Antiarrhythmic effects are due mainly to beta-adrenergic receptor blockade. Normally, sympathetic drive results in increased in Ca²⁺ ,K⁺ ,and Cl^- currents.

Increased sympathetic tone:

• Increases phase 4 depolarization (heart rate goes up), and

• Increases DAD (delayed afterdepolarizations) and EAD (early afterdepolarization) mediated arrhythmias. These effects are blocked by β-adrenergic receptor blockers.

β-adrenergic receptor blockers increase AV conduction time and increase AV nodal refractoriness, thereby helping to terminate nodal reentrant arrhythmias.

β-adrenergic receptor blockade can also help reduce ventricular following rates in atrial flutter and fibrillation, by acting at the AV node.