High altitude illness (HAI) occurs in the unique environment of hypobaric hypoxia and is generally thought to be due to hypoxia. A recent sheep study by Levine suggested that hypobaria and hypoxia together, but neither alone, produced a protein-rich pulmonary vascular leak, which is similar to high altitude pulmonary edema (HAPE). Many investigators have shown that hypoxia alone does not produce a high protein edema. Decades of clinical observations suggest that descent is more effective than oxygen for treatment of high altitude illness, also pointing to a possible role for hypobaria in addition to hypoxia. We hypothesize that decreased barometric pressure exerts an effect on capillary fluid dynamics which in combination with hypoxia produces vascular leak. As the first step in answering this question, we propose to compare oxygen and pressurization for treatment of HAI to document whether descent is truly superior to oxygen therapy. More rapid recovery from HAI with pressurization, compared to supplying the same PI02 by oxygen therapy, would be evidence for a role of hypobaria per se in the pathogenesis of high altitude illness. To answer these questions climbers ill with acute mountain sickness or HAPE will receive either hyperbaric therapy in a small, portable pressure chamber for six hours duration, or oxygen therapy at the same PI02 as the hyperbaric studies for the same duration. Changes in intravascular fluid volume and gas exchange will be studied. Alveolar PI02, alveolar PC02, arterial blood gases and pH, arterial oxygen saturation, fluid intake and output, electrocardiogram, respiratory rate, hemoglobin and hematocrit and signs and symptoms of HAI will be monitored throughout hyperbaric and oxygen therapy. This preliminary study may suggest mechanisms by which hypobaria per se contributes to HAI and indicate directions for further research into the pathogenesis of illness associated with hypobaric hypoxia. This question is important for all persons ascending to high altitude, for those in hypobaric environments such as during space travel, and perhaps for all hypoxic patients as well.
| Hackett, P H; Yarnell, P R; Hill, R et al. (1998) High-altitude cerebral edema evaluated with magnetic resonance imaging: clinical correlation and pathophysiology. JAMA 280:1920-5 |
| Levine, B D; Grayburn, P A; Voyles, W F et al. (1991) Intracardiac shunting across a patent foramen ovale may exacerbate hypoxemia in high-altitude pulmonary edema. Ann Intern Med 114:569-70 |
