capillary because partial pressure of 02m the alveoli, PA02 > partial pressure of 02 in the lung capillary blood.

the availability of 02 for the pulmonary capillary blood is poor. Thus, it is seen classically in conditions where the inspiratory P02 (PI02) is poor as in high altitude (vide infra) sickness. In the following description, for the sake of simplicity, it will be presumed that there is deficiency of P1 02. In hypoxic hypoxia, PI02 is low therefore alveolar P02 (PA 02) is also low -+ therefore, Pa02 becomes low, therefore, the Pa02 at the arterial end of capillary blood in a peripheral tissue (normally about 95 mm Hg) is also low and the gradient between the Pa02 of peripheral capillary and P02 of the tissue (Ptiss 02) is poor. As a result the diffusion of 02 to the tissue is poor and the tissue suffers from 02 lack. Theoretically this condition develops in all the tissues of the body but brain deserves special consideration. Brain cannot survive 02 lack even for a brief spell. If 02 lack develops, within a few seconds, the functions of the brain begin to deteriorate and if the hypoxia is of sufficient inten The diffusivity of C02 is 20 times greater than that of 02 (chap 4 sec N). The pressure gradient (between lung capillary am alveolus) of C02 (APC02) is 6 mm Hg.:. For the same ease for diffusion, A P02 should have been (6 x 20) =120 mm Hg, but it is only 60 mm Hg sity, within two minutes, irreversible (permanent) damage of the brain occurs. Therefore, symptoms of acute hypoxia are primarily due to lack of 02 in the brain. The symptoms include, confusion, error of judgement, emotiona upsets, false and often dangerous self-confidence. In fulminant cases, the patient suddenly becomes unconscious and in absence of treatment dies. In conditions like cardiac arrest of a few minutes duration the brain remains anoxic for those few minutes and as a result, the man, even if he recovers from the episode may become vegetative throughout the rest of his life. [To prevent this, no time must be lost for starting emergency resuscitation). As stated already, high altitude sickness is a typical example of hypoxic hypoxia The following condition is seen typically in the high altitude sickness : after a sudden and rapid ascent to a mountain over 3 km altitude, hyperventilation develops { EMBED Equation.3 } after a variable period, there may be slight decrease in respiratory drive, but after about 3 days the drive increases again. The (probable) causes of this secondary rise in respiratory drive have been discussed later on (see 'high altitude sickness', later, this chapter). Another rather funny aspect regarding high altitude physiology is that persons who live in high altitude since their childhood, have a blunted response to hypoxic drive. The brain hypoxia mentioned above can, apart from the symptoms mentioned above produce many other symptoms. Following open hearl surgery, there may be development of 'psychosis' due to hypoxic hypoxia in the post operative period. Compensatory mechanisms The following facts may be remembered : 1. The partia pressure of 02 in the inspired (atmospheric) air, PI02, must fall sharply before symptoms of hypoxic hypoxia develop. Thus to produce symptoms, the PI02 must fall below 90 mm Hg (normal value, about 158 mm Hg, see table 4.4.1). Stated in another way, at sea level, the percentage of 02 must be below 12% (normal value about 21%), in the inspired air. (Recall, on the other hand, slight increase of PIC02 causes hyperventilation). 2. Pure hypoxic hypoxia causes increased respiratory drive no doubt but this drive is increased if there is, concomitant presence of excess C02 (hypercapma). Recall, asphyxia = hypoxia + hypercapnia. 3. The compensatory mechanism develops better when the exposure to the hypoxia is rather chronic or subacute (but not acute). The compensatory mechanisms are discussed below: 1. The first compensatory mechanism is development of hyperventilation. It is apparently (but only apparently) funny that hyperventilation should help the subject of hypoxic hypoxia. Because, according to our theory, 02 flows from alveolus tothe lung capillary because partial pressure of 02m the alveoli, PA02 > partial pressure of 02 in the lung capillary blood. In hypoxic hypoxia, problem is that the PI02 has fallen acutely so that PA02 is also falling. Where the PA02 is very low, 02 diffusion should not occur no matter how much ventilation is occurring. The answer to the problem is hyperventilation can and does increase the alveolar PA02 (for details, see 'alveolar gas equation', below). In short, normally 5.5% of the alveolar air volume is accounted by C02 Hyperventilation, by removing alveolar C02 ('C02 washing out'), causes reduction of the proportion of space occupied by C02 and thus proportion of 02 (and hence the P02) increases in alveolar air. The hyperventilation appears almost immediately on exposure to the hypoxia. Its mechanism is, low PI02 { EMBED Equation.3 } low PA02 { EMBED Equation.3 } low Pa02. Now recall (chap 3 sec IV), the carotid body chemoreceptors are stimulated whenever there is fall of Pa02. And also stimulation of carotid body chemoreceptors { EMBED Equation.3 } stimulation of respiratory center (= increased respiratory drive){ EMBED Equation.3 } hyperventilation. So, hyperventilation of hypoxia is due to stimulation of glomus caroticum cells (and not due to direct stimulation of respiratory center. Indeed, directly, hypoxia on respiratory center has a depressant action ). This hyperventilation causes, as stated above, rise of PA02 (for further details, see 'alveolar gas eqaaauation' ){ EMBED Equation.3 } elevation of Pa 02 correction of the 02 deficiency. But after some time, the PaC