in this condition, blood flow per minute, in the pulmonary circglalion increases( EMBED Equation 3 )grealer axtraction

02 (= partial pressure of CO2 in It blood) begins to fall because of The hyperventilation This causes withdrawal of The respwatory drive some decrease in Ihe hyprvenlilatron 2 Soon, there develops Hyperkinesia of tha circulatory systen Benefits of hyrperkinetic circulation are as follows Hyperkmetic circulatory state means a state where the velocity of the blood circtilalion is high, tachycardia and cardiac stimulation are present Obviously, in this condition, blood flow per minute, in the pulmonary circglalion increases( EMBED Equation 3 )grealer axtraction of 02 from the alveolar air by the blood, thus, is now possible Cause of this hyperkiunsia is increased sympathetic activrty which in turn, is due to vaso motar center (VMC) stimulation due to hypoxia Recall, when the blood feeding the VMC is mildly or moderately hypoiemit the VMC is stimulated (gross hypotemic blood, however, causes death of VMC{ EMBED Equation 3 )sympathetic paralysis] The blood pressure (BP) however may fall or may rise of may show no change This is because, the BP is subjected to two opposing forces, (a) vasconstndion due to VMC overacrrvity (h) vasodilatalian due to local anoxia The resultant of these two opposing forces determine the outcome In addition, the concomitanl polycythernia also raises the BP 3 Thare is erythropoielin elaboration (for details, see chap 1 sec ll{ EMBED Equation 3 }rise of RBC count This also aids in extraction of greater 02 from the lung alveoli 4 Besides the above, kidneys also contribute But this is Largely to counteract, the (ill) side effects of hyperventrtation, as follows hypervenilation {EMBED Equation 3 } loss ofC02 from the body { EMBED Equation 3 ) loss of H2CO3 or rather H+ ions ( EMBED Equation 3 threatened alkalosis But gross alkalosis does not develop because the kidneys remove the HCO-3ions and the hnmeoslasis 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 catabolized by the glycotytic pathway; (also called the Embden Meyerhof pathway, EMP) to pyruvic acid (T 7.6.1, sec VII chip 6) On its way, in the EMP, one of the miermediate products is 1,3 diphosphoglycerate, (1.3 DPG.T7.6.1) The 1,3,DPG normally is first converted into 3 PG and then into pyruvic acid Sometimes nowever. 1.3. DPG is attacked by an enzyme 'diyhosphoglycerate rnutase' which converts the 1,3, DPG into 23, DPG This 2,3. DPG has some mportant effects Normally, 2.3. DPG is again converted into 3 phosphogtycerate (3 PG) (EMBED Equation 3 )pyruvic acid, a phenomenon called reentry of2,3, DPG mlo EMPcycle For-mation of 2.3 DPG therefore, occurs via a biochemical shunt which is also called The Papaport Bulbrmg Shunt' 2, 3r DPG shifts the O2 dissoc-anon curve to the rig ht That is. it lowers the affinity of Hb for ovygen so that 02 unloading at the hssue level becomes easier (P.50 increases) After about 2 days at a madertfely high attiude (eg, 15000 ft above the sea level), the 2.3. DPG concerntration in RBCs nses (EMBED Equation 3 } 02 unloading at the penpheral tissues facilitated Bui this rise (of2,3, DPG) also causes difficulty in catching 02 at The alveofar level Therefore rise of 23. DPG cannot be viewed as a pure unmixed advantage [ N B (1) Recall, 2, 3, DPG also rises in stored blood in blood bank and is one of the prsservaiion injuries' 2,3. DPG also rises in muscular exercise (2) Note, in table 4.6.1, that hypoxia hypoxia is the only type of hypoxia which causes arterial hypoxia (that is. a condition characterized by low Pa O2 )] Anemrc 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 affinity for Hb of CO is about 250 times stronger than thet of 02 Therefore the combination 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 O2 contenl of artenial blood is lew but Pa02 is normal (that is, 02 tension of attend blood is normal) This is because, there is no obstacle to the development of physical solution of 02 in the plasma Because ol the fact that Pa02 is normal. The carotid bodies are not stimulated and there is no (or very little)dyspnea in anemia (unless it 13 very severe) at rest However, dyspnea is quick to appear on exertion (Recall, the carotid bodies are susceptible. only to Pa02 values and nor the oxygen conten) Compsnsatory mechanism (ij Hyperkinesia oirculation, as dsscnbed under hypoxia hypoxia is also seen here (ii) There is increase o' 2.3. DPG within the R8C causing a shrft to ihe right of the O2 dissociation curve, (m) the Q2 lack slimulates rhe production ol erythropoietm. which in Turn raises the PBC count WHEN carbonmoonxide) is inhaled, the CO combines with the Hb to form carboxyhemoglobin (carboxy Hb, COHb) The affinity of CD for Hb it tome 250 times higherthanthat 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, in. in CO poisoning, the Pa02b is normal bul 02 saturation of Hb is very poor As the dissolved 02 alone is unable to meet the demand of the body.the symptoms and signs of hypoxia develop Trealment consist of high pressur* 02 therapy which raises the dissolved O2 (= PaO2) as will at by mass action replaces