Confirmation of the Pulse Oximetry Gap in Carbon Monoxide Poisoning,☆☆,

Presented at the Society for Academic Emergency Medicine Annual Meeting, Denver, Colorado, May 1996.
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Abstract

Study objective: To demonstrate the degree to which pulse oximetry overestimates actual oxyhemoglobin (O 2Hb) saturation in patients with carbon monoxide (CO) poisoning. This phenomenon has been reported in fewer than 20 humans in the English medical literature. Methods: A retrospective chart review of 191 patients evaluated for CO poisoning at a regional hyperbaric center identified 124 patients 10 years of age and older who had had both arterial blood gas and pulse oximetry measurements and who had received either high-flow oxygen through a nonrebreather mask or 100% inspired oxygen through an endotracheal tube. Blood gas measurements, including direct spectrophotometric determination of O 2Hb and carboxyhemoglobin (COHb) saturation values, were compared with finger-probe pulse oximetry readings. Results: Measured O 2Hb saturation (mean±SD, 88.7±10.2%; range, 51.4% to 99.0%) decreased linearly and predictably with rising COHb levels (10.7±10.4%; range, .2% to 46.4%). Pulse oximetry saturation (99.2%±1.3%; range, 92% to 100%) remained elevated across the range of COHb levels and failed to detect decreased O 2Hb saturation. The pulse oximetry gap, defined as the difference between pulse oximetry saturation and actual O 2Hb saturation (10.5%±9.7%; range, 0% to 40.6%), approximated the COHb level. Conclusion: There is a linear decline in O 2Hb saturation as COHb saturation increases. This decline is not detected by pulse oximetry, which therefore overestimates O 2Hb saturation in patients with increased COHb levels. The pulse oximetry gap increases with higher levels of COHb and approximates the COHb level. In patients with possible CO poisoning, pulse oximetry must be considered unreliable and interpreted with caution until the COHb level has been measured. [Bozeman WP, Myers RAM, Barish RA: Confirmation of the pulse oximetry gap in carbon monoxide poisoning. Ann Emerg Med November 1997;30:608-611.]

Section snippets

INTRODUCTION

The development of pulse oximetry has had an enormous impact on the ability of physicians to safely and reliably monitor arterial oxyhemoglobin saturation noninvasively in most situations. However, the inability of pulse oximetry saturation measurements (Sao 2) to detect even markedly reduced true oxyhemoglobin (O 2Hb) saturation in the setting of carbon monoxide (CO) poisoning is an important physiologic principle that has been demonstrated in animals but reported infrequently in humans.

MATERIALS AND METHODS

The records of 191 patients evaluated for CO exposure at a regional trauma and hyperbaric referral center between July 1993 and June 1995 were retrospectively reviewed. Inclusion criteria were age 10 years or older, documented treatment with high-flow oxygen by reservoir-equipped nonrebreather mask (at 10 L/minute or greater) or with 100% inspired oxygen by endotracheal tube, pulse oximetry measurement, and arterial blood gas (ABG) measurement.

Exclusion criteria for this study were determined

RESULTS

From the 191 charts reviewed, full data from 124 patients meeting inclusion criteria were available and analyzed. Mean age was 40±16.8 years (range, 11 to 83 years). Seventy percent of patients were male, 30 percent were female.

Measured oxyhemoglobin saturation by ABG (88.7%± 10.2%; range, 51.4% to 99.0%) decreased linearly with rising COHb levels (10.7%±10.4%; range, .2% to 46.4%). A linear regression model was defined: O 2Hb Saturation= 99.0−(.95×COHb) (R2, .94; F, 2018; P<.0001; Figure 1).

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DISCUSSION

CO competitively inhibits oxygen binding by the hemoglobin molecule, producing a linear decline in O 2Hb saturation as COHb levels increase. Death from CO intoxication is thought to result from hypoxia and impaired tissue perfusion. Other mechanisms of toxicity, such as cellular toxicity due to cytochrome binding, free radical generation producing reperfusion injury, and brain lipid peroxidation, have also been implicated.7 The relative contribution of these mechanisms to CO toxicity remains an

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From the R Adams Cowley Shock Trauma Center, University of Maryland Medical System, Baltimore, Maryland.

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Reprint no. 47/1/85038

Address for reprints: William P Bozeman, MD, Division of Emergency Medicine, University of Florida Health Science Center/Jacksonville, 655 West Eighth Street, Jacksonville, FL 32209-6511

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