Oswald Oelz

Prevention of High-Altitude Pulmonary Edema by Nifedipine

Abstract Background. 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. Methods. 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. The diagnosis of pulmonary edema was based on chest radio...

Endothelin-1 in Pulmonary Hypertension Associated With High-Altitude Exposure

BACKGROUNDnEndothelin-1 is involved in chronic pulmonary hypertension. Its role in acute pulmonary hypertension due to hypoxia in humans is not clear. We therefore studied the influence of hypoxia caused by exposure to high altitude on plasma endothelin-1 levels, arterial blood gases, and pulmonary arterial pressure in subjects taking nifedipine or placebo.nnnMETHODS AND RESULTSnTwenty-two healthy volunteers were investigated at low altitude (490 m) and high altitude (4559 m). Arterial blood gases were analyzed immediately, endothelin-1 was measured by radioimmunoassay, and pulmonary artery pressure was assessed by Doppler echocardiography. After baseline investigations, the mountaineers were allocated in a randomized double-blind fashion to receive either placebo or nifedipine (20 mg TID) during rapid ascent to high altitude within 22 hours. Tests were repeated at the high-altitude research laboratories located in the Capanna Regina Margherita (Italy, 4559 m). Plasma endothelin-1 was increased twofold at high altitude (5.9 +/- 2.2 pg/mL compared with 2.9 +/- 1.1 pg/mL, P < .05), was inversely related to arterial PO2 (r = -.46, P < .001), and correlated with pulmonary artery pressure (r = .52, P < .002). At high altitude, arterial endothelin-1 was lower (4.3 +/- 1.6 pg/mL) than venous endothelin-1 (5.9 +/= 2.2 pg/mL, P < .001), indicating either predominant production in the venous vasculature or pronounced clearance in the pulmonary circulation. The calcium antagonist nifedipine, which lowered pulmonary artery pressure at high altitude (32 +/- 5 versus 42 +/- 11 mm Hg, P < .05), had no influence on plasma endothelin-1 levels. The administration of 35% O2 at high altitude normalized arterial PO2, tended to decrease endothelin-1, and decreased pulmonary artery pressure accordingly.nnnCONCLUSIONSnWe conclude that plasma endothelin-1 is increased at high altitude, but whether or not it represents an important pathogenetic factor for pulmonary hypertension remains to be investigated.

Successful treatment of acute mountain sickness with dexamethasone.

A double blind, randomised, placebo controlled trial of treatment with dexamethasone for acute mountain sickness was performed in the Capanna Regina Margherita at an altitude of 4559 m in the Alps Valais. After 12-16 hours of treatment (8 mg dexamethasone initially, followed by 4 mg every six hours) the mean acute mountain sickness score decreased significantly from 5.4 to 1.3, and eight of 17 patients became totally asymptomatic. Mean arterial oxygen saturation rose from 75.5% to 82.0%, and there was a small increase in standard spirometric measurements. In the placebo group none of these variables changed significantly. It is concluded that dexamethasone may be used as emergency treatment for acute mountain sickness to facilitate safe descent to a lower altitude.

Treatment of acute mountain sickness by simulated descent: a randomised controlled trial.

OBJECTIVE--To evaluate the therapeutic efficacy of a portable hyperbaric chamber for treatment of acute mountain sickness. DESIGN--Controlled randomised trial over two mountaineering seasons. SETTING--High altitude research laboratory at 4559 m above sea level. SUBJECTS--64 climbers with acute mountain sickness randomly allocated to different treatments. INTERVENTIONS--One hour of treatment in the hyperbaric chamber at a pressure of 193 mbar or 20 mbar as control or bed rest. MAIN OUTCOME MEASURES--Symptoms of acute mountain sickness before, immediately after, and 12 hours after treatment. Permitted intake of analgesic and antiemetic drugs in the follow up period. RESULTS--Treatment with 193 mbar caused greater relief of symptoms than did control treatment or bed rest. During the 12 hour follow up period intake of analgesics was similar (58-80% of subjects in each group). Symptom scores had improved in all subjects after 12 hours with no significant differences between groups. CONCLUSIONS--One hour of treatment with 193 mbar in a portable hyperbaric chamber, corresponding to a descent of 2250 m, leads to a short term improvement in symptoms of acute mountain sickness but has no beneficial long term effects attributable to pressurisation.

Simulated descent v dexamethasone in treatment of acute mountain sickness: a randomised trial.

Abstract Objective: Evaluation and comparison of the therapeutic efficacy of a portable hyperbaric chamber and dexamethasone in the treatment of acute mountain sickness. Design: Randomised trial during the summer mountaineering season. Setting: High altitude research laboratory in the Capanna Regina Margherita at 4559m above sea level (Alps Valais). Subjects: 31 climbers with symptoms of acute mountain sickness randomly assigned to different treatments. Interventions: One hour of treatment in the hyperbaric chamber at a pressure of 193 mbar or oral administration of 8mg dexamethasone initially, followed by 4 mg after 6 hours. Main outcome measures: Symptoms of acute mountain sickness (Lake Louise score, clinical score, and AMS-C score) before one and about 11 hours after beginning the different methods of treatment. Permitted intake of mild analgesics before treatment and in the follow up period. Results: After one hour of treatment compression with 193mbar caused a significantly greater relief of symptoms of acute mountain sickness than dexamethasone (Lake Louise score: mean (SD) -4.6 (1.9) v -2.5 (1.8); clinical score: -4.0 (1.2) v -1.5 (1.4); AMS-C score: -1.24 (0.51) v -0.54 (0.59)). In contrast after about 11 hours subjects treated with dexamethasone suffered from significantly less severe acute mountain sickness than subjects treated with the hyperbaric chamber (-7.0 (3.6) v -1.6 (3.0); -4.1 (1.9) v -1.0 (1.5); -1.78 (0.73) v -0.75 (0.82) respectively). Intake of analgesics was similar in both groups. Conclusion: Both methods were efficient in treatment of acute mountain sickness. One hour of compression with 193mbar in the hyperbaric chamber, corresponding to a descent of 2250m, led to short term improvement but had no long term beneficial effect. On the other hand, treatment with dexamethasone in an oral dose of 8mg initially followed by 4mg every 6 hours resulted in a longer term clinical improvement. For optimal efficacy the two methods should be combined if descent or evacuation is not possible. Key messages Key messages Simulated descent in a hyperbaric chamber quickly relieves symptoms but the effect is short lived The drug dexamethasone takes longer to work but the effect is longer lasting A combination of the two methods may be the treatment of choice when the subject cannot be transported to lower altitudes

Relationship of mountain sickness to physical fitness and exercise intensity during ascent

The purpose of the study was to investigate whether susceptibility to acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) is related to differences of physical fitness and /or the level of exercise during ascent. Work capacity at a heart rate of 170 min −1 (PWC 170 ) was assessed on a bicycle ergometer prior to high-altitude exposure, and the heart rate was continuously registered during the ascent from 3610 to 4559 m in 41 mountaineers. During the subsequent stay of 3 days at 4559 m, 12 subjects developed AMS, 13 subjects showed radiographic evidence of HAPE, and 16 subjects remained without significant illness. PWC 170 (group means between 238 and 247 W) and heart rate during ascent (group means between 134 and 141 min −1 ) did not significantly differ between these groups. PWC 170 correlated negatively with two independent symptoms scores (clinical score, environmental symptom questionnaire) on day 3 at 4559 m, whereas heart rate during ascent correlated positively only with clinical score on days 2 and 3 at 4559 m. Correlations, however, were minor, with correlation coefficients of r =0.32–0.43 (p

Characteristics of the ventilatory response in subjects susceptible to high altitude pulmonary edema during acute and prolonged hypoxia.

The present study compares the changes in ventilation in response to sustained hypobaric hypoxia and acute normobaric hypoxia between subjects susceptible to high altitude pulmonary edema (HAPE-S) and control subjects (C-S). Seven HAPE-S and five C-S were exposed to simulated high altitude of 4000 m for 23 h in a hypobaric chamber. Resting minute ventilation (V(E)), tidal volume (V(T)), and respiratory frequency (f(R)), as well as the end-tidal partial pressures of oxygen (P(ET(O2))) and carbon dioxide (P(ET(CO2))) were measured in all subjects sitting in a standardized position. Six measurement periods were recorded: ZH1 at 450 m at Zurich level, HA1 on attaining 3600 m altitude, HA2 after 20 min at 4000 m, HA3 after 21 h and HA4 after 23 h at 4000 m altitude, and ZH2 immediately after recompression to Zurich level. At ZH1 and HA3, the measurements were first done in lying, then in sitting, and afterwards in standing. Peripheral arterial oxygen saturation (Sa(O2)) was continuously recorded. All respiratory parameters were also measured during exercise lasting 30 min, the work load being 50% of maximal oxygen consumption (V(O2max)) at Zurich level and 26% of the Zurich V(O2max) at 4000 m. V(E), P(ET(O2)) and P(ET(CO2)) did not significantly differ between HAPE-S and C-S at rest and during exercise periods at Zurich level and at high altitude. However, Sa(O2) was significantly lower in HAPE-S than in C-S at rest and during exercise at 4000 m. Breathing through the mouthpiece during ventilation measurements increased significantly the Sa(O2) in HAPE-S in posture tests at HA3. This effect was most pronounced in the supine posture, in which HAPE-S had the lowest Sa(O2) values. These data provide evidence that (1) gas exchange might be impaired on the level of ventilation-perfusion mismatch or due to diffusion limitation in HAPE-S during the first 23 h of exposure to a simulated altitude of 4000 m, and (2) contrary to C-S, the Sa(O2) in HAPE-S is significantly affected by body position and by mouthpiece breathing.

Accident on Mt Kenya

The following account first appeared in 1999 in the autobiography of Dr Oswald Oelz. In addition to being an Editor Emeritus of Wilderness and Environmental Medicine, Dr Oelz was the Chief of the Medical Staff of Triemli Hospital in Zürich, Switzerland. He is also known for his accomplishments as an extreme climber, expedition doctor, and expert in high altitude medicine. From Mit Eispickel und Stethoskop (With Ice Axe and tethoscope) by Oswald Oelz, MD (©1999 AS Verlag, ürich) Translated from the original German by Ken afren, MD.