CO2transport in normovolemic anemia: complete compensation and stability of blood CO2tensions

Abstract

Deem, Steven A., Michael K. Alberts, Michael J. Bishop, Akhil Bidani, and Erik R. Swenson.CO2transport in normovolemic anemia: complete compensation and stability of blood CO2tensions. J. Appl. Physiol. 83(1): 240–246, 1997.—Isovolemic hemodilution does not appear to impair CO2elimination nor cause CO2retention despite the important role of red blood cells in blood CO2transport. 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[Formula: see text] and[Formula: see text], and blood pressure; also, O2consumption, CO2production, 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 [Formula: see text]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 O2extraction ratio increased 61% without a decline in CO2production or a rise in alveolar ventilation. The dominant compensations maintaining CO2transport in normovolemic anemia include an increasedQ˙ and an augmented Haldane effect arising from the accompanying greater O2extraction.