Establishing a venoarterial extracorporeal membrane oxygenation (vaECMO) in cardiac arrest is known as extracorporeal cardiopulmonary resuscitation (eCPR). After eCPR, patients commonly present with a combined respiratory and metabolic acidosis [1].… Click to show full abstract
Establishing a venoarterial extracorporeal membrane oxygenation (vaECMO) in cardiac arrest is known as extracorporeal cardiopulmonary resuscitation (eCPR). After eCPR, patients commonly present with a combined respiratory and metabolic acidosis [1]. It is clear that acidosis negatively impacts survival after eCPR [2] and that a respiratory acidosis can be easily corrected by vaECMO. Current guidelines for conventional CPR suggest normocapnia as targeted after return of spontaneous circulation [3]. This recommendation is based on heterogeneous data. While a recent meta-analysis found adverse outcome in both hyperand hypocapnia [4], a randomized trial reported no difference in survival in low normal and high normal paCO2 [5]. The aim of the present study was to correlate arterial paCO2 and pH with hospital survival in eCPR. A single-center retrospective register analysis was performed. All eCPR patients treated between 2010 and 2017 were included. We analyzed arterial blood gases after 1 h, 3 h, 6 h, 12 h, and 24 h as well as hospital mortality. We detected a total of 186 eCPR. The mean age was 58.6 ± 14.9 years, and total hospital survival rate was 26.3%. After cannulation, paCO2 and pH values were (mean ± standard deviation) 38.3 ± 8.9 mmHg/7.28 ± 0.14 (+ 1 h), 38.5 ± 8.5 mmHg/7.30 ± 0.11 (+ 3 h), 38.72 ± 7.42mmHg/7.31 ± 0.11 (+ 6 h), 38.62 ± 7.26mmHg/7.34 ± 0.10 (+ 12 h), and 38.22 ± 5.62mmHg/ 7.38 ± 0.09 (+ 24 h), respectively. When comparing patients with paCO2 < 35, 35–45, and > 45mmHg, survival was statistically similar for all observed time points. There was however a highly significant association between hospital survival and pH when comparing groups with pH < 7.3, 7.3–7.4, and > 7.4 (see Fig. 1). As secondary endpoint and surrogate for neurological outcome, neuron-specific enolase (NSE) was analyzed. Maximum NSE measured within 72 h after eCPR was 150.8 ± 145.1 μg/l (mean ± standard deviation). When correlating maximum NSE with paCO2 at 1, 3, 6, 12, and 24 h after eCPR, no statistical significant linear correlation was found (p > 0.4 for all time points). There was however a significant linear correlation of maximum NSE and pH at 1, 3, and 6 h after eCPR (p = 0.037, 0.029, and 0.018, respectively). In this registry study, we found a strong correlation between hospital survival and arterial pH but no such
               
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