Gallen, Switzerland) between January 1st of 2014 and December 31st of 2019. This retrospective observational single-center cohort study included all consecutive patients with TBI who were intubated on the scene and transported by the helicopter emergency medical service (HEMS) (Swiss Air-Rescue, Rega) to a Level 1 trauma center (Kantonsspital St. Study participants, setting and ethics approval Furthermore, we investigated the predictive value of tension difference of CO 2 between EtCO 2 and PaCO 2 (CO 2 gap) for in-hospital mortality. The primary aim of this study is to describe the correlation between EtCO 2 and PaCO 2 at the time of admission in patients hospitalized with TBI. As expected, subgroup analyses have shown the best correlation between EtCO 2 and PaCO 2 in isolated TBI when compared to other trauma patients 20. However, major trauma accompanying TBI can negatively influence ventilation and perfusion, making the interpolation of PaCO 2 from EtCO 2 in trauma patients unreliable 17, 18, 19. The assumed correlation between EtCO 2 and PaCO 2 has been known to be accompanied by a tension difference of CO 2 ranging anywhere between 0.26 and 0.66 kPa (2 and 5 mmHg) in otherwise healthy individuals undergoing anesthesia 11, 12, 13, 14, 15, 16. Therefore end-tidal CO 2 (EtCO 2) determined by capnography has been used as a surrogate marker to estimate PaCO 2 assuming a reliable correlation between EtCO 2 and PaCO 2 8.Ĭapnography is considered the gold standard, both to determine correct placement of a definitive airway and to guide ventilation during emergency care 9, 10. Using PaCO 2 to monitor ventilation requires arterial blood gas (ABG) analyses, but the necessary lab equipment is not yet widely available in the prehospital environment. The effects of hypo- or hyperventilation on cerebral blood flow (CBF), with the potential for hypoxemia or hyperemia of cerebral tissue and their negative impact on outcome, have been widely studied 3, 4, 5, 6, 7. Treatment recommendations in traumatic brain injury (TBI) include early definitive airway protection as well as normoventilation with a target arterial partial pressure of CO 2 (PaCO 2) of 4.6–5.9 kPa (35–45 mmHg) 1, 2. The CO2 gap can lead to iatrogenic hypoventilation when normocapnic ventilation is aimed and might thereby increase in-hospital mortality. ![]() EtCO 2 was significantly lower than PaCO 2, making it an unreliable proxy for PaCO 2 when aiming for normocapnic ventilation. 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. 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). 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 correlation between EtCO 2 and PaCO 2 at admission was low (Pearson's r = .287). 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. 105 patients were included in this study. 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. 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 whether the difference between end tidal CO 2 and PaCO 2 at hospital admission is associated with in-hospital mortality. These are currently guided by end tidal CO 2 as a proxy for PaCO 2. Early definitive airway protection and normoventilation are key principles in the treatment of severe traumatic brain injury.
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