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Randomized Controlled Trial
. 2023 Feb 6;23(1):41.
doi: 10.1186/s12871-023-01982-9.

There is no evidence that carbon dioxide-enriched oxygen before apnea affects the time to arterial desaturation, but it might improve cerebral oxygenation in anesthetized obese patients: a single-blinded randomized crossover trial

Affiliations
Randomized Controlled Trial

There is no evidence that carbon dioxide-enriched oxygen before apnea affects the time to arterial desaturation, but it might improve cerebral oxygenation in anesthetized obese patients: a single-blinded randomized crossover trial

Marc T Schmidt et al. BMC Anesthesiol. .

Abstract

Purpose: Carbon dioxide (CO2) increases cerebral perfusion. The effect of CO2 on apnea tolerance, such as after anesthesia induction, is unknown. This study aimed to assess if cerebral apnea tolerance can be improved in obese patients under general anesthesia when comparing O2/Air (95%O2) to O2/CO2 (95%O2/5%CO2).

Methods: In this single-center, single-blinded, randomized crossover trial, 30 patients 18-65 years, with body mass index > 35 kg/m2, requiring general anesthesia for bariatric surgery, underwent two apneas that were preceded by ventilation with either O2/Air or O2/CO2 in random order. After anesthesia induction, intubation, and ventilation with O2/Air or O2/CO2 for 10 min, apnea was performed until the cerebral tissue oxygenation index (TOI) dropped by a relative 20% from baseline (primary endpoint) or oxygen saturation (SpO2) reached 80% (safety abortion criterion). The intervention was then repeated with the second substance.

Results: The safety criterion was reached in all patients before cerebral TOI decreased by 20%. The time until SpO2 dropped to 80% was similar in the two groups (+ 6 s with O2/CO2, 95%CI -7 to 19 s, p = 0.37). Cerebral TOI and PaO2 were higher after O2/CO2 (+ 1.5%; 95%CI: from 0.3 to 2.6; p = 0.02 and + 0.6 kPa; 95%CI: 0.1 to 1.1; p = 0.02).

Conclusion: O2/CO2 improves cerebral TOI and PaO2 in anesthetized bariatric patients. Better apnea tolerance could not be confirmed.

Keywords: Hypoxia; apnea tolerance; cerebral oxygenation; tissue oxygenation.

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Conflict of interest statement

Sandro Studer, Andres Kunz, Marc Schmidt, Sarah Haile, Lucas Kook, Andreas Pregernig, and Marco Bueter declare no conflicts of interest.

Beatrice Beck-Schimmer: BBS received a grant from Baxter AG (not related to this work). BBS was a participant in an Advisory Board Meeting of Baxter AG (not related to this topic). BBS has a patent 04/10/14 – 20140100278: Injectable formulation for treatment and protection of patients having an inflammatory reaction or an ischemia–reperfusion event; M. Urner, L.K. Limbach, I.K. Herrmann, W.J. Stark, B. Beck Schimmer, applied as Patent Cooperation Treaty (PCT) (internationally), July 2009, as well as a patent application on bioconjugates of antibodies and functionalized magnetic nanoparticles. BBS and Martin Schläpfer have received Sedana Medical AB, Danderyd, Sweden, grant money as collaborators of a large multicenter study ‘Inhaled Sedation in COVID-19-related acute respiratory distress syndrome (ISCA): an international research data study in the recent context of widespread disease resulting from the 2019 (SARS-CoV2) coronavirus pandemics (COVID-19), not related to this topic.

Martin Schläpfer has received research money for an investigator-initiated trial from Roche AG, Switzerland, not related to this study, and travel support from Baxter AG, Switzerland, as well as research money from Sedana Medical AB, Danderyd, Sweden, for another investigator-initiated trial, not related to this study. Martin Schläpfer, Beatrice Beck-Schimmer, and Marc Studer have submitted a patent for the application of CO2/O2 mixtures to mitigate negative effects of surgery and anesthesia.

Figures

Fig. 1
Fig. 1
Study intervention. This graphic displays the patient’s study intervention
Fig. 2
Fig. 2
CONSORT flowchart diagram. The adapted CONSORT flowchart diagram shows the patient flow in this cross-over trial
Fig. 3
Fig. 3
Values at the end of the apnea. The time until the peripheral oxygen saturation (SpO2) reached 80% (A), cerebral tissue oxygenation index (TOI) (B), arterial oxygen pressure (PaO2) (C), and arterial carbon dioxide pressure (PaCO2) (D) at the end of the apnea phase are displayed. The time until SpO2 reached 80% was similar after the two treatments, while TOI (p = 0.02), PaO2 (p = 0.02), and PaCO2 (p < 0.001) increased under O2/CO2 administration
Fig. 4
Fig. 4
TOI-values at the different time points. The graph illustrates the brain tissue oxygenation (TOI) values in the sequence O2/Air—O2/CO2 (A, n = 17) and the sequence O2/CO2—O2/Air (B, n = 13)

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