Hypocapnia in acute carbon monoxide poisoning: A complex interaction beyond metabolic compensation.

Abstract

Acute 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. We 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. The 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). In 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.