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How to treat combined respiratory and metabolic acidosis after extracorporeal cardiopulmonary resuscitation?
Critical Care volume 23, Article number: 183 (2019)
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 . It is clear that acidosis negatively impacts survival after eCPR  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 . This recommendation is based on heterogeneous data. While a recent meta-analysis found adverse outcome in both hyper- and hypocapnia , a randomized trial reported no difference in survival in low normal and high normal paCO2 .
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 ± 7.42 mmHg/7.31 ± 0.11 (+ 6 h), 38.62 ± 7.26 mmHg/7.34 ± 0.10 (+ 12 h), and 38.22 ± 5.62 mmHg/7.38 ± 0.09 (+ 24 h), respectively. When comparing patients with paCO2 < 35, 35–45, and > 45 mmHg, 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 correlation with paCO2. Also elevated NSE as a marker for neural injury did correlate with pH but not with paCO2. Being a retrospective, observational, single-center study, inherent limitations and biases are to be presumed and findings are to be considered hypothesis generating. Until further data are available however, it might be reasonable to correct both respiratory and metabolic acidosis in eCPR patients.
Extracorporeal cardiopulmonary resuscitation
- paCO2 :
Partial pressure of carbon dioxide in arterial blood
Venoarterial extracorporeal membrane oxygenation
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This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.
Availability of data and materials
The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.
Ethics approval and consent to participate
This retrospective study was approved by the ethics committee of the University of Freiburg, Germany (525/17).
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The authors declare that they have no competing interests.
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This comment refers to the article available at https://doi.org/10.1186/cc9976
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Bemtgen, X., Schroth, F., Wengenmayer, T. et al. How to treat combined respiratory and metabolic acidosis after extracorporeal cardiopulmonary resuscitation?. Crit Care 23, 183 (2019). https://doi.org/10.1186/s13054-019-2461-2
- Carbon dioxide