The pathophysiology of cyanotic/apnoeic episodes in preterm infants was investigated using overnight tape recordings of beat-to-beat arterial oxygen saturation (SaO2), plethysmographic waveforms from the oximeter, breathing movements and nasal airflow. Recordings were made in 16 preterm infants with recurrent cyanotic episodes of unknown cause that had received stimulation or resuscitation, and 15 preterm controls, matched for birth weight, post-conceptional and postnatal age. The recordings were analysed for baseline SaO2, the number of hypoxaemic episodes (SaO2 < or = 80% for > or = 4 s) and the breathing patterns associated with each episode. There was a significant difference in the total number of hypoxaemic episodes between patients and controls (520 versus 100; p < 0.01), but no difference was found for mean baseline SaO2 (98.6 versus 99.0%; p > 0.05). The mean duration of each hypoxaemic episode in the patients was 9.5 s compared with 5.8 s in the controls (p < 0.01). Although most hypoxaemic episodes (62 and 76%) were associated with pauses in breathing movements, a proportion (8 and 18%, respectively) occurred despite continuous airflow and breathing movements in both patients (6 of 16) and preterm controls (2 of 15). The rate of decrease in SaO2 was significantly more rapid during these latter hypoxaemic episodes than during episodes associated with isolated apnoeic pauses (8.5 versus 3.2% per second, p = 0.02). Preterm infants with cyanotic episodes have increased numbers of clinically unapparent hypoxaemic episodes, some of which have continued ventilation and rapid desaturation. The pathogenesis of these episodes warrants further investigation.