CO2 TRANSPORT IN NORMOVOLEMIC ANEMIA - COMPLETE COMPENSATION AND STABILITY OF BLOOD CO2 TENSIONS

Isovolemic hemodilution does not appear to impair CO2 elimination nor cause CO2 retention despite the important role of red blood cells in b lood CO2 transport. We studied this phenomenon and its physiological b asis in eight New Zealand White rabbits that were anesthetized, paraly zed, and mechanically ventilated at a fixed minute ventilation. Isovol emic anemia was induced by simultaneous blood withdrawal and infusion of 6% hetastarch in sequential stages; exchange transfusions ranged fr om 15-30 ml in volume. Variables measured after each hemodilution incl uded hematocrit (Hct), arterial and venous blood gases, mixed expired PCO2 and PO2, and blood pressure; also, O-2 consumption, CO2 productio n, cardiac output ((Q) over dot) and physiological dead space were cal culated. Data were analyzed by comparison of changes in variables with changes in Hct and by using the model of capillary gas exchange descr ibed by Bidani (J. Appl. Physiol. 70: 1686-1699, 1991). There was comp lete compensation for anemia with stability of venous and arterial PCO 2 between Hct values of 36 +/- 3 and 12 +/- 1%, which was predicted by the mathematical model. Over this range of hemodilution, (Q) over dot rose 50%, and the O-2 extraction ratio increased 61% without a declin e in CO2 production or a rise in alveolar ventilation. The dominant co mpensations maintaining CO2 transport in normovolemic anemia include a n increased (Q) over dot and an augmented Haldane effect arising from the accompanying greater O-2 extraction.