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PubMed · 7075784

Diffusion at high altitude.

Abstract

The problems posed by exercise at high altitude for oxygen diffusion across the blood-gas barrier have been recognized since the early part of this century. But the successful ascent of Mt. Everest (altitude 8848 m) by two climbers without supplementary oxygen in 1978 focused attention on this issue. We have therefore carried out a theoretical study of gas exchange under these conditions of extreme hypoxia. Calculations of oxygenation along the pulmonary capillaries show that, even at rest, there is an alveolar-end capillary PO2 of about 6 torr caused by diffusion limitation, and this widens rapidly on mild exercise. As the oxygen uptake is increased, the PO2 of mixed venous blood falls to very low values. If we assume a minimal value of 15 torr, a maximal oxygen uptake on the summit of less than 700 ml/min is predicted. VO2max is extremely sensitive to barometric pressure, and to a lesser extent to lung diffusing capacity.

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BibTeXRIS

J B West. 1982. Diffusion at high altitude.. https://pubmed.ncbi.nlm.nih.gov/7075784/

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Arterial oxygen saturation in Tibetan and Han infants born in Lhasa, Tibet.

BACKGROUND: Reduced oxygen availability at high altitude is associated with increased neonatal and infant mortality. We hypothesized that native Tibetan infants, whose ancestors have inhabited the Himalayan Plateau for approximately 25,000 years, are better able to maintain adequate oxygenation at high altitude than Han infants, whose ancestors moved to Tibet from lowland areas of China after the Chinese military entered Tibet in 1951. METHODS: We compared arterial oxygen saturation, signs of hypoxemia, and other indexes of neonatal wellbeing at birth and during the first four months of life in 15 Tibetan infants and 15 Han infants at 3658 m above sea level in Lhasa, Tibet. The Han mothers had migrated from lowland China about two years previously. A pulse oximeter was placed on each infant's foot to provide measurements of arterial oxygen saturation distal to the ductus arteriosus. RESULTS: The two groups had similar gestational ages (about 38.9 weeks) and Apgar scores. The Han infants had lower birth weights (2773 +/- 92 g) than the Tibetan infants (3067 +/- 107 g), higher concentrations of cord-blood hemoglobin (18.6 +/- 0.8 g per deciliter, vs. 16.7 +/- 0.4 in the Tibetans), and higher hematocrit values (58.5 +/- 2.4 percent, vs. 51.4 +/- 1.2 percent in the Tibetans). In both groups, arterial oxygen saturation was highest in the first two days after birth and was lower when the infants were asleep than when they were awake. Oxygen saturation values were lower in the Han than in the Tibetan infants at all times and under all conditions during all activities. The values declined in the Han infants from 92 +/- 3 percent while they were awake and 90 +/- 5 percent during quiet sleep at birth to 85 +/- 4 percent while awake and 76 +/- 5 percent during quiet sleep at four months of age. In the Tibetan infants, oxygen saturation values averaged 94 +/- 2 percent while they were awake and 94 +/- 3 percent during quiet sleep at birth and 88 +/- 2 percent while awake and 86 +/- 5 percent during quiet sleep at four months. Han infants had clinical signs of hypoxemia--such as cyanosis during sleep and while feeding--more frequently than Tibetans. CONCLUSIONS: In Lhasa, Tibet, we found that Tibetan newborns had higher arterial oxygen saturation at birth and during the first four months of life than Han newborns. Genetic adaptations may permit adequate oxygenation and confer resistance to the syndrome of pulmonary hypertension and right-heart failure (subacute infantile mountain sickness).

Altitude

[Lung problems in acute to subacute exposure to medium altitudes].

The hypobaric hypoxia of moderate altitude elicits various mechanisms of acute to subacute physiologic adaptations of the healthy lung: First of all it causes a hyperventilation, which increases the diminished arterial pO2. Because of hypoxemia-induced vasoconstriction, pulmonary arterial hypertension develops. The adrenergic stimulation of the cardiac output also increases the pulmonary perfusion. Most likely because of the diminished density of ambient air there is a measurable increase of exspiratory bronchial flow or, respectively, a diminution of the peripheral airway resistance. In higher altitudes, limitation of oxygen-diffusion under physical exertion is observed. The consequences of acute hypobaric hypoxia for diseased lungs depend on preexisting ventilation/perfusion mismatch or diffusion impairment. Arterial hypoxemia and hence also pulmonary arterial hypertension are increased. In the presence of normal chemoreceptor sensitivity (type pink puffer), a hyperventilation, which is often perceived as dyspnea by the patient, is induced. Mostly patients with chronic obstructive pulmonary disease adapt, however, surprisingly well to moderate altitude. Bronchial asthma improves frequently because allergen concentrations are low and air density is diminished. On the other hand, physical exertion in dry and cold ambient air may also elicit acute asthmatic exacerbations. The assessment of moderate altitude tolerance by patients with chronic lung diseases and prophylactic precautions before the ascent are discussed. The only altitude-specific disease of the healthy lung is the so-called high-altitude pulmonary edema. The major pathogenetic factor for its development is an inadequate or overshooting response to hypobaric hypoxia (nonuniform pulmonary arterial vasoconstriction, diminished hypoxic ventilatory drive, retention of fluid, centralization of blood volume and capillary leak). Prophylactic and therapeutic implications are discussed.

Altitude