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.

Abstract

In a previous study, low and high-normal arterial carbon dioxide tension (PaCO₂) were not associated with serum neuron-specific enolase (NSE) in cardiac arrest survivors. We assessed the effect of PaCO₂ on NSE in cerebrospinal fluid (CSF) and serum. This was a retrospective study. PaCO₂ 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 (LCO₂) and high PaCO₂ (HCO₂) groups defined as PaCO₂ ≤ 35.3 and PaCO₂ > 43.5 mmHg, respectively. NSE was measured at 24, 48, and 72 h (sNSE_24,48,72 and cNSE_24,48,72) from return of spontaneous circulation (ROSC). The primary outcome was the association between PaCO₂ and the NSE measured at 24 h after ROSC. Forty-two subjects (male, 33; 78.6%) were included in total cohort. PaCO₂ in TWA subgroup was associated with cNSE_24,48,72, while PaCO₂ in the other subgroup were only associated with cNSE₂₄. PaCO₂ 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 PaCO₂ in all analysis. Poor neurological outcome in LCO₂ was significantly higher than HCO₂ in qES, TWA, and median subgroups (p < 0.01, p < 0.01, and p = 0.02). Association was found between NSE and PaCO₂ using CSF, despite including normocapnic ranges; TWA of PaCO₂ may be most strongly associated with CSF NSE levels. A prospective, multi-centre study is required to confirm our results.