[Sudden infant death--the QT interval in ECG and bradyarrhythmias]

Prolongation of ventricular repolarization, as evidenced from an increased QT-interval, makes the ventricles more susceptible to fibrillation. The theory has previously been advanced that some cases of sudden infant death syndrome may be due to a non-hereditary QT-prolongation, resulting in fibrillation and cardiac death. This theory has been seriously doubted, since in subsequent long series of recordings in newborns the QT-interval has been found normal at rest. However, the QT-theory has recently been revived by a report that in some babies with sudden infant death syndrome the ability to shorten the QT-interval as the heart rate increases is impaired, an observation which is consistent with the QT-theory. The present experiments on infant and adult rodents have shown that during the innate fear paralysis reflex, elicited by a variety of frightening stimuli of a type that commonly occur during ordinary daily life, the QT-interval may be transiently prolonged and is usually associated with bradycardia and changes of the ST-segment and T-wave. The fear paralysis reflex has previously been proposed as a triggering mechanism for SIDS. These findings lend support both to the fear paralysis theory and the QT-theory. The reflex may represent an external cause of QT-prolongation which adds to the intrinsic impairment of repolarization resulting in a condition which favours ventricular fibrillation. A second unfavourable intrinsic factor is chronic hypoxia.