Confirmation of the Pulse Oximetry Gap in Carbon Monoxide Poisoning☆,☆☆,★
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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).
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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Cited by (0)
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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
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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