Purkinje system. This results in a right or left bundle branch block pattern,
depending on which bundle or fascicle is involved. The mechanism is similar to
Ashman’s phenomenon. (See "ECG tutorial: Intraventricular block", section on
'Ashman's phenomenon'.)
ATRIAL FIBRILLATION AND ATRIAL FLUTTER These topics are
discussed in detail elsewhere. (See "The electrocardiogram in atrial

fibrillation" and "Electrocardiographic and electrophysiologic features of atrial flutter".)
ATRIOVENTRICULAR NODAL REENTRANT
TACHYCARDIA Atrioventricular nodal reentrant tachycardia (AVNRT, also
called "junctional reciprocating tachycardia") is a supraventricular tachyarrhythmia that

originates within the AV node and adjacent atrial myocardium and is the result of dual
pathways entering the compact AV node (waveform 10). (See "Atrioventricular nodal
reentrant tachycardia" and "Narrow QRS complex tachycardias: Clinical manifestations,
diagnosis, and evaluation".)
The rate is generally between 140 to 220 beats per minute and there is usually 1:1 AV
association; as a result, every QRS complex has an associated P wave. Rarely is there
2:1 AV block (due to lower common pathway, infra-nodal or infra-Hisian block) with two
P waves and one QRS, or 2:1 VA block (due to upper common pathway block) with two
QRS complexes for every P wave.
Atrial and ventricular activation are usually simultaneous; as a result, a P wave is

superimposed upon the QRS complex and therefore not obvious on the surface
electrocardiogram. In some cases, the P wave may fuse with the terminal portion of the
QRS complex producing a pseudo-r' in lead V1 and/or a pseudo-S in the inferior leads
(figure 1). This is referred to as "typical" or "slow-fast" tachycardia since the antegrade
limb to the ventricles is a slow pathway while the retrograde limb back to the atrium is a
fast pathway. Less frequently, AVNRT will be associated with a long RP interval, also
called “atypical AVNRT” (figure 2). This occurs when there are two slow pathways and
no fast pathway (termed "slow-slow") or there is antegrade conduction via the fast
pathway with retrograde conduction to the atrium via the slow pathway (called "fast-
slow").
In contrast to an atrial tachycardia, AVNRT usually starts and stops abruptly and does
not usually manifest a warm-up or cool-down period. (See "Narrow QRS complex
tachycardias: Clinical manifestations, diagnosis, and evaluation".)
Since this arrhythmia is usually initiated by a PAC, there is an initial ectopic atrial P wave
and prolonged PR interval. Infrequently, a premature ventricular complex/contraction
(PVC; also referred to as premature ventricular beats or premature ventricular
depolarizations) initiates AVNRT as a result of retrograde conduction through the AV
node.
ATRIOVENTRICULAR REENTRANT
TACHYCARDIA Atrioventricular reentrant tachycardia (AVRT), or
atrioventricular reciprocating tachycardia, is a supraventricular tachycardia that utilizes

an accessory pathway between the atria and ventricles. It is frequently, but not
exclusively, associated with a preexcitation syndrome (ie, the Wolff-Parkinson-White
syndrome) (waveform 11), since pathways may conduct antegrade only, retrograde
only, or antegrade and retrograde. Retrograde only pathways cannot be seen on the
ECG. The circuit involved in this reentrant arrhythmia includes the accessory bypass
tract, AV node, and His Purkinje system, as well as the atria and ventricles.
(See "Anatomy, pathophysiology, and localization of accessory pathways in the
preexcitation syndrome".)
The most common type of AVRT uses the AV node and His Purkinje system (which has
a relatively short refractory period) for antegrade conduction to the ventricles and the
accessory pathway (which in these patients has a relatively long antegrade refractory
period when compared to the node) for retrograde conduction. During this type of
arrhythmia, called "orthodromic AVRT," QRS complexes are narrow (figure
3 and waveform 12). There is always 1:1 conduction of the impulse between the atria
and ventricles since both structures, along with the AV node and accessory pathway,
are a necessary part of the circuit. Since there is retrograde activation of the atrium
during orthodromic AVRT, a negative P wave may be seen in the inferior leads with a
short RP interval.
Less commonly, particularly when the refractory period of the accessory pathway is
shorter than that of the AV node and the His Purkinje system, the antegrade limb of the
circuit activating the ventricle is the accessory pathway and the impulse is conducted
retrogradely to the atrium via the His-Purkinje and AV node (figure 4). In this
tachycardia, called "antidromic AVRT," the QRS complexes are maximally pre-excited
and very wide, and there is a retrograde (and negative) P wave in lead II (waveform 13).
This form of AVRT may be difficult to distinguish from ventricular tachycardia.
(See "Wide QRS complex tachycardias: Approach to the diagnosis".)
ATRIOFASCICULAR AND MAHAIM FIBER
TACHYCARDIAS Atriofascicular pathways are rare types of bypass tracts. In
contrast to atrioventricular bypass pathways in the classic Wolff-Parkinson-White

syndrome, atriofascicular pathways are typically found along the tricuspid annulus and
connect directly into the right bundle branch system. Conduction is decremental, like
that in the atrioventricular (AV) node, such that faster heart rates (eg, with atrial pacing)
or spontaneous premature atrial complexes can lead to a prolongation of the PR
interval. Since the tachycardia circuit only conducts down the atriofascicular pathway
and then up the AV node (antidromic pathway), clinicians usually observe a wide QRS
with a left bundle branch block morphology, an R wave in lead I, and a QRS transition
zone usually at or to the left of lead V4. (See "Anatomy, pathophysiology, and
localization of accessory pathways in the preexcitation syndrome" and "General
principles of asynchronous activation and preexcitation".)
Mahaim fibers, which include nodoventricular or nodofascicular pathways, may also be
an unusual cause of supraventricular tachycardia. (See "Atriofascicular ("Mahaim")
pathway tachycardia".)
JUNCTIONAL ECTOPIC RHYTHM Junctional ectopic rhythm is most
often the result of an acceleration of impulse generation from the atrioventricular (AV)
junction, which, if more rapid than the sinus node rate, assumes control as the dominant
pacemaker of the heart (figure 5). In such cases, there are no P waves seen before the
QRS complexes; instead, they occur either simultaneously with the QRS complexes or
more commonly are retrograde (seen after the QRS complex located in the ST segment
or T wave). Sinus node activity is suppressed by the retrograde atrial activation. If there
is retrograde AV block of the impulse to the atrium, sinus node activity is not suppressed
by the junctional rhythm, and sinus P waves can be seen occurring independently at a
slower rate than the QRS complexes. This is known as AV dissociation. When the
junctional rhythm is faster than 100 beats/min, it is called junctional tachycardia. In some
cases, the junctional ectopic rhythm develops because there is failure of the sinus node.
Since the rate is slower than the expected sinus rate, it is known as a junctional escape
rhythm.
JUNCTIONAL PREMATURE BEATS Junctional premature beats are
early ectopic beats that originate in or near the atrioventricular (AV) junction and have a
QRS morphology that resembles the sinus complex (waveform 14). Although their timing
and morphology are similar to that of a premature atrial complexes, there is no P wave
present before the QRS complex, though a P wave may be noted after the QRS
complex if there is retrograde conduction through the AV node.
As with atrial premature beats, junctional premature beats may occasionally be

conducted with a bundle branch block pattern. In addition, junctional premature beats
may occur with a bigeminal or trigeminal pattern.
JUNCTIONAL ESCAPE BEATS Junctional escape beats or rhythm occur
when there is failure of upper pacemaker tissue (in other words, the absence of impulse
generation from the sinus node or atrial myocardium or with complete AV block). These
beats occur after a variable pause that is longer than the underlying sinus cycle length
(waveform 15).
In this arrhythmia, there are one or more normal QRS complexes that are not preceded
by a P wave. If there is retrograde conduction through the atrioventricular (AV) node,
retrograde P waves may be seen after each QRS complex, in the ST segment, or in the
T wave.
The rate is slower than that of the underlying sinus rate. An escape junctional rhythm
may occur during sinus arrest or when there is a complete AV block, preventing the
sinus impulse from reaching the ventricles. In this case, there are P waves that are
disassociated with the QRS complexes, and the PR intervals are variable. Such P
waves occur at a rate that is more rapid than the ventricular rate, resulting in AV
dissociation.
SUMMARY
●Atrialtachycardia occurs at 140 to 220 beats per minute and usually has 1:1
atrioventricular (AV) conduction. In some situations, there may be block within
the AV node, leading to variable or repetitive block patterns. P wave
morphology can be used to determine the atrial tachycardia site of origin.
●Wandering atrial pacemaker and multifocal atrial tachycardia demonstrate
three or more different P wave morphologies with no dominant P wave.
●AV reentrant tachycardia must have 1:1 atrial and ventricular conduction,
and, therefore, a P wave follows every QRS, even if not well seen.
●Junctional beats have a QRS morphology similar to a natively conducted
QRS, but have no P wave preceding it.
●Junctional escape beats or rhythm can occur with sinus arrest or complete
AV block.
Close
 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

 CME5.0
 Log Out

 Contents
 Calculators


Find

 Patient

 Print

 Share



 Bookmark

F
eedback
Back
Topic Outline
 SUMMARY
 INTRODUCTION
 RISK FACTORS AND DISEASE ASSOCIATIONS
 PATHOGENESIS
 NONVALVULAR VERSUS VALVULAR HEART DISEASE
 CLASSIFICATION
o General classification
o Lone atrial fibrillation
o Subclinical atrial fibrillation
 EVALUATION
o History and physical examination
o Electrocardiogram
o Echocardiogram
o Additional cardiac testing
o Baseline laboratory testing
 TREATMENT ISSUES
o Hospitalization
o New onset atrial fibrillation
 Prevention of systemic embolization
 Rate versus rhythm control
o Paroxysmal, persistent, longstanding persistent, or permanent atrial fibrillation
 Routine care
 Urgent care
 PREVENTION OF ATRIAL FIBRILLATION
 LONG-TERM OUTCOME
o Recurrence of atrial fibrillation
o Embolization
 Silent cerebral ischemia
o Mortality
o Predictors of poor outcome
o Myocardial infarction
o Prevention of adverse outcomes
 SCREENING/DETECTION
 SUMMARY
 ACKNOWLEDGMENT
 REFERENCES
GRAPHICS view all
 Figures
oPrevalence of atrial fibrillation by sex and age
oMortality men women AF
 Tables
oCHA2DS2-VASc score and risk factors
RELATED TOPICS
 Ambulatory ECG monitoring
 Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Clinical trials
 Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation: Recommendations
 Atrial fibrillation: Atrioventricular node ablation
 Atrial fibrillation: Catheter ablation
 Atrial fibrillation: Risk of embolization
 Auscultation of cardiac murmurs in adults
 Chronic kidney disease and coronary heart disease
 Control of ventricular rate in atrial fibrillation: Pharmacologic therapy
 Cryptogenic stroke
 Epidemiology of and risk factors for atrial fibrillation
 Examination of the arterial pulse
 Examination of the jugular venous pulse
 Examination of the precordial pulsation
 Goal blood pressure in adults with hypertension
 Mechanisms of atrial fibrillation
 Overview of the prevention of cardiovascular disease events in those with established disease
(secondary prevention) or at high risk
 Paroxysmal atrial fibrillation
 Patient education: Atrial fibrillation (Beyond the Basics)
 Patient education: Atrial fibrillation (The Basics)
 Patient education: Coping with high drug prices (Beyond the Basics)
 Patient education: Coping with high drug prices (The Basics)
 Patient education: Heart failure and atrial fibrillation (The Basics)
 Patient education: Medicines for atrial fibrillation (The Basics)
 Prevention of embolization prior to and after restoration of sinus rhythm in atrial fibrillation
 Role of echocardiography in atrial fibrillation
 The management of atrial fibrillation in patients with heart failure
Overview of atrial fibrillation

Author:
Kapil Kumar, MD
Section Editor:
Deputy Editor:
INTRODUCTION Atrial fibrillation (AF) is the most common cardiac arrhythmia
that has the following electrocardiographic characteristics (see "The electrocardiogram

in atrial fibrillation", section on 'Common findings'):
●The RR intervals follow no repetitive pattern. They have been labeled as
"irregularly irregular."
●While electrical activity suggestive of P waves is seen in some leads, there
are no distinct P waves. Thus, even when an atrial cycle length (the interval
between two atrial activations or the P-P interval) can be defined, it is not
regular and often less than 200 milliseconds (translating to an atrial rate
greater than 300 beats per minute).
AF can have adverse consequences related to a reduction in cardiac output and to atrial
and atrial appendage thrombus formation [1-4]. In addition, affected patients may be at
increased risk for mortality. (See 'Long-term outcome' below.)
AF is more prevalent in men and with increasing age (figure 1) [5]. (See "Epidemiology
of and risk factors for atrial fibrillation", section on 'Epidemiology'.)
This topic will provide a broad overview of AF, including the management of the patient.
The reader will be referred to more detailed discussions when appropriate.
RISK FACTORS AND DISEASE ASSOCIATIONS Hypertensive heart
disease and coronary heart disease (CHD) are the most common underlying disorders
in patients with atrial fibrillation (AF) in developed countries. Rheumatic heart disease,
although now uncommon in developed countries, is associated with a much higher
incidence of AF. (See "Epidemiology of and risk factors for atrial fibrillation", section on
'Chronic disease associations'.)
PATHOGENESIS Irrespective of the underlying risk factor(s), changes in the
electrophysiology of the atrial myocardium are likely important. The pathophysiology of

atrial fibrillation (AF) is discussed in detail elsewhere. (See "Epidemiology of and risk
factors for atrial fibrillation", section on 'Pathogenesis' and "Mechanisms of atrial
fibrillation", section on 'Basic atrial electrophysiology'.)
NONVALVULAR VERSUS VALVULAR HEART DISEASE Patients
with atrial fibrillation may or may not have valvular heart disease. This issue is of
particular importance in choosing antithrombotic therapy; it is discussed in detail
elsewhere. (See "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism",
section on 'Patients with valvular heart disease'.)
CLASSIFICATION
General classification — Historically, the terms "acute" and "chronic" atrial fibrillation

(AF) were used to describe the temporal nature of a patient’s AF. These two terms have
been replaced with the following classification schema provided in the 2014 American
Heart Association/American College of Cardiology/Heart Rhythm Society guidelines on
AF management [6-11]:
●Paroxysmal (ie, self-terminating or intermittent) AF – Paroxysmal AF is
defined as AF that terminates spontaneously or with intervention within seven
days of onset. Episodes may recur with variable frequency. (See "Paroxysmal
atrial fibrillation".)
●Persistent AF – Persistent AF is defined as AF that fails to self-terminate
within seven days. Episodes often require pharmacologic or electrical
cardioversion to restore sinus rhythm. While a patient who has had persistent
AF can have later episodes of paroxysmal AF, AF is generally considered a
progressive disease.
●Long-standing persistent AF – AF that has lasted for more than 12 months.
●Permanent AF – "Permanent AF" is a term used to identify individuals with
persistent atrial fibrillation where a joint decision by the patient and clinician
has been made to no longer pursue a rhythm control strategy.
While AF typically progresses from paroxysmal to persistent states, patients can present
with both types throughout their lives. Additionally, this classification applies to recurrent
episodes of AF that last more than 30 seconds and that are unrelated to a reversible
cause. If the AF is secondary to cardiac surgery, pericarditis, myocardial infarction (MI),
hyperthyroidism, pulmonary embolism, pulmonary disease, or other reversible causes,
therapy is directed toward the underlying disease as well as the AF. (See "Epidemiology
of and risk factors for atrial fibrillation".)
Lone atrial fibrillation — The term "lone AF" is less often used than in the past. We
and others do not think that the use of the term improves the understanding of the
mechanism of AF or the care of the patient [12].
Lone AF has generally referred to patients with paroxysmal, persistent, or permanent AF
who have no structural heart disease. It has primarily been applied to patients ≤60 years
of age and identifies a group of individuals at lowest risk of complications associated
with AF, including embolization. By definition, such patients have a CHA 2DS2-VASc
score of "0". (See "Atrial fibrillation: Risk of embolization", section on 'Epidemiology'.)
Subclinical atrial fibrillation — Subclinical AF (SCAF) is defined as episodes of AF
detected by intracardiac, implantable, or wearable monitors and confirmed by
intracardiac electrogram or review of the recorded rhythm on the ECG [13]. SCAF
usually occurs in individuals without characteristic symptoms of AF and without a prior
diagnosis. Most of these individuals will have paroxysmal AF. A scientific statement from
the American Heart Association on subclinical and device-detected AF was published in
2019 [13]. (See "Paroxysmal atrial fibrillation", section on 'Signs and symptoms of AF'.)
The prevalence of SCAF depends on the population studied as well as the duration,
sensitivity, and specificity of screening techniques. The following studies investigated the
prevalence of subclinical AF in different populations, using different monitoring
techniques:
●In the STROKESTOP observational study of 7173 individuals 75 to 76 years

of age in Sweden, previously unknown AF was detected using intermittent
electrocardiographic recordings over three weeks in 3 percent [14].
●The ASSERT study monitored (using a dual chamber pacemaker or
implantable cardioverter defibrillator) 2580 patients (65 years or older) with
hypertension and no history of AF for the development of AF (defined as
episodes of atrial rate >190 beats per minute for more than six minutes) [15].
The following findings were noted:
•At three months, subclinical AF was detected in about 10 percent of
patients. The median number of episodes was two, and the median time
to detection of the first episode was 36 days.
•At 2.5 years, SCAF was detected in about 35 percent of individuals.
Clinical AF developed in about 16 percent of patients with SCAF.
•This study also evaluated the relationship between the presence of
SCAF and stroke. This issue is discussed elsewhere. (See "Cryptogenic
stroke", section on 'Occult atrial fibrillation'.)
●In the ASSERT-II study of 256 patients (mean age of 74 years; mean
CHA2DS2-VASc score of 4.1) with an implanted subcutaneous
electrocardiographic monitor who were followed for about 16 months, one or
more episodes of SCAF lasting ≥5 minutes occurred in 34 percent [16]. This
was a high-risk population, as 48 percent (of the 256 patients) had prior
stroke, transient ischemic attack, or systemic embolism.
●Two studies have evaluated the prevalence of AF specifically in individuals
with cryptogenic transient ischemic attack or stroke (see "Cryptogenic stroke",
section on 'Occult atrial fibrillation'):
•In a study of 56 patients who were evaluated with an outpatient mobile
cardiac monitor for a mean of 21 days, AF was detected in 23 percent
[17].
•In a study of 149 patients who were evaluated with either a 24-hour
Holter monitor or, if that study was normal, an event-loop recording device
for seven days, AF was detected in 11 percent [18].
●Ina study of 590 individuals with stroke risk factors but without AF who
underwent screening with an implantable loop recorder for an average of 40
months, 35 percent of participants were found to have AF [19].
Additional information is as follows:
●Multiple studies have generally found that a higher CHA 2DS2-VASc score
(table 1) is predictive [13]. The individual studies were inconsistent regarding
the predictive ability of the individual components of the score.
●SCAF often progresses to clinical AF [20].
●SCAF is often found in patients with heart failure [13]. (See "The
management of atrial fibrillation in patients with heart failure" and "The
management of atrial fibrillation in patients with heart failure", section on
'Prevalence'.)
●SCAF is associated with an increased risk of stroke. (See "Cryptogenic
stroke", section on 'Occult atrial fibrillation'.)
Finally, it is not known whether the approach to anticoagulation in patients with SCAF
should be identical to that in patients with symptoms. This issue is discussed separately.
(See "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism", section on
'Short duration atrial fibrillation'.)
EVALUATION The history, physical examination, and specific laboratory and
cardiologic testing are all part of the evaluation of the patient with atrial fibrillation (AF).
History and physical examination — Not all patients with AF are symptomatic. Among
those that are, symptoms associated with AF are variable and the history should focus
on obtaining the following information:
●A description of the symptoms: onset or date of discovery, the frequency and
duration, severity, and qualitative characteristics.
Typical symptoms include palpitations, tachycardia, fatigue, weakness,
dizziness, lightheadedness, reduced exercise capacity, increased urination, or
mild dyspnea. More severe symptoms include dyspnea at rest, angina,
presyncope, or infrequently, syncope. In addition, some patients present with
an embolic event or the insidious onset of heart failure (as manifested by
pulmonary edema, peripheral edema, weight gain, and ascites).
A semi-quantitative method to classify symptoms has been developed, but the
clinical utility of such a system has not been demonstrated [21].
●Precipitating causes: exercise, emotion, or alcohol.
●The presence of the following disease associations: cardiovascular or
cerebrovascular disease, diabetes, hypertension, chronic obstructive
pulmonary disease, obstructive sleep apnea, or potentially reversible causes
(eg, hyperthyroidism, excessive alcohol ingestion). (See "Epidemiology of and
risk factors for atrial fibrillation".)
●A complete examination of the cardiovascular system should be performed in
all individuals with newly diagnosed AF and in those with a change in
symptom status. Abnormal findings may inform healthcare providers about
either contributing factors for (eg, murmur of mitral stenosis) or the impact of
(eg, evidence of heart failure) AF. (See "Examination of the precordial
pulsation" and "Auscultation of cardiac murmurs in adults" and "Examination of
the jugular venous pulse" and "Examination of the arterial pulse".)
Electrocardiogram — The electrocardiogram (ECG) is used to verify the presence of
AF and is necessary to make the diagnosis. AF has the following electrocardiographic
characteristics (see "The electrocardiogram in atrial fibrillation", section on 'Common
findings'):
●The RR intervals follow no repetitive pattern. They have been labeled as
"irregularly irregular."
●While electrical activity suggestive of P waves may be seen in some leads,
there are no distinct P waves. Thus, even when an atrial cycle length (the
interval between two atrial activations or the P-P interval) can be defined, it is
not regular and often less than 200 milliseconds (translating to an atrial rate
greater than 300 beats per minute).
There are a number of potential pitfalls in the electrocardiographic diagnosis of AF.
Errors in the diagnosis of AF are especially common with computerized ECG
interpretation and in patients who are continuously or intermittently paced. Hence, it is
important that the automated ECG interpretation provided by the machine is confirmed
by a skilled reader. (See "The electrocardiogram in atrial fibrillation", section on
'Difficulties in diagnosis'.)
A baseline ECG, preferably in sinus rhythm, should also be evaluated for the following
information:
●Markers of nonelectrical cardiac disease, such as left ventricular hypertrophy

(possible hypertension) or Q waves (possible coronary artery disease).
●Markers of electrical heart disease, including the presence of ventricular pre-
excitation or infranodal conduction disease (bundle branch block).
●The QT interval (to identify the potential risk of antiarrhythmic therapy)
●Evidence of severe bradycardia or sinus node dysfunction
Echocardiogram — The transthoracic echocardiogram (TTE) is performed to evaluate
the size of the right and left atria and the size and function of the right and left ventricles;
to detect possible valvular heart disease, left ventricular hypertrophy, and pericardial
disease; and to assess peak right ventricular pressure.
The TTE may also identify left atrial thrombus, although the sensitivity is low.
Transesophageal echocardiography is much more sensitive for identifying thrombi in the
left atrium or left atrial appendage and can be used to determine the need for
anticoagulation prior to any attempt at pharmacologic or electrical cardioversion.
(See "Role of echocardiography in atrial fibrillation" and 'Prevention of systemic
embolization' below.)
Additional cardiac testing — Exercise testing is reasonable for patients with signs or
symptoms of ischemic heart disease. It is also useful to help guide pharmacotherapy for
AF, as some antiarrhythmic medications are contraindicated in patients with coronary
artery disease. In addition, stress testing may be helpful in gauging adequacy of heart
rate control in AF during exercise. Insufficient heart rate control in AF is a major factor
for exercise intolerance in AF. (See "Antiarrhythmic drugs to maintain sinus rhythm in
patients with atrial fibrillation: Recommendations", section on 'Selecting an
antiarrhythmic drug'.)
Ambulatory cardiac monitoring with event recorders, adhesive extended time event
monitors, or insertable cardiac monitors (ICM; also sometimes referred to as implantable
cardiac monitor or implantable loop recorder) can be used to identify the arrhythmia if it
is intermittent and not captured on routine electrocardiography. Ambulatory ECG
monitoring can also be utilized to correlate symptoms to the arrhythmia along with
assessment of the AF burden. Twenty-four- to 48-hour Holter monitoring mainly aids in
the evaluation of overall ventricular response rates in individuals where a rate control
strategy has been chosen and there is concern for inadequate heart rate control or
bradycardia. (See "Ambulatory ECG monitoring".)
Baseline laboratory testing — Clinical or subclinical hyperthyroidism is present in less
than 5 percent of patients with AF [22]. A thyroid-stimulating hormone (TSH) and free T4
levels should be obtained in all patients with a first episode of AF, or in those who
develop an increase in AF frequency. (See "Epidemiology of and risk factors for atrial
fibrillation", section on 'Hyperthyroidism'.)
Other important baseline tests include a complete blood count, a serum creatinine, and
a test for diabetes mellitus [23].
TREATMENT ISSUES Healthcare providers are presented with two broad
types of patients with atrial fibrillation (AF): those with newly diagnosed AF and those
who have been previously diagnosed and managed. Care of the former includes
decisions regarding the need for anticoagulation and the choice between rate or rhythm
control strategies. For patients with established diagnosis, periodic assessment of the
adequacy of treatment is necessary.
Hospitalization — Some patients with AF may require care at an acute care facility or
an inpatient unit of a hospital. Common indications for care at one or both of these
facilities include:
●Management of heart failure, hypotension, or difficulty with rate control.
●Initiation of antiarrhythmic drug therapy.
●Treatment of an associated medical problem, which is often the reason for
the arrhythmia. Examples include the treatment of hypertension, infection,
thyroid storm, exacerbation of chronic obstructive pulmonary disease,
pulmonary embolism, persistent myocardial ischemia, or acute pericarditis.
Other indications for hospitalization are discussed separately. (See "New onset atrial
fibrillation", section on 'Indications for hospitalization'.)
New onset atrial fibrillation — Most patients with new onset (ie, first detected or
diagnosed) AF present with symptoms related to the arrhythmia. (See 'History and
physical examination' above.) Except for embolization, the symptoms associated with
new onset AF are primarily due to a rapid ventricular response. Thus, many patients
have dramatic improvement in their sense of well-being when the ventricular rate is
slowed. (See "New onset atrial fibrillation", section on 'Rate control'.)
There are two broad management issues that must be addressed early in patients with
new onset AF: the prevention of systemic embolization and the choice between a
rhythm or rate control strategy, both of which may improve symptoms. These issues will
be addressed briefly here. More detailed discussions are found elsewhere.
(See "Rhythm control versus rate control in atrial fibrillation" and "Atrial fibrillation:
Anticoagulant therapy to prevent thromboembolism".)
Prevention of systemic embolization — Every patient with AF should be evaluated for
the need of antithrombotic therapy to prevent systemic embolization even for the first AF
episode. This is accomplished by use of the CHA 2DS2-VASc score (table 1). Patients
who require antithrombotic therapy include those in whom cardioversion (whether
electrically or pharmacologically) to sinus rhythm is being considered (regardless of the
CHA2DS2-VASc score or method of cardioversion [electrical or pharmacologic]) and
those who meet criteria for long-term anticoagulation. All patients whose risk of
embolization exceeds the risk of bleeding are candidates for long-term antithrombotic
therapy. These issues are discussed in detail elsewhere. (See "Prevention of
embolization prior to and after restoration of sinus rhythm in atrial fibrillation" and "Atrial
fibrillation: Anticoagulant therapy to prevent thromboembolism".)
Rate versus rhythm control — Most patients who present with AF will require slowing
of the ventricular rate to improve symptoms. (See "Control of ventricular rate in atrial
fibrillation: Pharmacologic therapy".)
Once ventricular rate control is achieved, a decision regarding the long-term
management (rhythm versus rate control) of AF should be made. A rhythm control
strategy uses either antiarrhythmic drug therapy, percutaneous catheter ablation, and/or
a surgical procedure. Electrical cardioversion may be necessary to restore sinus rhythm.
Antiarrhythmic medications are generally started before cardioversion and continued to
maintain sinus rhythm (in the event of AF recurrence). (See "Surgical ablation to prevent
recurrent atrial fibrillation", section on 'Maze procedure' and "Atrial fibrillation: Catheter
ablation", section on 'Efficacy'.)
A rate control strategy generally uses drugs that slow conduction across the
atrioventricular (AV) node, such as beta blockers, non-dihydropyridine calcium channel
blockers, or digoxin. (See "Rhythm control versus rate control in atrial fibrillation",
section on 'Definitions'.)
Data suggest that rhythm and rate control strategies are associated with similar rates of
mortality and serious morbidity, such as embolic risk. However, there are several
reasons why pursuing a rhythm-control strategy would be preferred, including symptom
improvement, younger patient age, and irreversible structural and electrical remodeling
that can occur with longstanding persistent AF. (See "Rhythm control versus rate control
in atrial fibrillation", section on 'Comparative studies'.)
The decision to adopt a rhythm or rate control strategy is often dictated by the (1)
presence of symptoms associated with atrial fibrillation and/or (2) development of left
ventricular systolic dysfunction thought secondary to the arrhythmia. Some patients with
new onset AF who report being asymptomatic may have some subtle symptoms such as
fatigue, especially when palpitations are not a prominent component of the presentation.
These more subtle symptoms are sometimes only realized after restoration of sinus
rhythm, which is why many physicians will at least offer a rhythm control approach to
new onset AF patients. (See "Rhythm control versus rate control in atrial fibrillation",
section on 'Preference for rate control' and "Rhythm control versus rate control in atrial
fibrillation", section on 'Preference for rhythm control'.)
The methods to achieve either rate or rhythm control are discussed in detail elsewhere.
(See "New onset atrial fibrillation" and "Antiarrhythmic drugs to maintain sinus rhythm in
patients with atrial fibrillation: Recommendations" and "Atrial fibrillation:
Cardioversion" and "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial
fibrillation: Clinical trials" and "Atrial fibrillation: Atrioventricular node
ablation" and "Control of ventricular rate in atrial fibrillation: Pharmacologic
therapy" and "Surgical ablation to prevent recurrent atrial fibrillation" and "Atrial
fibrillation: Catheter ablation".)
Paroxysmal, persistent, longstanding persistent, or permanent atrial
fibrillation — Patients with paroxysmal, persistent, longstanding persistent, or
permanent AF will need periodic care as well as occasional urgent evaluation during the
natural history of their disease. (See 'Classification' above.)
We suggest routine follow-up every 12 months in stable patients and sooner if there are
changes in symptoms. Patients on high-risk antiarrhythmic therapy, such
as dofetilide or sotalol, are often seen every six months.
Routine care — From time to time, patients should be monitored for the following:
●Efficacy and safety of antithrombotic therapy (International Normalized Ratio
for patients on warfarin and creatinine clearance for patients on antiarrhythmic
therapy and other newer anticoagulants). (See "Atrial fibrillation: Anticoagulant
therapy to prevent thromboembolism", section on 'Select an anticoagulant'.)
●Functional status, including change in symptoms (history).
●Efficacy and safety of antiarrhythmic drug therapy (electrocardiogram [ECG],
assessment of renal and hepatic function, and perhaps other tests).
(See "Antiarrhythmic drugs to maintain sinus rhythm in patients with atrial
fibrillation: Recommendations".)
●Efficacy of rate control (history, ECG, and perhaps extended Holter
monitoring). (See "Control of ventricular rate in atrial fibrillation: Pharmacologic
therapy".)
Urgent care — Urgent care is necessary in patients who present with symptoms or
signs of symptomatic AF. (See 'History and physical examination' above.)
In addition to evaluating the efficacy of rate or rhythm control, the healthcare provider
may need to evaluate and manage changes in the symptoms and signs of coronary
artery disease or heart failure.
PREVENTION OF ATRIAL FIBRILLATION Risk factors for the
development of new or recurrent AF have been identified (see "Epidemiology of and risk

factors for atrial fibrillation"). However, for many of these, preventive strategies that
significantly reduce the risk have not been identified. The following are possible
preventive strategies:
●There is weak evidence that dietary modifications, such as extra virgin olive
oil or n-3 polyunsaturated fatty acids (n-3 PUFA) in fish oil, lower the risk of the
development of AF [24,25].
●The PREDIMED primary prevention trial found that a Mediterranean diet
enriched with either extra virgin olive oil or mixed nuts reduces the incidence
of stroke, myocardial infarction, and cardiovascular mortality [26]
(see "Overview of the prevention of cardiovascular disease events in those
with established disease (secondary prevention) or at high risk", section on
'Diet'). In a post-hoc analysis of PREDIMED, the group that received the
Mediterranean diet supplemented with extra virgin olive oil had a lower risk of
development of AF compared to the control group (hazard ratio 0.62; 95% CI
0.45-0.85) [27].
●Physical activity and weight loss can significantly reduce AF burden [28,29].
●Alcohol is a modifiable risk factor for AF, and abstinence (or a significant
reduction in weekly consumption) in those who consume an excessive amount
appears to decrease the risk of recurrent AF or the time in AF. The issue was
evaluated in a study of 140 symptomatic patients with paroxysmal or
persistent AF who were in sinus rhythm at baseline and who consumed 10 or
more standard drinks per week (about 120 grams of pure alcohol). Individuals
were randomly assigned to alcohol abstention or usual alcohol consumption
and followed for six months [30]. All patients underwent comprehensive
rhythm monitoring. Individuals in the abstinence group reduced their alcohol
intake from 16.8 to 2.1 standard drinks per week, while those in the usual
consumption group reduced their consumption from 16.4 to 13.2 per week.
After a two-week blanking period, AF recurred in 53 and 73 percent of the two
groups, respectively, during follow-up. In addition, recurrence of AF was
delayed in the abstinence group, and the AF burden was significantly lower.
●There is some evidence that lowering blood pressure in hypertensive patients
reduced the risk of the development of AF. In the SPRINT trial, intensive
compared with standard blood pressure lowering was associated with a lower
risk of developing new AF (hazard ratio 0.74, 95% CI 0.56-0.98) [31].
(See "Goal blood pressure in adults with hypertension", section on 'Patients
with established atherosclerotic cardiovascular disease'.)
LONG-TERM OUTCOME
Recurrence of atrial fibrillation — Continuous monitoring studies have shown that

approximately 90 percent of patients have recurrent episodes of atrial fibrillation (AF)
[32]. However, up to 90 percent of episodes are not recognized by the patient [33], and
asymptomatic episodes lasting more than 48 hours are not uncommon, occurring in 17
percent of patients in a report using continuous monitoring [32]. The latter study also
showed that 40 percent of patients had episodes of AF-like symptoms in the absence of
AF [32]. (See "Paroxysmal atrial fibrillation".)
Embolization — Systemic embolization, and particularly stroke, is the most frequent
major complication of AF. This issue is discussed separately. (See "Atrial fibrillation:
Risk of embolization" and "Atrial fibrillation: Anticoagulant therapy to prevent
thromboembolism".)
Silent cerebral ischemia — Silent cerebral ischemia (SCI) occurs in a patient who has
specific lesions on imaging studies in the absence of clinical complaints or findings.
These lesions have a radiographic appearance consistent with cerebral infarction.
In a systematic review and meta-analysis of 17 studies, the overall prevalence of SCI
lesions on magnetic resonance imaging and computed tomography among patients with
AF was 40 and 22 percent, respectively [34]. In this review, AF was associated with
more than a twofold increased risk of SCI in patients with no history of symptomatic
stroke (odds ratio, 2.62, 95% CI 1.81-3.80) in 11 studies. However, most studies pooled
in this meta-analysis were cross-sectional, making uncertain the causal link between AF
and silent cerebral infarction.
The potential relationship of SCI to cognitive performance in patients with AF was
studied in a registry that included 90 patients with paroxysmal and 90 patients with
persistent AF, as well as 90 matched controls [35]. Patients received clinical
assessment, which included a medical history, physical examination with standardized
neurologic examination, brain magnetic resonance imaging, and the Repeatable Battery
for the Assessment of Neuropsychological Status (RBANS) test for cognitive impairment
[36]. At least one SCI was present in 89, 92, and 46 percent of the three groups,
respectively (p<0.01 for both groups compared to controls), and the number of SCI
lesions per person was significantly higher in the persistent group than the paroxysmal
group (with both groups higher than controls). Cognitive impairment was significantly
greater in persistent and paroxysmal AF patients compared to controls.
Further evidence in support of the relationship between AF and development of
dementia, as well as the impact of anticoagulation, comes from two population cohort
studies. Age- and sex-matched individuals from the United Kingdom Clinical Practice
Research Datalink (2008 to 2016) with and without a diagnosis of AF were selected and
followed for development of new dementia [37]. Over 193,082 person-years, the AF
group had a higher rate of dementia. Furthermore, after excluding patients with a history
of transient ischemic attack/stroke, only those AF patients not on anticoagulants had a
significantly higher rate of dementia than non-AF patients (adjusted HR 1.42, 95% CI
1.18–1.72 without anticoagulation and HR 1.09, 95% CI 0.87–1.36 with
anticoagulation). Anticoagulation protected against the development of dementia,
presumably by a reduction of SCI. Similarly, 2685 dementia-free participants from the
Swedish National Study on Aging and Care were followed for nine years [38]. AF was
associated with a significantly faster annual Mini-Mental State Examination decline and
an increased HR of all-cause dementia (HR 1.40, 95% CI 1.11-1.77) and vascular and
mixed dementia (HR 1.88, 95% CI 1.09-3.23), but not Alzheimer disease (HR 1.33, 95%
CI 0.92-1.94). In addition, the use of anticoagulants, but not antiplatelet medications,
was associated with a 60 percent decrease in the risk of cognitive decline (HR 0.40,
95% CI 0.18-0.92).
It is unclear if episodes of AF are acute triggers of stroke or if AF is simply a marker of
left atrial dysfunction that predisposes an increased risk for stroke [39]. This was
highlighted in an analysis of the ASSERT trial that showed very few individuals with
subclinical AF who developed a stroke had AF in the month prior to their embolic event
[40]. Another concern is that patients with paroxysmal AF felt to be at high risk for stroke
also have a high risk for atherosclerosis, and as indicated above, there may be other
non-cardiac reasons for stroke in these patients, especially aortic plaques.
Mortality — AF is an independent risk factor for mortality across a wide age range and
in both men and women. However, we and others believe the evidence is insufficient to
label AF as causal [41]. The following studies illustrate the range of risk:
●In a secondary analysis of the randomized controlled AFFIRM trial of rhythm
versus rate control in AF, the presence of sinus rhythm was associated with a
significant reduction in mortality (hazard ratio 0.53) [42]. A similar benefit from
being in sinus rhythm (relative risk 0.44) was noted in the DIAMOND trial that
compared dofetilide to placebo in patients with reduced left ventricular function
[43].
●In a retrospective observational study of 272,186 patients with incidental AF
at the time of hospitalization and 544,344 matched AF-free controls, the
adjusted relative risk of death for women and men <65 years was 2.15 and
1.76 (respectively); 65 to 74 years was 1.72 and 1.36; and 75 to 85 years was
1.44 and 1.24 [44]. All values were statistically significant.
●In a report from the Framingham Heart Study 621 subjects between the ages
of 55 and 94 who developed AF were compared to those who did not [45]. AF
almost doubled the risk of death in both men and women (figure 2). After
adjustment for the pre-existing cardiovascular diseases with which AF was
associated, AF was still associated with a significantly increased risk of death
(odds ratio 1.9 for women and 1.5 for men). Both heart failure (HF) and stroke
contributed to the excess mortality.
●In a 20-year follow-up of over 15,000 men and women between the ages of
45 and 64 in which 47 women and 53 men had AF on a single
electrocardiogram (ECG) at baseline, the presence of AF was associated with
a marked increase in the risk of a cardiovascular event (death or
hospitalization) (89 versus 27 percent in women and 66 versus 45 percent in
men) and was a significant independent predictor of all-cause mortality
(relative risk 2.2 in women and 1.5 in men) [46].
In a post-hoc analysis of the Women’s Health Study of 34,772 women with a median
age of 53 who were free of AF, about 3 percent developed AF at a median follow-up of
15.4 years [47]. New onset AF was associated with a significantly increased adjusted
risk of all-cause, cardiovascular, and non-cardiovascular mortality (hazard ratios [HR]
2.14, 95% CI 1.64-2.77; 4.18, 95% CI 2.69-6.51; and 1.66, 95% CI 1.19-2.30,
respectively). Adjustment for nonfatal cardiovascular events, such as myocardial
infarction, stroke, or heart failure, lowered these risks but incident AF remained
significantly associated with all types of mortality (HR 1.7, 2.57, and 1.42, respectively).
The coexistence of cardiovascular disease and chronic AF worsens the patient's
prognosis, doubling the cardiovascular mortality [48]:
●In patients with a recent myocardial infarction (MI), the development of AF
increases mortality [49,50]. This effect is primarily due to associated risk
factors, such as HF and cardiogenic shock, not AF itself [50,51].
●The effect of AF in the setting of HF is less clear, since published studies
have yielded conflicting results and any effect of AF to increase mortality may
have diminished with better treatment of HF. (See "The management of atrial
fibrillation in patients with heart failure", section on 'Prevalence'.)
In addition, in an observational study of over 20,000 individuals in two cohorts, incident
AF was associated with an increased risk of sudden cardiac death (hazard ratio 2.47,
95% CI 1.95-3.13) as well as non-sudden cardiac death (hazard ratio 2.98, 95% CI 2.52-
3.53) [52]. This study reconfirms that AF is associated with increased all-cause mortality
(with death often attributable to events related to coronary artery disease and stroke)
and it advances our knowledge in that it demonstrates that there is a proportional
increase in sudden death as well.
None of these nonrandomized observations prove that AF directly causes an increase in
mortality, since they cannot distinguish this possibility from AF being a marker of a
confounding factor or factors that affect survival.
The specific causes of death, as well as their frequency and predictors, were evaluated
using follow-up data from the RE-LY trial comparing dabigatran to warfarin [53].
(See "Atrial fibrillation: Anticoagulant therapy to prevent thromboembolism", section on
'Select an anticoagulant'.) Among 18,113 randomized patients with a median follow-up
of two years, the annual mortality rate was 3.84 percent. Cardiac deaths (sudden
cardiac death and progressive heart failure) accounted for 37.4 percent of these; stroke
and hemorrhagic death accounted for 9.9 percent.
Predictors of poor outcome — In the RE-LY trial (see 'Mortality' above), the strongest
independent clinical predictors of cardiac death were heart failure, intraventricular
conduction delay on an electrocardiogram, and prior myocardial infarction [53].
In a post-hoc analysis of the RACE II trial, the risk of cardiovascular morbidity and
mortality was highest in those with the greatest symptom burden as assessed with the
Toronto AF Severity Scale [54]. This finding was driven by the increased rate of heart
failure hospitalizations.
Beta-trace protein (BTP), which is found in myocardial cells, is a proposed marker for
renal damage. (See "Chronic kidney disease and coronary heart disease", section on
'Cystatin C and other markers of kidney function'.) In a study of 1279 anticoagulated AF
patients, elevated BTP was associated with mortality (hazard ratio 2.08, 95% CI 1.49-
2.90), even after adjusting for CHA2DS2-VASc factors (table 1) and renal function [55].
The significance of this association will need to be validated in larger, independent
cohorts. The findings are intriguing and potentially point to a risk factor that has yet to be
recognized by the CHA2DS2-VASc score. (See "Atrial fibrillation: Risk of embolization",
section on 'Options for estimating risk in the individual patient'.)
Myocardial infarction — MI is a risk factor for AF. (See "Epidemiology of and risk
factors for atrial fibrillation", section on 'Coronary disease'.)
Although there have been observations of MI after AF, including proven cases of MI due
to thromboembolism, the association between AF and MI has not been formally
evaluated [56,57]. This relationship was evaluated using data from the prospective
cohort (the REGARDS cohort) study of nearly 24,000 United States citizens without
coronary heart disease [58]. After adjustment for multiple risk factors, AF at baseline
was associated with an increased risk of incident MI (hazard ratio [HR] 1.70, 95% CI
1.26-2.30). In subgroup analysis, the risk was significantly higher in women and blacks
(HR 2.16 and 2.53) but not men or whites. Mechanisms to explain the relationship are
speculative.
Prevention of adverse outcomes — There is some evidence that a higher level of
physical activity and overall cardiorespiratory fitness are associated with a lower rate of
these outcomes. In a prospective study of over 1100 individuals with AF, patients
meeting physical activity guidelines had a lower risk of cardiovascular mortality
compared with inactive patients (hazard ratio 0.54, 95% CI 0.34-0.86) over a median
follow-up of seven years [59,60]
SCREENING/DETECTION Despite the known increase in morbidity, such
as stroke, and mortality in patients with atrial fibrillation (AF), the issues of how or
whether to screen for AF have not been well studied. No studies have demonstrated
improved outcomes with a screening strategy [61]. We do not recommend screening
asymptomatic patients for AF [62,63].
At some time in the future, screening for AF may have merit. The following studies
provide information that may bear on which screening tool should be chosen:
●A 2018 United States Preventive Services Task Force (USPSTF) review of

randomized trials and observational studies (17 studies and 135,300 patients
age 65 years and older) found that systematic screening with ECG identified
more cases of AF than no screening (absolute increase from 0.6 to 2.8
percent over 12 months) [61]. Systematic screening with ECG did not detect
more cases than a systematic approach using pulse palpation (two trials and
17,803 patients).
●The sensitivity and negative predictive value for AF detection of the following
tools were evaluated in a 2020 study (see 'Subclinical atrial fibrillation' above):
10-second ECGs, twice daily 30-second ECG strips, and external monitoring
at 24 hours, 48 hours, 7 days, and 30 days. Detection rates with these tools
were compared with data gathered from 590 individuals with stroke risk factors
but without AF who underwent screening with an implantable loop recorder for
an average of 40 months. [19]. All tools were significantly less sensitive than
the implantable device.
●The mSToPS trial randomly assigned 2659 individuals with risk factors for AF
to immediate continuous active monitoring with a wearable, self-applied patch
for two weeks or to delayed monitoring at four months [64]. Immediate active
monitoring found a higher rate of a new diagnosis of AF at four months
compared with delayed monitoring (3.9 versus 0.9 percent; absolute difference
3 percent, 95% CI 1.8-4.1 percent). Although a higher incidence of AF was
found with this monitoring tool, treatment based on this information has not
been studied.
●The Apple Heart Study evaluated a novel technology for the detection of AF
[65]. Over 400,000 individuals without a history of AF who owned both an
Apple Watch and iPhone were recruited to participate. The watch is capable of
detecting irregular heart rhythms using an optical sensor that uses pulse wave
data. Participants downloaded an iPhone application that identifies episodes
(recorded by the watch) suggestive of AF and prompted them to initiate a
telemedicine visit. If possibility of AF was confirmed, participants were sent an
ECG patch to wear for seven days. In the study, 419,297 participants were
recruited, 2161 received irregular pulse notification, 658 had an ECG patch
sent to them, and 450 returned the patch containing data that could be
analyzed. (See "Ambulatory ECG monitoring", section on 'Patch monitor'.)
AF was present in 34 percent of patients who returned the patch. Among
those who were notified of an irregular pulse on the watch, 84 percent were
concordant with AF; that is, the positive predictive value for AF was 0.84.
This study provides evidence that the technology used could be adapted for
the detection, screening, evaluation and treatment of AF. Further research is
in process. However, as mentioned in the opening paragraph of this section,
there are no good data that intervention based on screening with this or other
similar device improves clinical outcomes. For patients who have downloaded
the application used in the trial and are concerned that they might have
findings suggestive of AF, it is reasonable to use traditional methods (such as
ambulatory monitoring) to detect AF. (See "Evaluation of palpitations in
adults", section on 'Ambulatory cardiac rhythm monitoring'.)
The role of evaluating patients with cryptogenic stroke for AF is discussed
separately. (See "Cryptogenic stroke", section on 'Occult atrial fibrillation'.)
Arrhythmias in adults".)
education materials, “The Basics” and “Beyond the Basics.” The Basics patient
articles on a variety of subjects by searching on “patient info” and the keyword(s) of
interest.)
●Basics topics (see "Patient education: Atrial fibrillation (The

Basics)" and "Patient education: Medicines for atrial fibrillation (The
Basics)" and "Patient education: Coping with high drug prices (The
Basics)" and "Patient education: Heart failure and atrial fibrillation (The
Basics)")
●Beyond the Basics topics (see "Patient education: Atrial fibrillation (Beyond
the Basics)" and "Patient education: Coping with high drug prices (Beyond the
Basics)")
SUMMARY The following are essential points addressed in this topic:
●Atrial fibrillation (AF) is the most common cardiac arrhythmia that can have
adverse consequences related to a reduction in cardiac output (symptoms)
and to atrial and atrial appendage thrombus formation (stroke and peripheral
embolization). In addition, affected patients may be at increased risk for
mortality. (See 'Long-term outcome' above.)
●Hypertensive heart disease and coronary heart disease are the most
common underlying disorders in developed countries associated with atrial
fibrillation. (See 'Risk factors and disease associations' above.)
●Patients are classified as having new onset, paroxysmal, persistent,
longstanding persistent, or permanent AF. (See 'Classification' above.)
●Essential information from the patient's history, physical examination,
electrocardiogram, and a transthoracic echocardiogram should be obtained at
the time of diagnosis and periodically during the course of the disease.
Additional laboratory testing, such as thyroid stimulating hormone assay, and
ambulatory ECG monitoring may be necessary. (See 'Evaluation' above.)
●The two principal management decisions for patients are:
•Does the patient need long-term antithrombotic therapy? All patients
whose risk of embolization exceeds the risk of bleeding are candidates for
such therapy. (See 'Prevention of systemic embolization' above.)
•Should the patient be managed with either a rate or a rhythm control
strategy? This should be determined based on severity of symptoms,
presence of structural heart disease, adequacy of rate control during
episodes of atrial fibrillation, and the patient’s preference for using
antiarrhythmic drug therapy or undergoing ablation-based interventions.
(See 'Rate versus rhythm control' above.)
●In the absence of a reversible precipitant, AF is typically recurrent.
ACKNOWLEDGMENT The UpToDate editorial staff would like to thank Dr.
Alan Cheng for his prior contributions as an author to this topic review.
REFERENCES
1. Pritchett EL. Management of atrial fibrillation. N Engl J Med 1992; 326:1264.
2. Atrial fibrillation: current understandings and research imperatives. The
National Heart, Lung, and Blood Institute Working Group on Atrial
Fibrillation. J Am Coll Cardiol 1993; 22:1830.
3. Lip GY, Metcalfe MJ, Rae AP. Management of paroxysmal atrial fibrillation.
Q J Med 1993; 86:467.
4. Disch DL, Greenberg ML, Holzberger PT, et al. Managing chronic atrial
fibrillation: a Markov decision analysis comparing warfarin, quinidine, and
low-dose amiodarone. Ann Intern Med 1994; 120:449.
5. Go AS, Hylek EM, Phillips KA, et al. Prevalence of diagnosed atrial
fibrillation in adults: national implications for rhythm management and stroke
prevention: the AnTicoagulation and Risk Factors in Atrial Fibrillation
(ATRIA) Study. JAMA 2001; 285:2370.
6. Wann LS, Curtis AB, January CT, et al. 2011 ACCF/AHA/HRS focused
update on the management of patients with atrial fibrillation (Updating the
2006 Guideline): a report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines.
7. American College of Cardiology Foundation, American Heart Association,
European Society of Cardiology, et al. Management of patients with atrial
fibrillation (compilation of 2006 ACCF/AHA/ESC and 2011 ACCF/AHA/HRS
recommendations): a report of the American College of
Cardiology/American Heart Association Task Force on practice guidelines.
the management of patients with atrial fibrillation: a report of the American
College of Cardiology/American Heart Association Task Force on practice
guidelines and the Heart Rhythm Society. Circulation 2014; 130:e199.
the management of patients with atrial fibrillation: executive summary: a
report of the American College of Cardiology/American Heart Association
Task Force on practice guidelines and the Heart Rhythm Society.
10. Kirchhof P, Benussi S, Kotecha D, et al. 2016 ESC Guidelines for the
management of atrial fibrillation developed in collaboration with EACTS. Eur
Heart J 2016; 37:2893.
11. January CT, Wann LS, Calkins H, et al. 2019 AHA/ACC/HRS Focused
Update of the 2014 AHA/ACC/HRS Guideline for the Management of
Patients With Atrial Fibrillation: A Report of the American College of
Cardiology/American Heart Association Task Force on Clinical Practice
Guidelines and the Heart Rhythm Society in Collaboration With the Society
of Thoracic Surgeons. Circulation 2019; 140:e125.
12. Wyse DG, Van Gelder IC, Ellinor PT, et al. Lone atrial fibrillation: does it
exist? J Am Coll Cardiol 2014; 63:1715.
13. Noseworthy PA, Kaufman ES, Chen LY, et al. Subclinical and Device-
Detected Atrial Fibrillation: Pondering the Knowledge Gap: A Scientific
Statement From the American Heart Association. Circulation 2019;
140:e944.
14. Svennberg E, Engdahl J, Al-Khalili F, et al. Mass Screening for Untreated
Atrial Fibrillation: The STROKESTOP Study. Circulation 2015; 131:2176.
15. Healey JS, Connolly SJ, Gold MR, et al. Subclinical atrial fibrillation and the
risk of stroke. N Engl J Med 2012; 366:120.
16. Healey JS, Alings M, Ha A, et al. Subclinical Atrial Fibrillation in Older
Patients. Circulation 2017; 136:1276.
17. Tayal AH, Tian M, Kelly KM, et al. Atrial fibrillation detected by mobile
cardiac outpatient telemetry in cryptogenic TIA or stroke. Neurology 2008;
71:1696.
18. Jabaudon D, Sztajzel J, Sievert K, et al. Usefulness of ambulatory 7-day
ECG monitoring for the detection of atrial fibrillation and flutter after acute
stroke and transient ischemic attack. Stroke 2004; 35:1647.
19. Diederichsen SZ, Haugan KJ, Kronborg C, et al. Comprehensive Evaluation
of Rhythm Monitoring Strategies in Screening for Atrial Fibrillation: Insights
From Patients at Risk Monitored Long Term With an Implantable Loop
Recorder. Circulation 2020; 141:1510.
20. Mahajan R, Perera T, Elliott AD, et al. Subclinical device-detected atrial
fibrillation and stroke risk: a systematic review and meta-analysis. Eur Heart
J 2018; 39:1407.
21. Wynn GJ, Todd DM, Webber M, et al. The European Heart Rhythm
Association symptom classification for atrial fibrillation: validation and
improvement through a simple modification. Europace 2014; 16:965.
22. Krahn AD, Klein GJ, Kerr CR, et al. How useful is thyroid function testing in
patients with recent-onset atrial fibrillation? The Canadian Registry of Atrial
Fibrillation Investigators. Arch Intern Med 1996; 156:2221.
23. European Heart Rhythm Association, European Association for Cardio-
Thoracic Surgery, Camm AJ, et al. Guidelines for the management of atrial
fibrillation: the Task Force for the Management of Atrial Fibrillation of the
24. Abdelhamid AS, Brown TJ, Brainard JS, et al. Omega-3 fatty acids for the
primary and secondary prevention of cardiovascular disease. Cochrane
Database Syst Rev 2018; 11:CD003177.
25. Abdelhamid AS, Martin N, Bridges C, et al. Polyunsaturated fatty acids for
the primary and secondary prevention of cardiovascular disease. Cochrane
Database Syst Rev 2018; 11:CD012345.
26. Estruch R, Ros E, Salas-Salvadó J, et al. Primary prevention of
cardiovascular disease with a Mediterranean diet. N Engl J Med 2013;
368:1279.
27. Martínez-González MÁ, Toledo E, Arós F, et al. Extravirgin olive oil
consumption reduces risk of atrial fibrillation: the PREDIMED (Prevención
con Dieta Mediterránea) trial. Circulation 2014; 130:18.
28. Pathak RK, Middeldorp ME, Lau DH, et al. Aggressive risk factor reduction
study for atrial fibrillation and implications for the outcome of ablation: the
ARREST-AF cohort study. J Am Coll Cardiol 2014; 64:2222.
29. Abed HS, Wittert GA, Leong DP, et al. Effect of weight reduction and
cardiometabolic risk factor management on symptom burden and severity in
patients with atrial fibrillation: a randomized clinical trial. JAMA 2013;
310:2050.
30. Voskoboinik A, Kalman JM, De Silva A, et al. Alcohol Abstinence in Drinkers
with Atrial Fibrillation. N Engl J Med 2020; 382:20.
31. Soliman EZ, Rahman AF, Zhang ZM, et al. Effect of Intensive Blood
Pressure Lowering on the Risk of Atrial Fibrillation. Hypertension 2020;
75:1491.
32. Israel CW, Grönefeld G, Ehrlich JR, et al. Long-term risk of recurrent atrial
fibrillation as documented by an implantable monitoring device: implications
for optimal patient care. J Am Coll Cardiol 2004; 43:47.
33. Page RL, Wilkinson WE, Clair WK, et al. Asymptomatic arrhythmias in
patients with symptomatic paroxysmal atrial fibrillation and paroxysmal
34. Kalantarian S, Ay H, Gollub RL, et al. Association between atrial fibrillation
and silent cerebral infarctions: a systematic review and meta-analysis. Ann
Intern Med 2014; 161:650.
35. Gaita F, Corsinovi L, Anselmino M, et al. Prevalence of silent cerebral
ischemia in paroxysmal and persistent atrial fibrillation and correlation with
cognitive function. J Am Coll Cardiol 2013; 62:1990.
36. Mooney S, Hasssanein TI, Hilsabeck RC, et al. Utility of the Repeatable
Battery for the Assessment of Neuropsychological Status (RBANS) in
patients with end-stage liver disease awaiting liver transplant. Arch Clin
Neuropsychol 2007; 22:175.
37. Field TS, Weijs B, Curcio A, et al. Incident Atrial Fibrillation, Dementia and
the Role of Anticoagulation: A Population-Based Cohort Study. Thromb
Haemost 2019; 119:981.
38. Ding M, Fratiglioni L, Johnell K, et al. Atrial fibrillation, antithrombotic
treatment, and cognitive aging: A population-based study. Neurology 2018;
91:e1732.
39. Martin DT, Bersohn MM, Waldo AL, et al. Randomized trial of atrial
arrhythmia monitoring to guide anticoagulation in patients with implanted
defibrillator and cardiac resynchronization devices. Eur Heart J 2015;
36:1660.
40. Brambatti M, Connolly SJ, Gold MR, et al. Temporal relationship between
subclinical atrial fibrillation and embolic events. Circulation 2014; 129:2094.
41. Leong DP, Eikelboom JW, Healey JS, Connolly SJ. Atrial fibrillation is
associated with increased mortality: causation or association? Eur Heart J
2013; 34:1027.
42. Corley SD, Epstein AE, DiMarco JP, et al. Relationships between sinus
rhythm, treatment, and survival in the Atrial Fibrillation Follow-Up
Investigation of Rhythm Management (AFFIRM) Study. Circulation 2004;
109:1509.
43. Pedersen OD, Bagger H, Keller N, et al. Efficacy of dofetilide in the
treatment of atrial fibrillation-flutter in patients with reduced left ventricular
function: a Danish investigations of arrhythmia and mortality on dofetilide
(diamond) substudy. Circulation 2001; 104:292.
44. Andersson T, Magnuson A, Bryngelsson IL, et al. All-cause mortality in
272,186 patients hospitalized with incident atrial fibrillation 1995-2008: a
Swedish nationwide long-term case-control study. Eur Heart J 2013;
34:1061.
45. Benjamin EJ, Wolf PA, D'Agostino RB, et al. Impact of atrial fibrillation on
the risk of death: the Framingham Heart Study. Circulation 1998; 98:946.
46. Stewart S, Hart CL, Hole DJ, McMurray JJ. A population-based study of the
long-term risks associated with atrial fibrillation: 20-year follow-up of the
Renfrew/Paisley study. Am J Med 2002; 113:359.
47. Conen D, Chae CU, Glynn RJ, et al. Risk of death and cardiovascular
events in initially healthy women with new-onset atrial fibrillation. JAMA
2011; 305:2080.
48. Kannel WB, Abbott RD, Savage DD, McNamara PM. Epidemiologic features
of chronic atrial fibrillation: the Framingham study. N Engl J Med 1982;
306:1018.
49. Crenshaw BS, Ward SR, Granger CB, et al. Atrial fibrillation in the setting of
acute myocardial infarction: the GUSTO-I experience. Global Utilization of
Streptokinase and TPA for Occluded Coronary Arteries. J Am Coll Cardiol
1997; 30:406.
50. Eldar M, Canetti M, Rotstein Z, et al. Significance of paroxysmal atrial
fibrillation complicating acute myocardial infarction in the thrombolytic era.
SPRINT and Thrombolytic Survey Groups. Circulation 1998; 97:965.
51. Goldberg RJ, Seeley D, Becker RC, et al. Impact of atrial fibrillation on the
in-hospital and long-term survival of patients with acute myocardial
infarction: a community-wide perspective. Am Heart J 1990; 119:996.
52. Chen LY, Sotoodehnia N, Bůžková P, et al. Atrial fibrillation and the risk of
sudden cardiac death: the atherosclerosis risk in communities study and
cardiovascular health study. JAMA Intern Med 2013; 173:29.
53. Marijon E, Le Heuzey JY, Connolly S, et al. Causes of death and influencing
factors in patients with atrial fibrillation: a competing-risk analysis from the
randomized evaluation of long-term anticoagulant therapy study. Circulation
2013; 128:2192.
54. Vermond RA, Crijns HJ, Tijssen JG, et al. Symptom severity is associated
with cardiovascular outcome in patients with permanent atrial fibrillation in
the RACE II study. Europace 2014; 16:1417.
55. Vílchez JA, Roldán V, Manzano-Fernández S, et al. β-Trace protein and
prognosis in patients with atrial fibrillation receiving anticoagulation
treatment. Chest 2013; 144:1564.
56. Schmitt J, Duray G, Gersh BJ, Hohnloser SH. Atrial fibrillation in acute
myocardial infarction: a systematic review of the incidence, clinical features
and prognostic implications. Eur Heart J 2009; 30:1038.
57. Garg RK, Jolly N. Acute myocardial infarction secondary to
thromboembolism in a patient with atrial fibrillation. Int J Cardiol 2007;
123:e18.
58. Soliman EZ, Safford MM, Muntner P, et al. Atrial fibrillation and the risk of
myocardial infarction. JAMA Intern Med 2014; 174:107.
59. Garnvik LE, Malmo V, Janszky I, et al. Physical activity, cardiorespiratory
fitness, and cardiovascular outcomes in individuals with atrial fibrillation: the
HUNT study. Eur Heart J 2020; 41:1467.
60. Piepoli MF, Hoes AW, Agewall S, et al. 2016 European Guidelines on
cardiovascular disease prevention in clinical practice: The Sixth Joint Task
Force of the European Society of Cardiology and Other Societies on
Cardiovascular Disease Prevention in Clinical Practice (constituted by
representatives of 10 societies and by invited experts)Developed with the
special contribution of the European Association for Cardiovascular
Prevention & Rehabilitation (EACPR). Eur Heart J 2016; 37:2315.
61. Jonas DE, Kahwati LC, Yun JDY, et al. Screening for Atrial Fibrillation With
Electrocardiography: Evidence Report and Systematic Review for the US
Preventive Services Task Force. JAMA 2018; 320:485.
62. US Preventive Services Task Force, Curry SJ, Krist AH, et al. Screening for
Atrial Fibrillation With Electrocardiography: US Preventive Services Task
Force Recommendation Statement. JAMA 2018; 320:478.
63. Freedman B, Camm J, Calkins H, et al. Screening for Atrial Fibrillation: A
Report of the AF-SCREEN International Collaboration. Circulation 2017;
135:1851.
64. Steinhubl SR, Waalen J, Edwards AM, et al. Effect of a Home-Based
Wearable Continuous ECG Monitoring Patch on Detection of Undiagnosed
Atrial Fibrillation: The mSToPS Randomized Clinical Trial. JAMA 2018;
320:146.
65. Perez MV, Mahaffey KW, Hedlin H, et al. Large-Scale Assessment of a
Smartwatch to Identify Atrial Fibrillation. N Engl J Med 2019; 381:1909.
Close
 Language

 Policies

 Support Tag
 Contact Us

 About Us

 UpToDate News

 Mobile Access

 Help & Training

 Demos








 Emmi®


 Lexicomp®

 Medi-Span®

Uptodte TSV

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Uptodte TSV

Uploaded by

Copyright:

Available Formats

Skip to OutlineSkip to TopicSkip to ReferencesSkip to Help

 Ilinca SavulescuIlinca Savulescu

Overview of the acute management of

INTRODUCTION Tachyarrhythmias, defined as abnormal heart rhythms with

INITIAL DIAGNOSTIC AND TREATMENT DECISIONS In anyone

who presents with a symptomatic tachyarrhythmia, a 12-lead electrocardiogram (ECG)

●Hemodynamically unstable and not sinus rhythm – If a patient has

treatment of wide QRS complex tachycardias, similar to narrow QRS complex

SOCIETY GUIDELINE LINKS Links to society and government-sponsored

INFORMATION FOR PATIENTS UpToDate offers two types of patient

●Basics topics (see "Patient education: Tachycardia (The

SUMMARY AND RECOMMENDATIONS

●For hemodynamically unstable patients, urgent cardioversion should be

ACKNOWLEDGMENT The authors and UpToDate would like to thank Dr.

Skip to OutlineSkip to TopicSkip to ReferencesSkip to Help

Narrow QRS complex tachycardias: Clinical

INTRODUCTION Tachyarrhythmias, defined as abnormal heart rhythms with

DEFINITIONS Tachycardias, with a ventricular heart rate exceeding 100 beats

TYPES OF NARROW QRS COMPLEX TACHYCARDIA

Differential diagnosis of narrow QRS complex tachycardias — Narrow QRS

The narrow QRS complex tachycardias include:

●Sinus tachycardia (ST) (see "Sinus tachycardia: Evaluation and

PATHOGENESIS Reentry is the most common cause of narrow QRS

CLINICAL MANIFESTATIONS The response to a rapid heart rate can be

DIAGNOSIS The diagnosis of a narrow QRS complex tachycardia is usually

EVALUATION Evaluation of a patient with a narrow QRS complex tachycardia

involves two primary components:

Assessing the patient for hemodynamic stability — The most important clinical

●Hemodynamically unstable and not sinus rhythm – If a patient has clinically

Examples of regular and irregular rhythms include:

●Regular – sinus tachycardia, AV nodal reentrant tachycardia, AV

●AF, where no discernible discrete P waves (waveform 1 and waveform 2) can

●Similarto sinus rhythm

●ST(see "Sinus tachycardia: Evaluation and management", section on

Electrophysiologic testing — In some cases, narrow QRS complex tachycardias

Diagnostic EP may be indicated to determine the mechanism of the arrhythmia in the

●Those with severe symptoms such as syncope or presyncope in association

SOCIETY GUIDELINE LINKS Links to society and government-sponsored

INFORMATION FOR PATIENTS UpToDate offers two types of patient

●Basicstopic (see "Patient education: Supraventricular tachycardia (SVT)

SUMMARY AND RECOMMENDATIONS

●Tachycardias, defined as abnormal heart rhythms with a ventricular rate of

© 2020 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Skip to OutlineSkip to TopicSkip to ReferencesSkip to Help

Atrioventricular nodal reentrant tachycardia

INTRODUCTION Atrioventricular nodal reentrant tachycardia (AVNRT) is a

EPIDEMIOLOGY AVNRT is the most common form of regular, sustained,

paroxysmal supraventricular tachycardia (PSVT), accounting for nearly two-thirds of all

ANATOMY AND PATHOPHYSIOLOGY The physiologic substrate for

This proposed mechanism explains a number of clinical observations in AVNRT:

●A single PAC (or retrograde penetration of the AV node from a junctional or

Symptoms — Patients with AVNRT most commonly report palpitations, dizziness or

DIAGNOSIS The diagnosis of AVNRT should be suspected in a patient with

DIFFERENTIAL DIAGNOSIS The differential diagnosis of palpitations is

Sustained narrow QRS complex tachycardias are generally divided according to

Sinus tachycardia — Sinus tachycardia is the most common narrow QRS complex

INITIAL MANAGEMENT The initial management of a patient presenting with

SUBSEQUENT MANAGEMENT The approach to the management of

subsequent AVNRT episodes is based around acute management of recurrent episodes

SOCIETY GUIDELINE LINKS Links to society and government-sponsored

INFORMATION FOR PATIENTS UpToDate offers two types of patient

●Basicstopic (see "Patient education: Supraventricular tachycardia (SVT)

SUMMARY AND RECOMMENDATIONS