[Comparative pathophysiology of the atrioventricular node].

The apparent mismatch between size and electrical function of the mammalian heart can be exemplified by the relation between ventricular rate during atrial fibrillation in dog, human, and horse, and bodyweight. The same is true for the relation between atrioventricular transmission time and heart size. While heart size may increase with a factor of 10(8), PR interval (on the surface ECG) will only increase with a factor 30. The curve of the PR interval versus the third root of heart weight has an S-shape. This form of relation cannot easily be explained on the basis of current electrophysiological theories. The contribution of the AV nodal delay to AV transmission time probably diminishes with increasing heart size. The mechanism of AV nodal delay is therefore not clear. Right ventricular pacing with intervals twice as long as the shortest PR-intervals in patients with atrial fibrillation results in complete block of anterograde conduction. The AV node as an unprotected pacemaker, entrained during sinus rhythm and electrotonically modulated during atrial fibrillation, rather than a cable with conduction properties, may offer an explanation for the non-linear and non-conductive behaviour of the AV node. This may well have consequences for the treatment of patients with atrial fibrillation.