Atrioventricular Nodal Reentry Tachycardia

Background

Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of reentrant supraventricular tachycardia (SVT). The substrate for AVNRT is the presence of dual AV nodal pathways. (See Etiology.)[1, 2]

Because of the abrupt onset and termination of the reentrant SVT, the nonspecific term paroxysmal supraventricular tachycardia (or even the misleading term paroxysmal atrial tachycardia [PAT]) has been used to refer to these tachyarrhythmias. With improved knowledge of the electrophysiology of reentrant SVT, greater specificity in nomenclature, based on the mechanism of reentry, has been possible. Such improved classification aids in the choice of appropriate therapies. (See Etiology, Prognosis, Treatment, and Medication.)

AVNRT is usually well tolerated, often occurring in patients with no structural heart disease. (See Prognosis, Presentation, and Workup.)

Patient education

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

For patient education information, see the Heart Health Center, as well as Supraventricular Tachycardia.

NextEtiology

The substrate for AVNRT may be functional rather than anatomic. These arrhythmias occur in young, healthy patients and in those with chronic heart disease.

In patients with atrioventricular (AV) nodal reentry, the AV node is functionally divided into 2 longitudinal pathways that form the reentrant circuit. (In contrast to a bypass tract, dual AV nodal physiology is often an acquired abnormality.) In the majority of patients, during AVNRT, antegrade conduction occurs to the ventricle over the slow (alpha) pathway, and retrograde conduction occurs over the fast (beta) pathway. (See the image below.)

Electrophysiological mechanism of atrioventricular nodal reentry tachycardia.

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

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

Atypical atrioventricular nodal reentry tachycardia. Typical atrioventricular nodal reentry tachycardia. PreviousNextEpidemiology

In the United States, AVNRT occurs in 60% of patients (with a female predominance) presenting with paroxysmal SVT. The prevalence of SVT in the general population is likely several cases per thousand persons. Internationally, the occurrence of AVNRT is similar to that in the United States.

AVNRT may occur in persons of any age. It is common in young adults, but some patients do not present until their seventh or eighth decade or later.

PreviousNextPrognosis

The prognosis for patients with AVNRT is usually good in the absence of structural heart disease. Most patients respond to medications to prevent recurrence or to radiofrequency ablation, which is approximately 95% curative and has a low risk of complications. It is the preferred method of treatment for most patients.

Complications of AVNRT include hemodynamic compromise, congestive heart failure, syncope, tachycardia-induced angina, cardiomyopathy, myocardial ischemia, and myocardial infarction.

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