ArticlePloS one2026
Hypocapnia in acute carbon monoxide poisoning: A complex interaction beyond metabolic compensation.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionAcute carbon monoxide poisoning frequently induces complex acid-base disturbances; however, whether hypocapnia serves solely as a compensatory response to metabolic acidosis or involves additional factors remains insufficiently characterized.
methodsWe retrospectively analyzed 940 emergency department patients with acute carbon monoxide poisoning (January 2019-February 2025), stratified by base excess into an acidosis group (<-3 mmol/L) and a non-acidosis group (≥ -3 mmol/L). Group comparisons used Mann-Whitney U tests, Spearman's correlations assessed bivariate relationships, and hierarchical regression modeled PaCO2 determinants.
resultsThe acidosis group (n = 169) showed higher carboxyhemoglobin (26.5% vs. 21.6%) and lactate (4.4 vs. 1.7 mmol/L), and lower pH (7.37 vs. 7.41) and PaCO2 (33 vs. 39 mmHg) (all P < 0.001). Base excess correlated positively with PaCO2 (ρ = 0.489) and pH (ρ = 0.498), and negatively with lactate (ρ = -0.414) (all P < 0.001). Base excess was the strongest independent predictor of PaCO2 (β = 0.866), with each 1 mmol/L decrease associated with a 1.57 mmHg reduction (95% CI: 1.47-1.68). These associations were more pronounced in acidotic patients (β = 1.289 vs. 0.453) and males (β = 1.106 vs. 0.750). Curve-fitting showed only a modest linear relationship (R2 = 0.211).
conclusionIn acute carbon monoxide poisoning, metabolic acidosis is associated with hypocapnia, but the relationship is modest and context-dependent. The limited linear association between base excess and PaCO2, together with effect modification by acidosis status and sex, indicates hypocapnia involves factors beyond simple metabolic compensation.
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