Assessment of end-tidal CO₂ levels in the diagnosis and management of patients with pulmonary embolism
- 1Department of Pulmonary Diseases, Ataturk University School of Medicine, Yakutiye, Erzurum, 25240 Turkey
- 2Department of Pulmonary Diseases, Aksaray University School of Medicine, Aksaray, Turkey
- 3Department of Radiology, Ataturk University School of Medicine, Yakutiye, Erzurum, 25240 Turkey
Abstract
Background: Pulmonary embolism (PE) is a life-threatening emergency associated with acute cardiopulmonary deterioration. This study evaluated the clinical utility of end-tidal carbon dioxide (EtCO₂) for assessing disease severity and monitoring treatment response in high- and intermediate–high-risk PE.
Methods: This prospective study (registry ID: NCT07241130) included 120 individuals presenting between February and July 2025, categorized into four groups: high-risk PE with thrombolysis, intermediate–high-risk PE with thrombolysis, intermediate–high-risk PE without thrombolysis, and healthy controls. Physiological parameters were measured using the Rad-97 monitor under standardized conditions.
Results: Baseline EtCO₂ levels differed significantly among the groups (p < 0.001). The lowest mean EtCO₂ value was observed in the high-risk PE group (15.2 ± 1.9 mmHg) and the highest in the control group (31.8 ± 3.1 mmHg). After 24 h of treatment, there were no significant differences among the groups in terms of EtCO₂, peripheral oxygen saturation (SpO₂), or perfusion index (PI) values (p > 0.05). EtCO₂ was negatively correlated with pulmonary artery obstruction index (r = − 0.358, p = 0.01) and positively correlated with SpO₂ (r = 0.594, p < 0.001) and PI (r = 0.431, p < 0.001). ROC analysis identified an optimum EtCO₂ cutoff of 17.5 mmHg to discriminate between patients with and without thrombolytic therapy (97% sensitivity, 85% specificity).
Conclusion: EtCO₂ is a simple, noninvasive physiological marker associated with thrombus burden and treatment-related changes in PE. Rather than determining therapeutic decisions, EtCO₂ may complement established clinical and imaging parameters by providing supportive physiological information in acute settings.
Clinical trial number: ClinicalTrials.gov Identifier: NCT07241130. Retrospectively registered.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12890-026-04570-y.
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BibTeX
@article{celik2026assessment,
title = {{Assessment of end-tidal CO₂ levels in the diagnosis and management of patients with pulmonary embolism}},
author = {Kadir Çelik and Buğra Kerget and Alperen Aksakal and Elif Yılmazel Uçar and Mustafa Yeşilyurt and Leyla Sağlam},
journal = {BMC Pulmonary Medicine},
year = {2026},
month = aug,
doi = {10.1186/s12890-026-04570-y},
url = {https://doi.org/10.1186/s12890-026-04570-y},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Assessment of end-tidal CO₂ levels in the diagnosis and management of patients with pulmonary embolism
AU - Kadir Çelik
AU - Buğra Kerget
AU - Alperen Aksakal
AU - Elif Yılmazel Uçar
AU - Mustafa Yeşilyurt
AU - Leyla Sağlam
PY - 2026
DA - 2026/08/07
JO - BMC Pulmonary Medicine
DO - 10.1186/s12890-026-04570-y
UR - https://doi.org/10.1186/s12890-026-04570-y
AB - Background: Pulmonary embolism (PE) is a life-threatening emergency associated with acute cardiopulmonary deterioration. This study evaluated the clinical utility of end-tidal carbon dioxide (EtCO₂) for assessing disease severity and monitoring treatment response in high- and intermediate–high-risk PE. Methods: This prospective study (registry ID: NCT07241130) included 120 individuals presenting between February and July 2025, categorized into four groups: high-risk PE with thrombolysis, intermediate–high-risk PE with thrombolysis, intermediate–high-risk PE without thrombolysis, and healthy controls. Physiological parameters were measured using the Rad-97 monitor under standardized conditions. Results: Baseline EtCO₂ levels differed significantly among the groups (p < 0.001). The lowest mean EtCO₂ value was observed in the high-risk PE group (15.2 ± 1.9 mmHg) and the highest in the control group (31.8 ± 3.1 mmHg). After 24 h of treatment, there were no significant differences among the groups in terms of EtCO₂, peripheral oxygen saturation (SpO₂), or perfusion index (PI) values (p > 0.05). EtCO₂ was negatively correlated with pulmonary artery obstruction index (r = − 0.358, p = 0.01) and positively correlated with SpO₂ (r = 0.594, p < 0.001) and PI (r = 0.431, p < 0.001). ROC analysis identified an optimum EtCO₂ cutoff of 17.5 mmHg to discriminate between patients with and without thrombolytic therapy (97% sensitivity, 85% specificity). Conclusion: EtCO₂ is a simple, noninvasive physiological marker associated with thrombus burden and treatment-related changes in PE. Rather than determining therapeutic decisions, EtCO₂ may complement established clinical and imaging parameters by providing supportive physiological information in acute settings. Clinical trial number: ClinicalTrials.gov Identifier: NCT07241130. Retrospectively registered. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12890-026-04570-y.
SN - 1471-2466
ER -