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Nitrous Oxide and the Second Gas Effect on Emergence from Anesthesia. Molly Orr, BS, BSN, CCRN, SRNA Oakland University-Beaumont Graduate Program of Nurse Anesthesia.
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Nitrous Oxide and the Second Gas Effect on Emergence from Anesthesia Molly Orr, BS, BSN, CCRN, SRNA Oakland University-Beaumont Graduate Program of Nurse Anesthesia
Peyton, P. J., Chao, I., Weinberg, L., Robinson, G. J. B., & Thompson, B. R. (2011). Nitrous oxide and the second gas effect on emergence from anesthesia. Anesthesiology, 114(3), 596-602. Departments of Anesthesia and Surgery, Austin Hospital, Melbourne, Australia Department of Surgery, University of Melbourne, Melbourne, Australia
Definition • What is second gas effect? • What do we know about it? • Why is it important?
Study concept • Does the elimination of N2O affect the rate of decrease in end-tidal and arterial sevofluraneconcentrations (…and thus speed emergence)? • The null hypothesis: The rapid diffusion of N2O at the end of inhalational anesthesia has no effect on the rate of reduction in end-tidal and arterial concentrations of volatile anesthetic (i.e. sevoflurane)
Study design • Randomized controlled study • Patients randomly assigned to experimental or control group via sealed envelope (N=20) • Control group (n=10): Gas mixture of sevo in air-oxygen • Experimental (nitrous oxide) group (n=10): Gas mixture of sevo in a 2:1 mixture of nitrous oxide-oxygen
Inclusion criteria • Adults (> 18 yo) capable of giving informed consent • General surgery at least 1 hour duration • Requires arterial line for hemodynamic monitoring • Arterial line samples used for gas analysis
Exclusion criteria • History of severe lung disease (PFT criteria) • Symptomatic ischemic heart disease • Super obesity (BMI>45) • Pregnancy • H/O severe PONV • Critically ill/immunologically compromised • Vit B12 or folate deficiency • Presence of gas-filled, space occupying lesion
Methods used • Premed: 1-2 mg midazolam IV • Standard monitoring + arterial line + BIS • Preoxygenated • Induction: 1.5-2.5 mg/kg propofol IV, opioids (1-2 mcg/kg fentanyl and/or morphine 0.05-0.1 mg/kg), nondepolarizing neuromuscular blocker • Endotracheal intubation, controlled ventilation 12-15 breaths/min, EtCO2 maintained 28-33 mmHg • Maintenance: Inhalational anesthetic mixture (with air-oxygen or with nitrous-oxygen) initiated and sevo concentration adjusted to maintain BIS 40-60 (N2O does not affect BIS!) • Normothermia with forced air warming device
Methods cont’d At conclusion of surgery: • Baseline 10 mL arterial blood sample + 1 mL sample for respiratory blood gas analysis • End-tidal gas concentrations over 20 sec recorded simultaneously with gas analyzer • Baseline hemodynamic, ventilation data, SpO2, temp and BIS numbers recorded • After baseline obtained, neuromuscular blockade reversed with 2.5 mg neostigmine and 0.4 mg glycopyrrolate, fresh gas mixture changed to 100% O2 at 9 L/min
Methods cont’d • Arterial blood gas samples drawn, end-tidal gas analysis, and other vital data collected at 2 min and 5 min • Patient then loudly commanded to open his or her eyes, command repeated every 30 sec until response; time from command until eye opening was noted • Extubation after standard criteria met; time to extubation noted • Final arterial blood gas sample obtained in PACU at 30 min
The dependent variables: Primary and Secondary Endpoints • “Primary study endpoints”: • Differences in the fraction of baseline partial pressures of sevofluranein arterial blood at 2 min and 5 min • End-tidal sevo partial pressures at 2 min and 5 min • End-tidal and arterial concentrations of CO2 were also determined at 2 min and 5 min • “Secondary study endpoints”: • BIS number comparisons between the two groups at 2, 5, and 10 min • Time to eye opening • Time to extubation
Statistical Analysis • Estimated 20 patients required for analysis • Two-tailed t test for unpaired data (with Bonferroni correction for multiple measurements in each patient) • Two-way ANOVA to determine whether any measured differences changed significantly over time • Best-fit curves for primary endpoints were generated using least squares method • Two-tailed t test used for secondary endpoints (after Kolmogorov-Smirnov normality testing) • P value of 0.05 or less considered statistically significant
Results/Conclusion • During the first 5 min after conclusion of anesthesia, the arterial partial pressure of sevo was 39% higher in the control group than in the nitrous oxide group (P<0.04), but was not found to be statistically significant at 2 min and 30 min • End-tidal differences in sevo were not significant between the two groups at 2 min and 5 min • PaCO2 decline at 2 min was significant in N2O group vs. the control group (d/t diffusion hypoxia), but no sig diff remained at 5 min • No significant diff in BIS at 2 and 5 min between two groups • Times to eye opening and extubation were significantly shorter in nitrous oxide group (8 min and 10 min, respectively) compared to control group (11 min and 13 min). [P<0.04]
Strengths of study • Independent variables were consistent between the two groups (e.g. age, sex, weight, operative time, baseline vent parameters, baseline VS, baseline temps and BIS numbers) • Anesthetic technique was standardized between two groups (apart from administration of nitrous oxide) • Measurements conducted in identical manner between two groups
Limitations of study • Small sample size (N=20, two outliers later excluded) • Variations in characteristics of people whoenrolled in study (e.g. age, end organ function, smoker vs. non-smoker, V/Q mismatching, etc.) • Confounding variables as identified by authors, such as trend toward lower HR and BP in nitrous oxide group, which correlates to 10-20% lower cardiac output and may affect alveolar anesthetic concentrations • Use of nitrous with volatile anesthetic reduces volatile anesthetic dose; has “MAC sparing” effect • No statistical significance was found in end-tidal sevo (i.e. alveolar) concentrations between the two groups
Overall takeaway • How can we use this in practice? • A more rapid emergence?