Velocity of CO₂ exchange in blood

Carbon dioxide exchange involves multiple interrelated processes. Approximately half of CO₂ exchange is independent of oxygen exchange and is initiated as soon as blood enters the capillary. The hydration-dehydration reaction initially limits the velocity of CO₂ exchange in blood, but shortly thereafter the transmembrane exchange of bicarbonate and chloride ions emerges as the major factor affecting the rate of CO₂ movement. The remainder of CO₂ exchange, which is dependent upon prior oxygenation of hemoglobin, is achieved via oxylabile carbamate and oxylabile bicarbonate pathways. The carbamate pathway is of lesser importance. Oxylabile bicarbonate exchange occurs as a result of the liberation of Bohr protons that accompanies oxygenation of hemoglobin. The series of reactions involved in this pathway are similar to those involved in non-oxygen-dependent bicarbonate exchange, except that prior oxygenation of hemoglobin is required. CO₂ exchange via both oxylabile pathways may not reach completion during capillary transit, especially if oxygenation is delayed. The kinetics of CO₂ reactions depend critically upon the length of time blood spends in the capillary bed. During CO₂ uptake in tissues, capillary transit times are usually somewhat greater than during CO₂ unloading in the lung. Therefore, any limitation of CO₂ exchange that might occur on a kinetic basis would probably occur in the lung as opposed to peripheral tissues. Exercising muscle may provide a possible exception to this general role. Finally, relatively little experimental data have been acquired in vivo. Diffusion and convective mixing in the capillary itself have not been studied extensively. These factors may have a substantial effect on the velocity of CO₂ exchange in blood. Further study is needed in this area.