Mechanisms of atypical atrioventricular Wenckebach periodicity. A theoretical model derived from the concepts of inhomogeneous excitability and electrotonically mediated conduction.

To explain the mechanisms of atypical atrioventricular (AV) Wenckebach periodicity, a model of the AV node was theoretically derived from the concepts of "inhomogeneous excitability" and "electrotonically mediated conduction." The theoretical model of the AV node has the following characteristics: (1) increased vagal tone depresses excitability in the AV node, (2) depressed excitability in the AV node is inhomogeneous in both transverse and longitudinal directions, and (3) electrotonically mediated conduction occurs across inexcitable gaps in the AV node. Many features in atypical AV Wenckebach periodicity are explained by the use of this model. Delayed AV conduction is caused mostly by electrotonically mediated conduction across a much-depressed region in the AV node, and thereafter AV conduction is blocked at the same region, resulting in the occurrence of an AV Wenckebach period with gradual lengthening of PR intervals. Occasionally, longitudinal dissociaton and concealed reentry in the AV node occur in the part below (distal to) the above depressed region, resulting in the occurrence of an AV Wenckebach period with sudden marked lengthening of a PR interval. The sinus impulse following such suddenly delayed AV conduction is usually blocked in the AV node as the result of concealed reentry of the preceding impulse.