Abstract
Normovolemic hemodilution can progress to a classic form of hypoxia called anemic anoxia in the terminology first used by Barcroft (1920). It differs from anoxic anoxia, or hypoxic hypoxia in more modern terminology, in that arterial PO2 can be quite normal but the arterial O2 concentration is rower than normal. The question naturally arises, therefore, of why one would intentionally hemodilute in a clinical setting. The reason becomes clearer when consideration isgiven to the desirability of sparing as much as possible the use of allogeneic blood because of its additional risk factors. Furthermore, hemodilution within specified limits may actually be desirable by virtue of increased blood fluidity and consequently better tissue oxygenation under some circumstances. There is even evidence that tissue PO2 in various organ systems may actually increase with mild hemodilution (Messmer et al., 1973). Given the desirability of preoperative autologous blood donation and/or volume expansion with cell-free diluents such as dextran, albumin, and hetastarch, it is worthwhile to ask what the lower limits of hemodilution might be. Such limits are set to some extent by the ability of the body to compensate for the decrease in oxygen carrying capacity. The nature of those compensatory actions, their effectiveness, and the net effect upon tissue oxygenation in health and disease states are the topics that will be discussed.
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© 1994 Springer Science+Business Media New York
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Cain, S.M. (1994). Oxygen Delivery and Intentional Hemodilution. In: Hogan, M.C., Mathieu-Costello, O., Poole, D.C., Wagner, P.D. (eds) Oxygen Transport to Tissue XVI. Advances in Experimental Medicine and Biology, vol 361. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1875-4_45
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DOI: https://doi.org/10.1007/978-1-4615-1875-4_45
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