* Numbers in parentheses are acclimatized values.
* Numbers in parentheses are acclimatized values.
Alveolar Po2 at Different Altitudes. The fifth column of Table 43-1 shows the approximate Po2s in the alveoli at different altitudes when one is breathing air for both the unacclimatized and the acclimatized person. At sea level, the alveolar P02 is 104 mm Hg; at 20,000 feet altitude, it falls to about 40 mm Hg in the unacclimatized person but only to 53 mm Hg in the acclimatized. The difference between these two is that alveolar ventilation increases much more in the acclimatized person than in the unacclimatized person, as we discuss later.
Saturation of Hemoglobin with Oxygen at Different Altitudes.
Figure 43-1 shows arterial blood oxygen saturation at different altitudes while a person is breathing air and while breathing oxygen. Up to an altitude of about 10,000 feet, even when air is breathed, the arterial oxygen saturation remains at least as high as 90 per cent. Above 10,000 feet, the arterial oxygen saturation falls rapidly, as shown by the blue curve of the figure, until it is slightly less than 70 per cent at 20,000 feet and much less at still higher altitudes.
Effect of Breathing Pure Oxygen on Alveolar PO2 at Different Altitudes
When a person breathes pure oxygen instead of air, most of the space in the alveoli formerly occupied by nitrogen becomes occupied by oxygen. At 30,000 feet, an aviator could have an alveolar Po2 as high as 139 mm Hg instead of the 18 mm Hg when breathing air (see Table 43-1).
The red curve of Figure 43-1 shows arterial blood hemoglobin oxygen saturation at different altitudes when one is breathing pure oxygen. Note that the saturation remains above 90 per cent until the aviator ascends to about 39,000 feet; then it falls rapidly to about 50 per cent at about 47,000 feet.
The "Ceiling" When Breathing Air and When Breathing Oxygen in an Unpressurized Airplane
Comparing the two arterial blood oxygen saturation curves in Figure 43-1, one notes that an aviator
Breathing pure oxygen Breathing air
10 20 30 40 Altitude (thousands of feet)
Effect of high altitude on arterial oxygen saturation when breathing air and when breathing pure oxygen.
breathing pure oxygen in an unpressurized airplane can ascend to far higher altitudes than one breathing air. For instance, the arterial saturation at 47,000 feet when one is breathing oxygen is about 50 per cent and is equivalent to the arterial oxygen saturation at 23,000 feet when one is breathing air. In addition, because an unacclimatized person usually can remain conscious until the arterial oxygen saturation falls to 50 per cent, for short exposure times the ceiling for an aviator in an unpressurized airplane when breathing air is about 23,000 feet and when breathing pure oxygen is about 47,000 feet, provided the oxygen-supplying equipment operates perfectly.
Some of the important acute effects of hypoxia in the unacclimatized person breathing air, beginning at an altitude of about 12,000 feet, are drowsiness, lassitude, mental and muscle fatigue, sometimes headache, occasionally nausea, and sometimes euphoria.These effects progress to a stage of twitchings or seizures above 18,000 feet and end, above 23,000 feet in the unaccli-matized person, in coma, followed shortly thereafter by death.
One of the most important effects of hypoxia is decreased mental proficiency, which decreases judgment, memory, and performance of discrete motor movements. For instance, if an unacclimatized aviator stays at 15,000 feet for 1 hour, mental proficiency ordinarily falls to about 50 per cent of normal, and after 18 hours at this level it falls to about 20 per cent of normal.
A person remaining at high altitudes for days, weeks, or years becomes more and more acclimatized to the low Po2, so that it causes fewer deleterious effects on the body. And it becomes possible for the person to work harder without hypoxic effects or to ascend to still higher altitudes.
The principal means by which acclimatization comes about are (1) a great increase in pulmonary ventilation, (2) increased numbers of red blood cells, (3) increased diffusing capacity of the lungs, (4) increased vascularity of the peripheral tissues, and (5) increased ability of the tissue cells to use oxygen despite low Po2.
Increased Pulmonary Ventilation—Role of Arterial Chemore-ceptors. Immediate exposure to low Po2 stimulates the arterial chemoreceptors, and this increases alveolar ventilation to a maximum of about 1.65 times normal. Therefore, compensation occurs within seconds for the high altitude, and it alone allows the person to rise several thousand feet higher than would be possible without the increased ventilation. Then, if the person remains at very high altitude for several days, the chemoreceptors increase ventilation still more, up to about five times normal.
The immediate increase in pulmonary ventilation on rising to a high altitude blows off large quantities of carbon dioxide, reducing the Pco2 and increasing the pH of the body fluids. These changes inhibit the brain stem respiratory center and thereby oppose the effect of low PO2 to stimulate respiration by way of the peripheral arterial chemoreceptors in the carotid and aortic bodies. But during the ensuing 2 to 5 days, this inhibition fades away, allowing the respiratory center to respond with full force to the peripheral chemore-ceptor stimulus from hypoxia, and ventilation increases to about five times normal.
The cause of this fading inhibition is believed to be mainly a reduction of bicarbonate ion concentration in the cerebrospinal fluid as well as in the brain tissues. This in turn decreases the pH in the fluids surrounding the chemosensitive neurons of the respiratory center, thus increasing the respiratory stimulatory activity of the center.
An important mechanism for the gradual decrease in bicarbonate concentration is compensation by the kidneys for the respiratory alkalosis, as discussed in Chapter 30. The kidneys respond to decreased Pco2 by reducing hydrogen ion secretion and increasing bicarbonate excretion. This metabolic compensation for the respiratory alkalosis gradually reduces plasma and cerebrospinal fluid bicarbonate concentration and pH toward normal and removes part of the inhibitory effect on respiration of low hydrogen ion concentration. Thus, the respiratory centers are much more responsive to the peripheral chemoreceptor stimulus caused by the hypoxia after the kidneys compensate for the alkalosis.
Increase in Red Blood Cells and Hemoglobin Concentration During Acclimatization. As discussed in Chapter 32, hypoxia is the principal stimulus for causing an increase in red blood cell production. Ordinarily, when a person remains exposed to low oxygen for weeks at a time, the hematocrit rises slowly from a normal value of 40 to 45 to an average of about 60, with an average increase in whole blood hemoglobin concentration from normal of 15 g/dl to about 20 g/dl.
In addition, the blood volume also increases, often by 20 to 30 per cent, and this increase times the increased blood hemoglobin concentration gives an increase in total body hemoglobin of 50 or more per cent.
Increased Diffusing Capacity After Acclimatization. It will be recalled that the normal diffusing capacity for oxygen through the pulmonary membrane is about 21 ml/mm Hg/min, and this diffusing capacity can increase as much as threefold during exercise. A similar increase in diffusing capacity occurs at high altitude.
Part of the increase results from increased pulmonary capillary blood volume, which expands the capillaries and increases the surface area through which oxygen can diffuse into the blood. Another part results from an increase in lung air volume, which expands the surface area of the alveolar-capillary interface still more. A final part results from an increase in pulmonary arterial blood pressure; this forces blood into greater numbers of alveolar capillaries than normally—especially in the upper parts of the lungs, which are poorly perfused under usual conditions.
Peripheral Circulatory System Changes During Acclimatization—Increased Tissue Capillarity. The cardiac output often increases as much as 30 per cent immediately after a person ascends to high altitude but then decreases back toward normal over a period of weeks as the blood hematocrit increases, so that the amount of oxygen transported to the peripheral body tissues remains about normal.
Another circulatory adaptation is growth of increased numbers of systemic circulatory capillaries in the nonpulmonary tissues, which is called increased tissue capillarity (or angiogenesis). This occurs
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