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(Stroke. 2006;37:3008.)
© 2006 American Heart Association, Inc.

Original Contributions

Oximetry-Guided Reoxygenation Improves Neurological Outcome After Experimental Cardiac Arrest

Irina S. Balan, PhD; Gary Fiskum, PhD; Julie Hazelton, MS; Cynthia Cotto-Cumba, MD Robert E. Rosenthal, MD

From the Departments of Anesthesiology (I.S.B., G.F., J.H., R.E.R.) and Surgery (C.C.-C., R.E.R.), Program in Trauma, University of Maryland School of Medicine, Baltimore, Md.

Correspondence to Robert E. Rosenthal, MD, Section of Hyperbaric Medicine, R. Adams Cowley Shock Trauma Center, University of Maryland Medical Center, 22 S Greene St, Baltimore, MD 21201. E-mail rrosenthal{at}umm.edu

Background and Purpose— Current guidelines suggest that cardiac arrest (CA) survivors should be ventilated with 100% O₂ after resuscitation. Breathing 100% O₂ may worsen neurological outcome after experimental CA. This study tested the hypothesis that graded reoxygenation, with oximetry guidance, can safely reduce FiO₂ after resuscitation, avoiding hypoxia while promoting neurological recovery.

Methods— Mature dogs underwent 10 minutes of CA and restoration of spontaneous circulation with100% O_2. Animals were randomized to 1-hour additional ventilation on 100% FiO₂ or to rapid lowering of arterial O₂ 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.

Results— 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 mm³; P<0.001).

Conclusions— 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.

Key Words: canine model • cerebral ischemia • neurological deficit • oxygen utilization

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