This difference is due to the hyperventilation produced as a result of hypoxia. Thus, the immediate compensation

In persons living in unpolluted environment and of non smoking habits the concentration of carboxy Hb in the blood is negligible. However, people in modern cities/ heavy smokers/professional car drivers/ industrial workers might have a carboxy hemoglobin concentration as high as 10% The affinity for Mgb of CO is even higher. Result is tissue damage (eg. myocardial damage, brain damage) can occur. Dyspnea does not occur because Pa02 remains normal, for which, the patient may not become conscious to his ailments. In many Western world cities regular medical check up for CO poisoning of some category of people (eg. taxi drivers) is compulsory. Stagnant hypoxia This develops when the velocity of blood flow is very poor. As a result, the blood stays in the peripheral capillaries for a longer time and 02 extraction by the tissue continues but after some time the 02 extraction can no longer occur (as the 02 of capillary blood is now almost exhausted) and the tissue suffers Thus, this type of hypoxia is seen in cardiac failure and circulatory shock. In this type of hypoxia Pa02 is normal but arterio venous difference [A-V difference, normal value, about 4 ml/100 ml, (arterial blood containing 19 ml/100 ml and mixed venous blood about 15 ml/100 ml of oxygen)] is very great (i.e. it becomes more than 4 ml/100 ml). Histotoxic hypoxia Typical example is cyanide poisoning. In this type of hypoxia, there is fault of the enzyme system which catalyzes the tissue oxidation, viz , the cytochrome system (fig. 7.2.1) and the other iron containing enzyme systems. As a result, the tissues can extract little or no oxygen. In this type of hypoxia, the Pa02 is normal but venous blood contains a high concentration of 02, i.e. , the A-V difference of 02 is nil or very little. The venous blood in this condition is bright red in appearance (as it remains fully oxygenated. Oxygenated blood is bright red in appearance). Table 4.6.1 summarizes some of the highlights of the four types of hypoxia. HIGH ALTITUDE SICKNESS, ACCLIMATIZATION When a man, who resides in the plane, ascends suddenly to sufficiently high altitude, he develops signs and symptoms due to hypoxic type of hypoxia. This hypoxic hypoxia. due to sudden ascent to high altitude, is called high altitude sickness. If the ascent is, however, slow, some physiological ad-aptations develop, so that the man develops no symptom (or minimal symptoms and signs) when he reaches the same altitude at which he felt severely sick when the ascent was rapid. These adaptative changes are called acclimatization. Cause of the sickness when the ascent is rapid (pathogenesis Typically, this occurs if the ascent to a mountain is very rapic (hence this used to be spoken of, as 'mountain sickness' in the yesteryears of physiology). Alternatively, this can happen, when an aircraft, without a pressure cabin ascents swiftly to lofty altitude, as used to happen before the introduction of pressurized cabins in the air craft, before modern times. The cause of sickness is low Pa02, which in turn is due to low PI02. It should be clearly borne in mind, that the percentage composition of the atmospheric air, whether it is in the top o> Mount Everest (over 29000 ft = about 10 km) or at sea level, is always same. But due to changes in the barometric pressure the PI02 falls. Thus, at the top of Mt. Everest (barometric pressure about 200 mm Hg), assuming somewhat arbitrarily, the water vapour tension is 10 mm Hg, the PI02 is (the 02 percentage is assumed to be 21 %), 21 x (200 -10) = 39.9 mm Hg. At sea level, where the percentage composition is same, the PI02 is, PI02 values. 100 x (760 -10) =158 mm Hg. Fig. 4.6.1. Barometric pressure at different altitudes with their corresponding This means that the PA02 at high altitude will be still lower (lower than PI02). The PA02 can be calculated by the alveolar gas equation, which states : (PA02 = PI02 - PA C02 + F R where, R = respiratory exchange ratio, i.e. { EMBED Equation.3 }C02/{ EMBED Equation.3 }02 normal value, about 0.8. F = a correction factor, of approximately 2 mm Hg value. Therefore, at top of Mt. Everest, the value of PA02 on theo-retical grounds will be : PI02 - PA C02 + F = (39.9 - 50 +2) -8.1 mm Hg (Normally, the value of PAC02 is 40 mm Hg- see earlier chapters). This should cause flow of 02 from the blood to the atmosphere, technically spoken of as "boiling of the blood". In practice, however, because of the compensatory mechanisms (see below), the PA02 is much higher (Ώ 30 mm Hg at the top of Mt. Everest). At still higher altitudes of course, despite all compensatory mechanisms, the blood will "boil". Table A and B of 4.6.2 show the position in tabulated form. Mark in the table 4.6.2 A and B the following: 1) Although the volume percentage of the gases of the inspired air remain same whether the atmosphere is at sea level or at high altitude, the partial pressures of oxygen greatly falls at high altitudes. 2) Theoretically predicted values (calculated by alveolar gas equation) of the tensions of the respiratory gases of the alveolar air (assuming no hyperventilation is present) are substantially different from the values obtained in practice This difference is due to the hyperventilation produced as a result of hypoxia. Thus, the immediate compensation is achieved by increasing the ventilation. Hy- perventilation, is due to the reflex stimulation of the carotid bodies, due to low Pa02. Signs and symptoms of the high altitude sickness are same as those of hypoxic hypoxia described earlier in this chapter. They are essentially due to cerebral