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Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial

PURPOSE: We assessed the effects of targeting low-normal or high-normal arterial carbon dioxide tension (PaCO(2)) and normoxia or moderate hyperoxia after out-of-hospital cardiac arrest (OHCA) on markers of cerebral and cardiac injury. METHODS: Using a 2(3) factorial design, we randomly assigned 123...

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Autores principales: Jakkula, Pekka, Reinikainen, Matti, Hästbacka, Johanna, Loisa, Pekka, Tiainen, Marjaana, Pettilä, Ville, Toppila, Jussi, Lähde, Marika, Bäcklund, Minna, Okkonen, Marjatta, Bendel, Stepani, Birkelund, Thomas, Pulkkinen, Anni, Heinonen, Jonna, Tikka, Tuukka, Skrifvars, Markus B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6280824/
https://www.ncbi.nlm.nih.gov/pubmed/30430209
http://dx.doi.org/10.1007/s00134-018-5453-9
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author Jakkula, Pekka
Reinikainen, Matti
Hästbacka, Johanna
Loisa, Pekka
Tiainen, Marjaana
Pettilä, Ville
Toppila, Jussi
Lähde, Marika
Bäcklund, Minna
Okkonen, Marjatta
Bendel, Stepani
Birkelund, Thomas
Pulkkinen, Anni
Heinonen, Jonna
Tikka, Tuukka
Skrifvars, Markus B.
author_facet Jakkula, Pekka
Reinikainen, Matti
Hästbacka, Johanna
Loisa, Pekka
Tiainen, Marjaana
Pettilä, Ville
Toppila, Jussi
Lähde, Marika
Bäcklund, Minna
Okkonen, Marjatta
Bendel, Stepani
Birkelund, Thomas
Pulkkinen, Anni
Heinonen, Jonna
Tikka, Tuukka
Skrifvars, Markus B.
author_sort Jakkula, Pekka
collection PubMed
description PURPOSE: We assessed the effects of targeting low-normal or high-normal arterial carbon dioxide tension (PaCO(2)) and normoxia or moderate hyperoxia after out-of-hospital cardiac arrest (OHCA) on markers of cerebral and cardiac injury. METHODS: Using a 2(3) factorial design, we randomly assigned 123 patients resuscitated from OHCA to low-normal (4.5–4.7 kPa) or high-normal (5.8–6.0 kPa) PaCO(2) and to normoxia (arterial oxygen tension [PaO(2)] 10–15 kPa) or moderate hyperoxia (PaO(2) 20–25 kPa) and to low-normal or high-normal mean arterial pressure during the first 36 h in the intensive care unit. Here we report the results of the low-normal vs. high-normal PaCO(2) and normoxia vs. moderate hyperoxia comparisons. The primary endpoint was the serum concentration of neuron-specific enolase (NSE) 48 h after cardiac arrest. Secondary endpoints included S100B protein and cardiac troponin concentrations, continuous electroencephalography (EEG) and near-infrared spectroscopy (NIRS) results and neurologic outcome at 6 months. RESULTS: In total 120 patients were included in the analyses. There was a clear separation in PaCO(2) (p < 0.001) and PaO(2) (p < 0.001) between the groups. The median (interquartile range) NSE concentration at 48 h was 18.8 µg/l (13.9–28.3 µg/l) in the low-normal PaCO(2) group and 22.5 µg/l (14.2–34.9 µg/l) in the high-normal PaCO(2) group, p = 0.400; and 22.3 µg/l (14.8–27.8 µg/l) in the normoxia group and 20.6 µg/l (14.2–34.9 µg/l) in the moderate hyperoxia group, p = 0.594). High-normal PaCO(2) and moderate hyperoxia increased NIRS values. There were no differences in other secondary outcomes. CONCLUSIONS: Both high-normal PaCO(2) and moderate hyperoxia increased NIRS values, but the NSE concentration was unaffected. REGISTRATION: ClinicalTrials.gov, NCT02698917. Registered on January 26, 2016. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s00134-018-5453-9) contains supplementary material, which is available to authorized users.
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spelling pubmed-62808242018-12-26 Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial Jakkula, Pekka Reinikainen, Matti Hästbacka, Johanna Loisa, Pekka Tiainen, Marjaana Pettilä, Ville Toppila, Jussi Lähde, Marika Bäcklund, Minna Okkonen, Marjatta Bendel, Stepani Birkelund, Thomas Pulkkinen, Anni Heinonen, Jonna Tikka, Tuukka Skrifvars, Markus B. Intensive Care Med Original PURPOSE: We assessed the effects of targeting low-normal or high-normal arterial carbon dioxide tension (PaCO(2)) and normoxia or moderate hyperoxia after out-of-hospital cardiac arrest (OHCA) on markers of cerebral and cardiac injury. METHODS: Using a 2(3) factorial design, we randomly assigned 123 patients resuscitated from OHCA to low-normal (4.5–4.7 kPa) or high-normal (5.8–6.0 kPa) PaCO(2) and to normoxia (arterial oxygen tension [PaO(2)] 10–15 kPa) or moderate hyperoxia (PaO(2) 20–25 kPa) and to low-normal or high-normal mean arterial pressure during the first 36 h in the intensive care unit. Here we report the results of the low-normal vs. high-normal PaCO(2) and normoxia vs. moderate hyperoxia comparisons. The primary endpoint was the serum concentration of neuron-specific enolase (NSE) 48 h after cardiac arrest. Secondary endpoints included S100B protein and cardiac troponin concentrations, continuous electroencephalography (EEG) and near-infrared spectroscopy (NIRS) results and neurologic outcome at 6 months. RESULTS: In total 120 patients were included in the analyses. There was a clear separation in PaCO(2) (p < 0.001) and PaO(2) (p < 0.001) between the groups. The median (interquartile range) NSE concentration at 48 h was 18.8 µg/l (13.9–28.3 µg/l) in the low-normal PaCO(2) group and 22.5 µg/l (14.2–34.9 µg/l) in the high-normal PaCO(2) group, p = 0.400; and 22.3 µg/l (14.8–27.8 µg/l) in the normoxia group and 20.6 µg/l (14.2–34.9 µg/l) in the moderate hyperoxia group, p = 0.594). High-normal PaCO(2) and moderate hyperoxia increased NIRS values. There were no differences in other secondary outcomes. CONCLUSIONS: Both high-normal PaCO(2) and moderate hyperoxia increased NIRS values, but the NSE concentration was unaffected. REGISTRATION: ClinicalTrials.gov, NCT02698917. Registered on January 26, 2016. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s00134-018-5453-9) contains supplementary material, which is available to authorized users. Springer Berlin Heidelberg 2018-11-14 2018 /pmc/articles/PMC6280824/ /pubmed/30430209 http://dx.doi.org/10.1007/s00134-018-5453-9 Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/), which permits any noncommercial use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Original
Jakkula, Pekka
Reinikainen, Matti
Hästbacka, Johanna
Loisa, Pekka
Tiainen, Marjaana
Pettilä, Ville
Toppila, Jussi
Lähde, Marika
Bäcklund, Minna
Okkonen, Marjatta
Bendel, Stepani
Birkelund, Thomas
Pulkkinen, Anni
Heinonen, Jonna
Tikka, Tuukka
Skrifvars, Markus B.
Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial
title Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial
title_full Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial
title_fullStr Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial
title_full_unstemmed Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial
title_short Targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial
title_sort targeting two different levels of both arterial carbon dioxide and arterial oxygen after cardiac arrest and resuscitation: a randomised pilot trial
topic Original
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6280824/
https://www.ncbi.nlm.nih.gov/pubmed/30430209
http://dx.doi.org/10.1007/s00134-018-5453-9
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