[Dual atrioventricular nodal pathways: physiology, arrhythmic findings, and electrocardiographic manifestations]

The atrioventricular (AV) node is an anatomically well-defined structure, conveniently housed in the triangle of Koch. There are two distinct atrial impulse approaches to the AV node, one of which (in the anterior portion of triangle of Koch) has a faster conduction, while the other one (in the posterior portion) has a slower conduction. However, it is not said that such a conductive duality translates into any arrhythmic phenomena. Actually, these arrhythmias are due to an imbalance of the two pathways electrophysiological properties, which does not always exist. In the presence of such an imbalance, the dual AV nodal physiology is, however, the substrate for various arrhythmias and curious electrocardiographic behaviors. Often the fast pathway is characterized by a relatively long refractory period. In contrast, the slow approach is often characterized by shorter refractoriness.The unbalanced refractoriness of the two nodal pathways constitutes the prerequisite for the most common form of paroxysmal supraventricular tachycardia: the AV nodal reentrant tachycardia (AVNRT). In subjects prone to this type of arrhythmia, during sinus rhythm, nodal conduction usually occurs from the anterior approach (fast pathway). However, a premature atrial beat may find this pathway refractory and cross the AV node through the posterior approach (slow pathway), resulting in a sudden prolongation of the AV conduction time ("jump"). This allows the impulse, once it reaches the common end, to excitate the fast pathway in a retrograde direction and to return backwards to the atrium, thus triggering a circus movement that can result in a "slow-fast" AVNRT. More rarely, an AVNRT can take place in an opposite direction of the reentrant impulse ("fast-slow" variety of AVNRT). A paroxysmal supraventricular tachycardia may seldom occur with a regularly alternating RR cycle, if the reentrant mechanism involves retrogradely an accessory AV pathway and, in anterograde direction, a fast and a slow AV nodal pathway, alternately. Among the mechanisms underlying the total RR irregularity during atrial fibrillation, there is probably also the possibility that the AV node may offer to the atrial impulses two distinct pathways to reach the His bundle. Not too rarely, a dual AV nodal physiology can occur during sinus rhythm, through unexpected and sudden changes in the AV conduction time, so that two distinct PR families can be observed. It is likely that the presence of dual AV nodal pathways can facilitate or promote a Wenckebach conduction mechanism at nodal site.