Paradoxical Inhalational Anesthetics, Nitrous Oxide, Ketamine, and Propofol
摘要
There are large differences between volatile anesthetic agents and other drugs such as ketamine or Nitrous Oxide (N2O). This is where the processed Electroencephalography-Depth Of Anesthesia (pEEG-DOA) monitors start to diverge from clinical signs of anesthesia. Cortical electroencephalography (EEG) is mainly the target of γ-amino butyric acid (GABA) receptors agonists that modulate sedation and consciousness. However, ketamine and N2O, two N-methyl-D-aspartate (NMDA) receptor inhibitors induce loss of consciousness without depressing the cortical EEG. Ketamine induces loss of consciousness through a completely different mechanism of “dissociative anesthesia” other than GABA receptors. Each individual anesthetic agent, such as sevoflurane or propofol, has their own characteristic EEG “footprint” profile for calculating pEEG-DOA algorithms, that is different than other anesthetic agents: xenon, N2O, and ketamine with their unique EEG patterns than that commonly seen with other conventional general anesthetic agents.