In a stressed A-V node decremental conduction, a normally very long RP and its increase by electrotonus and temporal shifts induced by slow conduction result in a delay of conduction which increases with each beat until finally one impulse is blocked. The recovery of cells proximal to the block is accelerated by electrotonus, while the distal cells enjoy a longer recovery time. The next impulse finds fully recovered tissue in all parts and is conducted rapidly. The second impulse of the cycle encounters decremental conduction, prolongation of the RP due to electrotonus and temporal shift, and postbradysystolic hypoconductivity. It suffers the largest increment of delay. Retrograde Wenckebach cycles always end in an obligatory ventricular echo if the rate is slow. Wenckebach cycles and ventricular echoes are inherent in the node and are often present at the same times. In the A-N region spokes of nodal cells accompanied by connective tissue radiate into the atrium. They are the distal path for the retrograde impulse. When the impulse undergoes a Wenckebach delay it will traverse some spokes slowly (alpha path) and block in others (beta). The spokes are insulated from each other by the weak transverse electrotonus due to the small AP of nodal cells and to the increased connective tissue. The atrium returns the impulse through beta. The fast conduction in beta has the same mechanism as the fast conduction of the first beat of the Wenckebach cycle.