Neonatal electrocortical brain activity and cerebral tissue oxygenation during non-acidotic, normocarbic and normotensive graded hypoxemia

Objective: Neonates are commonly exposed to isolated hypoxemic episodes. In order to identify the risk of this, we correlated cerebral oxygen delivery and electrocortical brain activity during isolated graded and repetitive hypoxemia in 1-week-old piglets. Methods: Six halothane-anesthetized piglets were subjected to two episodes of graded hypoxemia of 45 min duration. The fractional concentration of inspired oxygen (FiO2) was stepwise decreased at 15 min intervals from 0.21 to 0.15, 0.10 and 0.05. A second identical hypoxemic event was induced after 1 h of normoxemia (FiO2 0.21). Mean arterial pressure (MAP) and pH were maintained at baseline values during the whole experiment. We measured near infrared spectroscopy parameters (cerebral oxidized cytochrome aa3 (Cytaa3), total hemoglobin (tHb: oxy- +deoxyhemoglobin)) corresponding to cerebral blood volume (CBV), carotid blood flow (Qcar), intra-arterial oxygen saturation (SaO2), and mean maximal EEG amplitude and relative spectral power. Results: Delta (δ) power increased significantly and the EEG amplitude dropped below 10 and 5 μV at the end of the first and the second hypoxemic period (PaO2 2.68±1.08 (P<0.05) and 2.87±0.58 kPa, respectively). Both EEG variables normalized during recovery (FiO2 0.21). Qcar, CBV and Cytaa3 were not changed. Conclusion: Acute isolated hypoxemia has to be sustained to induce neuronal hypofunction in normotensive animals. Hypoxic hypoxemia led to acute changes in neuronal activity, whereas cellular oxygenation remained unaffected.