Impact of a β-blocker and/or acute hemodilution on cerebral oxygenation during apneic hypoxia

Background β‐blockers reduce the tolerance for acute hemodilution by decreasing cerebral oxygenation and may contribute to the incidence of stroke. We hypothesized that β‐blockers also increase the risk for cerebral hypoxia when apneic hypoxia occurs. Methods After induction of isoflurane, 14 swine (mean ± SD =25.3 ± 0.8 kg) were studied using 200 μg/kg/min of landiolol or saline (control group) in three sequential stages: before, during, and after landiolol (saline) infusion. In each stage, after 5 min of mechanical ventilation with 100% oxygen, apnea was induced until the time to < 70% oxygen saturation. Hemodynamic and blood gas variables were measured, and the cerebral tissue oxygenation index (TOI) was recorded by near infrared spectroscopy (apnea experiment). After these steps, hemodilution was induced by hemorrhage of 600 ml and infusion of the same volume of hydroxyethylstarch, and the apnea experiments were then conducted before, during, and after landiolol (saline) infusion similarly to before hemodilution. Results Landiolol decreased TOI at 1 min after apnea and at SpO2 < 70% by 3.3% and 7.0% from each corresponding value at baseline, and by 13.1% and 20.3% during hemodilution. Landiolol shifted the relationship between TOI and arterial hemoglobin oxygen saturation (SaO2) or arterial partial pressure of oxygen (PaO2) to the left; and reduced TOI at similar arterial blood oxygenation. This phenomenon was marked during hemodilution. Conclusions Landiolol reduces cerebral tissue oxygenation during apneic hypoxia. β‐blockers increase the risk for cerebral hypoxia when apneic hypoxia occurs, especially during acute hemodilution.