Objective To test the hypothesis that a higher pulsoximetric arterial oxygen saturation (SpO₂) target range is associated with reduced cerebral tissue oxygen desaturations from baseline during events of hypoxaemia or bradycardia.

Design Randomised crossover trial.

Setting Single tertiary care neonatal intensive care unit.

Patients Sixteen preterm infants with severe intermittent hypoxaemia or bradycardia.

Interventions SpO₂ target was set to 80–92% and 85–96% for 4 h each in random sequence. On a subsequent day, the target sequence was reversed and the study was repeated.

Main outcome measures We simultaneously recorded cerebral tissue oxygen saturation (cerebral StO₂), SpO₂ and heart rate. Cerebral StO₂ was measured by near infrared spectroscopy. The primary outcome was the cumulative cerebral StO₂ desaturation score representing the area below a cerebral StO₂ baseline value before onset of each hypoxaemic or bradycardic event.

Results During low SpO₂ target range the median (IQR) cumulative cerebral StO₂ desaturation score was higher (27384 (15825–37396) vs 18103 (6964–32946), p=0.011) and the mean (±SD) number of events was higher (29.1 (±15.3) vs 21.1 (±11.4), p=0.001). More time was spent with SpO₂ below 80% (57.2 (±24.8) min vs 34.0 (±29.6) min, p=0.006). Total time of hyperoxaemia (defined as SpO₂ ≥97% and ≥99%, respectively) and total time with cerebral StO₂ <60% and <55% were similar.

Conclusions A lower SpO₂ target range was associated with a greater cumulative cerebral StO₂ desaturation score, caused by more frequent SpO₂ desaturations. However, time at very low cerebral StO₂ was not affected. Episodes of hyperoxaemia were not reduced.