may show some features of pulmonary hypertension. Pulmonary edema is another serious hazard

hypoxia. (*) Calculated alv. air composition, assuming Ihere is no hypervenlilalion. (**) Actual alv. air composition, commonly found at thise altitudes when hyperventilation is fully operating saturation of Hb of arterial blood in presence of hyper-ventilation (i.e. alveolar air as in **). In addition, some symptoms due to the low barometric pressure may also develop. Thus, expansion of air in the middle ear cavity may be troublesome and aircraft passengers use cotton plug in the ear as a remedy. There may be distension of the intestine due to expansion of gas in the intestine. In 1985 an Air India plane, 'Kamshka' due to some yet unidentified reason, exploded in the mid air, high aver the Atlantic Sea. As because the victims were exposed to that severely rarefied air, gases in their body expanded immediately (and before death) and caused bursting of their bodies most probably long before those bodies touched the sea water level. Compensatory (acclimatization) mechanisms 1. The first major compensatory mechanism is as stated above, hyperventilation. Once it develops, the Pa02 is sub { EMBED Equation. 3 } stantially increased and PAC02 is lowered. As a result the Pa02 is raised. How the hyperventilation can raise the Pa02 ? The answer is, hyperventilation washes away C02 from the alveoli and as a result the value of alveolar equation changes: as the value of the PAC02 decreases due to hyperventilation, the value of PA02 rises It has already been pointed out that the hyperventilation (i e. stimulation to breathing due 02 lack) starts when the volume percent of 02 in the inspired air has fallen to about 12 ml/100 ml ({ EMBED Equations.3 } 90 mm Hg) and not before. 2. Consequences of the hyperventilation are as follows: hyperventilation washing out of C02 fall of PaC02. Now as Pa C02 falls, some alkalosis develops in the brain and CSF. Recall (fig. 4. 3 .8), H+ is a powerful stimulator of respiration. Therefore, with the onset of alkalosis in CSF & brain, the respiratory drive falls to some extent (the anoxic drive, however, persists) After about 3 days, the V{ EMBED Equation 3 }E again rises ('secondary rise). Its (probable) mechanisms are: (i) the extra HCO-3 ions in the brain tissue fluid and CSF (which caused their pH to rise) are removed by an active process (n) hypoxia of brain produces lactic acid Factors (i) and (n) together correct the alkalosis of the CSF and brain tissue fluid so that their pH returns to normal value " secondary rise of ( EMBED Equation .3 }E. (iii) in addition, for some undetermined reason, the respiratory center becomes more sensitive to C02 so that even if the PaC02 value is low yet it is sufficient to drive the respiration. The hyperventilation causes a generalized rise of HC03 ions in the body and thus an alkalosis is threatened. But the kidneys secrete highly alkaline urine pH homeostasis is regained. 3. Hyperkmesia of the circulation develops. This is due, probably to the stimulation of the sympathetic system, which in turn is due to stimulation of vasomotor center (VMC). Features of hyperkmetic circulation have been described in connection with hypoxic hypoxia. The arterial blood pressure, however, as stated in hypoxic hypoxia, usually does not rise. 4. Polycythemia develops due to excessive production of erythropoietm. This erythropoietm generation is due to 02 lack. As a result, the RBC count may shoot up to such values like 8 x 106 /cmm of blood (normal value 5 x 106 cmm). Polycythemia causes increased viscosity of blood, which in turn (a) slows down the circulation and (b) increases the blood pressure. BP however is not necessarily raised because of vasodilatation by the hypoxia. Let alone military supersonic Jet bombers, even modem passenger Jet planes fly at fairly high altitudes, sometimes over 40000 ft (well over the height of Mt. Everest) and the barometric pressure there is very low and the air rarefied. However, the cabins are pressurized although the cabins are kept in a simulated altitude of about 1. 5 km or so. For a healthy person, this altitude is nothing because at this level of rarefication, percentage saturation of Hb is still over 90% and the 02 dissociation curve still operates in the upper flat region (fig. 4.5.1). But in a man suffering from advanced emphysema or heart disease (whose Hb saturation with 02 is already low), this 1.5 km altitude may cause a saturation (with 02) of only 80% or even lower. This means, if now there is (for some or other reason) still further fall of PI02, the dissociation of 02 from the Hb will be extremely rapid (as the curve will be now operating at its steep part) and hypoxic condition will result because at this stage, the affinity (for 02) of Hb is grossly reduced and 02 loading at lungs is hampered. For this reason, passengers are given a lesson on how to use 02 (from the source adjacent to his seat) before the plane takes off. Pulmonary hypertension. Hypoxia produces pulmonary hypertension, which in turn may cause right ventricular hypertrophy and even failure Persons who have been residing in high altitude, although acclimatized, may show some features of pulmonary hypertension. Pulmonary edema is another serious hazard of high altitude People who live at high altitudes since birth show a few anatomical and physiological peculiarities: 1their right ventricle is often bigger and hypertrophied. This is due to the concomitant pulmonary hypertension and polycythemia present so often in them, (ii) their carotid bodies are bigger probably due to overuse) (iii) their Pa02 as well as PaC02 are slightly lower than that of their brothers