“…Using canine models of acute ischemic injury, Scherlag et al [2] and El-Sherif et al [20] found paroxysmal AV block to be tachycardiadependent, with sites of block at both the His-Purkinje and AV node level. The tachycardia-dependent, or phase 3 block occurs due to abnormally prolonged refractoriness in the His-Purkinje system and prolongation of action potential duration (repetitive concealed conduction) [18,20,23]. Bradycardia-dependent, or phase 4 block, has also been reported as a mechanism of paroxysmal AV block [3,14,21], and it has been explained by prolonged recovery, hypopolarization and spontaneous diastolic depolarization in the injured distal conduction system [3,23].…”