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Clinical Investigations in Critical Care |

Carboxyhemoglobin Half-life in Carbon Monoxide-Poisoned Patients Treated With 100% Oxygen at Atmospheric Pressure*

Lindell K. Weaver, MD, FCCP; Steve Howe, MA, MS; Ramona Hopkins, PhD; Karen J. Chan, BS
Author and Funding Information

*From the Hyperbaric Medicine and Pulmonary Division (Dr. Weaver and Mr. Howe) and the Statistical Data Center (Ms. Chan), LDS Hospital, Salt Lake City; and the Psychology Department (Dr. Hopkins), Brigham Young University, Provo, UT.

Correspondence to: Lindell K. Weaver, MD, FCCP, Critical Care Medicine, LDS Hospital, Eighth Ave and C St, Salt Lake City, UT 84143; e-mail: lweaver@ihc.com



Chest. 2000;117(3):801-808. doi:10.1378/chest.117.3.801
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Study objectives: There are large reported differences for the carboxyhemoglobin (COHb) half-life (COHb t1/2) in humans breathing 100% atmospheric O2 following CO inhalation in tightly controlled experiments compared to the COHb t1/2 observed in clinical CO poisoning (range, 36 to 131 min, respectively). Other reports have suggested that the COHb t1/2 may be affected by gender differences, age, and lung function. We wished to test the hypothesis that the COHb t1/2 might also be influenced by CO poisoning vs experimental CO exposure, by a history of loss of consciousness (LOC), concurrent tobacco smoking, and by Pao2. The purpose of the present study was to measure the COHb t1/2 in a cohort of CO-poisoned patients and to determine if those listed factors influenced the COHb t1/2.

Design: Retrospective chart review from 1985 to 1995. We calculated the COHb t1/2 of CO-poisoned patients who were treated with high-flow supplemental atmospheric pressure O2 delivered by nonrebreather face mask or endotracheal tube.

Setting: Hyperbaric medicine department of a tertiary-care teaching hospital.

Patients: Of 240 CO-poisoned patients, 93 had at least two COHb measurements > 2% (upper limit of normal) with recorded times of the measurements, permitting calculation of the COHb t1/2.

Results: The COHb t1/2 was 74 ± 25 min (mean ± 1 SD) with a range from 26 to 148 min. By stepwise multiple linear regression analysis, the Pao2 influenced the COHb t1/2 (R2 = 0.19; p < 0.001), whereas the COHb t1/2 was not influenced by gender, age, smoke inhalation, history of LOC, concurrent tobacco smoking, degree of initial metabolic acidosis (base excess), or initial COHb level.

Conclusions: The COHb t1/2 of 93 CO-poisoned patients treated with 100% O2 at atmospheric pressure was 74 ± 25 min, considerably shorter than the COHb t1/2 reported in prior clinical reports (approximately 130 ± 130 min) and was influenced only by the patient’s Pao2.

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