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Peer-reviewedCC BY 4.0PLOS One

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

  • Yongai Ling1
  • Xianwei Xiong2
  • Changsheng Ye3
  • Weiguang Wang
  1. 1Health Promotion Center, People’s Hospital of Anji, Huzhou, Zhejiang, China
  2. 2Department of Emergency Medicine, People’s Hospital of Anji, Huzhou, Zhejiang, China
  3. 3General Practice Department, People’s Hospital of Anji, Huzhou, Zhejiang, China
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Abstract

Introduction: 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. Methods: 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. Results: 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). Conclusion: 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.

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Cite

BibTeXRIS
BibTeX
@article{ling2026hypocapnia,
  title = {{Hypocapnia in acute carbon monoxide poisoning: A complex interaction beyond metabolic compensation}},
  author = {Yongai Ling and Xianwei Xiong and Changsheng Ye and Weiguang Wang},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0356796},
  url = {https://doi.org/10.1371/journal.pone.0356796},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Hypocapnia in acute carbon monoxide poisoning: A complex interaction beyond metabolic compensation
AU  - Yongai Ling
AU  - Xianwei Xiong
AU  - Changsheng Ye
AU  - Weiguang Wang
PY  - 2026
DA  - 2026/09/08
JO  - PLOS One
DO  - 10.1371/journal.pone.0356796
UR  - https://doi.org/10.1371/journal.pone.0356796
AB  - Introduction: 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. Methods: 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. Results: 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). Conclusion: 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.
SN  - 1932-6203
ER  -