Atrial fibrillation: a new look at an old arrhythmia

Abstract

The ventricular rhythm during atrial fibrillation in human beings is random because the excitatory process of atrial fibrillation itself is almost certainly a random phenomenon. It remains random because A V junctional memory is too short to inftuence the sequence of conducted impulses . In human beings, the longest intervals (seldom over 2,000 ms) are too short to cause autonomic nervous interference with either atrial excitation or A V junctional conduction. The role of the A V junction in atrial fibrillation in human subjects seems to be limited to scaling down the atrial impulses, because interventions that alter junctional electrophysiologic properties do not interfere with the random pattern of the ventricular rhythm. The effect of digitalis and quinidine on ventricular rate and rhythm in atrial fibrillation in patients can be satisfactorily explained by the direct action of the drugs on the rate of the atrial impulses (while leaving the other random characteristics of the atrial excitation process intact) and their effect on the functional refractory period of the A V junction. However, the dispute between Mackenzie and Lewis (1,2) during the early 1920s about whether or not digitalis in atrial fibrillation (also) acts via the vagal nerve is still unsettled. They were probably both right, although current evidence seems to support Lewis (11 , 15-17).