Regular readers know my interest for the influence of vasopressors, to correct mean arterial pressure during surgeries (whether it is during anesthesia or cardiopulmonary bypass), on cerebral oxygenation.
In some cases, vasopressors may not be necessary because evidence shows that cerebral oxygenation doesn’t always decrease during anesthesia-induced hypotension. We still don’t know the reason though.
In a recent study, Meng et al. tested the hypothesis that the reduction in brain perfusion, associated with hypotension during anesthesia, would be counterbalanced by a decrease in brain metabolism. As a consequence, frontal lobe oxygenation (or cerebral tissue oxygen saturation in this paper) measured by near-infrared spectroscopy would not be lowered.
To test this hypothesis, the authors recruited patients (data for 30 patients are presented) scheduled for elective non-neurological surgery under general anesthesia with tracheal intubation.
Anesthesia was induced with propofol and fentanyl. Cerebral tissue oxygen saturation, mean arterial pressure, heart rate, cardiac output and bispectral index were monitored before induction of anesthesia and after tracheal intubation.
Mean arterial pressure and cardiac output decreased from pre-anesthesia induction to tracheal intubation. Frontal lobe oxygenation after tracheal intubation remained similar to baseline (pre-anesthesia induction) in these patients.
Cerebral metabolism was not measured in this study. Based on previous findings showing that cerebral metabolism is decreased following induction of anesthesia, the authors inferred that brain oxygen demand and supply remained matched after induction of anesthesia with propofol and fentanyl, leading to an absence of significant change in cerebral tissue oxygen saturation in their patients.
Meng L, Gelb AW, McDonagh DL. Changes in cerebral tissue oxygen saturation during anaessthetic-induced hypotension: an interpretation based on neurovascular coupling and cerebral autoregulation. Anaesthesia 2013; 68(7):736-41.