Antiarrhythmic agents affect the generation and/or propagation of the cardiac rhythm by their actions on one or several ion channel currents and/or the autonomous nervous system. This chapter focuses on five antiarrhythmic agents: digoxin, flecainide, sotalol, amiodarone and adenosine. Due to their relative safety and efficacy, these agents are considered the foundation of transplacental and/or direct pharmacological therapy of fetal supraventricular tachyarrhythmias (SVT). SVT itself can be produced by four different mechanisms, namely: atrioventricular reentry (AVRT), atrial flutter (AF), atrial ectopic tachycardia (AET), and permanent junctional reciprocating tachycardia (PJRT). AVRT and PJRT involve the atrial and ventricular myocardium, the AV node, and accessory pathway(s) in the reentrant circuit. Suppression of AET and AF is possible by drugs like flecainide, sotalol, and amiodarone that directly act on atrial cells. The fetal response to antiarrhythmic therapy not unexpectedly is affected by fetal hemodynamics, arrhythmia mechanism, and the choice of drug management.