Background: Low-normal levels of arterial carbon dioxide (PaCO2) are recommended in the acute phase of traumatic brain injury (TBI) to optimize oxygen and CO2 tension, and to maintain cerebral perfusion. End-tidal CO2 (ETCO2) may be used as a surrogate for PaCO2 when arterial sampling is less readily available. ETCO2 may not be an adequate proxy to guide ventilation and the effects on concomitant injury, time, and the impact of ventilatory strategies on the PaCO2-ETCO2 gradient are not well understood. The primary objective of this study was to describe the correlation and agreement between PaCO2 and ETCO2 in intubated adult trauma patients with TBI.
Methods: This study was a retrospective analysis of prospectively-collected data of intubated adult major trauma patients with serious TBI, admitted to the East of England regional major trauma centre; 2015-2019. Linear regression and Welch's test were performed on each cohort to assess correlation between paired PaCO2 and ETCO2 at 24-hour epochs for 120 hours after admission. Bland-Altman plots were constructed at 24-hour epochs to assess the PaCO2-ETCO2 agreement.
Results: 695 patients were included, with 3812 paired PaCO2 and ETCO2 data points. The median PaCO2-ETCO2 gradient on admission was 0.8 [0.4-1.4] kPa, Bland Altman Bias of 0.96, upper (+2.93) and lower (-1.00), and correlation R2 0.149. The gradient was significantly greater in patients with TBI plus concomitant injury, compared to those with isolated TBI (0.9 [0.4-1.5] kPa vs. 0.7 [0.3-1.1] kPa, p<0.05). Across all groups the gradient reduced over time. Patients who died within 30 days had a larger gradient on admission compared to those who survived; 1.2 [0.7-1.9] kPa and 0.7 [0.3-1.2] kPa, p<0.005.
Conclusions: Amongst adult patients with TBI, the PaCO2-ETCO2 gradient was greater than previously reported values, particularly early in the patient journey, and when associated with concomitant chest injury. An increased PaCO2-ETCO2 gradient on admission was associated with increased mortality.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10836696 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0297113 | PLOS |
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Article Synopsis
- Cerebrovascular autoregulation (CA) can be disrupted after acute brain injuries, and different levels of carbon dioxide (PaCO₂) influence this regulation, though the specifics are not well understood.
- This study aimed to examine how changes in PaCO₂ affect pial vasodynamics using a porcine model, preparing for further research on cerebral blood flow (CBF) under varying PaCO₂ levels.
- Results showed that modifying respiratory rates to adjust PaCO₂ was effective, and while there were changes in pial arteriolar diameter with PaCO₂ variations, significant vasodilation only occurred in a hypercapnic environment, indicating a non-linear relationship.
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