Atrioventricular nodal reentrant tachycardia

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 most SVTs, the QRS complex in AVNRT is typically narrow (ie, ≤120 milliseconds), reflecting normal ventricular activation through the His-Purkinje system. However, rate-related aberrant conduction during SVT or an underlying bundle branch block can result in a wide QRS complex tachycardia.

This topic will review the mechanisms, clinical manifestations, diagnosis, and 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 — 

Atrioventricular nodal reentrant tachycardia (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 female patients [1-3]. AVNRT can present at any age; however, patients usually experience their first episode in adolescence or young adulthood. 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]. AVNRT usually occurs in patients with otherwise normal hearts; however, it can occur in patients with structural heart disease [5,6]. Rare cases of familial AVNRT have also been reported [7].

ANATOMY AND PATHOPHYSIOLOGY — 

Atrioventricular nodal reentrant tachycardia (AVNRT) generally requires the existence of dual electrical pathways in the AV node. A discussion of these pathways, as well as the two types of AVNRT, is found below.

Dual AV nodal pathways — The physiologic substrate for AVNRT usually involves dual (ie, fast and slow) electrical pathways that lead to the compact AV node (ie, the dense, functional core of the AV node) [8,9]. One pathway (ie, fast pathway), conducts rapidly and has a relatively long refractory period. The second pathway (ie, slow pathway) conducts relatively slowly and has a shorter refractory period. Approximately 10 to 20 percent of the general population has dual pathways [10].

The slow and fast pathways are located within Koch's triangle, an anatomical region that is bounded by the tricuspid ring, the tendon of Todoro, and the coronary sinus ostium (figure 1 and figure 2) [8,11]. The fast pathway is usually located in the anterior third of Koch’s triangle, near the tendon of Todaro, while the slow pathway is usually located in the posterior third of the triangle [8,12,13]. These pathways join and enter a final common pathway in the compact AV node. It is unclear whether the pathways are distinct anatomic structures or are anatomically continuous but functionally separate (ie, have different electrical properties). Regardless of whether they are anatomically distinct, they must have different conduction velocities and refractory periods in order for reentry to occur [14].

Not all patients with AVNRT have evidence of dual pathways during electrophysiology (EP) study (waveform 1A-B) [15]. Conversely, not all patients with dual AV nodal pathways have clinical AVNRT. 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 [16]. However, in the author's experience, the vast majority of patients with documented AVNRT have clear evidence of dual AV nodal pathways with an inferior rightward slow pathway extension.

When dual pathways are present, AV conduction occurs during sinus rhythm 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 final common pathway, it runs into the refractory wake of the impulse that had traveled down the fast pathway. The advent of ultra-high-density three-dimensional mapping has made it possible to detect this site of collision during sinus rhythm in patients with dual AV nodal pathways [17].

Typical and atypical AVNRT — AVNRT is a reentrant arrhythmia (table 1) (see "Reentry and the development of cardiac arrhythmias"). Approximately 80 to 90 percent of patients with AVNRT present with typical AVNRT, also known as "slow-fast" AVNRT. The other 10 to 20 percent of patients have uncommon forms of the arrhythmia, known as "atypical AVNRT." In rare cases, typical and atypical AVNRT have been found during EP studies to occur in the same patient [18].

●Typical AVNRT – Typical AVNRT usually initiates and perpetuates as follows (figure 3):

•A premature atrial complex (PAC; also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) arrives at the AV node when the fast pathway is in its refractory period, so antegrade conduction down the fast pathway is blocked. Occasionally, this process is initiated by a premature junctional or ventricular beat with retrograde conduction rather than a PAC.

•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 is 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 4).

The penetration of the reentrant circuit by another premature beat can abruptly terminate the arrhythmia.

●Atypical AVNRT – Mechanisms of atypical AVNRT include the following:

•Antegrade conduction can occur down the fast pathway with retrograde conduction up the slow pathway (figure 5) [19]. 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, conduction through the reentrant circuit is so slow that the heart rate is less than 100 beats per minute which, by definition, is not tachycardia. This arrhythmia, sometimes referred to as AV nodal reentrant arrhythmia, can be mistaken for a junctional rhythm. Despite the absence of tachycardia, patients can be symptomatic.

A more detailed discussion of the electrophysiology of AVNRT can be found in published reviews [8,9,20,21].

CLINICAL MANIFESTATIONS

●Symptoms – Patients with atrioventricular nodal reentrant tachycardia (AVNRT) often experience symptoms such as palpitations (98 percent), dizziness or lightheadedness (78 percent), dyspnea (47 percent), or chest pain (38 percent); less commonly, they report fatigue (19 percent) and syncope (16 percent) [22]. Because of the paroxysmal nature of the arrhythmia, the onset and termination of the symptoms are usually sudden. Those with significant underlying cardiac disease are more likely to experience dyspnea and chest pain. Patients may report a sensation of neck pounding, which reflects a sudden rise in jugular venous pressure due to the right atrium contracting while the tricuspid valve is closed. Some patients with AVNRT experience urination during or after AVNRT; the mechanism of this symptom is probably related to an elevated mean right atrial pressure and plasma level of atrial natriuretic peptide, which are present during the arrhythmia [23].

Syncope is uncommon with AVNRT and is most likely to occur in those with high heart rates (eg, heart rate ≥170 beats per minute). However, factors other than heart rate may also contribute to syncope. As an example, abnormal vasomotor adaptation during AVNRT has been reported, suggesting a role for neurally mediated (neurocardiogenic) responses [24,25]. In very rare cases, AVNRT can result in cardiac arrest [26].

●Triggers – Usually there is no apparent precipitating cause for episodes of AVNRT. However, in some patients, nicotine, alcohol, caffeine, amphetamines, exercise, or medications can initiate episodes. Drugs that may cause or exacerbate AVNRT include certain antipsychotics, bronchodilators, dobutamine, corticosteroids, furosemide (in children), and stimulants (eg, methylphenidate) [27].

Some patients experience the onset of AVNRT during sleep or after a particular motion (eg, bending forward, squatting) that enhances vagal tone. While vagal maneuvers (eg, Valsalva maneuver) can be used to terminate AVNRT, increased vagal tone may paradoxically facilitate the induction of AVNRT.

●Termination with maneuvers – Some patients with AVNRT will report they can terminate their symptoms by coughing, holding their breath, or bearing down. These are maneuvers that increase vagal tone. (See 'Valsalva maneuver (all patients)' below.)

DIAGNOSIS

When to suspect AVNRT — We suspect atrioventricular nodal reentrant tachycardia (AVNRT) when a young patient (<40 years of age) presents with the abrupt onset and offset of rapid palpitations. While older patients can present with AVNRT, other arrhythmias (eg, atrial fibrillation, atrial flutter) are more likely to cause these symptoms in older patients.

Diagnostic testing

Patients who are currently symptomatic — For symptomatic patients who present with tachyarrhythmia, a 12-lead electrocardiogram (ECG) is the first step in diagnosing AVNRT. ECG features that are characteristic of the arrhythmia include the following:

●Ventricular rate – The ventricular rate is usually between 140 and 180 bpm but may be outside this range.

●Abrupt onset following a premature atrial complex (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). At times, a brief run of atrial tachycardia can initiate typical AVNRT with the last beat of the atrial tachycardia conducting over the slow pathway.

●Relationship between QRS complexes and P waves – Because of the relationship between the QRS complex and the subsequent P wave, typical AVNRT is referred to as a "short RP tachycardia," while atypical AVNRT is a "long RP tachycardia" [21]. (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 (waveform 2). A component of the P wave is often evident slightly after (or, less commonly, before) the QRS. When the P wave occurs shortly after the QRS complex, the fused waveform can produce a pseudo-R' (ie, a second R wave) in lead V1 and a pseudo-S wave in the inferior leads (figure 6).

•In atypical AVNRT, retrograde atrial activation occurs long after ventricular activation, resulting in a P wave that occurs so late after the QRS complex that it appears to be occurring shortly before the next QRS complex (figure 5 and figure 7 and waveform 3). This pattern resembles that seen in atrial tachycardias. In such cases, an electrophysiology (EP) study may be required to define the arrhythmogenic mechanism.

●Narrow QRS complex – In most cases of AVNRT, the QRS complex is of normal width (<120 ms). However, it can appear wide (>120 ms) if the patient has an underlying bundle branch block or a rate-related bundle branch block.

●P wave morphology – When P waves can be clearly identified, the P wave axis in AVNRT is abnormal due to retrograde atrial activation. This is usually manifested on the ECG as a negative P wave axis with inverted P waves in leads II, III, and aVF [28].

●ST segment depression – 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 reciprocating (reentrant) tachycardia (AVRT) associated with an accessory pathway [29-31]. For most patients with AVNRT, the ST segment depression is not an indicator of myocardial ischemia; however, in older patients, especially those with chest pain during the arrhythmia, concurrent coronary artery disease may be present [32].

●T wave inversions following termination – After the acute termination of AVNRT and other paroxysmal supraventricular tachycardias (SVTs), T wave inversions may be seen in the anterior or inferior leads in approximately 40 percent of patients [33]. Inverted T waves may be seen immediately upon termination or may develop within the first six hours and persist for hours to days. The occurrence of negative T waves is not predicted by clinical parameters, tachycardia rate, duration, or the presence and extent of ST segment depression during the tachycardia. They are not the result of coronary artery disease but are likely due to ionic current alterations resulting from the rapid rate.

Patients who are currently asymptomatic — Patients who are currently asymptomatic but who report symptoms suggestive of AVNRT (see 'When to suspect AVNRT' above) can be managed in the outpatient setting. For these patients, we order an event (loop) recorder (see "Ambulatory ECG monitoring", section on 'Event (loop) monitor'). We choose the monitoring duration based on the frequency of symptoms. Findings on the event recorder that suggest AVNRT are discussed below. (See 'Establishing the diagnosis' below.)

Establishing the diagnosis — A diagnosis of AVNRT can usually be made if the ECG or event recorder show the following characteristics:

●A regular, narrow QRS complex tachycardia.

●Short RP interval with the P wave fused at the end of the QRS complex, or absent P wave.

●Abnormal P wave axis (if P waves are present):

•On a 12-lead ECG, P waves are inverted in the inferior leads.

•On an event recorder, P wave axis is different from the axis of the sinus P waves.

●Sudden onset and termination of the arrhythmia (if these are captured). The onset of the arrhythmia is immediately preceded by a PAC.

It is important to note that the absence of one or more of these characteristics does not rule out AVNRT. As an example, as discussed above (see 'Patients who are currently symptomatic' above), AVNRT can sometimes have a long RP interval. If the diagnosis is unclear, using the Valsalva maneuver or intravenous (IV) adenosine to temporarily slow AV nodal conduction can be a helpful diagnostic maneuver. AVNRT and other reentrant arrhythmias (eg, AVRT) are usually terminated with the Valsalva maneuver and adenosine, whereas other common SVTs (eg, atrial flutter, atrial tachycardia, sinus tachycardia) are not. The use of the Valsalva maneuver and adenosine as diagnostic maneuvers is discussed in more detail elsewhere. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'ECG identification of atrial activity'.)

If the diagnosis remains uncertain despite the Valsalva maneuver and adenosine, an invasive electrophysiology (EP) study may be necessary. (See "Invasive diagnostic cardiac electrophysiology studies".)

DIFFERENTIAL DIAGNOSIS — 

The list of conditions that cause palpitations is extensive (table 2) (see "Evaluation of palpitations in adults"). However, once an electrocardiogram (ECG) or event recorder is available and reveals a regular, narrow QRS complex tachycardia, the differential diagnosis is limited to regular supraventricular tachycardias (SVTs). In addition to atrioventricular nodal reentrant tachycardia (AVNRT), these include sinus tachycardia, atrioventricular reentrant tachycardia (AVRT), focal atrial tachycardia, atrial flutter, and several rare SVTs. These arrhythmias are discussed briefly below.

●Sinus tachycardia – Sinus tachycardia is the most common regular, narrow QRS complex tachycardia. In contrast to AVNRT, which has an abrupt onset and offset, sinus tachycardia has a gradual onset and offset that typically occurs over 30 seconds to several minutes. Additionally, for most patients, sinus tachycardia does not result in symptoms. Sinus tachycardia is usually secondary to an underlying noncardiac condition. However, it is occasionally persistent in otherwise healthy patients, in which case it is known as “inappropriate sinus tachycardia.” (See "Sinus tachycardia: Evaluation and management" and "Sinus tachycardia: Evaluation and management", section on 'Inappropriate sinus tachycardia'.)

●AVRT – Both AVRT and AVNRT have abrupt onset and termination. However, if an ECG is performed when the patient is in sinus rhythm, most patients with AVRT have evidence of preexcitation (ie, short PR interval and delta wave) consistent with an accessory pathway, whereas those with AVNRT will not have this finding. For the minority of patients with AVRT who have concealed conduction (ie, an accessory pathway that does not cause a delta wave), invasive electrophysiology (EP) study is required to distinguish AVNRT from AVRT. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)

●Focal atrial tachycardia – As with AVNRT and AVRT, focal atrial tachycardia has an abrupt onset. In contrast to AVNRT, the P wave morphology during atrial tachycardia may 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. Atrial tachycardia usually terminates with a QRS complex. (See "Focal atrial tachycardia".)

●Atrial flutter – When atrial flutter is conducted 2:1, it can be mistaken for AVNRT if the flutter waves are not easily seen. Atrial flutter should be suspected if the ventricular rate is approximately 150 bpm and the patient is older (ie, >50 years of age). (See "Electrocardiographic and electrophysiologic features of atrial flutter".)

●Rare SVTs – Several rare types of SVT are in the differential diagnosis:

•Junctional ectopic tachycardia (JET) – 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 [34]. JET can be difficult to differentiate from typical AVNRT. However, it 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 [35].

•Dual AV nodal nonreentrant tachycardia (DAVNNT) – Patients with dual AV nodal pathways can rarely develop DAVNNT during sinus rhythm. This tachycardia occurs when each sinus beat is followed by two ventricular depolarizations due to consecutive double antegrade conduction via the fast and slow pathways. Unlike AVNRT, DAVNNT is usually associated with alternating R-R intervals on ECG [36].

•Sinoatrial nodal reentrant tachycardia (SANRT) – SANRT has an identical appearance to sinus tachycardia and to some atrial tachycardias. In contrast to sinus tachycardia, SANRT can have an abrupt onset. An invasive EP study is required for diagnosis. (See "Sinoatrial nodal reentrant tachycardia (SANRT)".)

•Intraatrial tachycardia – 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 "Intraatrial reentrant tachycardia".)

•Idiopathic left ventricular tachycardia – 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'.)

INITIAL MANAGEMENT

Unstable patients — It is rare for atrioventricular nodal reentrant tachycardia (AVNRT) to cause hemodynamic or clinical instability (ie, hypotension, shock, decreased level of consciousness, heart failure). However, for patients with AVNRT who are unstable, immediate synchronized electrical cardioversion is appropriate (algorithm 1). If sinus rhythm is not restored following an initial 50- to 100-joule shock, subsequent shocks should be at higher energy levels. Electrical cardioversion is usually successful but may require relatively high energy levels, probably due to the deep location of the reentrant pathway. (See "Cardioversion for specific arrhythmias".)

After the arrhythmia is terminated, patients do not usually require further management of the AVNRT (eg, intravenous [IV] antiarrhythmic drugs) in the acute setting. However, because AVNRT does not usually lead to hemodynamic compromise, it is possible that AVNRT was not the cause of the patient’s instability. If the patient remains unstable after cardioversion, they should be evaluated for other etiologies of hemodynamic compromise. (See "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock".)

Stable patients — For stable patients with AVNRT (ie, those without hypotension, shock, decreased level of consciousness, or heart failure), we adhere to the following sequential approach to terminating the arrhythmia (algorithm 1) [37,38]:

●Step 1: Valsalva maneuver – As the initial treatment of AVNRT, we attempt one or more vagal maneuvers. We typically start with a standard Valsalva maneuver, followed by a modified Valsalva maneuver if the standard one is ineffective. Carotid sinus massage is another option. In a standard Valsalva maneuver, the patient is placed in a supine or semirecumbent position and instructed to inhale normally, close their mouth, pinch their nose, and push their breath out against the closed mouth for 10 to 15 seconds. The modified Valsalva maneuver consists of the standard Valsalva maneuver followed by supine positioning and passive leg raising. Additional information on the Valsalva maneuver and other vagal maneuvers is presented separately. (See "Vagal maneuvers".)

The Valsalva maneuver is safe, easily performed, and effective for AVNRT. It increases parasympathetic tone, gradually slowing conduction in the antegrade slow pathway [39]; in addition, it can produce an abrupt block in the retrograde fast pathway. In one systematic review, which included 316 patients with a total of 965 episodes of AVNRT and AV reciprocating tachycardia (AVRT), the standard Valsalva maneuver successfully terminated 45 percent of supraventricular tachycardia (SVT) episodes and was more effective than carotid sinus massage [40]. In a trial in 428 patients with SVT, those who were randomly assigned to the modified Valsalva maneuver were more likely to have restoration of sinus rhythm at one minute than those assigned to the standard Valsalva maneuver (adjusted odds ratio 3.7; 95% CI 2.3-5.8) [41]. While the modified Valsalva maneuver is more effective than the standard one, it is reasonable to perform the simpler standard maneuver first.

For patients whose arrhythmia is terminated with vagal maneuvers, further management focuses on preventing and treating recurrent AVNRT. (See 'Further management' below.)

For those whose arrhythmia persists after vagal maneuvers, we administer IV adenosine, which is discussed below.

●Step 2: Adenosine – For patients with AVNRT that persists following vagal maneuvers, or in whom these maneuvers cannot be adequately performed, we suggest IV adenosine rather than longer-acting AV nodal blockers. The protocol for administering adenosine is described in the algorithm (algorithm 2), with more details presented separately. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Intravenous adenosine'.)

The advantages of adenosine over other agents (eg, beta blockers, calcium channel blockers) include its rapid onset and short half-life. Adenosine terminates AVNRT in most cases [42-45]. As an example, in an observational study of 95 patients with AVNRT, adenosine terminated the arrhythmia in 86 percent of patients [42]. Adenosine is safe and generally well tolerated.

For patients in whom adenosine terminates the arrhythmia, further management focuses on preventing and treating recurrent AVNRT. (See 'Further management' below.)

For those in whom adenosine fails to terminate the arrhythmia, we administer a beta blocker or calcium channel blocker, which is discussed below.

●Step 3: Beta blocker or calcium channel blocker – If vagal maneuvers and adenosine are ineffective, or AVNRT recurs shortly after the arrhythmia was terminated, we suggest administering IV nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) or IV beta blockers (eg, metoprolol, esmolol) [46,47]. We prefer these medications over cardioversion, which requires that the patient receive moderate sedation by specially trained personnel in a monitored setting. Calcium channel blockers have been shown to terminate SVT (not specifically AVNRT) in 64 to 98 percent of patients, while data on the effectiveness of beta blockers are more limited [37]. Both classes of drugs are usually well tolerated but have potential adverse effects, including hypotension and bradycardia [48,49]. We choose among these drugs based on familiarity with and availability of the agents. Calcium channel blockers are preferred for patients with reactive airway disease and active wheezing. We do not use oral medications in the acute setting because they will take longer to terminate AVNRT than IV medications. Initial IV dosing options include:

•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.

•Esmolol – 500 mcg/kg IV bolus over one minute, followed by a 50 to 150 mcg/kg/minute infusion if necessary. Infusion rate can be adjusted as needed to maintain the desired heart rate (up to 300 mcg/kg/minute).

•Verapamil – 5 to 10 mg IV bolus over two 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 two 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.

Clinical trials of an intranasally administered calcium channel blocker, etripamil, have shown it to be highly effective, leading to termination of SVT in up to 95 percent of patients [50,51]; however, this drug is not yet available in the United States or Europe.

For patients in whom beta blockers and/or calcium channel blockers terminate the arrhythmia, further management focuses on preventing and treating recurrent AVNRT. (See 'Further management' below.)

For those in whom these agents fail to terminate the arrhythmia, we perform electrical cardioversion, which is discussed above and elsewhere. (See 'Unstable patients' above and "Cardioversion for specific arrhythmias".)

FURTHER MANAGEMENT — 

After acute atrioventricular nodal reentrant tachycardia (AVNRT) has been terminated, further management focuses on treating and preventing recurrences.

Patient-initiated treatment of recurrent AVNRT — For all patients with AVNRT, we develop a plan for patient-initiated treatment of arrhythmia recurrence in the outpatient setting.

Valsalva maneuver (all patients) — We instruct all patients with AVNRT to perform the standard Valsalva maneuver. Patients who have been educated on the proper performance of this maneuver are often able to terminate subsequent episodes of AVNRT on their own. If the maneuver is successful, patients generally do not need to seek urgent medical attention. However, patients should seek medical attention if the arrhythmia persists despite several attempts. Details about the Valsalva maneuver are discussed above and elsewhere. (See 'Stable patients' above and "Vagal maneuvers", section on 'Valsalva maneuver'.)

Pill-in-the-pocket (select patients) — For patients who are having infrequent, well-tolerated episodes of AVNRT that are not terminated by the Valsalva maneuver, and who do not want catheter ablation or chronic suppressive medication (see 'Choosing between options' below), an alternative strategy is to take a single dose of an oral medication (eg, beta blocker, nondihydropyridine calcium channel blocker) to terminate recurrent arrhythmia [37,52,53]. This “pill-in-the-pocket” approach may reduce the need for emergency department visits and help a patient avoid chronic medical therapy or catheter ablation. Although data in support of this strategy are limited, in small studies in patients with supraventricular arrhythmias, single doses of an oral beta blocker or calcium channel blocker have been associated with rates of termination ranging from 60 to 90 percent [52,53]. While this approach has also been evaluated with the class IC antiarrhythmic drug flecainide [53], flecainide is rarely used in the management of AVNRT due to the possible toxicities (eg, arrhythmia). The choice of a particular agent will vary from patient to patient depending on comorbidities and patient preference.

Prevention of recurrence

Choosing between options — Our approach to the prevention of recurrent AVNRT is based on the nature of symptoms (eg, frequency, severity) and patient preference.

●We suggest radiofrequency catheter ablation rather than chronic suppressive medications for the prevention of recurrent AVNRT for patients with any of the following:

•Frequent recurrences of AVNRT

•AVNRT that is refractory to the Valsalva maneuver

•AVNRT that is poorly tolerated (eg, associated with near-syncope, syncope, angina, severe dyspnea)

•Presentation to the emergency department with AVNRT

In a trial of 61 patients with AVNRT diagnosed by electrophysiology (EP) study that compared catheter ablation with antiarrhythmic therapy (eg, calcium channel blocker, beta blocker), 100 percent of patients randomly assigned to ablation remained free from recurrent AVNRT over five years of follow-up compared with only 25 percent of patients assigned to antiarrhythmic therapy [54]. Observational studies have demonstrated that catheter ablation is a definitive cure for AVNRT in greater than 95 percent of patients, with high rates of success with both typical and atypical AVNRT [55-57]. Catheter ablation is discussed in detail below. (See 'Catheter ablation' below.)

For those who are not good candidates for ablation or do not wish to undergo the procedure, chronic suppressive medication is an appropriate alternative. A pill-in-the pocket approach is another acceptable option in patients with occasional episodes of AVNRT that do not terminate with Valsalva maneuvers. (See 'Chronic suppressive therapy' below and 'Pill-in-the-pocket (select patients)' above.)

●For the prevention of recurrent AVNRT in patients without any of the above characteristics (ie, patients with infrequent, mild episodes that are terminated with the Valsalva maneuver), we base our approach on the patient’s preference. Management options include the following:

•No preventive therapy – Some patients, particularly those who can rapidly terminate episodes with the Valsalva maneuver, may decline preventive therapy. These patients may wish to keep a dose of an oral beta blocker or calcium channel blocker on hand (ie, “pill-in-the-pocket” approach) to take in the event that they experience persistent AVNRT despite the Valsalva maneuver. (See 'Pill-in-the-pocket (select patients)' above.)

•Preventive therapy – For patients who prefer to receive preventive therapy, there are two options: catheter ablation and chronic suppressive medication.

-Catheter ablation – For patients who do not want to take daily medication indefinitely, or cannot take those medications, catheter ablation is reasonable. (See 'Catheter ablation' below.)

-Chronic suppressive medication – For patients who do not want to undergo a procedure, an oral beta blocker or nondihydropyridine calcium channel blocker is appropriate. (See 'Chronic suppressive therapy' below.)

Catheter ablation — Radiofrequency catheter ablation prevents AVNRT by eliminating one of the dual AV nodal pathways responsible for the arrhythmia. The efficacy of catheter ablation and our approach to selecting appropriate patients for the procedure are discussed above. (See 'Choosing between options' above.)

The most significant potential complication of radiofrequency ablation for AVNRT is AV block; however, this complication is infrequent, occurring in less than 1 percent of patients, primarily in patients of older age and with baseline PR interval prolongation [56,58-63]. (See "Overview of catheter ablation of cardiac arrhythmias", section on 'Complications'.)

For patients with AVNRT, catheter ablation usually targets the posterior slow pathway (figure 8). Compared with ablation of the anterior fast pathway, ablation of the slow pathway carries a lower risk of AV block, preserves fast pathway function (and a normal PR interval post-ablation), and is facilitated by reliable anatomic and electrophysiologic landmarks. While the fast pathway can also be ablated, this approach is 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. The slow pathway is rarely in a nonposterior location, which will impact the approach during ablation [64]; as an example, the slow pathway may be a leftward rather than rightward inferior AV nodal extension, requiring ablation from the left atrial septum or within the coronary sinus [65].

Chronic suppressive therapy — For patients with AVNRT who are not good candidates for catheter ablation, or who have declined the procedure, an oral beta blocker (eg, metoprolol) or nondihydropyridine calcium channel blocker (eg, verapamil, diltiazem) may be helpful to suppress recurrent arrhythmias, although these medications are not as effective for preventing AVNRT as catheter ablation [54]. Both of these classes of drugs are generally well tolerated. While there are limited data comparing the efficacy of different agents, one small study found that propranolol, verapamil, and digoxin were all similarly effective in reducing the number and duration of SVT episodes [66]. We choose a medication based on the patient’s comorbidities (eg, reactive airway disease, depression). The choice of a starting dose will vary depending upon the baseline heart rate and blood pressure, and doses can be titrated upward as needed.

For patients who do not respond to optimally titrated beta blockers or calcium channel blockers and who do not want to pursue ablation, a class IC (eg, flecainide, propafenone) or class III (eg, sotalol, dofetilide, amiodarone) antiarrhythmic drug may be considered. The choice of a particular agent should be individualized based on the patient’s comorbidities. However, due to the potential for significant toxicities, including proarrhythmia, the use of class I and III antiarrhythmic drugs for the management of AVNRT should be reserved for rare cases and should be administered in consultation with an electrophysiologist. 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".)

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: Arrhythmias in adults" and "Society guideline links: Catheter ablation of arrhythmias" 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 6^th 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 12^th 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 topic (see "Patient education: Supraventricular tachycardia (SVT) (The Basics)")

SUMMARY AND RECOMMENDATIONS

●General principles – Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common regular, narrow complex, supraventricular tachycardia (SVT). Most patients first present in adolescence or young adulthood. (See 'Introduction' above and 'Epidemiology' above.)

●Anatomy and pathophysiology – AVNRT is a reentrant arrhythmia occurring in patients who have dual AV nodal electrical pathways. In typical AVNRT, there is antegrade conduction down the slow pathway and retrograde conduction up the fast pathway. The arrhythmia is triggered by a premature atrial complex (PAC). (See 'Anatomy and pathophysiology' above.)

●Clinical manifestations – Most patients with AVNRT experience palpitations and lightheadedness. Many have dyspnea or chest pain, while syncope is uncommon. (See 'Clinical manifestations' above.)

●Diagnosis

•When to suspect AVNRT – We suspect AVNRT when a young patient (<40 years of age) presents with the abrupt onset of palpitations. Similar symptoms in an older patient are more likely to be due to other arrhythmias. (See 'When to suspect AVNRT' above.)

•Diagnostic testing

-Patients who are currently symptomatic – For symptomatic patients who present with a tachyarrhythmia, a 12-lead electrocardiogram (ECG) is the first step in diagnosing AVNRT. Several ECG features are characteristic of AVNRT. (See 'Patients who are currently symptomatic' above.)

-Patients who are currently asymptomatic – For asymptomatic patients, we order an event (loop) recorder. (See 'Patients who are currently asymptomatic' above.)

•Establishing the diagnosis – AVNRT can often be diagnosed on an ECG or event recorder. Characteristic findings include:

-Regular, narrow QRS complex tachycardia

-Short RP interval with the P wave fused at the end of the QRS complex, or absent P wave

-If P waves are seen, their axis is abnormal

-Sudden onset and termination of the arrhythmia (if these are captured). The onset is immediately preceded by a PAC

The Valsalva maneuver and adenosine can be useful for diagnosis, but electrophysiology (EP) testing is sometimes necessary. (See 'Establishing the diagnosis' above.)

●Differential diagnosis – The differential diagnosis for AVNRT includes sinus tachycardia, AV reciprocating (reentrant) tachycardia, focal atrial tachycardia, atrial flutter, and several rare SVTs. (See 'Differential diagnosis' above.)

●Initial management – Unstable patients require immediate cardioversion. For stable patients, we follow a sequential approach to terminating the arrhythmia, starting with the Valsalva maneuver. If this is ineffective, we suggest intravenous (IV) adenosine (Grade 2C). For patients in whom adenosine fails to break the arrhythmia, we suggest IV beta blockers or calcium blockers (Grade 2C), reserving cardioversion for cases refractory to these measures, given the special resources and time required to implement the latter. (See 'Initial management' above.)

●Further management

•Patient-initiated treatment of recurrent AVNRT – We instruct all patients to perform a Valsalva maneuver. For some patients, we prescribe an oral AV nodal-blocking medication to be taken if the Valsalva maneuver is ineffective (“pill-in-the-pocket” approach). (See 'Patient-initiated treatment of recurrent AVNRT' above.)

•Prevention of recurrence – We suggest radiofrequency catheter ablation rather than chronic suppressive medications for the prevention of recurrent AVNRT for patients who have any of the following (Grade 2C):

-Frequent recurrences of AVNRT

-AVNRT that is refractory to the Valsalva maneuver

-AVNRT that is poorly tolerated (eg, associated with near-syncope, syncope, angina, severe dyspnea)

-Presentation to the emergency department with AVNRT

For those who choose not to undergo ablation, chronic suppressive medications (eg, beta blockers, calcium channel blockers) are an appropriate alternative. A pill-in-the-pocket approach is another acceptable option in patients with occasional episodes of AVNRT that do not terminate with the Valsalva maneuver.

For patients without any of these characteristics, we base our approach on the patient’s preference. Options include no preventive therapy, catheter ablation, or chronic suppressive medications. (See 'Prevention of recurrence' above.)