Hypoxia and Postoperative Stroke: The Picture Is Still Not Clear

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The methodology and findings of the study by Dunham et al1 published in the July 2017 issue of Anesthesia & Analgesia do not support the concluding statement: “we believe our study provides valuable information about the possible role of hypoxia in the development of postoperative stroke,” for the following reasons:
The possibility of confounding decreases the confidence in accepting that a 10-mm Hg decrease in mean nadir PaO2 would result in a 23% increase in OR of stroke, and the nonlinear shape of the oxy-hemoglobin dissociation curve decreases the likelihood that such OR would be sustained across the whole range of PaO2 values. A potential risk of accepting the study findings and implementing them would be to aim to increase PaO2 values in an attempt to decrease stroke risk. A multicenter cohort study, found that, in ventilated stroke patients admitted to the intensive care unit, arterial hyperoxia (PaO2 ≥300 mm Hg) was independently associated with increased in-hospital death as compared with either hypoxia (PaO2 ≤60 mm Hg) or normoxia (PaO2 60–300 mm Hg).2 Further investigation is needed before any conclusions can be made about the association of hypoxia and postoperative stroke in cardiac surgery.

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