Carbon dioxide (CO2) is produced in tissues as a byproduct of normal metabolism. It dissolves in the solution of blood plasma and into red blood cells (RBC), where carbonic anhydrase catalyzes its hydration to carbonic acid (H2CO3). Carbonic acid then spontaneously dissociates to form bicarbonate Ions (HCO3−) and a hydrogen ion (H+). In response to the decrease in intracellular pCO2, more CO2 passively diffuses into the cell. Cell membranes are generally impermeable to charged ions (i.e. H+, HCO3− ) but RBCs are able to exchange bicarbonate for<unk>  using the anion exchanger protein Band 3. Thus, the rise in intracellular bicarbonate leads to bicarbonate export and<unk>  intake. The term<unk> " refers to this exchange. Consequently,<unk>  concentration is lower in systemic venous blood than in systemic arterial blood: high venous pCO2 leads to bicarbonate production in RBCs, which then leaves the RBC in exchange for<unk>  coming in. The opposite process occurs in the pulmonary capillaries of the lungs when the PO2 rises and PCO2 falls, and the Haldane effect occurs (release of CO2 from hemoglobin during oxygenation). This releases hydrogen ions from hemoglobin, increases free H+ concentration within RBCs, and<unk> s the equilibrium towards CO2 and water formation from bicarbonate. The subsequent decrease in intracellular bicarbonate concentration reverses<unk> -bicarbonate exchange: bicarbonate moves into the cell in exchange for<unk>  moving out. Inward movement of bicarbonate via the Band 3 exchanger allows carbonic anhydrase to convert it to CO2 for expiration. The<unk>  may also regulate the affinity of hemoglobin for oxygen through the<unk>  ion acting as an allosteric effector.
Chloride shift
Osmosis
Demineralization 
Closing the Gap
Contraction alkalosis
Isobaric counterdiffusion
Alkaline tide
Enhanced permeability and retention effect