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Emergency Medicine News:
doi: 10.1097/01.EEM.0000411483.89983.ff
Journal Scan

Journal Scan: High-Flow Oxygen Safely Reduces Propofol-Related Hypoxia

Lovato, Luis MD

Free Access

As the art of ED procedural sedation has matured, two schools of thought have emerged about routine oxygenation during sedation.

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Some physicians preoxygenate patients with high-flow oxygen using a reservoir mask to maximize the fraction of inspired oxygen (FiO2) and the partial pressure of oxygen (pO2) in the lung space. The high-oxygen content in the lungs is transferred to the bloodstream effectively, increasing the time it will take to reach critical desaturation should respiratory insufficiency or apnea occur.

One study showed that healthy adolescents undergoing induction and paralysis prior to intubation who had at least two minutes of manual ventilation at maximum FiO2 took more than six minutes to develop critical desaturation after the onset of apnea. (Can J Anaesth 1994;41(9):771.) Given the ultrashort effect of sedatives like propofol, even if apnea occurs transiently, adequate ventilatory function is likely to resume in these patients before desaturation ever takes place.

The other school of thought cautions against the routine use of oxygen with sedation, however. Proponents of no preoxygenation argue that a slowly decreasing oxygen saturation actually forewarns the clinician of impending respiratory insufficiency, and this critical alert becomes unreliable when a patient is preoxygenated. For a falsely reassuring oxygen saturation, a physician might downplay clinical signs of respiratory depression such as decreased alertness, reduced chest rise, or insufficient respiratory effort. In the worst-case scenario, overzealous sedation might even occur.

Although hypoxia might be more common without preoxygenation, it is generally managed easily when it occurs, often reversed merely by administering oxygen or repositioning the airway. When respiratory insufficiency occurs in a preoxygenated patient who is already receiving maximum FiO2, however, any episodes of hypoxia are more likely to require more vigorous interventions such as manual ventilation.

A recent randomized controlled trial attempts to shed some light on this controversy.

The Utility of High-Flow Oxygen during Emergency Department Procedural Sedation and Analgesia with Propofol:

A Randomized, Controlled Trial

Deitch K, et al

Ann Emerg Med

2011;58(4):360

This randomized, placebo-controlled trial enrolled consecutive adult patients undergoing procedural sedation with propofol in the ED of a Level I trauma center. Notable exclusion criteria included COPD, home oxygen, respiratory distress, pregnancy, hemodynamic instability, or inability to consent. All patients received sedation with propofol at an initial dose of 1.0 mg/kg and subsequent doses at 0.5 mg/kg at the discretion of the treating physician.

The study group was administered oxygen at 15L/min via reservoir mask, while the control group received compressed room air using a similar set-up. Physicians performing sedation were provided with standard cardiac monitoring, continuous pulse oximetry, and capnography, but were blinded to the type of gas being delivered. A separate, blinded research team, which did not interact with the treating physician, observed all study procedures and recorded all data.

The study was powered to measure a primary outcome of hypoxia assuming that a 20 percent absolute decrease in the incidence of hypoxia was clinically relevant. Clinically significant hypoxia was defined as an oxygen saturation less than 93% for more than 15 seconds. A secondary outcome of respiratory depression was defined as an end-tidal CO2 greater than 50 mmHg, a change from baseline of greater than 10 percent, or loss of a waveform for more than 15 seconds.

Hypoxia occurred 41 percent of the time (24 of 58 patients) in the compressed air placebo group and only 19 percent of the time (11 of 59 patients) in the high FiO2 group. This represented an absolute reduction in the incidence of hypoxia of 23 percent (95% CI:6% to 38%; p=0.007). Respiratory depression and adverse events were similar in both groups.

In analyzing the study results, a few points are worth mentioning. It seems that administering high-flow oxygen with a reservoir mask before and during sedation with propofol does indeed reduce the incidence of clinically significant hypoxia. This benefit does not appear to come at the expense of alternate forms of respiratory depression or other adverse events, although the study was not specifically powered to measure these outcomes.

Despite preoxygenation, almost 20 percent of patients in this study who received propofol for sedation had transient hypoxia requiring an intervention. Although ACEP clinical policy gave propofol sedation in the ED a Level B safety recommendation (meaning it was considered safer than etomidate), it is important to emphasize that propofol sedation should only be administered with physicians who have experience with emergent airways and are capable of intervening at a moment's notice. (Ann Emerg Med 2005;45[2]:177.)

It should be mentioned that all patients in this study had capnographic monitoring. ACEP clinical policy considers capnometry a Level C recommendation during procedural sedation. (Ann Emerg Med 2005;45[2]:177.) Capnometry may have alerted physicians of impending respiratory insufficiency, may have altered decision-making in this study, and may have played a role in the study outcome.

This article provides convincing data that administering high-flow oxygen during ED procedural sedation with propofol results in a significantly lower incidence of hypoxia. This benefit did not appear to come at the expense of other adverse events.

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▪ Read an abstract of the Annals of Emergency Medicine article, “The Utility of High-Flow Oxygen during Emergency Department Procedural Sedation and Analgesia with Propofol: A Randomized, Controlled Trial,” at http://bit.ly/HighFlow.

▪ Read all of Dr. Lovato's past columns in the EM-News.com archive.

▪ Comments about this article? Write to EMN at emn@lww.com.

© 2012 Lippincott Williams & Wilkins, Inc.

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