Targeting low-normal or high-normal mean arterial pressure after cardiac arrest and resuscitation: a randomised pilot trial View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-12

AUTHORS

Pekka Jakkula, Ville Pettilä, Markus B. Skrifvars, Johanna Hästbacka, Pekka Loisa, Marjaana Tiainen, Erika Wilkman, Jussi Toppila, Talvikki Koskue, Stepani Bendel, Thomas Birkelund, Raili Laru-Sompa, Miia Valkonen, Matti Reinikainen, COMACARE study group

ABSTRACT

PURPOSE: We aimed to determine the feasibility of targeting low-normal or high-normal mean arterial pressure (MAP) after out-of-hospital cardiac arrest (OHCA) and its effect on markers of neurological injury. METHODS: In the Carbon dioxide, Oxygen and Mean arterial pressure After Cardiac Arrest and REsuscitation (COMACARE) trial, we used a 23 factorial design to randomly assign patients after OHCA and resuscitation to low-normal or high-normal levels of arterial carbon dioxide tension, to normoxia or moderate hyperoxia, and to low-normal or high-normal MAP. In this paper we report the results of the low-normal (65-75 mmHg) vs. high-normal (80-100 mmHg) MAP comparison. The primary outcome was the serum concentration of neuron-specific enolase (NSE) at 48 h after cardiac arrest. The feasibility outcome was the difference in MAP between the groups. Secondary outcomes included S100B protein and cardiac troponin (TnT) concentrations, electroencephalography (EEG) findings, cerebral oxygenation and neurological outcome at 6 months after cardiac arrest. RESULTS: We recruited 123 patients and included 120 in the final analysis. We found a clear separation in MAP between the groups (p < 0.001). The median (interquartile range) NSE concentration at 48 h was 20.6 µg/L (15.2-34.9 µg/L) in the low-normal MAP group and 22.0 µg/L (13.6-30.9 µg/L) in the high-normal MAP group, p = 0.522. We found no differences in the secondary outcomes. CONCLUSIONS: Targeting a specific range of MAP was feasible during post-resuscitation intensive care. However, the blood pressure level did not affect the NSE concentration at 48 h after cardiac arrest, nor any secondary outcomes. More... »

PAGES

2091-2101

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00134-018-5446-8

DOI

http://dx.doi.org/10.1007/s00134-018-5446-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1109912634

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30443729


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