This chapter provides a logical approach to diagnosis of fetal dysrhythmias and discusses the current management of fetal dysrhythmias. Echocardiography, the main diagnostic tool in the fetus, allows recording of the mechanical consequences of the electrical stimulation, registered as myocardial wall movement and blood flow signals. Other techniques such as fetal electrocardiography (f-ECG) or fetal magnetocardiography (f-MCG) allow recording of the electrical cardiac impulses. Rhythm irregularities are common and often associated with premature contraction of the atrium. The most frequent tachycardias are supraventricular tachyarrhythmias including supraventricular tachycardia (SVT) and atrial flutter (AF). Neither heart rate nor fetal heart rate (FHR) variability allows clear distinction among the various types although they may aid diagnosis. Fetal bradycardia may be a manifestation of fetal distress and require emergency Cesarean section. Hydrops increases morbidity and mortality for both tachycardias and bradycardias.

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.