Airway/original research
The Utility of Supplemental Oxygen During Emergency Department Procedural Sedation With Propofol: A Randomized, Controlled Trial

https://doi.org/10.1016/j.annemergmed.2007.11.040Get rights and content

Study objective

We determine whether supplemental oxygen reduces the incidence of hypoxia by 20% compared with breathing room air in adult study patients receiving propofol for emergency department procedural sedation.

Methods

Patients were randomized to receive either supplemental oxygen or compressed air by nasal cannula at 3 L per minute. Physicians were blinded to the gas used and end tidal CO2 (etco2) data. Respiratory depression was defined a priori as oxygen saturation less than or equal to 93%, an etco2 level of greater than or equal to 50 mm Hg, an absolute etco2 change from baseline of greater than or equal to 10 mm Hg, or loss of the etco2 waveform.

Results

Of the 110 patients analyzed, 56 received supplemental oxygen and 54 received room air. Ten (18%) patients in the supplemental oxygen group and 15 (28%) patients in the compressed air group experienced hypoxia (P=.3, effect size=10%, 95% confidence interval −24% to 7%). Twenty-seven patients (20 supplemental oxygen; 7 room air) met etco2 criteria for respiratory depression but did not become hypoxic. Physicians identified respiratory depression in 23 of 25 patients who developed hypoxia compared with only 1 of 27 patients who met etco2 criteria for respiratory depression but who did not have hypoxia. One patient in the supplemental oxygen group experienced a transient arrhythmia and had a short apneic episode, both of which resolved spontaneously. The patient was admitted for observation.

Conclusion

Supplemental oxygen (3 L/minute) trended toward reducing hypoxia in adult study patients; however, the 10% difference observed was not statistically significant and was below our a priori 20% threshold. Blinded capnography frequently identified respiratory depression undetected by the treating physicians.

Introduction

Throughout the past decade, the need to provide safe and effective procedural sedation has prompted an increasing number of emergency department (ED) clinical trials and the introduction of new agents, techniques, and monitoring devices. Yet, despite the knowledge gained by scientific study and clinical experience, early detection of respiratory depression and prevention of hypoxia remains a challenge.1 To reduce the incidence of hypoxia, the American Society of Anesthesiology recommends the use of supplemental oxygen for patients undergoing deep sedation and suggests it be considered during moderate sedation.2 Although these recommendations seem intuitive, there is a paucity of information about the risks and benefits of supplemental oxygen during ED procedural sedation.

The goal of supplemental oxygen is to increase oxygen reserves, thereby delaying or preventing the onset of hypoxia. However, increasing oxygen reserves is not without risk. It has been shown that superoxygenated patients desaturate only after prolonged apnea.3, 4 This negates the use of pulse oximetry as an early warning device for respiratory depression,2, 5, 6 which is concerning in light of the fact that emergency physicians rarely recognize respiratory depression in sedated patients who do not become hypoxic.7

In the only other prospective study specifically designed to evaluate the use of supplemental oxygen during ED procedural sedation and analgesia, we found that 2 L of supplemental oxygen did not reduce the incidence of hypoxia by 20% in adult patients receiving midazolam and fentanyl.7 It is not clear whether these results can be extrapolated to other agents, particularly propofol, which has a higher incidence of respiratory depression.8

If supplemental oxygen can limit the incidence or severity of hypoxia during procedural sedation with propofol, without hindering early recognition of respiratory depression, it should be incorporated into standard ED procedural sedation protocols. If supplemental oxygen prevents hypoxia but interferes with the physician's ability to detect respiratory depression, then additional precautions such as monitoring end tidal carbon dioxide (etco2) may be indicated. If supplemental oxygen does not reduce the incidence of hypoxia, its use should be abandoned.

The goal of this study was to determine whether supplemental oxygen delivered at 3 L per minute by nasal cannula would reduce the incidence of hypoxia by 20% in adult patients receiving propofol for procedural sedation. We also evaluated whether physicians blinded to capnographic data are able to recognize respiratory depression during procedural sedation. Finally, in a preplanned secondary analysis, we compared the relative accuracy of capnography in predicting hypoxia when the criterion of a 10-mm Hg absolute change in etco2 from baseline is narrowed to a 10% absolute change in etco2 from baseline.

Section snippets

Study Design

This was a prospective, randomized, double-blind, placebo-controlled study conducted between November 2005 and October 2006. The institutional review board approved the study.

Setting and Selection of Participants

The study was performed in the ED at the Albert Einstein Medical Center, a Level I trauma center located in Philadelphia, PA. The ED features a well-established emergency medicine residency program and has an annual census of approximately 75,000 patient visits.

All patients older than 18 years and receiving propofol to

Characteristics of Study Subjects

Research associates screened 175 patients during the 12-month study period. Of these, 112 were enrolled in the study. Two patients were subsequently excluded because they received a nonstudy medication (etomidate) for sedation, leaving 110 patients for analysis (Figure). The 2 groups were similar with respect to age, sex, and weight. Abscess incision and drainage and fracture and joint reduction accounted for all procedures. There were no significant differences between the groups in the type

Limitations

We administered 3 L per minute of oxygen to the subjects in the treatment group. Providing a higher concentration of supplemental oxygen may have resulted in a lower incidence of hypoxia.

The mean initial and total propofol doses were slightly higher in the room air group (Table 1), which may have contributed to the difference in the incidence of hypoxia observed between the 2 groups.

We defined hypoxia as an oxygen saturation of less than 93%. Although this level is higher than the traditional

Discussion

Supplemental oxygen (3 L/minute) trended toward reducing hypoxia in adult study patients; however, the 10% difference observed was not statistically significant and was below our a priori 20% threshold. To our knowledge, this is the first study specifically designed to evaluate the use of supplemental oxygen during procedural sedation that has shown a potential benefit to its use. We performed a previous study of procedural sedation and analgesia with midazolam and fentanyl, in which the use of

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  • J.R. Miner et al.

    Bispectral electroencephalographic analysis of patients undergoing procedural sedation in the emergency department

    Acad Emerg Med

    (2003)
  • Cited by (0)

    Supervising editor: Steven M. Green, MD

    Funding and support: By Annals policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article, that may create any potential conflict of interest. The authors have stated that no such relationships exist. See the Manuscript Submission Agreement in this issue for examples of specific conflicts covered by this statement.

    Author contributions: KD and CRC conceived the study and designed the trial. KD, CRC, and PD supervised the conduct of the trial and data collection. KD, CRC, and PD managed the data, including quality control. PD provided statistical advice on study design and analyzed the data. KD drafted the article. CRC provided editorial support and contributed substantially to its revisions. KD takes responsibility for the paper as a whole.

    Earn CME Credit: Continuing Medical Education for this article is available at: www.ACEP-EMedHome.com.

    Reprints not available from the authors.

    Publication dates: Available online March 4, 2008.

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