Impact of low and high partial pressure of carbon dioxide on neuron-specific enolase derived from serum and cerebrospinal fluid in patients who underwent targeted temperature management after out-of-hospital cardiac arrest: A retrospective study.

Aim: In a previous study, low and high-normal arterial carbon dioxide tension (PaCO) were not associated with serum neuron-specific enolase (NSE) in cardiac arrest survivors. We assessed the effect of PaCO on NSE in cerebrospinal fluid (CSF) and serum.

Methods: This was a retrospective study. PaCO for the first 24 h was analysed in four means, qualitative exposure state (qES), time-weighted average (TWA), median, and minimum-maximum (Min-Max). These subgroups were divided into low (LCO) and high PaCO (HCO) groups defined as PaCO ≤ 35.3 and PaCO > 43.5 mmHg, respectively. NSE was measured at 24, 48, and 72 h (sNSE and cNSE) from return of spontaneous circulation (ROSC). The primary outcome was the association between PaCO and the NSE measured at 24 h after ROSC.

Results: Forty-two subjects (male, 33; 78.6%) were included in total cohort. PaCO in TWA subgroup was associated with cNSE, while PaCO in the other subgroup were only associated with cNSE. PaCO and cNSE in qES subgroup showed good correlation (r = -0.61; p < 0.01), and in TWA, median, and Min-Max subgroup showed moderate correlations (r = -0.57, r = -0.48, and r = -0.60; p < 0.01). Contrastively, sNSE was not associated and correlated with PaCO in all analysis. Poor neurological outcome in LCO was significantly higher than HCO in qES, TWA, and median subgroups (p < 0.01, p < 0.01, and p = 0.02).

Conclusion: Association was found between NSE and PaCO using CSF, despite including normocapnic ranges; TWA of PaCO may be most strongly associated with CSF NSE levels. A prospective, multi-centre study is required to confirm our results.