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 the majority of SVTs, the QRS complex in AVNRT is usually 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. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Paroxysmal and incessant SVT'.)

This topic will review the mechanisms, clinical manifestations, diagnosis, and the management of AVNRT. A detailed discussion of the broader approach to narrow QRS complex tachycardias is presented separately. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation".)

EPIDEMIOLOGY — AVNRT is the most common form of regular, sustained, paroxysmal supraventricular tachycardia (PSVT), accounting for nearly two-thirds of all PSVTs, and is more common in women compared with men [1-3]. AVNRT can present at any age, but as with AV reentrant tachycardia (AVRT) that involves an accessory pathway, it is more likely to begin in young adults. In a series of 231 patients with AVNRT, the mean age of symptom onset was 32 years, with two-thirds of cases beginning after the age of 20 [4].

ANATOMY AND PATHOPHYSIOLOGY — The physiologic substrate for AVNRT involves dual electrical pathways that lead to the compact AV node (table 1) [5,6]. The arrhythmia usually develops in hearts that are otherwise normal, although it can also occur in the presence of underlying structural heart disease [7,8]. A more detailed discussion of the electrophysiology of AVNRT can be found in published reviews [5,6,9,10]. (See 'Dual AV nodal physiology' below.)

Anatomy — The exact anatomic distribution of these pathways is uncertain. Koch's triangle is bounded by the tricuspid ring and the tendon of Todoro, which bracket the coronary sinus at the base of the triangle and are in close proximity forming the apex near the His bundle at the membranous septum (figure 1 and figure 2) [5,11]. As an approximation, Koch's triangle can be divided into thirds:

●The anterior third, which contains the AV node and fast pathways

●The middle third

●The posterior third, the usual site of slow pathways

Dual AV nodal physiology — The simplest concept of AV nodal physiology that allows for reentry involves separate electrical pathways proximal to the AV node (figure 3). This model is supported by clinical observations as well as animal and human mapping studies [5,12,13]. These pathways may be distinct anatomic structures, or they may be functionally separate (ie, regions that appear anatomically continuous but have different electrical properties). It is possible that some cases of AVNRT are acquired when there is right atrial pressure overload leading to changes in the electrophysiologic properties of the AV nodal inputs. Rare cases of familial AVNRT have also been reported [14]. Whether the dual pathways are anatomic or functional, in order for reentry to occur, they must have different conduction velocities and refractory periods [15]:

●One pathway conducts rapidly and has a relatively long refractory period. This is called the fast pathway.

●The second pathway conducts relatively slowly and has a shorter refractory period. This is called the slow pathway.

The origins of the fast and slow pathways are probably in perinodal atrial tissue. These pathways join and enter a final common pathway in the compact AV node. While atrial tissue above the AV node appears to be part of the reentrant circuit, the bundle of His below the node is not a necessary part of the circuit. This can be illustrated by the following observations:

●AVNRT is associated with 2:1 AV block in approximately 10 percent of patients [16]. The AV block in this setting is probably a functional infranodal block within the bundle of His [16].

●His bundle electrograms indicate that reentry is proximal to the recording site [17,18].

Not all patients with AVNRT have evidence of dual pathways during electrophysiology (EP) studies. Conversely, not all patients with dual AV nodal pathways have clinical AVNRT (waveform 1A-B). The imperfect association between dual AV nodal physiology and clinical AVNRT was illustrated in a series of 180 patients undergoing EP studies for a variety of indications [19]. In the authors' experience, however, a vast majority of patients with documented AVNRT have clear evidence of dual AV nodal pathways with an inferior rightward slow pathway extension at the time of an EP procedure. A concealed atrio-Hisian tract that bypasses the AV node may constitute the retrograde fast pathway in up to a third of all apparently "typical" AVNRT cases [20]. Thus, the anatomic and electrophysiologic mechanism of AVNRT may be more complex than the dual AV nodal physiology model suggests [21,22].

Dual AV nodal pathways during normal sinus rhythm — During normal sinus rhythm, AV conduction occurs as follows (figure 3):

●The normal sinus beat enters the AV node and the impulse travels down both the fast and slow pathways.

●The impulse traveling down the fast pathway reaches the His bundle first, creating a refractory wake.

●The impulse traveling down the slow pathway is extinguished when, in the area of the final common pathway, it runs into the refractory wake of the impulse that had traveled down the fast pathway. The advent of ultrahigh-density three-dimensional mapping has made it possible to detect this site of collision during sinus rhythm in patients with dual AV nodal pathways [23].

Typical AVNRT — Approximately 80 to 90 percent of patients with AVNRT present with what is called the common form of the arrhythmia. The common form is also called "typical AVNRT" or "slow-fast" AVNRT.

Typical AVNRT usually initiates as follows (figure 3):

●A premature atrial complex (PAC; also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) (or less commonly, a premature junctional or ventricular beat with retrograde conduction) arrives at the AV node when the fast pathway is in its refractory period. Thus, antegrade conduction down the fast pathway is blocked.

●If the premature beat arrives in a specific time window (ie, a "critically timed" premature beat), the slow pathway, with a shorter refractory period than the fast pathway, is available for conduction to the ventricle.

●The premature beat conducts via the slow pathway, through the final common pathway, to the bundle of His. As a result, the PR interval of the premature beat will be longer than those of normal beats conducted through the fast pathway.

●If the fast pathway has recovered its excitability by the time the slow pathway impulse reaches the distal junction of the two pathways, the impulse can conduct retrograde up the fast pathway. The circuit may then become repetitive with antegrade conduction back down the slow pathway and retrograde conduction up the fast pathway resulting in a sustained tachycardia (figure 3 and figure 4).

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

●A single PAC (or retrograde penetration of the AV node from a junctional or premature ventricular complex/contraction [PVC; also referred to a premature ventricular beats or premature ventricular depolarizations]) can initiate the arrhythmia.

●Penetration of the reentrant circuit by a premature beat can abruptly terminate the arrhythmia.

Atypical AVNRT — Up to 20 percent of patients with AVNRT have uncommon forms of the arrhythmia, referred to as "atypical AVNRT." As examples:

●Antegrade conduction can occur down the fast pathway with retrograde conduction up the slow pathway (figure 5 and figure 6 and waveform 2) [24]. This is referred to as "fast-slow" AVNRT.

●Some patients have multiple slow pathways, resulting in "slow-slow AVNRT" variants in which both the antegrade and retrograde limbs of the circuit utilize slow AV nodal pathways.

●Rarely during AVNRT, conduction through the reentrant circuit is so slow that the heart rate is less than 100 beats per minute, by definition not a tachycardia. Despite the absence of tachycardia, patients can be symptomatic and may be treated with a slow pathway ablation. This arrhythmia, sometimes referred to as AV nodal reentrant arrhythmia (AVNRA), has been mistaken for a junctional rhythm. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Undetectable P waves'.)

Typical and atypical AVNRT have rarely been found to coexist in the same patient during electrophysiology studies [25].

CLINICAL MANIFESTATIONS

Symptoms — Patients with AVNRT most commonly report palpitations, dizziness or lightheadedness, and dyspnea. Because of the paroxysmal nature of the arrhythmia, the onset and termination of the symptoms are usually sudden. Those with significant heart disease may have additional symptoms such as dyspnea and chest pain. Because atrial activation occurs coincident with ventricular activation during typical AVNRT, atrial contraction occurs when the tricuspid valve is closed, causing rhythmic abrupt rises in venous pressure, and can result in a sensation of neck pounding. Some patients with AVNRT have a feeling of polyuria and experience a diuresis during or after AVNRT; the mechanism probably is related to an elevated mean right atrial pressure and plasma level of atrial natriuretic peptide, which are present during the arrhythmia [26].

In a series of 167 supraventricular tachycardia (SVT) patients referred for radiofrequency ablation, the 64 patients with AVNRT reported the following symptoms [27]:

●Palpitations – 98 percent

●Dizziness – 78 percent

●Dyspnea – 47 percent

●Chest pain – 38 percent

●Fatigue – 19 percent

●Syncope – 16 percent

Syncope is an uncommon feature of AVNRT and appears to be more likely with high heart rates (eg, heart rate ≥170 beats per minute). However, factors other than heart rate also contribute to syncope. As an example, abnormal vasomotor adaptation during AVNRT has been reported, suggesting a role for neurally mediated (neurocardiogenic) responses [28,29].

In very rare cases, AVNRT can result in cardiac arrest [30].

Triggers — Most often there is no apparent precipitating cause for episodes of AVNRT.

In some patients, nicotine, alcohol, stimulants, and exercise can initiate episodes. A 2020 scientific statement from the American Heart Association details drugs associated with AVNRT [31].

Some patients experience the onset of AVNRT during sleep or after sudden bending forward or squatting, all of which can enhance vagal tone. In contrast to using vagal maneuvers to terminate AVNRT, increased vagal tone may facilitate the induction of AVNRT in some circumstances. In one series of 10 patients with AVNRT, electrophysiologic data were measured before and during continuous enhancement of vagal tone induced by infusing phenylephrine [32]. Vagal enhancement markedly prolonged the effective refractory period and functional refractory period of antegrade conduction in the fast pathway. However, the refractoriness of antegrade conduction in the slow pathway and retrograde conduction in the fast pathway were unchanged.

Electrocardiographic characteristics — All patients with palpitations should undergo 12-lead electrocardiography (ECG), ideally while symptomatic. There are several ECG features that are helpful in confirming the diagnosis of AVNRT.

●Ventricular rate – The ventricular rate is generally between 120 and 220 beats per minute.

●Abrupt onset following PAC – If the initiation of the tachycardia is captured on a tracing, the tachycardia often begins with a PAC with sudden prolongation of the PR interval (figure 4). (See 'Typical AVNRT' above.) 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 relationships between the QRS complex and the following P wave, typical AVNRT is referred to as a "short RP tachycardia," while atypical AVNRT is a "long RP tachycardia" [10]. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'RP relationship'.)

•In typical AVNRT, retrograde atrial activation and antegrade ventricular activation occur almost simultaneously (figure 4). The P wave, therefore, is usually buried within or fused with the QRS complex.

A component of the P wave is often evident slightly after, or less commonly before, the QRS (figure 7 and waveform 3). When the P wave occurs shortly after the QRS complex, the fused waveform can produce a pseudo-R' (a second R wave) in lead V1 and a pseudo-S wave in the inferior leads. (See 'Typical AVNRT' above.)

•In atypical AVNRT, retrograde atrial activation occurs long after ventricular activation, resulting in a P wave so late after the QRS complex that it appears to be occurring shortly before the next QRS complex (figure 5 and figure 6 and waveform 2). This pattern resembles that seen in atrial tachycardias. In such cases, an electrophysiology (EP) study may be required to define the arrhythmogenic mechanism. (See 'Atypical AVNRT' above and "Invasive diagnostic cardiac electrophysiology studies".)

●P wave morphology – The P wave axis, when P waves can be clearly identified, is abnormal due to retrograde atrial activation. This is usually manifested on the electrocardiogram as a negative P wave axis with inverted P waves in leads II, III and aVF [33].

●ST segment depression – Significant ST segment depression during tachycardia has been observed in 25 to 50 percent of patients with AVNRT, although it is more commonly seen in those with an AV reentrant tachycardia associated with an accessory pathway [34-36]. The ST segment depression does not represent myocardial ischemia in most patients (although it may in patients with significantly underlying coronary heart disease), but rather represents abnormalities of repolarization [37].

●T wave inversions following termination – After acute termination of AVNRT and other paroxysmal SVTs, T wave inversions may be seen in the anterior or inferior leads in approximately 40 percent of patients [38]. Inverted T waves may be seen immediately upon termination or may develop within the first six hours, and can persist for hours to days. The occurrence of negative T waves is not predicted by clinical parameters, tachycardia rate or duration, or the presence and extent of ST segment depression during the tachycardia. They are not the result of coronary artery disease, but are repolarization abnormalities, likely due to ionic current alterations resulting from the rapid rate.

DIAGNOSIS — The diagnosis of AVNRT should be suspected in a patient with the abrupt onset and offset of rapid sustained palpitations, often associated with lightheadedness or dyspnea. The ability for a patient to terminate the symptoms with a vagal maneuver is also suggestive of AVNRT as a potential etiology of symptoms. (See 'Symptoms' above and 'Vagal maneuvers' below.)

The diagnosis of AVNRT is typically confirmed following the review of an ECG acquired during the arrhythmia. When possible, review of the ECG at the onset or termination of the arrhythmia should be performed as this frequently provides additional information (ie, initiation following an PAC with sudden prolongation of the PR interval (figure 4)). When there is sudden termination of a regular paroxysmal supraventricular tachycardia (PSVT) that has 1:1AV conduction associated with AV block but not due to a PAC (last beat of the tachycardia is a P wave rather than a QRS complex that occurs at the expected timing), then an atrial tachycardia is very unlikely.

●In typical AVNRT, the P wave is usually buried within or fused with the QRS complex, resulting in a pseudo-R' (a second R wave) in lead V1 and a pseudo-S wave in the inferior leads.

●In atypical AVNRT, the P wave occurs late after the QRS complex, often appearing shortly before the next QRS complex, resulting in a pattern that resembles atrial tachycardia.

If the diagnosis cannot be confirmed following review of the surface ECG, invasive electrophysiology studies can be performed in an effort to confirm the diagnosis. (See "Invasive diagnostic cardiac electrophysiology studies".)

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of palpitations is extensive (table 2), and the etiology varies depending upon the population studied. The approach to palpitations is discussed separately. (See "Evaluation of palpitations in adults".)

Once a tachycardia with a narrow QRS complex has been identified, the differential diagnosis is generally limited to SVTs, although on rare occasions idiopathic left ventricular tachycardia (a ventricular tachycardia arising from septum) can present as a narrow complex tachycardia. (See "Ventricular tachycardia in the absence of apparent structural heart disease", section on 'Idiopathic left ventricular tachycardia'.)

Sustained narrow QRS complex tachycardias are generally divided according to whether the QRS complexes occur regularly or irregularly:

●Irregular QRS complexes – Atrial fibrillation, atrial flutter with variable conduction, multifocal atrial tachycardia.

●Regular QRS complexes – Sinus tachycardia, atrial flutter, AVNRT, atrioventricular reentrant tachycardia (AVRT), atrial tachycardia, and junctional ectopic tachycardia (JET). The term PSVT generally refers to AVNRT, AVRT, atrial tachycardia, and JET.

Because AVNRT is a regular tachycardia, the tachycardias with irregular QRS complexes can be excluded immediately. The remainder of the differential diagnosis discussion will focus on the other regular narrow QRS complex tachycardias.

Sinus tachycardia — Sinus tachycardia is the most common narrow QRS complex tachycardia. Typically, sinus tachycardia is a response to another condition in which catecholamine release is physiologically enhanced or, less commonly, the parasympathetic nervous system withdrawn. In contrast to the abrupt onset and termination of AVNRT, sinus tachycardia has a gradual onset and offset, which typically occurs over 30 seconds to several minutes. Additionally, for the vast majority of patients, sinus tachycardia does not result in symptoms. (See "Sinus tachycardia: Evaluation and management".)

Atrioventricular reentrant tachycardia — Patients with AVRT can present in a similar fashion to patients with AVNRT. Both arrhythmias are associated with the abrupt onset of palpitations, and the surface ECG may appear very similar with regular QRS complexes and inverted P waves and a short RP interval that is less than one-half of the RR interval. AVNRT is most easily distinguished from AVRT when evidence of pre-excitation (short PR interval and delta wave) can be identified on prior ECGs during normal sinus rhythm (when available) consistent with an accessory pathway and the potential for AVRT. In the event of concealed pre-excitation, invasive electrophysiology studies may be required to distinguish AVNRT from AVRT. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)

Atrial tachycardia — As with AVNRT and AVRT, most patients with focal atrial tachycardia report an abrupt onset of palpitations associated with their episodes of tachycardia. In contrast to AVNRT, the P wave morphology during atrial tachycardia can appear normal or abnormal, depending upon the site of origin of the tachycardia, and the P waves tend to occur prior to the QRS complex, resulting in a long RP tachycardia. (See "Focal atrial tachycardia".)

Junctional ectopic tachycardia — Junctional ectopic tachycardia (JET) is a focal ectopic arrhythmia arising from the AV node region itself. It is a rare arrhythmia most often seen in young children as a congenital arrhythmia or after surgery for congenital heart disease [39]. JET can be difficult to differentiate from typical AVNRT. However, JET should be suspected when there is ventriculoatrial block during tachycardia and when the tachycardia is initiated by a premature junctional beat. Because the substrate related to JET is near the compact AV node, there is a greater concern for AV block during catheter ablation of JET compared with AVNRT [40].

Dual AV nodal nonreentrant tachycardia (DAVNNT) — Patients with dual AV nodal pathways can rarely develop dual AV nodal nonreentrant tachycardia (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 and is usually is associated with alternating RR intervals [41].

Other SVTs — Other than sinus tachycardia, AVRT, and atrial tachycardia, the remaining SVTs occur far less commonly. Inappropriate sinus tachycardia and sinoatrial nodal reentrant tachycardia have an identical appearance to sinus tachycardia. In contrast to sinus tachycardia, sinoatrial nodal reentrant tachycardia can have an abrupt onset (making it look identical to atrial tachycardia) and requires invasive electrophysiology studies to diagnose. Inappropriate sinus tachycardia tends to persist for days to weeks without the typical associations seen with sinus tachycardia (eg, pain, fever, hypovolemia, etc) and is relatively refractory to rate-slowing medications. Intraatrial tachycardia is a type of reentrant tachycardia seen almost exclusively in patients with underlying structural heart disease and prior cardiac procedures resulting in scar formation (eg, repair of congenital heart disease, catheter ablation for atrial fibrillation, etc). (See "Sinus tachycardia: Evaluation and management", section on 'Inappropriate sinus tachycardia' and "Sinoatrial nodal reentrant tachycardia (SANRT)" and "Intraatrial reentrant tachycardia".)

INITIAL MANAGEMENT — The initial management of a patient presenting with a narrow QRS tachycardia and suspected AVNRT is guided by whether or not the patient is experiencing signs and symptoms of hemodynamic instability (algorithm 1) related to the rapid heart rate (eg, hypotension, shortness of breath, chest pain suggestive of coronary ischemia, shock, and/or decreased level of consciousness). Unstable patients require urgent electrical cardioversion. However, it is very rare that a patient with paroxysmal supraventricular tachycardia (PSVT) requires electrical cardioversion.

There are several effective therapies for the acute termination of AVNRT, but few data regarding the optimal sequence of therapies for the acute termination of AVNRT [42,43]. These treatment options include:

●Vagal maneuvers (see "Vagal maneuvers")

●Intravenous (IV) adenosine

●IV calcium channel blockers or beta blockers

Management recommendations are based upon an understanding of the properties and risks of the treatment options. Almost all patients, including those who are severely symptomatic, can be treated first with several attempts at vagal maneuvers or IV adenosine [42,43]. Our recommendations are in general agreement with published professional society recommendations [42,43].

Electrical cardioversion — AVNRT almost always terminates with vagal maneuvers, spontaneously, or with intravenous antiarrhythmic therapy using adenosine, calcium channel blockers, or beta blockers. Very rarely, the patient is hemodynamically unstable or AVNRT persists in spite of vagal maneuvers and AV nodal blocking medications and electrical cardioversion should be considered (algorithm 1). Electrical cardioversion is usually successful but may require relatively high energy levels, probably due to the deep location of the reentrant pathway. If sinus rhythm is not restored following an initial 50 to 100 joule shock, subsequent shocks should be at higher energy levels (algorithm 2). (See "Cardioversion for specific arrhythmias".)

Vagal maneuvers — Vagal maneuvers (eg, Valsalva maneuver or carotid sinus massage) are safe, easily performed, and effective first-line therapies for patients with AVNRT (algorithm 1). For patients who are hemodynamically stable and able to effectively perform the vagal maneuvers, we recommend at least one or two attempts at a standard Valsalva maneuver, followed by at least one or two attempts using the modified Valsalva maneuver (if AVNRT persists), as the initial treatment for AVNRT rather than another vagal maneuver or adenosine.

Vagal maneuvers increase parasympathetic tone, which produces a gradual slowing of conduction in the antegrade slow pathway. Slowing and eventual block in the antegrade slow pathway are the usual cause for arrhythmia termination with these interventions [44], although they can also produce abrupt block in the retrograde fast pathway. In one systematic review, which included 316 patients with a total of 965 episodes of supraventricular tachycardia (SVT; which included both AVNRT and atrioventricular reciprocating tachycardia), the standard Valsalva maneuver (exhaling forcefully against a closed glottis for 10 to 15 seconds) successfully terminated 45 percent of SVT episodes and was more successful than carotid sinus massage [45].

To perform a standard Valsalva maneuver, the patient is placed in a supine or semi-recumbent position and instructed inhale normally and then to exhale forcefully against a closed glottis for 10 to 15 seconds. A modified Valsalva maneuver (which begins with the standard Valsalva maneuver and is followed by supine positioning and passive leg raising) has been proposed as an improvement on the standard Valsalva maneuver. In the largest randomized trial of vagal maneuvers for the treatment of SVT, 428 patients with hemodynamically stable SVT were randomly assigned to perform the standard Valsalva maneuver (strain generating 40 mmHg pressure for 15 seconds while in a semi-recumbent position) or to perform the standard Valsalva maneuver followed by supine repositioning (placing the patient supine from the upright or semi-recumbent position) and passive leg raise for 15 seconds (214 patients per group) [46]. Patients performing the modified Valsalva maneuver with supine repositioning and passive leg raise were significantly more likely to have restoration of sinus rhythm at one minute (43 versus 17 percent in the standard Valsalva group; adjusted odds ratio 3.7; 95% CI 2.3-5.8). When feasible, we recommend the modified Valsalva maneuver given the greater likelihood of successful restoration of sinus rhythm.

Additional information on the performance and use of vagal maneuvers is presented separately. (See "Vagal maneuvers".)

Adenosine — If vagal maneuvers cannot be performed or if they fail to terminate the arrhythmia, IV medical therapy that blocks AV nodal conduction is indicated as the next step (algorithm 1). For patients with AVNRT that persists following vagal maneuvers (or in whom vagal maneuvers cannot be adequately performed), we recommend IV adenosine rather than a calcium channel blocker or a beta blocker. The protocol for administration of adenosine is described in the algorithm (algorithm 3).

The advantages of adenosine over other agents include rapid onset and a short half-life. Adenosine terminates AVNRT in over 80 percent of cases [47-49]. It is well tolerated in most patients, with the exception of those with severe bronchospastic asthma or severe coronary artery disease.

The use of adenosine for the evaluation and termination of SVTs is presented separately. (See "Narrow QRS complex tachycardias: Clinical manifestations, diagnosis, and evaluation", section on 'Intravenous adenosine'.)

Other AV nodal blocking drugs — If vagal maneuvers and adenosine have been ineffective or terminate the tachycardia but are followed by an immediate recurrence, IV nondihydropyridine calcium channel blockers (eg, verapamil and diltiazem) or IV beta blockers (eg, metoprolol, esmolol) can be used (algorithm 1) to terminate AVNRT and prevent an immediate recurrence [50,51]. Clinical trials of an intranasally administered calcium channel blocker, etripamil, have shown it to be effective, with termination of SVT in up to 95 percent of patients [52,53]

The choice between these drugs is usually based on familiarity with and availability of the particular agents, although a calcium channel blocker would be preferred for a patient with reactive airway disease and active wheezing. Calcium channel and beta blockers are generally well tolerated, although potential adverse effects include hypotension (due to both negative inotropic and vasodilatory effects) and bradycardia [54-56]. Initial IV dosing options include:

●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.

●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 desired heart rate (up to 300 mcg/kg/minute).

Because of their longer half-lives, verapamil, diltiazem, and beta blockers have the potential to suppress arrhythmia recurrence. Thus, these drugs should be used in patients who have early arrhythmia recurrence after termination with adenosine.

SUBSEQUENT MANAGEMENT — The approach to the management of subsequent AVNRT episodes is based around acute management of recurrent episodes and/or preventive therapy to reduce or eliminate recurrences. Because AVNRT is usually well tolerated in the majority of patients, with a variety of safe and effective treatment options, and there are no compelling data favoring one therapy over another, the choice of long-term management strategies is largely influenced by patient preference. When working with a patient to select a treatment strategy, the following issues should be considered:

●Frequency of episodes

●Severity of symptoms

●Comorbid conditions

●Medication compliance

●Medication side effects

Patients who have had syncope in the setting of AVNRT may be subject to driving restrictions, which vary between municipalities. (See "Syncope in adults: Management and prognosis", section on 'Driving restrictions'.)

Acute management of recurrent episodes — For the initial management of recurrent AVNRT, we generally work with the patient to develop a patient-directed treatment approach using either vagal maneuvers or an oral medication ("pill-in-the-pocket" approach). For most patients, we suggest a combination of one or more vagal maneuvers rather than the pill-in-the-pocket approach.

Patients who have experienced prior episodes and who have been educated on the proper performance of vagal maneuvers are frequently able to terminate subsequent episodes by performing vagal maneuvers on their own. If one or more vagal maneuvers successfully terminate the arrhythmia, patients generally do not need to seek urgent medical attention. Conversely, patients should be instructed to consult with their clinician or seek medical attention if the arrhythmia persists in spite of several attempts at patient-directed vagal maneuvers. (See 'Vagal maneuvers' above.)

An alternative patient-directed approach to the management of recurrent AVNRT is the pill-in-the-pocket approach. For selected patients with infrequent, well-tolerated, and long-lasting episodes of AVNRT, a single dose of an antiarrhythmic agent that was previously evaluated under observation can be effective for acute termination of the arrhythmia [42,57,58]. This strategy can both reduce the need for emergency department visits and avoid chronic medical therapy or invasive procedures. This approach has been evaluated with the nondihydropyridine calcium channel blockers, beta blockers, and the class IC antiarrhythmic drug flecainide [58]. However, based upon the efficacy of alternative, lower-risk therapies, and the efficacy of catheter ablation, flecainide is rarely used in the management of AVNRT. The choice of a particular agent will vary from patient to patient depending on comorbidities and patient preference.

Preventive therapy — The decision to treat with long-term preventive therapy is based upon the following factors:

●The frequency of the arrhythmia

●The severity of the symptoms

●Patient tolerance of medications

●Patient preference

Many patients with infrequent episodes of AVNRT, or those with minimal or well-tolerated symptoms, may prefer a more conservative management approach with either no specific therapy or pharmacologic suppression. If pharmacologic therapy fails or if the side effects result from chronic medical therapy, catheter ablation remains an option. Conversely, for patients with significant symptoms, or for patients who prefer definitive therapy, even for rare, well-tolerated episodes, catheter ablation may be considered early in the patient's management [42,43].

No treatment — Patients with infrequent and well-tolerated episodes of AVNRT may choose no chronic therapy. For these patients, we emphasize the patient-directed approach to the termination of recurrent episodes using one or more vagal maneuvers, with the ability to reassess long-term management options at any time should there be a change in the frequency or severity of recurrences. (See 'Acute management of recurrent episodes' above and "Vagal maneuvers".)

Catheter ablation — For patients with episodes of AVNRT that are either frequently occurring, refractory to medical therapy, poorly tolerated (eg, associated with near-syncope or syncope, angina, or severe dyspnea), or result in presentation to the emergency department or admission to the hospital, we recommend catheter ablation rather than chronic medical therapy as initial long-term management strategy. In such cases, the risks associated with recurrent arrhythmic events (eg, syncope with associated trauma) outweigh the procedural risks. In addition, the potential for definitive therapy makes ablation preferable to medical therapy in this setting.

Catheter ablation offers the opportunity for definitive cure of AVNRT in greater than 95 percent of patients, with high rates of success in both the typical and atypical forms [59-61]. However, ablation is associated with a small but non-trivial rate of procedural complications. The most significant potential complication of radiofrequency ablation for AVNRT is AV block (approximately 1 percent). Historically, the risk of AV block requiring permanent pacing following ablation ranged from 1 to 3 percent, but in multiple contemporary cohorts involving experienced electrophysiologists, the need for permanent pacing following the procedure has consistently been <1 percent [60,62,63]. Older age and baseline PR interval prolongation are predictors of an increased risk of post-ablation AV block [64-67]. However, due to its high success rate in curing AVNRT by successful slow pathway ablation and low complication rate, catheter ablation is increasingly favored among patients with recurrent AVNRT [42,43]. (See "Overview of catheter ablation of cardiac arrhythmias", section on 'Complications'.)

The general approach to the catheter ablation of AVNRT is based upon the concept of dual AV nodal pathways. The most common AVNRT circuit (80 to 90 percent) involves antegrade conduction down the slow pathway and retrograde conduction up the fast pathway. The ablation target is the posterior slow pathway (figure 8) since ablation here carries the lowest risk of AV block, preserves fast pathway function (and a normal PR interval post-ablation), and is facilitated by reliable anatomic and electrophysiologic landmarks. The anterior fast pathway can also be ablated, but this approach is now limited to a few special circumstances since fast pathway ablation results in a long PR interval during sinus rhythm and is associated with a higher risk of heart block. During ablation for atypical "fast-slow" AVNRT, the slow pathway is the usual target. The slow pathway in these patients tends to be posteriorly located near the coronary sinus ostium as with patients who have typical AVNRT. However, there are reports of rare cases of atypical AV nodal reentry where the slow retrograde limb of the circuit is located more superiorly near the compact AV node [68]. The slow AV nodal pathway in patients with AVNRT can rarely be a leftward rather than rightward inferior AV nodal extension requiring ablation from the left atrial septum or within the coronary sinus [69].

The relative efficacy and costs of catheter ablation and medical therapy were compared in a series of 79 patients with newly documented supraventricular tachycardia (SVT) who were treated with either ablation or pharmacologic therapy, based upon patient preference [70]. After a follow-up period of 12 months, both medication and ablation decreased the frequency of arrhythmia-related symptoms, but ablation was more likely to result in complete abolition of symptoms (74 versus 33 percent). (See 'Chronic suppressive therapy' below.)

Chronic suppressive therapy — For patients with symptomatic episodes of AVNRT who are not candidates for or who have declined catheter ablation, chronic medical therapy using beta blockers, nondihydropyridine calcium channel blockers, or antiarrhythmic drugs can be initiated in an effort to suppress recurrent arrhythmias.

There are few data comparing the relative efficacy of various agents used for chronic suppressive therapy of AVNRT. Because they are effective and well tolerated, the medications that are most commonly used for the chronic suppression of AVNRT are beta blockers (eg, metoprolol) and nondihydropyridine calcium channel blockers (eg, verapamil and diltiazem). Traditionally, beta blockers were preferred rather than calcium channel blockers unless the patient has reactive airway disease or another contraindication, although calcium channel blockers may have fewer side effects. The choice of a starting dose for chronic suppressive medication will vary depending upon the baseline heart rate and blood pressure. The dose of beta blocker or calcium channel blocker is titrated as tolerated with the dose limited to avoid hypotension (symptomatic hypotension or asymptomatic systolic blood pressure <100 mmHg) and bradycardia (heart rate <55 beats per minute).

Among patients who do not respond to optimally titrated diltiazem, verapamil, or beta blockers and who do not want to pursue ablation, the following antiarrhythmic drugs may be considered:

●Flecainide (class IC)

●Propafenone (class IC)

●Sotalol (class III)

●Dofetilide (class III)

●Amiodarone (class III)

The choice of a particular agent will need to be individualized in each patient based on other comorbidities. However, due to the potential for significant toxicities, including proarrhythmia, the use of class I and class III antiarrhythmic drugs for the management of AVNRT should be reserved for rare cases and should be administered in consultation with an electrophysiologist. In particular, because of the risk of toxicities with long-term use, amiodarone is usually avoided in young patients. (See "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring".)

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

●Definition and prevalence – Atrioventricular nodal reentrant tachycardia (AVNRT) is a regular tachycardia that results from the formation of a reentry circuit confined to the AV node and perinodal atrial tissue. The physiologic substrate for AVNRT involves dual electrical pathways in or near the AV node. It is the most common form of regular, sustained, paroxysmal supraventricular tachycardia (PSVT), and it accounts for nearly two-thirds of all PSVTs. (See 'Introduction' above and 'Epidemiology' above.)

●Pathophysiology – The simplest concept of AV nodal physiology that allows for reentry involves separate electrical pathways within or proximal to the AV node (figure 3). The fast pathway conducts rapidly and has a relatively long refractory period, while the slow pathway conducts relatively slowly and has a shorter refractory period. Both typical and atypical forms of AVNRT can result from reentry involving the fast and slow pathways. Tachycardia is initiated by a premature beat. (See 'Anatomy and pathophysiology' above.)

●Symptoms – Patients with AVNRT most commonly report palpitations, dizziness or lightheadedness, and dyspnea. Because of the paroxysmal nature of the arrhythmia, the onset and termination of the symptoms are usually sudden. Those with significant heart disease may have additional symptoms such as dyspnea and chest pain. (See 'Symptoms' above.)

●ECG features – There are several features seen on an ECG that are helpful in confirming the diagnosis of AVNRT, including the ventricular rate, abrupt onset following a PAC, the relationship between QRS complexes and P waves, and spontaneous termination with AV block in the absence of a PAC. (See 'Electrocardiographic characteristics' above.)

●Initial management – The initial management (algorithm 1) of a patient presenting with a narrow QRS tachycardia and suspected AVNRT is guided by whether or not the patient is experiencing signs and symptoms of hemodynamic instability related to the rapid heart rate (eg, hypotension, shortness of breath, chest pain suggestive of coronary ischemia, shock, and/or decreased level of consciousness).

•Hemodynamically unstable – Rare patients who are severely hemodynamically unstable should undergo urgent cardioversion. (See 'Electrical cardioversion' above.)

•Hemodynamically stable – For patients who are hemodynamically stable and able to effectively perform the vagal maneuvers, we recommend at least one or two attempts of a standard Valsalva maneuver, followed by at least one or two attempts using the modified Valsalva maneuver (if AVNRT persists), as the initial treatment for AVNRT rather than another vagal maneuver or adenosine (Grade 1B). (See 'Vagal maneuvers' above.)

If vagal maneuvers cannot be performed or if they fail to terminate the arrhythmia, intravenous (IV) medical therapy that blocks AV nodal conduction is indicated as the next step. For patients with AVNRT that persists following vagal maneuvers (or in whom vagal maneuvers cannot be adequately performed), we recommend IV adenosine (algorithm 3) rather than a calcium channel blocker or a beta blocker (Grade 1B). (See 'Adenosine' above.)

If both vagal maneuvers and adenosine are ineffective, or when these options are followed by an immediate recurrence of the tachycardia, IV verapamil, diltiazem, or a beta blocker can be used to terminate or prevent recurrent AVNRT. (See 'Other AV nodal blocking drugs' above.)

●Management of recurrent episodes – The approach to the management of subsequent AVNRT episodes is based around acute management of recurrent episodes and/or preventive therapy to reduce or eliminate recurrences. Because AVNRT is usually well-tolerated in the majority of patients, with a variety of safe and effective treatment options, and there are no compelling data favoring one therapy over another, the choice of long-term management strategies is largely influenced by patient preference.

•Initial management – For the initial management of recurrent AVNRT, we generally work with the patient to develop a patient-directed treatment approach using either vagal maneuvers or an oral medication ("pill-in-the-pocket" approach). For most patients, we suggest a combination of one or more vagal maneuvers rather than the pill-in-the-pocket approach (Grade 2C). (See 'Acute management of recurrent episodes' above.)

•Infrequent and well-tolerated episodes – Patients with infrequent and well-tolerated episodes of AVNRT may choose no chronic therapy. For these patients, we emphasize the patient-directed approach to the termination of recurrent episodes using one or more vagal maneuvers. (See 'No treatment' above.)

•Frequent or poorly tolerated episodes – For patients with episodes of AVNRT that are either frequently occurring or poorly tolerated (eg, associated with near-syncope or syncope, angina, or severe dyspnea), we recommend catheter ablation rather than chronic medical therapy as initial long-term management strategy (Grade 1B). In such cases, the risks associated with recurrent arrhythmic events (eg, syncope with associated trauma) outweigh the procedural risks. In addition, the potential for definitive therapy makes ablation preferable to medical therapy in this setting. (See 'Catheter ablation' above.)

For patients with poorly tolerated symptomatic episodes of AVNRT who are not candidates for or who have declined catheter ablation, chronic medical therapy using beta blockers, nondihydropyridine calcium channel blockers, or antiarrhythmic drugs can be initiated in an effort to suppress recurrent arrhythmias. Our experts typical prefer beta blockers rather than calcium channel blockers or antiarrhythmic drugs as the initial option for chronic medical therapy. (See 'Chronic suppressive therapy' above.)