mountaineering and in the army. The second issue (ARDS), although highlighted only in recent times, carries a high mortality

carbamino hemoglobin is the principal agent of C02 transfer and the C02 transfer is always adequate. 3 Carbamino compounds are formed more readily when the Hb is reduced; this helps in more C02 uplake by the peripheral capillary blood. 4. Presence of 2,3 DPG depresses the formation of carbamino compound. 5. Although the amount of it is not much, because of the speed of its formation and dissociation, carbaminohemoglobin compound is a very important compound for uptake or release of C02. About 25% of the C02 that undergoes transfer is accounted by this compound. Fig. 4.5.4. C02 disassociation pattern of blood. C02, DISSOCIATION CURVE (fig. 4.5.4) Like the 02 dissociation curve, the C02 dissociation curve also can be constructed. The sludent should note however, that the ordinate represents volumes (in ml) of C02 present per 100 ml of blood instead of percentage saturation of Hb by 02 as in oxygen dissociation curve. Note, if the Hb is oxygenated, the C02 dissociation curve shifts to the right, that is, the blood begins to lose some C02 as it becomes oxygenated. This is usually called Haldane effect, although it is also known by its alternate name, viz, CDH (Christiansen, Douglas, Haldane) effect. SUMMARY & HIGHLIGHTS 02 contenl of arterial blood is about 19 ml/100 ml, 02 capacity of the same is 20 ml per 100 ml, hence percentage saturation of Hb (by 02) in arterial blood is around 95%. This means in healthy persons at sea level there is little scope to increase the 02 level. 02 in blood is carried in (i) physical solution (0.3 ml/100 ml in plasma, and (ii) as combined wilh Hb. It is the physical solution which exerts the 02 tension, the 02 of Hb02 merely acts as a sink. 02 dissociation curve is sigmoid (S) shaped; this means until the barometric pressure and the PI02 fall sharply, the oxygenation at the lung is not much affected Also, the Ptissue 02 need not be very low for unloading in the tissue level. Presence of excess C02, heat and acidity (the environment found in working tissues) favor unloading of 02 at tissue level. 2, 3, DPG also favors unloading excess 2,3 DPG develops when BMP path of glucose metabolism operates vigorously. C02 is carried mainly as (i) in plasma soln. (ii) plasma NaHC03 (iii) KHCo3 in RBC (iv) carbamino hemoglobin in RBC - the last named is most important for transfer. During C02 loading [chloride] increases within the RBC and is called Chloride Shift. Hypoxia, high altitude sickness and ARDS 2 Hypercapnia, hypouentitation 3. Asphyxia 4. Cyanosis 5. Periodic breathing 6. Voluntary hyperpnea and breath holding 7. Oxygen therapy 8. Decompression sickness 9. Emphysema, asthma 10. Airpollution Cigarette smoking 11. Artificial respiration 12. Dyspnea 13. Lung defence mechanism 14. Respiration during sleep 15. Spirometry and other lung function tesls 16. Breath sounds 17. Respiratory physiology in the infant & the old HYPOXIA AND HIGH ALTITUDE SICKNESS Hypoxia (also called anoxia) is a condition characterized by insufficient oxygen supply to the tissues. The term hypoxia (hypo = less) is preferred which means a state of insufficient oxygenation and not its older equivalent anoxia, which means no oxygen. Following terms should be clearly understood: (i) Hypoxia is lack of oxygen, (ii) hypercapnia means excess of C02 in the arterial blood, (iii) asphyxia means lack of oxygen plus retention of C02. However many authors of text books on physiology or medicine do not obey some of these distinctions. According to the traditional teaching, there are four classes of hypoxia, viz, (i) hypoxic (anoxic) hypoxia (anoxia) (ii) anemic hypoxia (iii) stagnant hypoxia, and (iv) hisloloxic hypoxia. A description of the different classes of hypoxias will be made first which will be followed by short accounts of high altitude sickness and ARDS, both being important examples of hypoxic hypoxia. High altitude sickness is important, because (apart from the fact that it gives insight to respiratory, cardiovascular, renal, neurophysiology etc. ) it has great applications in civil aviation, mountaineering and in the army. The second issue (ARDS), although highlighted only in recent times, carries a high mortality rate and is likely lo increase with industrialization. Hypoxic hypoxia Causes. Typical example is (i) sudden ascent to a very high altitude [10,000 ft. or above (= about 3 km). (ii) In in-fections of lung, eg. lobar pneumonia, where exudate collects into the alveoli and thickens the alveolo capillary membrane hypoxic hypoxia may develop. [Theoretically there should be both lack of 02 and retention of C02 in this condition (lobar pneumonia) but because C02 has a very high diffusivily compared to 02, C02 can manage to pass out of the alveolocapillary membrane satisfactorily, so that C02 retention is not appreciable* in early stages of this disease]. (iii) hypoxia of arterial blood is a characteristic feature of adult respiratory distress syndrome, (ARDS). [ Some authors prefer to call hypoxic hypoxia, to all conditions, whenever there is low P02 of arterial blood (Pa02). Thus, according to them, obstruction in respiratory passage, diaphragmatic paralysis, etc. are all examples of hypoxic hypoxia. But according to what has been written in the beginning of this chapter, these are actually examples of asphyxia. Mild or moderate hypoventilation, on the other hand, should better be described under the heading hypercapnia for reasons stated elsewhere in this book. ] Pathogenesis and pathophysiology of hypoxic hypoxia Hypoxic hypoxia is produced when FILE NO. 7418532