Arterial Blood Gases and Oxygen Content in Climbers on Mount Everest  

Oleh:

Grocott, Michael P.W. ; Martin, Daniel S. ; Levett, Denny Z.H. ; McMorrow, Roger ; Windsor, Jeremy

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The New England Journal of Medicine (keterangan: ada di Proquest) vol. 360 no. 02 (Jan. 2009), page 140-149.
Topik: hypobaric hypoxia

Ketersediaan

Perpustakaan FK Nomor Panggil: N08.K.2009.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Background The level of environmental hypobaric hypoxia that affects climbers at the summit of Mount Everest (8848 m [29,029 ft]) is close to the limit of tolerance by humans. We performed direct field measurements of arterial blood gases in climbers breathing ambient air on Mount Everest. Methods We obtained samples of arterial blood from 10 climbers during their ascent to and descent from the summit of Mount Everest. The partial pressures of arterial oxygen (PaO2) and carbon dioxide (PaCO2), pH, and hemoglobin and lactate concentrations were measured. The arterial oxygen saturation (SaO2), bicarbonate concentration, base excess, and alveolar–arterial oxygen difference were calculated. Results PaO2 fell with increasing altitude, whereas SaO2 was relatively stable. The hemoglobin concentration increased such that the oxygen content of arterial blood was maintained at or above sea-level values until the climbers reached an elevation of 7100 m (23,294 ft). In four samples taken at 8400 m (27,559 ft) — at which altitude the barometric pressure was 272 mm Hg (36.3 kPa) — the mean PaO2 in subjects breathing ambient air was 24.6 mm Hg (3.28 kPa), with a range of 19.1 to 29.5 mm Hg (2.55 to 3.93 kPa). The mean PaCO2 was 13.3 mm Hg (1.77 kPa), with a range of 10.3 to 15.7 mm Hg (1.37 to 2.09 kPa). At 8400 m, the mean arterial oxygen content was 26% lower than it was at 7100 m (145.8 ml per liter as compared with 197.1 ml per liter). The mean calculated alveolar–arterial oxygen difference was 5.4 mm Hg (0.72 kPa). Conclusions The elevated alveolar–arterial oxygen difference that is seen in subjects who are in conditions of extreme hypoxia may represent a degree of subclinical high-altitude pulmonary edema or a functional limitation in pulmonary diffusion.

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