Dual AV Nodal Physiology and AVNRT
In this section, we will cover the concept of dual AV nodal physiology, the phenomenon whereby a patient has two (or more) electrophysiologically distinct pathways in their AV node, and its related arrhythmias.
This section will go over:
The normal biology of the AV junction, which is normally meant to induce a conduction delay to allow left ventricular filling after atrial contraction and to prevent tachyarrhythmia. We will discuss the three distinct regions and cell types (AN, N, NH) and their individual properties, including how they are affected by medications and autonomic signalling.
The prevalence and structure of the dual pathways in this condition, such as the usual presence of both a fast and slow pathway, as well as a discussion about the common pathways proximal and distal to the dual pathways.
The various different manifestations of dual AV nodal physiology, including:
Atrioventricular nodal reciprocating tachycardia (AVNRT), which is a condition whereby the two pathways form the limbs of a reentrant circuit which can cause supraventricular tachycardia. This is the most well-known manifestation of dual AV nodal physiology. We will discuss the more prevalent "typical" (slow-fast) AVNRT, as well as the "atypical" variants (fast-slow and slow-slow).
Reciprocating beats, whereby impulses traverse down one pathway and return via the other pathway to re-excite the chamber that the impulse originated from.
Two families of PR intervals, where a patient will exhibit either a long or short PR interval depending on which pathway is being used for anterograde conduction. We will also discuss how the heart "switches" between the two pathways in the presence of premature beats, concealed conduction, or changes in autonomic tone. On a similar note, we will also discuss two families of RP intervals, where the RP interval of retrograde p waves switches between two values in the context of a ventricular rhythm.
Double fire tachycardia, wherein an atrial beat is conducted down both fast and slow pathways simultaneously, such that the ventricles are captured twice for each atrial beat.
Rapid atrial fibrillation, which, while not solely related to dual AV nodal physiology, can be more prevalent in this population. This is because the slow pathway tends to have a lower refractory period, and can hence conduct more atrial signals, causing tachycardia. In essence, this is the a compromise of the normal physiologic block of the AV node.