Atrioventricular Node Reentry Supraventricular Tachycardia

Updated: Jan 25, 2022
Author: Glenn T Wetzel, MD, PhD; Chief Editor: Stuart Berger, MD 



Atrioventricular node reentrant tachycardia (AVNRT) is a form of reentrant rhythm within the region of the atrioventricular (AV) node. Reentrant rhythms account for most episodes of supraventricular tachycardia (SVT) in children. A reentrant rhythm involves the presence of two distinct pathways, a zone of slow conduction and unidirectional block in one limb, allowing an electrical impulse to travel down the second limb and reenter the blocked pathway from the other direction. Reentrant rhythms can usually be initiated and terminated by pacing or premature beats. During AVNRT, the circuit typically involves both a fast and a slow pathway within the region of the AV node, which allows the impulses to proceed down the His-Purkinje system to the ventricles while simultaneously proceeding in a retrograde fashion to depolarize the atria and reenter the node.

Atrioventricular Node Reentry Supraventricular Tac Atrioventricular Node Reentry Supraventricular Tachycardia. Nonsustained atrioventricular node reentry tachycardia (AVNRT). This electrocardiogram is from a 10-year-old who is in sinus rhythm until a junction escape beat initiates a 5-beat run of supraventricular tachycardia. The heart rate is quite slow at 130 beats per minute, likely due to his resting state (higher vagal tone) and treatment with the beta-blocker atenolol. Note the pseudo R' waves in lead V1. These deflections represent retrograde atrial activation. Some patients may also exhibit pseudo S waves in the inferior leads. The R' waves are lost when the tachycardia ends, demonstrating that the R' wave is not associated with ventricular depolarization. The terminal QRS has no R' wave, indicating that the tachycardia terminated in the retrograde limb of the circuit (fast AV nodal pathway).


Two or more functionally and (usually) anatomically distinct pathways have been described connecting the atria to the atrioventricular (AV) node; they are known as the fast and the slow pathways and have different electrophysiologic (EP) characteristics. The fast pathway crosses the tendon of Todaro superiorly and is identified by its relatively shorter conduction time and longer effective refractory period (ERP). The slow pathway(s) approach the compact AV node from inferiorly and have a relatively longer conduction time and an ERP that typically is short when compared to the fast pathway ERP. The different EP characteristics of the fast and slow pathway(s) can be observed during EP studies as evidence of dual AV nodal physiology. However, dual AV nodal physiology is a common finding during EP studies[1] ; it is not synonymous with AV node reentrant tachycardia (AVNRT) because the incidental finding of dual AV nodal physiology does not predict AVNRT in children and adolescents after successful accessory pathway ablation.[2]

The two forms of AVNRT that are usually described are the typical form (ie, slow-fast) and the atypical form (ie, fast-slow or slow-slow), referring to the characteristic of antegrade-retrograde conduction during tachyarrhythmia. In the typical form, which represents 90% of clinical AVNRT episodes, the conduction moves in antegrade direction through the slow pathway from the atrium to the compact AVN and in retrograde direction through the fast pathway. In an atypical form, the conduction moves antegradely in the fast pathway and retrogradely in the slow pathway, resulting in a long RP interval. A third form also has been identified in which the conduction appears to be antegrade and retrograde through two discrete slow pathways.[3] Multiple atypical AVNRT circuits using rightward and leftward inferior extensions of the AV node have been described.[4] In such models, these extensions participate in the tachycardia by connections to the left atrium.[5]

Conduction during sinus rhythm usually occurs over the fast pathway, resulting in a normal PR interval. A premature atrial beat may cause a unidirectional block in the fast pathway (because of its longer ERP) but conduct via the slow pathway. The slow pathway has a longer conduction time than the fast pathway, providing a delay of the impulse; therefore, when it reaches the distal end of the fast pathway (which has by that time recovered from refractoriness), the impulse is conducted retrograde via the fast pathway. After traversing a short portion of the low septal right atrium, it then reenters the slow pathway again, creating a circus movement tachycardia.

The natural history of AVNRT in children is unknown, but some infants appear to exhibit spontaneous resolution. The substrate for atrioventricular tachycardia is not fully understood, but cell-to-cell interactions may play a role.[3]


The incidence of atrioventricular node reentrant tachycardia (AVNRT) appears to be increased in the setting of congenital heart disease. In addition, related conditions, such as twin AV node (AV node-to-node reentry) with a Mönckeberg sling, may occur in the setting of complex congenital heart disease. Finally, dual AV nodal physiology may be a bystander to accessory pathways, and accessory pathways, including Mahaim fibers, may be bystanders to AVNRT.

One report detailed evidence that AVNRT may have a familial inheritance in some cases, which is suggestive of a genetic mechanism.[6]


United States data

Atrioventricular node reentrant tachycardia (AVNRT) is the most common cause of paroxysmal supraventricular tachycardia (PSVT). Approximately 89,000 new cases are reported each year, and 570,000 persons with PSVT live in the United States.


PSVT has a prevalence of 2.25 per 1000 population and an incidence of 35 per 100,000 person-years.

Sex- and age-related demographics

Prevalence of AVNRT is more common in females than in males, particularly in adults.

AVNRT is considered less common in newborns and increases in prevalence throughout childhood. However, some reports suggest that AVNRT may be underrecognized in infancy.[7] AVNRT is the predominant mechanism (accounting for 40-50% of cases) of SVT in adults.[8]


The diagnosis of atrioventricular node reentrant tachycardia (AVNRT) is associated with unpredictable occurrences that pose a nuisance and interfere with quality of life more than they are life threatening.


Episodes of supraventricular tachycardia (SVT) caused by any mechanism, including AVNRT, have a minimal impact on mortality in children, although SVT may lead to some degree of morbidity. Rare cases of AVNRT in young infants may be associated with more significant morbidity and possible mortality. The presence of dual AV node physiology per se does not necessarily indicate morbidity. Discontinuous AV nodal conduction curves observed during an electrophysiologic study that suggest the presence of dual AV nodal pathways have been encountered in patients without SVT and occur in approximately 63% of children. However, the presence of dual AV node physiology with associated AVNRT is a common mechanism for SVT in children and adults. Thapar and Gillette's publication showed that dual AV node physiology was the mechanism in 46% of children who presented for evaluation of arrhythmias.[9]

Patients with dual antegrade conduction in the AV node generally have good long-term outcomes following catheter ablation. However, diagnosis and management may be challenging in the presence of autonomic tone-dependent changes in ante- vs retrograde conduction via the slow and/or fast pathway(s).[10]

Patient Education

Patients beyond infancy are usually informed that their condition, despite the severity of symptoms, is not significantly life threatening. Vagal maneuvers are taught, and the options of intermittent treatment (eg, vagal maneuvers, emergency department visits), long-term drug therapy, and slow pathway modification with radiofrequency or cryothermal energy are discussed.

For patient education resources, see Heart Health Center, as well as Supraventricular Tachycardia (SVT, PSVT), and SVT (Supraventricular Tachycardia) vs. Heart Attack.




Presenting symptoms vary depending on age, heart rate, duration, and underlying heart condition. Tachycardia rates can be very dependent on the adrenergic state. Children presenting with tachycardia during exercise may have much faster rates.

Patients with atrioventricular node reentrant tachycardia (AVNRT) may be more symptomatic than those with other mechanisms of supraventricular tachycardia (SVT) due to the simultaneous depolarization of the atrial and ventricular myocardium, which causes the occurrence of atrial contraction against a closed AV valve and loss of the atrial contribution to a complete diastolic filling.[11, 12] A pounding sensation in the neck (ie, neck pulsations) is fairly unique to the presence of AVNRT and considered to be the result of cannon A waves when the atrium contracts against a simultaneously contracting ventricle.

Symptoms of congestive heart failure in the infant may include restlessness, feeding problems, and diaphoresis. Shock may occur when a hemodynamically significant tachyarrhythmia goes unrecognized and untreated for variable amounts of time (from a few hours to days).

In the older child, symptoms may include chest pain, palpitations, shortness of breath, lightheadedness, and fatigue.

Occasionally, adult patients may present with syncope or severe presyncope.

Physical Examination

Promptly evaluate the hemodynamic state of children presenting with tachyarrhythmia. The degree of hemodynamic compromise is usually determined by numerous factors, including age, heart rate, duration of the arrhythmia, and the presence or absence of structural heart disease.

Note the following:

  • Evaluate infants for signs of congestive heart failure, such as tachypnea, retractions, rales, liver enlargement, decreased pulse, and poor perfusion.

  • Cardiogenic shock with hypotension, metabolic acidosis, ventricular dysfunction, and pulmonary edema may occur.

  • Physical examination findings of the older child without underlying heart disease may be normal except for the fast heart rate.

  • The patient may exhibit tachypnea, pallor, and evidence of jugular venous pulsations caused by asynchrony of atrial and ventricular contractions (ie, the atrium contracting against a closed atrioventricular valve).

  • Patients with structural heart disease and ventricular dysfunction may have more severe hemodynamic compromise upon presentation because they have limited myocardial reserves and do not tolerate tachycardia and the absence of AV synchrony for long periods.



Diagnostic Considerations

The permanent form of junctional reciprocating tachycardia (PJRT) can be difficult to distinguish from atypical (fast-slow) atrioventricular node reentrant tachycardia (AVNRT).[13, 14, 15] However, the response to premature atrial complexes (PACs) allows for differentiation between these two arrhythmias: His refractory PACs (HrPACs) perturbing the next His (resetting with fusion) is diagnostic of AVRNT, as late PACs that fuse with the native beats are not able to reset the focal source of junctional tachycardia.[15] However, simultaneous conduction through the AV nodal fast and slow pathways (ie, two-for-one response [TFOR]) can occur in both AVNRT and junctional tachycardia and, therefore, early PAC advancing the immediate His with continuation of tachycardia is not diagnostic of junctional tachycardia.[15]

Another rare mechanism is verapamil-sensitive atrial tachycardia originating from near the atrioventricular node.[16]

Differential Diagnoses



Laboratory Studies

Upon initial presentation of atrioventricular node reentrant tachycardia (AVNRT), assessments of serum electrolyte levels, thyroid function, and hemoglobin are often performed.

Other laboratory studies may be performed to monitor serum levels and adverse effects in children receiving antiarrhythmic medications.


The electrocardiogram (ECG) obtained during normal sinus rhythm shows a normal PR interval and the absence of ventricular preexcitation. Some patients may exhibit a slightly shortened PR interval or increased beat-to-beat variability of the PR interval, reflecting varying conduction through the fast or slow pathways. The typical atrioventricular node reentrant tachycardia (AVNRT) is characterized as a narrow complex regular tachycardia with rates that vary from 150 to 300 beats per minute.[17] Unlike AV reciprocating tachycardia (accessory pathway mediated tachycardia [eg, Wolff-Parkinson-White syndrome (WPW)]), AVNRT may exhibit AV dissociation with block to either the atrium (1:2 conduction) or to the ventricle (2:1 conduction).[18]

The His-atrial-ventricular (HAV) pattern, in which the atrial electrogram follows the His bundle electrogram and precedes the ventricular electrogram on the catheter placed in the His position, is observed in up to 74% of pediatric patients with AVNRT during an electrophysiologic (EP) study.[19]

Slow-fast form of AVNRT

Note the following:

  • The slow-fast form of AVNRT is typical.

  • Initiation of tachycardia usually occurs suddenly with a premature atrial beat. Sometimes, sudden sinus slowing is followed by a junctional escape beat as a trigger for the tachyarrhythmia.

  • The termination usually occurs with AV block, which can be spontaneous or induced by vagal maneuvers or medications.

  • The rhythm may terminate with a P wave or QRS complex, depending on the site of block.

  • Little variability in RR intervals is usually noted.

  • The time that the impulse takes to reach the atrium and the ventricle from the distal node is approximately the same, which causes the retrograde P waves to be buried within the QRS or appear immediately preceding or at the terminal end of the QRS.

  • The RP interval is usually less than 50-70 milliseconds, which often results in the P wave being hidden in the QRS complex.

  • When the P wave is visible at the end of the QRS, it exhibits a characteristic late-positive component in ECG lead V1 (ie, pseudo-R' wave), or the retrograde P waves may simulate an S wave in the inferior leads.

Fast-slow form of AVNRT

Note the following:

  • The fast-slow form of AVNRT is atypical.[20]

  • The trigger is usually a premature ventricular beat that blocks in the fast pathway and is conducted in a retrograde fashion through the slow pathway and then in an antegrade fashion through the fast pathway.

  • In this form, conduction to the atria takes longer than conduction to the ventricles and the RP interval is longer than the PR interval.

  • Another characteristic is that the P-wave axis is superior (ie, negative P waves in the inferior leads), because the impulse is retrograde and originates in the AV node.

  • Distinguishing this tachycardia from permanent form of junctional reciprocating tachycardia (PJRT) can be difficult. However, PJRT usually presents with a more incessant rather than paroxysmal pattern.[14]

Imaging Studies

Chest radiography and echocardiography are often performed to evaluate the degree of cardiopulmonary dysfunction associated with the tachyarrhythmia and to assess for structural abnormalities.

Clinical and experimental studies using electrophysiologic and electroanatomical mapping are adding to the understanding of the anatomy and physiology of this disorder.

Some studies suggest that the coronary sinus, imaged at the time of electrophysiologic study, may have a broader opening in pediatric patients with atrioventricular node reentrant tachycardia (AVNRT).[21]


The electrophysiologic characteristics of atrioventricular node reentrant tachycardia (AVNRT) include initiation and termination of tachycardia by extrastimulus or rapid pacing; normal antegrade and retrograde AV nodal conduction (with the earliest retrograde activation at the His bundle); and termination with AV block that, although uncommon, may allow the AVNRT to persist. These characteristics can be evaluated in patients through the electrophysiologic study (EPS), which may be semi-invasive (eg, esophageal electrode behind the heart) or intracardiac.

Note the following:

  • During the EPS, the presence of the two functionally distinct AV nodal pathways can usually be demonstrated with atrial extrastimulus testing in adult patients.

  • As the atrial extrastimulus-coupling interval (A1-A2) is shortened by 10-millisecond decrements, the AV nodal conduction time following the atrial extrastimulus (A2-H2) increases gradually.

  • At a critical atrial extrastimulus-coupling interval, a 10-millisecond decrease in A1-A2 results in a marked increase (>50 ms) in A2-H2. This abrupt increase in AV nodal conduction time is termed a jump in conduction (discontinuous AH conduction curve), and it often is associated with the appearance of atrial echo beats or initiation of AVNRT.

  • Further 10-millisecond decreases in the A1-A2 interval result in small additional increases (< 50 ms) in the A2-H2 interval, or, less commonly, additional AH jumps are evident.

Some data indicate that AV nodal physiology in children is different than in adults. Based on the traditional definition of a 50-millisecond AH jump after a decrement of 10 milliseconds in the extrastimulus coupling interval, only 62% of the children in one study met criteria for dual AV node physiology.[22] However, all patients had inducible AVNRT, and most of them were successfully ablated. The clinical importance of this finding is that children may not always fit the classic electrophysiologic criteria as it applies to adults; therefore, the endpoints for catheter ablation need to be readdressed and redefined in the pediatric population. Data from Dasgupta et al suggest that single echo beats without sustained slow pathway conduction or inducible AVNRT may be an acceptable endpoint for catheter ablation in the pediatric population.[23]



Medical Care

Patients with known supraventricular tachycardia (SVT) who are presenting with recurrence and receiving effective therapy usually do not require admission. New patients are frequently admitted for a period of observation and to provide teaching and reassurance to the parent or child. Often, certain antiarrhythmic medications are initiated in the hospital while the patient is monitored for adverse effects (eg, proarrhythmia).

Emergency treatment of patients with hemodynamic instability in the setting of atrioventricular node reentrant tachycardia (AVNRT) is directed at converting the rhythm to sinus through a brief episode of AV block.

Perform synchronized electrical cardioversion if patients have a deteriorating condition or if there is no response to the initial attempts of conversion (see below).

The use of vagal maneuvers can be very helpful in the acute setting. In the infant, apply a plastic bag containing ice cubes and water to the face for 25-30 seconds to induce the diving reflex, a vagal stimulus. Note that this maneuver may be stressful to the infant and parents alike. In older children, other vagal maneuvers can be attempted, such as breathholding or the Valsalva maneuver. If this is not successful, the next step is to administer medication. The drug of choice is adenosine, administered from an intravenous site as close as possible to the heart. Importantly, data have indicated low efficacy of the initial recommended doses of adenosine. Use of esmolol, a short-acting beta-blocker, also has been successful.

Esophageal overdrive atrial pacing is also quite safe and effective in converting to sinus rhythm.

Recording of a long 3- or 12-lead rhythm strip during attempts to terminate the tachycardia may be invaluable in subsequent efforts to define the mechanism of SVT and should be routinely performed.


Ideally, as with most tachycardias in children, transfer should take place after successful conversion has been achieved.


Patients with AVNRT should avoid caffeine-containing items so that SVT is not provoked by caffeine-induced premature beats.

Surgical Care

Catheter ablation

See also the Guidelines section for recommendations for the management of supraventricular tachycardia (SVT) by the European Society of Cardiology (ESC) and Association for European Paediatric and Congenital Cardiology (AEPC) (2019),[24] as well as those from the American College of Cardiology, American Heart Association, and the Heart Rhythm Society (ACC/AHA/HRS) (2015).[25]

Knowledge of the anatomy of the Koch triangle (ie, where the AV node is located) is needed to understand how slow pathway ablation is performed. The Koch triangle is defined by the ostium of the coronary sinus posteriorly. The apex of the triangle is defined anteriorly by the His bundle. The tendon of Todaro and the tricuspid valve annulus comprise the sides of the triangle. In the electrophysiology laboratory, landmarks of the Koch triangle are identified by one catheter recording the His deflection and a second catheter placed in the ostium of the coronary sinus. The Koch triangle is located between these two catheters.

The fast pathway is located anteriorly, along the tendon of Todaro. The slow pathway is generally located posterior-inferiorly, along the tricuspid annulus, near the ostium of the coronary sinus. However, less common variations have been described.[4, 26]

Ablation of atrioventricular node reentrant tachycardia (AVNRT) is accomplished by delivering either radiofrequency or cryothermal energy over the slow pathway. Because its location is more posterior and, thus, distant from the AV node, incidence of complete heart block with the use of radiofrequency energy is low (1.2%).[27] The overall success rate of radiofrequency ablation on AVNRT has been more than 98% over the past decade.

In adults with mild congenital heart disease, the European Society of Cardiology recommends catheter ablation over long-term medical therapy for symptomatic, sustained recurrent SVT (AVNRT, atrioventricular reciprocating tachycardia [AVRT], atrial tachycardia [AT], and intraatrial reentrant tachycardia [IART]), or if SVT is potentially related to sudden cardiac death (SCD).[28, 29]

Cryothermal energy has allowed catheter mapping of specific ablation targets. This is especially advantageous in children with AVNRT because it allows greater reversibility of conduction block, decreasing the risk of complete AV block. The use of cryothermal energy to map and ablate arrhythmia substrates has been shown to be safer than radiofrequency energy; however, early studies showed that this safety came at the expense of acutely lower success rates and higher recurrence rates at midterm follow-up.[30, 31, 32]

In 2005, success rates of 83% were achieved for pediatric AVNRT cryoablation for an international registry. No complications were reported, and, subsequently, the success rate for radiofrequency ablation in the four AVNRT cryoablation failures was 100% with the combined approach.[33] More recent studies have reported the initial success rate for AVNRT to be 96-100% although the recurrence rate remained high at 6-20%.[34, 35, 36, 37]

In a 2010 survey of physicians who were largely invasive pediatric electrophysiologists (94%) who practice at mid- to high-volume centers (>50 ablation procedures/year), 41% of responders use cryoablation as first-line therapy for AVNRT.[38]

One study demonstrated that the fast pathway effective refractory period (ERP) prolongs during AV node modification by cryotherapy, and this can be used as a marker of success. This study indicates that prolongation of more than 20 ms in the fast pathway ERP during cryotherapy application is 70% sensitive and 72% specific for predicting successful slow pathway modification. Subsequent to the procedure, the fast pathway ERP shortens to below baseline levels.[39, 40]

A study of pediatric patients showed a trend toward improved initial success rates (98% vs 93%) and lower early recurrence rates (9% vs 18%) using a 6-mm tip cryoablation catheter as compared with a 4-mm tip catheter.[41] Use of an 8-mm tip cryoablation catheter has also been compared with radiofrequency ablation.[42]

A study in adult patients emphasized the importance of eliminating AH jumps with retrograde atrial (echo) beats in reducing the recurrence rate.[43] The applicability of this finding to the pediatric population is unclear as the typical findings of dual AV nodal physiology described in adult patients are less common in pediatric patients.[22] Persistent single echo beats may be an acceptable endpoint for slow pathway ablation in children.[23] Pediatric patients also exhibit an increased prevalence of inducible atypical arrhythmias.[44]

With the use of radiofrequency energy, the AV node can be modified by ablation of the slow pathway. The approaches to AV node slow pathway modification are generally anatomic (ie, creating a line or lines of block across the usual site of the slow-pathway entrance) or guided by slow-pathway potentials.[45] Successful deliveries of energy often are associated with a smooth and gradual acceleration of junctional tachycardia.[46] AV conduction must be assessed carefully during energy application to ensure that heart block is not created. Successful ablation usually is associated with a loss of the jump in conduction, fewer or no AV nodal echo beats, and failure to reinduce tachycardia.

With cryothermal energy, the advantage of using a moderate temperature cryo map (eg, −30°C) to identify a a target for subsequent full cryoablation (< −70°C) has been partly obscured by the finding that, in some patients, the mapped location does not predict the actual successful site, with a reported negative predictive value of 66% in some series.[47] Also, transient AV block was noted in other patients, where the map has previously shown to be a safe location. So far, no permanent AV block has been described with cryomapping/ablation.

A meta-analysis concluded that cryoablation is a safe and effective treatment. Late recurrences were more common with cryoablation; however, avoidance of AV nodal block was noted.[34] One study showed early transient AV block following cryotherapy in 18% of patients; however, in all patients, there was no evidence of AV nodal dysfunction 24 hours following the procedure.[48] Cryoablation has been shown to be more successful with increased individual experience in one study, in which there was a decreased recurrence rate from 28% in the first 25 cases to 8.9% in the last 45 cases.[35]

Postcatheterization complications include hemorrhage from the sheath access sites, pain, nausea and vomiting, rhythm abnormalities, and arterial or venous obstruction from thrombosis or spasm. Although the long-term sequelae of AVNRT ablation are unknown, one study of pediatric patients has described changes in atrial size and electrophysiology 2-5 years following ablation.[49, 50]

Current electroanatomic mapping systems have led to a significant decrease in fluoroscopy use and thus radiation exposure during electrophysiology studies and ablation.[51, 52] Intracardiac echocardiography has also been used in conjunction with electroanatomic mapping to lower radiation exposure.[53]

Some authors have suggested that cryoablation has a lower recurrence rate when performed at a younger age.[54]

Historically the electrophysiologic signal was equally important to the anatomic location for determination of appropriate ablation targets. However, increased use of high density, three-dimensional, electroanatomic voltage mapping of the Koch triangle has led to the development of observation of areas of low-voltage or voltage gradients, described as low-voltage bridges, which often coincide with areas of successful slow pathway cryoablation. Cryoablation guided by the low-voltage bridge approach has been found to be safe and effective and may result in a lower rate of tachycardia recurrence.[55, 56, 57]

Atrioventricular Node Reentry Supraventricular Tac Atrioventricular Node Reentry Supraventricular Tachycardia. Low voltage bridge in atrioventricular node reentry tachycardia (AVNRT). The images are a three-dimensional electroanatomic voltage map of the right atrium in the left anterior oblique projection with caudal angulation. The purple regions represent areas of high ("normal") atrial electrogram voltage, whereas gray and red regions have lower amplitude signals. The red region projecting from the tricuspid annulus (cutout) posteriorly toward the coronary sinus (thin purple cylinder) is a potential target for slow pathway ablation. The white spherical images are locations where cryotherapy of lesions were performed. The lesion highlighted in yellow represents the location of the successful slow pathway ablation. The others are "insurance" lesions.


2019 ESC/AEPC Guidelines for the Management of Supraventricular Tachycardia

The recommendations on the management of supraventricular tachycardia (SVT) were released in August 2019 by the European Society of Cardiology (ESC) in collaboration with the Association for European Paediatric and Congenital Cardiology (AEPC).[24, 58]  Several changes from the previous guidelines (2003) include revised drug grades as well as medications that are no longer considered, and changes to ablation techniques and indications.

Recommendations for management of AVNRT

Acute management

For hemodynamically unstable patients, synchronized direct current (DC) cardioversion is recommended (class I: recommended or indicated)

For hemodynamically stable patients, note the following class I recommendations:

  • Vagal maneuvers; the supine position with leg elevation is preferred
  • If vagal maneuvers fail, administer adenosine (6-18 mg intravenous [IV] bolus)
  • Synchronized DC cardioversion in the setting of failed drug therapy to convert or control the tachycardia 

For hemodynamically stable patients, the following are class IIa (should be considered) recommendations:

  • If vagal maneuvers and adenosine fail, consider IV verapamil or diltiazem, or consider beta-blockers (IV esmolol or metoprolol)

Chronic management

Catheter ablation is recommended for symptomatic, recurrent AVNRT (class I).

If ablation is not desirable or feasible, consider diltiazem or verapamil, in patients without heart failure with reduced ejection fraction (HFrEF), or beta-blockers (class IIa).

Consider abstinence from therapy for minimally symptomatic patients with very infrequent, short-lived episodes of tachycardia (class IIa).

2019 New Recommendations

For detailed recommendations on specific types of SVTs, please consult the original guidelines.[24]

Class I (recommended or indicated)

For conversion of atrial flutter: IV ibutilide, or IV or oral (PO) (in-hospital) dofetilide

For termination of atrial flutter (when an implanted pacemaker or defibrillator is present): High-rate atrial pacing

For asymptomatic patients with high-risk features (eg, shortest pre-excited RR interval during atrial fibrillation [SPERRI] ≤250 ms, accessory pathway [AP] effective refractory period [ERP] ≤250 ms, multiple APs, and an inducible AP-mediated tachycardia) as identified on electrophysiology testing (EPS) using isoprenaline: Catheter ablation

For tachycardia responsible for tachycardiomyopathy that cannot be ablated or controlled by drugs: Atrioventricular nodal ablation followed by pacing (“ablate and pace”) (biventricular or His-bundle pacing)

First trimester of pregnancy: Avoid all antiarrhythmic drugs, if possible

Class IIa (should be considered)

Symptomatic patients with inappropriate sinus tachycardia: Consider ivabradine alone or with a beta-blocker

Atrial flutter without atrial fibrillation: Consider anticoagulation (initiation threshold not yet established)

Asymptomatic preexcitation: Consider EPS for risk stratification

Asymptomatic preexcitation with left ventricular dysfunction due to electrical dyssynchrony: Consider catheter ablation

Class IIb (may be considered)

Acute focal atrial tachycardia: Consider IV ibutilide

Chronic focal atrial tachycardia: Consider ivabradine with a beta-blocker

Postural orthostatic tachycardia syndrome: Consider ivabradine

Asymptomatic preexcitation: Consider noninvasive assessment of the AP conducting properties

Asymptomatic preexcitation with low-risk AP at invasive/noninvasive risk stratification: Consider catheter ablation

Prevention of SVT in pregnant women without Wolff-Parkinson-White syndrome: Consider beta-1 selective blockers (except atenolol) (preferred) or verapamil

Prevention of SVT in pregnant women with Wolff-Parkinson-White syndrome and without ischemic or structural heart disease: Consider flecainide or propafenone

Class III (not recommended)

IV amiodarone is not recommended for preexcited atrial fibrillation.

Table. Medications, Strategies, and Techniques Specified or Not Mentioned in the 2019 Guidelines (Open Table in a new window)

Type of Tachycardia Treatment (Grade) Not Mentioned in 2019 Guidelines
Narrow QRS tachycardias Verapamil and diltiazem; beta-blockers (now all are grade IIa) Amiodarone, digoxin
Wide QRS tachycardias Procainamide, adenosine (both grade IIa); amiodarone (IIb) Sotalol, lidocaine
Inappropriate sinus tachycardia Beta-blockers (IIa) Verapamil/diltiazem, catheter ablation
Postural orthostatic tachycardia syndrome Salt and fluid intake (IIb) Head-up tilt sleep, compression stockings, selective beta-blockers, fludrocortisone, clonidine, methylphenidate, fluoxetine, erythropoietin, ergotaminel octreotide, phenobarbitone
Focal atrial tachycardia Acute: beta-blockers (IIa); flecainide/propafenone, amiodarone (IIb) Acute: procainamide, sotalol, digoxin
Chronic: beta-blockers; verapamil and diltiazem (all IIa) Chronic: amiodarone, sotalol, disopyramide
Atrial flutter Acute: ibutilide (I); verapamil and diltiazem, beta-blockers (all IIa); atrial or transesophageal pacing (IIb); flecainide/propafenone (III) Acute: digitalis
Chronic: — Chronic: dofetilide, sotalol, flecainide, propafenone, procainamide, quinidine, disopyramide
Atrioventricular nodal reentrant tachycardia (AVNRT) Acute: — Acute: amiodarone, sotalol, flecainide, propafenone
Chronic: verapamil and diltiazem; beta-blockers (all IIa) Chronic: amiodarone, sotalol, flecainide, propafenone, “pill-in-the-pocket” approach
Atrioventricular reentrant tachycardia (AVRT) Beta-blockers (IIa); flecainide/propafenone (IIb) Amiodarone, sotalol, “pill-in-the-pocket” approach
SVT in pregnancy Verapamil (IIa); catheter ablation (IIa when fluoroless ablation is available) Sotalol, propafenone, quinidine, procainamide
Adapted from Brugada J, Katritsis DG, Arbelo E, et al, for the ESC Scientific Document Group. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2019 Aug 31;ehz467.

2015 ACC/AHA/HRS Guidelines for the Management of Supraventricular Tachycardia

In 2015, the American College of Cardiology, American Heart Association, and the Heart Rhythm Society (ACC/AHA/HRS) released joint guidelines for the management of supraventricular tachycardia that includes specific recommendations for both acute and ongoing ;management of atrioventricular node reentry tachycardia (AVNRT).[25]

Management of Acute AVNRT

Vagal maneuvers and/or IV adenosine are the recommended initial treatments for acute AVNRT. (Class I; level of evidence B-R)

Additional recommendations for acute treatment when adenosine and vagal maneuvers are ineffective or contraindicated are summarized below.

Hemodynamically unstable patients

  • Synchronized cardioversion (class I; level of evidence B-NR)

Hemodynamically stable patients

  • Synchronized cardioversion when beta blockers, diltiazem, or verapamil are ineffective or contraindicated (class I; level of evidence B-NR)
  • IV beta blockers, diltiazem, or verapamil (class IIa; level of evidence: B-R)
  • Oral beta blockers, diltiazem, or verapamil may be considered (class IIb; level of evidence: C-LD)
  • IV amiodarone may be considered when other therapies are ineffective or contraindicated (class IIb; level of evidence: C-LD)

The guidelines note that for rhythms that terminate or recur spontaneously, synchronized cardioversion is not appropriate.

Management of Ongoing AVNRT

Minimally symptomatic

Clinical follow-up without pharmacologic therapy or ablation is reasonable for minimally symptomatic patients with AVNRT. (Class IIa; level of evidence B-R)

Self-administered (“pill-in-the-pocket”) acute doses of oral beta blockers, diltiazem, or verapamil may be reasonable for patients with infrequent, well-tolerated episodes of AVNRT. (Class IIb; level of evidence C-LD)


Catheter ablation of the slow pathway is the recommended initial treatment for ongoing management of symptomatic AVNRT. (Class I; level of evidence B-R) Patients who are not candidates for, or prefer not to undergo, catheter ablation should be treated with verapamil, diltiazem, or oral beta blockers. (Class I; level of evidence B-R)

Additional treatment options for ongoing treatment of AVNRT include:

  • ​Flecainide or propafenone in patients without structural heart disease or ischemic heart disease when Class I therapies (catheter ablation; beta blockers, diltiazem, or verapamil) are ineffective or contraindicated. (Class IIa; level of evidence B-R)
  • Oral sotalol, dofetilide, oral digoxin, or amiodarone may be reasonable for patients who are not candidates for, or prefer not to, undergo catheter ablation. (Class IIb; level of evidence B-R)


Medication Summary

Emergency treatment in the patient with hemodynamic instability is directed at immediate synchronized cardioversion. If the patient is stable, then the goal is to convert the rhythm to sinus through a brief episode of atrioventricular (AV) block. Adenosine is the drug of choice for acute termination of AV nodal reentrant tachycardia (AVNRT).[59] Esmolol, other beta-adrenergic blockers, verapamil, and digoxin also have been used with some success.

Drugs used for long-term therapy that have some effect in AV node reentrant tachycardia include digoxin, beta-blockers, and verapamil.[60] Avoid intravenous verapamil use in infants because of its negative inotropic effects and avoid its use in combination with beta-blockers.

Digoxin has been used in cases of fetal supraventricular tachycardia (SVT) and atrial flutter (AF). However, it is sometimes ineffective, especially in cases of fetal hydrops. A retrospective review of pregnancies with fetal tachycardia at one center found sotalol, alone or combined with digoxin, to be an effective alternative treatment for fetal SVT and AF.[61]

Antiarrhythmic agents

Class Summary

These agents alter the electrophysiologic mechanisms responsible for arrhythmia.

Adenosine (Adenocard)

Slows conduction time through AV node. Can interrupt reentry pathways through AV node and restore normal sinus rhythm in PSVT.

Esmolol (Brevibloc)

Excellent drug 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. Short half-life of 8 min allows for titration to desired effect and quick discontinuation if needed. A loading dose is described to speed up the onset of effect but can be deferred, particularly if there is a concern for a poor hemodynamic response to acute beta blockade.

Digoxin (Lanoxin, Lanoxicaps)

Cardiac glycoside with direct inotropic effects in addition to indirect effects on the cardiovascular system. Acts directly on cardiac muscle, increasing myocardial systolic contractions. Its indirect actions result in increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increase in mean arterial pressure. Generally not an effective acute treatment for AVNRT since the vagotonic effect is centrally mediated and so is delayed by several hours by the blood-brain barrier.

Propranolol (Inderal)

Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.

Atenolol (Tenormin)

Selectively blocks beta1-receptors with little or no effect on beta2 types. The advantage is the requirement of administration only twice per day in young infants. Causes less central nervous system effects than propranolol because atenolol does not cross the blood brain barrier.

Verapamil (Calan)

Acts on the slow calcium current in SA and AV nodal cells. Decreases the rate of phase 4 automaticity and phase 0 depolarization, prolonging refractoriness and conduction time. Interrupts AVNRT by slowing conduction through the AV node.