Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of reentrant

supraventricular tachycardia (SVT). The substrate for AVNRT is the presence of dual AV
nodal pathways. (See Etiology.)[1, 2]
Because of the abrupt onset and termination of the reentrant SVT, the nonspecific term
paroxysmal supraventricular tachycardia (or even the misleading term paroxysmal atrial
tachycardia [PAT]) has been used to refer to these tachyarrhythmias. With improved
knowledge of the electrophysiology of reentrant SVT, greater specificity in nomenclature,
based on the mechanism of reentry, has been possible. Such improved classification aids in
the choice of appropriate therapies. (See Etiology, Prognosis, Treatment, and Medication.)
AVNRT is usually well tolerated, often occurring in patients with no structural heart disease.
(See Prognosis, Presentation, and Workup.)

Patient education
Patients should be instructed on vagal maneuvers (Valsalva, diving reflex), used to try to
terminate an episode of AVNRT. Patients with hemodynamic compromise or syncope should
be instructed on avoiding activities that could be dangerous to them or to others (eg, driving,
swimming) while the risk of an episode remains. Ablation obviates the need for any longterm restriction.

Etiology
The substrate for AVNRT may be functional rather than anatomic. These arrhythmias occur in
young, healthy patients and in those with chronic heart disease.
In patients with atrioventricular (AV) nodal reentry, the AV node is functionally divided into 2
longitudinal pathways that form the reentrant circuit. (In contrast to a bypass tract, dual AV
nodal physiology is often an acquired abnormality.) In the majority of patients, during
AVNRT, antegrade conduction occurs to the ventricle over the slow (alpha) pathway, and
retrograde conduction occurs over the fast (beta) pathway. (See the image below.)

Electrophysiological mechanism of atrioventricular

nodal reentry tachycardia.

In most patients with this arrhythmia, the tachycardia is initiated when an atrial premature
complex is blocked in the fast pathway with a longer refractory period and conducts in the
slow pathway with a shorter refractory period. While the impulse conducts to the ventricle in
the slow pathway (antegrade conduction), the fast pathway recovers so that the impulse can

conduct retrograde up the fast pathway to the atrium and the atrial end of the slow pathway
(retrograde conduction).
In approximately one third of patients, AVNRT is induced by premature ventricular
stimulation. In addition to the typical mechanism of AV nodal reentry described above,
atypical AV nodal reentry can occur in the opposite direction, with antegrade conduction in
the fast pathway and retrograde conduction in the slow pathway. Less commonly, the
reentrant circuit can be over 2 slow pathways, the so-called slow-slow AV nodal reentry. (See
the images below.)

Atypical atrioventricular nodal reentry tachycardia.

Typical atrioventricular nodal reentry tachycardia.

The prognosis for patients with AVNRT is usually good in the absence of structural heart
disease. Most patients respond to medications to prevent recurrence or to radiofrequency
ablation, which is approximately 95% curative and has a low risk of complications. It is the
preferred method of treatment for most patients.
Complications of AVNRT include hemodynamic compromise, congestive heart failure,
syncope, tachycardia-induced angina, cardiomyopathy, myocardial ischemia, and myocardial
infarction.

History
Atrioventricular nodal reentry tachycardia (AVNRT) is typically characterized by an abrupt
onset and termination. Episodes may last from seconds to minutes to days. In the absence of
structural heart disease, it is usually well tolerated.
Common symptoms include the following:

Palpitations

Nervousness

Anxiety

Lightheadedness

Neck pounding[3]

Neck and chest discomfort

Dyspnea

Polyuria - Can occur after termination of an episode (due to the release of

atrial natriuretic factor)

AVNRT may cause angina or myocardial infarction in patients with coronary artery disease
and may cause or worsen heart failure in patients with poor left ventricular function.
Syncope may occur in patients with a rapid ventricular rate or prolonged tachycardia due to
poor ventricular filling, decreased cardiac output, hypotension, and reduced cerebral
perfusion. Syncope may also occur because of transient asystole when the tachycardia
terminates, due to tachycardia-induced depression of the sinus node.

Physical Examination
The heart rate is usually rapid, ranging from 150-250 beats per minute (bpm). It is usually
180-200 bpm in adults; in children, the rate may exceed 250 bpm.
Hypotension may occur initially or with rapid ventricular rates and prolonged episodes.
Sometimes, initial hypotension evokes a sympathetic response that increases blood pressure
and may terminate the tachycardia by an increase in vagal tone.
Signs of left heart failure may develop or worsen in patients with poor left ventricular
function.
Automatic or triggered atrial tachycardia
This is a focal tachycardia originating in the atria. It may or may not be associated with
underlying heart disease. There may be AV block.
Multifocal atrial tachycardia
This is an irregular rhythm with at least 3 distinctly discernible P-wave morphologies.
Multifocal atrial tachycardia is often associated with pulmonary disease or medications such
as digoxin.
Bypass tract mediated macroreentrant tachycardia
Electrocardiographic findings may show evidence of preexcitation (if there is antegrade
conduction via the accessory pathway but this is often not present). Some bypass tracts do not
demonstrate antegrade conduction, so baseline preexcitation is not present on the surface

electrocardiogram (ECG). In orthodromic tachycardias (ie, due to a bypass tract), the P wave
typically falls after the QRS complex, in contrast to the superimposition most commonly seen
with atrioventricular nodal reentry tachycardia (AVNRT).
Orthodromic AV-reciprocating tachycardia (AVRT) tends to occur at an earlier age and more
frequently in males than AVNRT. In young males, AVRT tends to be a more rapid SVT than
are most AVNRTs. Women tend to have a greater risk for AVNRT than for AVRT, but there is,
nevertheless, a large overlap in the incidence of both conditions by age and sex.
Another potentially distinguishing factor in AVNRT is the sensation of neck pulsations. This
is more common in AVNRT, as there is simultaneous atrial and ventricular activation and
contraction.[3]
During the rapid SVTs, QRS alternans may occur. QRS alternans can occur during AVRT or
AVNRT and is more related to rate than mechanism.
Sinus node reentrant tachycardia
Normal P waves precede the QRS (electrocardiographic) complex.
Intra-atrial reentry tachycardia
Abnormal P waves precede each QRS complex. There may be AV block
Atrial fibrillation
This is an irregular ventricular rhythm without P waves, due to dyssynchronous and variable
atrial activation.
Atrial flutter
Flutter waves are present. The atrial rhythm is rapid and regular. The ventricular rate can be
variable but without treatment is approximately 150 bpm (with 2:1 AV block).
Automatic junctional tachycardia
This tachycardia originates from the AV node as an automatic rhythm. Atrioventricular
dissociation may occur.

Differential Diagnoses

Atrial Fibrillation

Atrial Flutter

Atrial Tachycardia

Multifocal Atrial Tachycardia

Paroxysmal Supraventricular Tachycardia

Wolff-Parkinson-White Syndrome

Approach Considerations
Atrioventricular nodal reentry tachycardia (AVNRT) can be initiated by ectopic atrial or
ventricular beats. Typically, it is initiated by atrial ectopic beats that block in the fast pathway
and travel antegrade via the slow pathway. There is a "jump" in AV nodal conduction at
tachycardia onset with retrograde activation, such that atrial activation is nearly simultaneous
or just after the ventricular activation.
Sometimes, SVT due to AVNRT can present with a wide QRS due to underlying conduction
system disease or aberration. A wide QRS tachycardia with a typical bundle branch block
morphology during SVT due to aberration is not uncommon.
Occasionally, distinguishing ventricular tachycardia from SVT can be difficult, but in most
instances this can be accomplished using the clinical scenario, the QRS morphology (owing
to the frequent occurrence of the aforementioned typical bundle branch block), evidence for
AV dissociation (this may be difficult if there is simultaneous activation), physical
examination (including the presence of neck vein pulsations[3] ), and lack of fusion and
capture.
In patients with an otherwise normal heart, considering carotid massage or adenosine is
reasonable unless the patient is hemodynamically unstable, in which case cardioversion may
be required.
If the diagnosis is in question, an electrophysiologic study helps to distinguish the potential
mechanisms for the tachycardia. Therefore, an electrophysiologic study may be indicated for
a patient with a wide QRS complex tachycardia in whom the mechanism is not clear, and is
also reasonable if the plan is to attempt to ablate the tachycardia and cure it.[4]
Echocardiography

Echocardiography can be used to evaluate for the presence of structural heart disease.

Electrocardiography
Evaluation usually reveals a supraventricular origin of QRS complexes at rates of 150-250
bpm and a regular rhythm. The QRS complex is usually narrow unless a conduction
abnormality is present or is functionally induced (aberrancy) from the rapid heart rate or the
abrupt change in rate. (See the images below.)

Atypical atrioventricular nodal reentry tachycardia.

Typical atrioventricular nodal reentry tachycardia.

P waves are not usually seen, because they are buried in the QRS complex. A pseudo R prime
may be seen in V1, or pseudo S waves may be seen in leads II, III, or aVF. The onset is
abrupt, with an atrial premature complex that conducts with a prolonged PR interval. Atypical
AV nodal reentry includes fast antegrade/slow retrograde conduction with a P wave before the
QRS complex. Slow-slow AV nodal reentry can occur, with a P wave occurring in
middiastole.
The PR interval may shorten over the first few beats at onset, or it may lengthen during last
few beats preceding termination of the tachycardia.
Abrupt termination occurs with a retrograde P wave, sometimes followed by a brief period of
asystole or bradycardia.
Although AVNRT is usually a short RP interval tachycardia (with the P wave buried in the
QRS complex), rarely, retrograde conduction can occur in the slow pathway, producing a
long RP tachycardia. The latter form of tachycardia is indistinguishable from automatic atrial
tachycardia or AV reciprocating tachycardia on typical surface electrocardiographic
recordings. This is important to recognize because AVNRT is usually fairly easily to cure
with catheter ablation,[5] while automatic atrial tachycardia may be more difficult to cure.

Electrophysiology
Typical findings in AVNRT on electrophysiologic studies include dual-node physiology, a
discontinuous pattern of atrial-to-ventricular conduction reflecting the differing conduction
properties of fast and slow antegrade conduction, and/or sustaining slow antegrade
conduction, which mimics the superimposition of the P wave and QRS complex observed in
the clinical arrhythmia. The most typical endpoint of ablation for AVNRT is modification or
elimination of slow pathway conduction associated with inability to induce the arrhythmia.[4]

During the electrophysiologic study, a "jump" in the AV-node function curve, demonstrating 2
distinct physiologic AV nodal pathways, is one of the key findings indicating the presence of
AV nodal reentry.
AV nodal reentry often starts with a premature atrial beat, a long AV interval followed by a
retrograde rapid beat that is simultaneous or near simultaneous to the QRS complex. During
ventricular pacing, retrograde activation is through the AV node and is demonstrated by early
atrial activation in the His bundle electrogram.
Atypical AVNRT has fast-activation antegrade through the AV node and slow-activation
retrograde that allows early atrial activation to occur at a distinct time after the QRS complex
and is earliest in the posterior septal right atrium. AVRT causes eccentric retrograde atrial
activation.
In some instances, if an accessory pathway is septal, retrograde activation can mimic
retrograde atrial activation through the AV node. This can be distinguished using adenosine
administration with ventricular pacing to assess ventriculoatrial conduction, and through the
use of ventricular extrastimuli during tachycardia that allows for preexcitation of the atria
once the His bundle is refractory. Other interventions during the electrophysiologic study
may further distinguish AVNRT from AVRT (such as para-Hisian pacing), as well as
determine if the tachycardia is atrial tachycardia, sinoatrial reentry, or ventricular tachycardia.

Approach Considerations
Rest, reassurance, sedation, and/or vagal maneuvers may terminate an attack of
atrioventricular nodal reentry tachycardia (AVNRT). The successful management of an acute
attack, however, depends on the symptoms, the presence of underlying heart disease, and the
natural history of previous episodes.
In the presence of a wide-complex tachycardia, the institution of therapy should always
follow a careful review of the patient's prior cardiac history, including left ventricular
function and previous ECGs, which are helpful tools for defining the origin of the arrhythmia
(ie, supraventricular vs ventricular).
The use of calcium channel blockers is contraindicated in patients with tachycardias of
ventricular origin and may cause hemodynamic compromise and death.
Vagal maneuvers

To terminate AVNRT, try vagal maneuvers (eg, carotid sinus massage, exposure of the face to
ice water, Valsalva maneuver) before initiating drug treatment. These maneuvers can also be
tried after each pharmacologic approach. Vagal maneuvers are unlikely to work and should
not be tried if hypotension is present. Sometimes, putting the patient in the Trendelenburg
position facilitates termination with a vagal maneuver.
Direct-current synchronized cardioversion

Direct-current (DC) synchronized cardioversion is used to terminate an attack if the patient

has hemodynamic compromise or if drug conversion fails and the patient continues to be
symptomatic. However, DC cardioversion is rarely necessary for AVNRT.
Competitive atrial or ventricular pacing may be used if DC cardioversion is contraindicated
(eg, if high doses of digitalis have been administered).
Diet

No specific recommendations or restrictions are necessary, but some patients' episodes are
exacerbated by caffeine, theophylline, or theobromine in selected foods (coffee, tea, or
chocolate, respectively). Alcohol may also be a trigger.
Activity

Advise the patient to rest during tachycardia, preferably in a supine position.

Consultations

Consultations include the following:

Cardiologist

Electrophysiologist

Transfer

Transfer to a facility capable of performing electrophysiologic studies and radiofrequency

ablation may be needed.

Pharmacologic Therapy
Drugs that can be used to terminate an attack include adenosine, calcium channel blockers
(eg, diltiazem, verapamil), beta-blockers, and digitalis.
Adenosine

Adenosine is the first-line drug used for termination of AVNRT. In rare cases, the
administration of adenosine may lead to atrial fibrillation or even asystole for a short period.
Adenosine-induced ventricular fibrillation results from transient block in the AV node and
rapid antegrade conduction through an accessory pathway, should one exist. This almost
never occurs and would only happen in the presence of atrial fibrillation. Defibrillation
equipment must be readily available when adenosine is administered. For AVNRT, if present,
adenosine will never initiate ventricular fibrillation in standard doses.
Adenosine administration should be given through a central, large bore intravenous (IV)
needle, as it has a very short half-life. It should be followed by a saline flush and elevation of

the extremity in which it is being injected. The initial dose is 6 mg followed by 12 mg and
occasionally 18 mg. It should not be used in heart transplantation patients, it may be
ineffective if given to a patient taking theophylline, and it may be potentiated by
dipyridamole.
Preventive therapy

Preventive therapy is needed for frequent, prolonged, or highly symptomatic episodes that do
not terminate spontaneously or for those that cannot be easily terminated by the patient.
Drugs that are used for prevention of recurrence include long-acting beta-blockers, calcium
channel blockers, and digitalis.

Radiofrequency Catheter Ablation

Radiofrequency catheter ablation[5] of the reentrant circuit should be considered in patients
who have frequent or highly symptomatic episodes, who do not want drug therapy, who
cannot tolerate the drugs, or in whom drug therapy fails.
Radiofrequency catheter ablation is associated with cure rates of greater than 95%, with very
low risk of AV block (< 1%) for patients with AVNRT.[5] This is an invasive procedure in
which catheter electrodes are placed percutaneously via central veins into the heart.
Tachycardia can be initiated by pacing and by programmed electrical stimulation delivered
from the atria or the ventricles.
An ablation catheter electrode can be placed in the location of the slow AV nodal pathway,
with radiofrequency energy delivered via the catheter to interrupt conduction via this pathway
and thus eliminate the circuit.
Drugs used to terminate an acute episode of atrioventricular nodal reentry tachycardia
(AVNRT) are given intravenously. These medications include the following:

Adenosine (first-line)

Calcium channel blockers - Eg, diltiazem and verapamil

Beta-blockers - Eg, esmolol, propranolol, metoprolol, and atenolol

Digitalis

Drugs used to prevent recurrences are given orally and include calcium channel blockers,
long-acting beta-blockers, and digitalis.
As previously mentioned, the administration of adenosine or other AV nodal blocking agents
may, in rare cases, lead to ventricular fibrillation or even asystole for a short period of time.

Medication Summary
Drugs used to terminate an acute episode of atrioventricular nodal reentry tachycardia
(AVNRT) are given intravenously. These medications include the following:

Adenosine (first-line)

Calcium channel blockers - Eg, diltiazem and verapamil

Beta-blockers - Eg, esmolol, propranolol, metoprolol, and atenolol

Digitalis

Drugs used to prevent recurrences are given orally and include calcium channel blockers,
long-acting beta-blockers, and digitalis.
As previously mentioned, the administration of adenosine or other AV nodal blocking agents
may, in rare cases, lead to ventricular fibrillation or even asystole for a short period of time.

Cardiovascular, Other
Class Summary

Antiarrhythmic drugs affect the electrophysiology of the pathways responsible for AVNRT.
View full drug information
Adenosine (Adenocard)

Adenosine transiently blocks conduction through the AV node. It can interrupt reentry
pathways through the AV node and restore normal sinus rhythm in paroxysmal SVT,
including paroxysmal SVT associated with Wolff-Parkinson-White (WPW) syndrome.
Adenosine has a short half-life. It is the preferred medication for IV administration to
terminate AVNRT because of its rapid metabolism and generally good safety profile.
View full drug information
Digoxin (Lanoxin)

Cardiac glycosides have direct and indirect inotropic effects on the cardiovascular system.
Digoxin acts directly on cardiac muscle, increasing myocardial systolic contractions. Indirect
actions result in increased vagal activity for any given increase in mean arterial pressure.
Digoxin is administered intravenously to terminate an acute attack, but it has a delayed onset
of action and is less effective than other therapies. The drug is given orally to prevent
recurrence. IV digoxin has generally been supplanted by other medications.

Calcium Channel Blockers

Class Summary

These drugs block the AV nodal pathways responsible for AVNRT (particularly, the slow
pathway).
View full drug information
Diltiazem (Dilacor XR, Tiazac, Cartia XT, Cardizem)

It is administered intravenously to terminate an acute attack, and orally to prevent recurrence.

View full drug information
Verapamil (Calan, Covera-HS, Verelan)

This is the second-line treatment for AVNRT after adenosine. Verapamil causes fewer adverse
effects, is less expensive, and lasts longer; however, its action is not as rapid, and
hypotension, bradycardia, and a negative inotropic effect may occur. The drug is good to use
in lieu of adenosine if AVNRT recurs after termination.

Beta-Blockers, Beta-1 Selective

Class Summary

These agents are used for AV nodal blockade.

View full drug information
Esmolol (Brevibloc)

Esmolol's short half-life of 8 minutes allows for titration to the desired effect and quick
discontinuation if necessary.
View full drug information
Atenolol (Tenormin)

Atenolol selectively blocks beta-1 receptors, with little or no effect on beta-2 types. Atenolol
is excellent for use in patients at risk for experiencing complications from beta-blockade,
particularly those with reactive airway disease, mild-to-moderate LV dysfunction, and/or
peripheral vascular disease.

View full drug information

Metoprolol (Lopressor, Toprol XL)

Metoprolol is a selective beta-1 adrenergic receptor blocker that decreases the automaticity of
contractions. During intravenous administration, carefully monitor blood pressure, heart rate,
and ECG