Objectives: to study the effect of apnea and bradycardia (A/B) on cerebral total haemoglobin (tHb), which is analogous to cerebral blood volume, and on EEG. To investigate whether alterations in tHb and/or EEG relate to bradycardia or hypoxia. Methods: 20 preterm newborn infants, 26-33 week of gestation, (median 29), were studied during 88 episodes of apnea. Changes in tHb were measured using near-infrared spectroscopy. Two channels(C3-O1, C4-O2) of EEG tracing were recorded. Respiration was monitored by chest movements using impedance pneumography and by nasal airflow using a thermistor. In addition instantaneous heart rate (HR) and arterial oxygen saturation (SaO2) were continuously recorded. The threshold of bradycardia was automatically set at a value which was 30% less than the baseline heart rate value, with a minimum of 100 b/min. All physiological variables were transferred to a cotside computer for analysis.Results: there was a significant decrease in tHb during A/B (3.35± 1.2 μmol/l vs 2.45 ± 1.1 μmol/l; p < 0.001). This decrease was accompanied by a significant depression of EEG (71.5 ± 15μvolt vs 44 ± 13 μvol/l; p < 0.001). Changes in tHb and EEG were correlated with heart rate (r =.46, p < 0.001; r =.35, p < 0.0025 respectively) but were not reflected in arterial oxygen saturation (r =.23, p=.06 ns, between tHb and SaO2; r =.13, p = 0.5 ns, between amplitude of EEG and SaO2). Conclusion: 1) In the preterm neonate bradycardia, more than hypoxia, was observed to have the strongest impact on tHb and EEG. This could be explained by a fall in cardiac output and thus cerebral perfusion. 2) Efforts must be made to improve heart rate monitoring(instantaneous vs mean HR). SaO2 alone may not reflect the severity of A/B and its potential deleterious effects on the brain.
