• Richard B Weiskopf, Pearl Toy, Harriet W Hopf, John Feiner, Heather E Finlay, Michelle Takahashi, Alan Bostrom, Christopher Songster, and Michael J Aminoff.
• Departments of Anesthesia and Physiology, Cardiovascular Research Institute, University of California, San Francisco, 94143-0648, USA. rbw@itsa.ucsf.edu
• Clin Neurophysiol. 2005 May 1;116(5):1028-32.

ObjectiveAcute anemia slows the responses to clinical tests of cognitive function. We tested the hypothesis that these slowed responses during acute severe isovolemic anemia in healthy unmedicated humans result from impaired central processing.MethodsA blinded operator measured the latency of the P300 peak in nine healthy volunteers at each volunteer's baseline hemoglobin concentration (Hb), and again after isovolemic hemodilution to Hb 5 g/dL. At both Hb concentrations, the P300 latency was measured twice: with the blinded subject breathing air or 100% oxygen, administered in random order.ResultsAnemia increased P300 latency significantly from baseline values (P < 0.05). Breathing oxygen during induced anemia resulted in a P300 latency not different from that at baseline when breathing air (P = 0.5) or oxygen (P = 0.8).ConclusionsImpaired central processing is, at least in part, responsible for the slowed responses and deficits of cognitive function that occur during acute isovolemic anemia at Hb 5-6 g/dL.SignificanceThe P300 latency appears to be a potential measure of inadequate central oxygenation. In healthy young adults with acute anemia, erythrocytes should be transfused to produce Hb>5-6 g/dL. As a temporizing measure, administration of oxygen can reverse the cognitive deficits and impaired central processing associated with acute anemia.

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