Abstract Body: Introduction
The difference between jugular venous and arterial carbon dioxide (CO₂) tension, the cerebral CO₂ gap reflects the coupling of cerebral perfusion to metabolism. When interpreted with jugular venous oxygen saturation (SjvO₂), the cerebral CO₂ gap may provide a nuanced understanding of hypoxic-ischemic brain injury (HIBI) pathophysiology.
Hypotheses
We hypothesized cerebral CO₂ gap could identify patients with abnormally elevated SjvO₂ responsive to treatment with hypertonic saline (HTS). Secondarily, we hypothesized CO₂ gap would be associated with electrographic and radiographic markers of HIBI severity.
Methods
This was a retrospective, single center study including post-cardiac arrest patients who had jugular bulb venous catheters placed for SjvO₂ monitoring. We quantified the relationship between CO₂ and SjvO₂ using hierarchical linear regression, adjusting for mean arterial pressure, partial pressure of oxygen, and temperature. Among patients with pathologically elevated SjvO₂, we tested if CO₂ gap predicted response to HTS (an indicator of diffusion-limited hypoxia) using an interaction between treatment and CO₂ gap dichotomized as normal or high (<=6 or >6 mmHg). Finally, we assessed the association between CO₂ gap and burst-suppression with identical bursts (BSIB) and grey-white ratio (GWR).
Results
Among 109 patients, cerebral CO₂ gap was significantly lower among patients with normal (β = -4.3; 95% CI, -5.6 to -3.1; p < 0.001) or high SjvO₂ (β = -7.8; 95% CI, -9.1 to -6.6; p < 0.001) compared to low SjvO₂ (Fig 1). Treatment with HTS was associated with a 14.4 mmHg decrease in SjvO₂ (95% CI, -18.4 to -10.4) among those with a high CO₂ gap, whereas SjvO₂ did not change in those with a normal CO₂ gap (Fig 2). CO₂ gap was lower among patients with BISB compared to those without BSIB (β = -1.8; 95% CI, -2.8 to -0.9; p < 0.001), but there was no association between CO₂ gap and GWR.
Conclusion
Cerebral CO₂ gap increased as SjvO₂ decreased. However, elevated CO₂ gap occurred even when SjvO₂ was normal or low, suggesting global cerebral perfusion may not be the sole determinant of CO₂ gap. Additionally, the CO₂ gap was significantly lower among those with EEG features of severe HIBI and those whose SjvO₂ failed to decrease in response to treatment with HTS. These findings suggest the CO₂ gap, combined with SjvO₂, may identify cerebral pathophysiology beyond inadequate oxygen delivery and be a useful adjunct to discern treatment-responsive phenotypes.