End-tidal to arterial carbon dioxide gradient is associated with increased mortality in patients with traumatic brain injury: a retrospective observational study

• Published in: Scientific reports Vol. 11; no. 1; p. 10391
• Main Authors: Doppmann, Pascal, Meuli, Lorenz, Sollid, Stephen J. M., Filipovic, Miodrag, Knapp, Jürgen, Exadaktylos, Aristomenis, Albrecht, Roland, Pietsch, Urs
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 17.05.2021; Nature Publishing Group; Nature Portfolio
• Subjects: 692/308; 692/699; Adult; Aged; Brain Injuries, Traumatic - metabolism; Brain Injuries, Traumatic - mortality; Brain Injuries, Traumatic - pathology; Carbon dioxide; Carbon Dioxide - isolation & purification; Carbon Dioxide - metabolism; Emergency Medical Services; Female; Hospital Mortality; Humanities and Social Sciences; Humans; Hypoventilation; Male; Middle Aged; Mortality; multidisciplinary; Observational studies; Patients; Regression analysis; Respiration; Respiration, Artificial - adverse effects; Retrospective Studies; Science; Science (multidisciplinary); Tidal Volume - physiology; Traumatic brain injury; Ventilation
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-021-89913-x

Early definitive airway protection and normoventilation are key principles in the treatment of severe traumatic brain injury. These are currently guided by end tidal CO 2 as a proxy for PaCO 2 . We assessed whether the difference between end tidal CO 2 and PaCO 2 at hospital admission is associated with in-hospital mortality. We conducted a retrospective observational cohort study of consecutive patients with traumatic brain injury who were intubated and transported by Helicopter Emergency Medical Services to a Level 1 trauma center between January 2014 and December 2019. We assessed the association between the CO 2 gap—defined as the difference between end tidal CO 2 and PaCO 2 —and in-hospital mortality using multivariate logistic regression models. 105 patients were included in this study. The mean ± SD CO 2 gap at admission was 1.64 ± 1.09 kPa and significantly greater in non-survivors than survivors (2.26 ± 1.30 kPa vs. 1.42 ± 0.92 kPa, p < .001). The correlation between EtCO 2 and PaCO 2 at admission was low (Pearson's r = .287). The mean CO 2 gap after 24 h was only 0.64 ± 0.82 kPa, and no longer significantly different between non-survivors and survivors. The multivariate logistic regression model showed that the CO 2 gap was independently associated with increased mortality in this cohort and associated with a 2.7-fold increased mortality for every 1 kPa increase in the CO 2 gap (OR 2.692, 95% CI 1.293 to 5.646, p = .009). This study demonstrates that the difference between EtCO 2 and PaCO 2 is significantly associated with in-hospital mortality in patients with traumatic brain injury. EtCO 2 was significantly lower than PaCO 2 , making it an unreliable proxy for PaCO 2 when aiming for normocapnic ventilation. The CO2 gap can lead to iatrogenic hypoventilation when normocapnic ventilation is aimed and might thereby increase in-hospital mortality.