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Many antiarrhythmics share a lipophilic or aromatic region, a linker, and a basic nitrogen. Protonation can support cationic binding within an ion-channel pore, while structural differences distinguish drug classes and individual agents. In Class I drugs, the aromatic–carbonyl–amine core resembles local anesthetics, and channel dissociation rate separates IA, IB, and IC profiles. Other notable structure–property relationships include ester hydrolysis of esmolol, the long persistence of highly lipophilic amiodarone, and the influence of chirality in agents such as quinidine, sotalol, and verapamil. These connections provide a foundation for understanding pharmacokinetics and safety considerations, including proarrhythmic risk associated with delayed repolarization and QT prolongation.