The inclusion of nitrous oxide in the prescription for general anesthesia continues to be widespread throughout the world. Nitrous oxide (a first gas) can accelerate the speed of induction of the general anesthetic state produced by simultaneous use of a potent inhalation agent (a second gas) as a result of the second gas, or concentration, effect. (Have you read classic descriptions of this phenomenon:ref 1
?) When nitrous oxide is transferred from alveoli to arterial blood, the alveolar concentration of the remaining volatile anesthetic agent is raised, as is its clinical effectiveness, consequently increasing depth of anesthesia. While the second gas effect was first described almost 50 years ago, understanding its physiology and relationship to hemodynamic and respiratory variables continues to be a topic studied by anesthesiologists
The March issue of ANESTHESIOLOGY presents a study
of the second gas effect focused not on the induction of anesthesia but rather on emergence. Peyton and colleagues investigated nitrous oxide’s effect (i.e., a dilution effect) during emergence, when nitrous oxide administration is discontinued and it diffuses out of the blood into the alveoli, reducing the amount of volatile anesthetic agent in the alveoli and blood. The additional clinical question asked was whether such a dilution alters (speeds) emergence.
Sevoflurane concentrations were measured in the arterial blood and alveoli at the end of an anesthetic administered to a constant depth gauged by the establishment of a relatively constant bi-spectral index of 40-60 in a control group (sevoflurane in air-oxygen) compared to a nitrous oxide group (2:1 mixture of nitrous oxide-oxygen). Clinical status was assessed in two ways: patients’ response to a command to open their eyes and time required for extubation. Arterial sevoflurane at 5 minutes compared to baseline was approximately 40% lower in the nitrous oxide group, a transient difference that had disappeared at 30 minutes. Alveolar sevoflurane was approximately 24% lower in the nitrous oxide group, though this was not statistically significant. Eye opening and extubation occurred more quickly in the nitrous oxide group (8.7 vs. 10.1 minutes) than in the control group (11.0 vs. 13.2 minutes).
This study demonstrates that during emergence, diffusion of nitrous oxide into the alveoli suggests a concomitant reduction in partial pressure of the volatile agent. The diffusion effect of nitrous oxide reduced the partial pressure of sevoflurane in arterial blood more than it affected alveolar concentration. The reduction in the concentration of potent inhalation agent in both blood and alveoli contribute to lower partial pressure of the anesthetic in the brain, changing both depth of anesthesia and speed of emergence. A benefit of reading and digesting this study is that it facilitates an understanding of minimum alveolar concentration (MAC) (i.e., the interplay of inspired, alveolar and arterial concentrations of an anesthetic agent that ultimately produce an anesthetic state). Have you read a classic discourse
on MAC? Do you use nitrous oxide? Is your decision to use nitrous oxide influenced by the second gas effect? Knowing that nitrous oxide can enhance emergence from anesthesia, will you utilize it for this specific purpose in the future? Tell us what you think
Posted by Alan Jay Schwartz, M.D.,MSEd