PURPOSE: Previous data indicate that 100% O(2) ventilation during early reperfusion after cardiac arrest (CA) and cardiopulmonary resuscitation (CPR) increases neuronal death. However, current guidelines encourage the use of 100% O(2) during resuscitation and for an undefined period thereafter. We retrospectively analyzed data from a porcine CA model and hypothesized that prolonged hyperoxic reperfusion would be associated with increased neurohistopathological damage and impaired neurological recovery.
METHODS: Fifteen male pigs underwent 8min of CA and 5min of CPR. After resuscitation animals were ventilated with either 100% oxygen for 60min (hyperoxia; n=8) or 10min (normoxia; n=7). Physiological variables were obtained at baseline and 10, 60 and 240min after resuscitation. Daily functional performance was assessed using an established neurocognitive test in parallel to a neurological deficit score (NDS). On day 5, brains of the re-anaesthetized pigs were harvested for neurohistopathological analyses.
RESULTS: At baseline there were no differences in hemodynamics and neurological status between groups. Post-arrest only PaO(2), as a result of the different inspired oxygen fractions, was significantly higher in the hyperoxia group. There was a numerical trend towards improved clinical recovery in both the NDS and the neurocognitive testing for animals exposed to 10min of 100% oxygen. However, hyperoxic animals showed a significantly greater degree of necrotic neurons and perivascular inflammation in the striatum in comparison to normoxic animals.
CONCLUSION: In this retrospective analysis prolonged hyperoxia after CA aggravated necrotic brain damage and perivascular inflammation in the striatum of pigs.
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doi:10.1016/j.resuscitation.2010.06.027 | How to Cite or Link Using DOI
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Reducing the duration of 100% oxygen ventilation in the early reperfusion period after cardiopulmonary resuscitation decreases striatal brain damagestar, open
Anne Brückena, 1, Corresponding Author Contact Information, E-mail The Corresponding Author, Aaref Bani Kaaba, 1, Kai Kottmanna, Rolf Rossainta, Kay Wilhelm Nolteb, Joachim Weisb and Michael Friesc
a Department of Anesthesiology, University Hospital RWTH Aachen, Pauwelsstraße 30, 52074 Aachen, Germany
b Institute of Neuropathology, University Hospital RWTH Aachen, Aachen, Germany
c Department of Intensive Care, University Hospital RWTH Aachen, Aachen, Germany
Received 10 May 2010;
revised 18 June 2010;
accepted 30 June 2010.
Available online 2 September 2010.