Latest & greatest articles for High Altitude Edema

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Top results for High Altitude Edema

1. Patent foramen ovale and high-altitude pulmonary edema. (Full text)

Patent foramen ovale and high-altitude pulmonary edema. Individuals susceptible to high-altitude pulmonary edema (HAPE) are characterized by exaggerated pulmonary hypertension and arterial hypoxemia at high altitude, but the underlying mechanism is incompletely understood. Anecdotal evidence suggests that shunting across a patent foramen ovale (PFO) may exacerbate hypoxemia in HAPE.We hypothesized that PFO is more frequent in HAPE-susceptible individuals and may contribute to more severe (...) was more than 4 times higher in HAPE-susceptible than in HAPE-resistant participants, both at low altitude (56% vs 11%, P = .004; odds ratio [OR], 10.9 [95% confidence interval {CI}, 1.9-64.0]) and high altitude (69% vs 16%, P = .001; OR, 11.7 [95% CI, 2.3-59.5]). At high altitude, mean (SD) arterial oxygen saturation prior to the onset of pulmonary edema was significantly lower in HAPE-susceptible participants than in the control group (73% [10%] vs 83% [7%], P = .001). Moreover, in the HAPE

2006 JAMA PubMed

2. Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor. (PubMed)

Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor. The pathogenesis of high-altitude pulmonary edema (HAPE) is considered an altered permeability of the alveolar-capillary barrier secondary to intense pulmonary vasoconstriction and high capillary pressure, but previous bronchoalveolar lavage (BAL) findings in well-established HAPE are also consistent with inflammatory etiologic characteristics.To determine whether inflammation is a primary event in HAPE (...) at 4559 m compared with HAPE-resistant subjects (66 vs 37 mm Hg; P =.004). Despite development of HAPE in the majority of HAPE-susceptible subjects, there were no differences in BAL fluid total leukocyte counts between resistant and susceptible subjects or between counts taken at low and high altitudes. Subjects who developed HAPE had BAL fluid with high concentrations of plasma-derived proteins and erythrocytes, but there was no increase in plasma concentrations of surfactant protein A and Clara cell

2002 JAMA

3. Salmeterol for the prevention of high-altitude pulmonary edema. (Full text)

Salmeterol for the prevention of high-altitude pulmonary edema. Pulmonary edema results from a persistent imbalance between forces that drive water into the air space and the physiologic mechanisms that remove it. Among the latter, the absorption of liquid driven by active alveolar transepithelial sodium transport has an important role; a defect of this mechanism may predispose patients to pulmonary edema. Beta-adrenergic agonists up-regulate the clearance of alveolar fluid and attenuate (...) pulmonary edema in animal models.In a double-blind, randomized, placebo-controlled study, we assessed the effects of prophylactic inhalation of the beta-adrenergic agonist salmeterol on the incidence of pulmonary edema during exposure to high altitudes (4559 m, reached in less than 22 hours) in 37 subjects who were susceptible to high-altitude pulmonary edema. We also measured the nasal transepithelial potential difference, a marker of the transepithelial sodium and water transport in the distal airways

2002 NEJM PubMed

4. Prevention of high-altitude pulmonary edema by nifedipine. (PubMed)

Prevention of high-altitude pulmonary edema by nifedipine. Exaggerated pulmonary-artery pressure due to hypoxic vasoconstriction is considered an important pathogenetic factor in high-altitude pulmonary edema. We previously found that nifedipine lowered pulmonary-artery pressure and improved exercise performance, gas exchange, and the radiographic manifestations of disease in patients with high-altitude pulmonary edema. We therefore hypothesized that the prophylactic administration (...) of nifedipine would prevent its recurrence.Twenty-one mountaineers (1 woman and 20 men) with a history of radiographically documented high-altitude pulmonary edema were randomly assigned to receive either 20 mg of a slow-release preparation of nifedipine (n = 10) or placebo (n = 11) every 8 hours while ascending rapidly (within 22 hours) from a low altitude to 4559 m and during the following three days at this altitude. Both the subjects and the investigators were blinded to the assigned treatment

1991 NEJM