Our understanding of the mechanisms of cardiac arrhythmias in infants and children112 has advanced greatly since the classic monograph by Langendorf and Pick in 1954.3 Ambulatory and transtelephonic monitoring have accurately defined the occurrence of arrhythmias and invasive electrophysiologic studies have elucidated many of their mechanisms. Hubbard4 first drew attention to “paroxysmal tachycardia” in young infants. He described 9 cases of supraventricular tachycardia @VT) in infancy and concluded that “digitalis or one of the digitalis preparations, when given in adequate amounts, has invariably been effective in stopping the tachycardia.” (He also reached the prescient conclusion that “until more is known about the dosage of digitalis for infants, caution should be used in giving infants and young children much larger amounts per pound of body weight than have been accepted for adult use.“) Gibson5 reported similar success with digitoxin in treating SVT. He speculated that the mechanism of the SVT was either an ectopic pacemaker in the auricles (sic) or in the atrioventricular node, the former site being the commoner. Modern intracardiac recording techniques have allowed classification of SVT based on either site of origin or presumed electrophysiologic mechanism. As pediatric electrophysiology has become established as a specialized branch within pediatric cardiology, it may appear to pediatricians and pediatric cardiologists that the management of many arrhythmias that was straightforward in the past has become fraught with pitfalls and overly reliant on complex invasive electrophysiologic studies. It is our purpose herein to review the management of SVT in infancy in the light of recent advances in diagnostic and therapeutic techniques. We confine our discussion to the commonest varieties of SVT: atrioventricular reentrant tachycardia with or without the Wolff-Parkinson-White (WPW) syndrome.