An “account” of digitalis and atrial fibrillation

This review deals with the mechanisms by which digitalis exerts its “opium-like” action on the ventricular rate in patients with atrial fibrillation. To understand the effect of digitalis on ventricular rate and rhythm, it is essential to learn more about the basic electrophysiologic principles responsible for: 1) atrial fibrillation as such, and 2) the scaling function of the atrioventricular (AV) node-His system. It may be assumed that during atrial fibrillation, the atrial excitatory process results In randomly spaced impulses that reach the AV junction from random directions with random strength. The refractory period of and concealed conduction in the AV node enable the AV conduction system to scale down the shower of atrial impulses to a random ventricular response with a considerably lower rate. Digitalis decreases the ventricular rate through two synergistic pharmacologic actions: 1) digitalis increases the refractory period of the AV node, and 2) digitalis decreases the refractory period of the atrial myocardium through a direct and indirect effect (vagotonic and vagomimetic). A decrease in the refractory period of the atrial myocardium results in more atrial impulses reaching the AV junction in a given unit of time. More atrial impulses result in a greater degree of concealed conduction in the AV node and, thus, in a slower ventricular rate. The ventricular rhythm remains random during digitalis treatment. Digitalis is the only drug that effects an increase in the refractory period of and concealed conduction within the AV node. Two hundred years after its discovery, digitalis remains the drug of choice for the treatment of patients with sustained atrial fibrillation.