The increased awareness of fetal arrhythmias by obstetricians and the development of sophisticated fetal echocardiography have established the basis for identification and treatment of these arrhythmias. The development of fetal hydrops is a recognized link to the severity of the arrhythmia. Fetal tachycardias have been diagnosed relatively early in gestation. They may be differentiated into sinus tachycardia, supraventricular tachycardia, atrial flutter or fibrillation, and ventricular tachycardia. The need for prenatal treatment is widely accepted and various modes of therapy are advocated. Oral maternal antiarrhythmic medication is often used, is considered convenient and safe, and provides adequate conversion. The drugs of choice at various centers have included digoxin, flecainide, amiodarone, and a host of combinations, as well as sotalol, which is gaining popularity. At birth, reentry mechanisms are often documented, with frequent relapses of tachycardia, warranting postpartum continuation of treatment. Fetal bradycardias consist of sinus bradycardia (generally related to obstetric pathology) and atrioventricular block. Atrioventricular block may occur secondary to severe congenital heart disease in the fetus or as an isolated phenomenon. The development of isolated total atrioventricular block has been seen to occur from a gestational age of 18 weeks up to term. It is invariably accompanied by the presence of SS-A and SS-B autoantibodies in the mother. Passage of these antibodies across the placenta causes inflammatory disease of fetal atrioventricular node tissue, resulting in fibrosis and atrioventricular block. Although prospective studies do not suggest the presence of abnormally increased antibody levels in these mothers during pregnancy, experimental preventive therapy has been instituted in pregnancies of SS-A and SS-B positive mothers who have had previous children with atrioventricular block. This preventive therapy consists mainly of corticosteroids or immunosuppressive drugs.