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J Appl Physiol 83: 240-246, 1997;
8750-7587/97 $5.00
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Journal of Applied Physiology
Vol. 83, No. 1, pp. 240-246, July 1997
GAS EXCHANGE, MECHANICS, AND AIRWAYS

CO2 transport in normovolemic anemia: complete compensation and stability of blood CO2 tensions

Steven Deem, Michael K. Alberts, Michael J. Bishop, Akhil Bidani, and Erik R. Swenson

Departments of Anesthesiology and Medicine, University of Washington, Seattle, 98195; Anesthesiology and Medical Services, Veterans Affairs Medical Center, Seattle, Washington 98108; and Department of Medicine, University of Texas Medical Branch, Galveston, Texas 77550

Received 20 September 1996; accepted in final form 7 March 1997.

Deem, Steven A., Michael K. Alberts, Michael J. Bishop, Akhil Bidani, and Erik R. Swenson. CO2 transport in normovolemic anemia: complete compensation and stability of blood CO2 tensions. J. Appl. Physiol. 83(1): 240-246, 1997.---Isovolemic hemodilution does not appear to impair CO2 elimination nor cause CO2 retention despite the important role of red blood cells in blood CO2 transport. We studied this phenomenon and its physiological basis in eight New Zealand White rabbits that were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Isovolemic anemia was induced by simultaneous blood withdrawal and infusion of 6% hetastarch in sequential stages; exchange transfusions ranged from 15-30 ml in volume. Variables measured after each hemodilution included hematocrit (Hct), arterial and venous blood gases, mixed expired PCO2 and PO2, and blood pressure; also, O2 consumption, CO2 production, cardiac output (Q), and physiological dead space were calculated. Data were analyzed by comparison of changes in variables with changes in Hct and by using the model of capillary gas exchange described by Bidani (J. Appl. Physiol. 70: 1686-1699, 1991). There was complete compensation for anemia with stability of venous and arterial PCO2 between Hct values of 36 ± 3 and 12 ± 1%, which was predicted by the mathematical model. Over this range of hemodilution, Q rose 50%, and the O2 extraction ratio increased 61% without a decline in CO2 production or a rise in alveolar ventilation. The dominant compensations maintaining CO2 transport in normovolemic anemia include an increased Q and an augmented Haldane effect arising from the accompanying greater O2 extraction.

anemia; carbon dioxide; hemodilution; pulmonary gas exchange




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