the kidneys remove Ihe HCO-3 ions and the homeostasis regarding the acid base balance is not disturbed

H2C03 or rather H+ ions { EMBED Equation 3 }threatened alkalosis. But gross alkalosis does not develop because the kidneys remove Ihe HCO-3 ions and the homeostasis regarding the acid base balance is not disturbed. 5. At this stage, role of 2, 3, DPG can be taken up. Normally, within the RBC, glucose is calabolized by the glycolytic pathway (also called Ihe Embden Meyerhof pathway, EMP) lo pyruvic acid (T.7.6.1, sec VII chap 6). On its way, in the EMP, one of the intermediate products is 1,3 diphosphoglycerate, (1,3 DPG, T.7.6.1). The 1,3, DPG, normally is first converted into 3 PG and then into pyruvic acid. Sometimes however, 1,3, DPG is attacked by an enzyme 'diyhosphoglycerate mutase' which converts the 1,3, DPG into 2,3, DPG. This 2,3, DPG has some important effects. Normally, 2,3, DPG is again converted into 3 phosphoglycerate (3 PG) { EMBED Equalion. 3 }pyruvic acid, a phenomenon called reentry of 2,3, DPG into EMP cycle. For-mation of 2,3, DPG, therefore, occurs via a biochemical shunt which is also called the 'Rapaport Bulbring Shunt'. 2, 3, DPG shifts Ihe 02 dissociation curve to the right. That is, it lowers the affinity of Hb for oxygen so that 02 unloading at the tissue level becomes easier (P.50 increases). After about 2 days at a moderately high altilude (eg, 15000 ft above the sea level), the 2,3, DPG concentration in RBCs rises { EMBED Equation.3 } 02 unloading at the peripheral tissues facilitated. But this rise (of 2,3, DPG) also causes difficulty in calching 02 at the alveolar level. Therefore rise of 2,3, DPG cannot be viewed as a pure unmixed advantage. [ N.B. (1) Recall, 2,3, DPG also rises m stored blood m blood bank and is one of the 'preservation injuries'. 2,3, DPG also rises m muscular exercise. (2) Note, in table 4.6.1, that hypoxic hypoxia is the only type of hypoxia which causes arterial hypoxia (that is, a condition characterized by low Pa 02 ) ] . Anemic hypoxia This is seen, in (1) anemia and (ii) in CO poisoning. In anemia, the concentration of Hb is deficient whereas in CO poisoning (recall that CO binds with Hb so that 02 cannot bind with Hb. Further, the affimly for Hb of CO is about 250 times stronger than that of 02. Therefore the combmation of CO and Hb is very difficult to dissociate) the Hb, although physically present, is not functionally available; hence it is anemic hypoxia. In anemic hypoxia, the 02 content of arterial blood is low but Pa02 is normal (that is 02 tension of arterial blood is normal). This is because, there is no obslacle to the development of physical solution of 02 in the plasma. Because of the fact that Pa02 is normal, the carotid bodies are not stimulated and there is no (or very little) dyspnea in anemia (unless it is very severe) at rest. However, dyspnea is quick to appear on exertion. (Recall, the carotid bodies are susceptible, only to Pa02 values and not the oxygen content). Compensatory mechanism (i) Hyperkinesia of circulation, as described under hypoxic hypoxia is also seen here (ii) there is increase of 2,3, DPG within the RBC causing a shift to the right of the 02dissociation curve, (iii) the 02 lack stimulates the production of erythropoietin, which in turn raises the RBC count. WHEN carbonmooxide) is inhaled, the CO combines with the Hb to form carboxyhemoglobin (carboxy Hb, COHb). The affiinty of CD for Hb is some 250 times higher than that of 02 (see above). Therefore once COHb is formed, it is not dissociated easily. As 02 competes for the same site, Hb02 thus, cannot be formed. Conclusion therefore, is, in CO poisoning, the Pa02, is normal but 02 saturation of Hb is very poor. As the dissolved 02 alone is unable to meet the demands of the body, the symptoms and signs of hypoxia develop. Treatment consists of high pressure 02 therapy whicl raises the dissolved 02 (= Pa02) as well as by mass action replaces the CO from Hb.