Fetal tachycardia is an important cause of fetal morbidity and mortality.1 ,2 Reliable diagnosis in utero has been possible only since the introduction of ultrasound examination of the fetal heart.2 ,3 In the early days little thought was given to the mechanism of tachycardia, and treatment involved maternal administration of drugs fashionable at the time for treating supraventricular tachycardia in infants and children. Drug treatment was often followed by a return to sinus rhythm, which was interpreted as a response to treatment. However, the natural history of fetal tachycardia was, and remains, unknown.

Resolution of tachycardia, sometimes many days after institution of treatment, may be spontaneous rather than a response to treatment. Digoxin was the mainstay of treatment and verapamil was often the second choice. Both of these drugs exert their main effect on the atrioventricular node. Some deaths occurred with treatment and it was not clear whether this was because treatment was ineffective or the drugs actually caused the death. Most antiarrhythmic drugs have a negative inotropic effect that might be poorly tolerated by the failing fetal myocardium. Digoxin has relatively little effect in suppressing infant supraventricular tachycardia4 ,5 and intravenous verapamil is recognised as potentially hazardous in early infancy. …