Oximetry-guided reoxygenation improves neurological outcome after experimental cardiac arrest

Abstract

Background and purpose: 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.

Methods: 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.

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 mm(3); 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.

Figures

Figure 1

Individual variation of NDSs 24 hours after CA/ROSC in animals ventilated with H or O protocols.

Figure 2

Cresyl violet (upper panel; white arrows denote necrotic neurons) or fluoro-Jade B (lower panel) staining demonstrates dying or degenerating neurons in the CA1 region of the dorsal hippocampus of sham (C, F), H (A, D), and O (B, E) ventilated dogs 24 hours after reperfusion.

Figure 3

Individual variation of neuronal injury in the dorsal CA1 region of the cresyl violet-stained hippocampus 24 hours after CA/ROSC.

Figure 4

Individual variation of neuronal injury in the dorsal CA1 region of the fluoro-Jade B-stained hippocampus 24 hours after CA/ROSC.