Atrioventricular node re-entrant tachycardia (AVNRT) is a form of re-entrant rhythm within the region of the atrioventricular (AV) node. Re-entrant rhythms account for most episodes of supraventricular tachycardia (SVT) in children. A re-entrant rhythm involves the presence of 2 distinct pathways, a zone of slow conduction and unidirectional block in one limb, allowing an electrical impulse to travel down the second limb and re-enter the blocked pathway from the other direction. Re-entrant rhythms can usually be initiated and terminated by pacing or premature beats. During AVNRT, the circuit typically involves both a fast and a slow pathway within the region of the AV node, which allows the impulses to proceed down the His-Purkinje system to the ventricles while simultaneously proceeding in a retrograde fashion to depolarize the atria and re-enter the node.
Two or more functionally and (usually) anatomically distinct pathways have been described connecting the atria to the AV node; they are known as the fast and the slow pathways and have different electrophysiologic characteristics. The fast pathway crosses the tendon of Todaro superiorly and is identified by its relatively shorter conduction time and longer effective refractory period (ERP). The slow pathway(s) approach the compact AV node from inferiorly and have a relatively longer conduction time and an ERP that typically is short when compared to fast pathway ERP. However, dual AV nodal physiology is a common finding during EP studies  and is not synonymous with AVNRT since the incidental finding of dual AV nodal physiology does not predict AVNRT in children and adolescents after successful accessory pathway ablation. 
The 2 forms of AV node reentry (AVNR) that usually are described are the typical form (ie, slow-fast) and the atypical form (ie, fast-slow or slow-slow), referring to the characteristic of antegrade-retrograde conduction during tachyarrhythmia. In the typical form, which represents 90% of clinical AVNRT episodes, the conduction moves in antegrade direction through the slow pathway from the atrium to the compact AVN and in retrograde direction through the fast pathway. In an atypical form, the conduction moves antegradely in the fast pathway and retrogradely in the slow pathway, resulting in a long RP interval. A third form also has been identified in which the conduction appears to be antegrade and retrograde through 2 slow pathways.  Nakagawa and Jackman have described multiple atypical AVNRT circuits using rightward and leftward inferior extensions of the AV node. In their model, these extensions participate in the tachycardia by connections to the left atrium. 
Conduction during sinus rhythm usually occurs over the fast pathway, and the PR interval is normal. A premature atrial beat may cause a block in the fast pathway (because of its longer ERP) but conduct by the slow pathway. The slow pathway has a longer conduction time than the fast pathway, providing a delay of the impulse; therefore, when it reaches the distal end of the fast pathway (which has by that time recovered from refractoriness), the impulse is conducted retrograde via the fast pathway. After traversing a short portion of the low septal right atrium, it then re-enters the slow pathway again, creating a circus movement tachycardia.
The natural history of AVNRT is unknown, but some infants appear to exhibit spontaneous resolution. The substrate for atrioventricular tachycardia is not fully understood, but cell-to-cell interactions may play a role. 
The diagnosis of AVNRT is associated with random unpredictable occurrences that pose a nuisance and interfere with quality of life more than they are life-threatening.
AVNRT is the most common cause of paroxysmal supraventricular tachycardia (PSVT). Approximately 89,000 new cases are reported each year, and 570,000 persons with PSVT live in the United States.
PSVT has a prevalence of 2.25 per 1000 population and an incidence of 35 per 100,000 person-years.
Episodes of SVT caused by any mechanism, including AVNRT, have a minimal impact on mortality rates in children, although SVT may lead to some degree of morbidity. Rare cases of AVNRT in young infants may be associated with more significant morbidity and possible mortality. The presence of dual AV node physiology per se does not necessarily indicate morbidity. Discontinuous AV nodal conduction curves on the electrophysiologic study that suggest the presence of dual AV nodal pathways have been encountered in patients without SVT and occur in approximately 63% of children. However, the presence of dual AV node physiology with associated AVNRT is a common mechanism for SVT in children and adults. Thapar and Gillette's publication showed that dual AV node physiology was the mechanism in 46% of children who presented for evaluation of arrhythmias. 
Prevalence of AVNRT is more common in females than in males, particularly in adults.
AVNRT is considered less common in newborns and increases in prevalence throughout childhood. AVNRT is the predominant mechanism (accounting for 40-50% of cases) of SVT in adults.  However, some reports suggest that AVNRT may be underrecognized in infancy. 
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