Oximetry-Guided Reoxygenation Improves Neurological Outcome After Experimental Cardiac Arrest

Department of Surgery, University of Maryland, Baltimore, Baltimore, Maryland, United States
Stroke (Impact Factor: 5.72). 01/2007; 37(12):3008-13. DOI: 10.1161/01.STR.0000248455.73785.b1
Source: PubMed


Current guidelines suggest that cardiac arrest (CA) survivors should be ventilated with 100% O(2) after resuscitation. Breathing 100% O(2) may worsen neurological outcome after experimental CA. This study tested the hypothesis that graded reoxygenation, with oximetry guidance, can safely reduce FiO(2) after resuscitation, avoiding hypoxia while promoting neurological recovery.
Mature dogs underwent 10 minutes of CA and restoration of spontaneous circulation with 100% O(2.) Animals were randomized to 1-hour additional ventilation on 100% FiO(2) or to rapid lowering of arterial O(2) saturation to <96% but >94% with pulse oximeter guidance. Animals were awakened at hour 23, and the neurological deficit score (0=normal; 100=brain-dead) was measured. Reanesthetized animals were perfusion-fixed and the brains removed for histopathology.
The neurological deficit score was significantly better in oximetry (O) dogs. O dogs appeared aware of their surroundings, whereas most hyperoxic (H) animals were stuporous (neurological deficit score=43.0+/-5.9 [O] versus 61.0+/-4.2 [H]; n=8, P<0.05). Stereological analysis revealed fewer injured CA1 neurons in O animals (cresyl violet: 35.5+/-4.3% [O] versus 60.5+/-3.3% [H]; P<0.05). There were also fewer fluoro-Jade B-stained degenerating CA1 neurons in O animals (3320+/-267 [O] versus 6633+/-356 [H] per 0.1 mm(3); P<0.001).
A clinically applicable protocol designed to reduce postresuscitative hyperoxia after CA results in significant neuroprotection. Clinical trials of controlled normoxia after CA/restoration of spontaneous circulation should strongly be considered.

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    • "Originally references " Balan et al, 2006; Brodbelt et al, 2008; Brücken et al, 2010; Fletcher et al, 2012; Hopper et al, 2012; Kilgannon et al, 2008; McMichael et al, 2012; Reynolds et al, 2007; Rozanski et al, 2012; Smarick et al, 2012 " were not cited in the text. Hence they have been combined with the citation of corresponding previous references. "
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    • "An example of how avoiding hyperoxia can provide neuroprotection comes from studies comparing neurochemical and neurologic outcomes after experimental cardiac arrest, for animals artificially ventilated using either 100% O 2 or 21% to 30% O 2 during the first hour of reperfusion . Compared with animals receiving normoxic resuscitation, those receiving hyperoxic ventilation display elevated markers of oxidative stress, e.g., nitrotyrosine, impaired mitochondrial respiration, inhibited pyruvate dehydrogenase enzyme activity, decreased cerebral aerobic energy metabolism, increased hippocampal neuronal death, and worse neurologic outcome (Vereczki et al, 2005; Balan et al, 2006; Richards et al, 2007; Fiskum et al, 2008). These findings illustrate the concept that simple avoidance of unnecessarily high levels of O 2 can defend against oxidative stress-induced mitochondrial bioenergetic dysfunction and provide neuroprotection in a clinically relevant model of acute brain injury. "
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    • "Recently, higher survival rates have been reported for patients treated with therapeutic hypothermia after successful resuscitation from cardiac arrest [2] [3], confirming that patient outcome is determined not only by the time of circulation recovery but also by the pathophysiologic processes triggered by cardiac arrest. Other treatments, such as early hemodynamic optimization [1], controlled reoxygenation [4], supportive care, and disease-specific interventions guided by the patients' conditions, have potential benefit for patients with post– cardiac arrest syndrome. One possible benefit of the above treatments is the prevention of an increase in the oxygen debt and a decrease in the systemic and cerebral metabolic rates of oxygen consumption [5]. "
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