Hemoglobin P(50) during a simulated ascent of Mt. Everest, Operation Everest II

The amount of O(2) available to tissues is essentially the product of cardiac output, [Hb], and O(2) saturation. Saturation depends on P(O2) and the O(2)Hb dissociation curve. With altitude, increased [2,3-DPG] shifts the dissociation curve rightward, but hypocapnia and alkalosis move it leftward. We determined both standard and in vivo P(50) in 5 fit subjects decompressed over 42 days in an altitude chamber to the equivalent of the Mt. Everest summit (Operation Everest II). Arterial and venous blood was sampled at five "altitudes " (P(B) = 760, 429, 347, 282, 253 mmHg), and P(O2), P(CO2), pH, O(2) saturation, [Hb] and [2,3-DPG] were measured. As reported previously, 2,3-DPG levels increased from 1.7 (P(B) = 760) to 3.8 mmol/L (P(B) = 282). Standard P(50) also increased (from 28.2 mmHg at sea level to 33.1 on the summit, p<0.001). Alone, this would have lowered saturation by 12 percentage points at a summit arterial P(O2) of approximately 30 mmHg. However, in vivo P(50) remained between 26 and 27 mmHg throughout due to progressive hypocapnia and alkalosis. Calculations suggest that the increase in standard P(50) did not affect summit V(O2 MAX)), alveolar, arterial and venous P(O2)'s, but reduced arterial and venous O(2) saturations by 8.4 and 17.4 points, respectively, and increased O(2) extraction by 7.9 percentage points. Reduced saturation was balanced by increased extraction, resulting in no significant overall O(2) transport benefit, thus leaving unanswered the question of the purpose of increased [2,3-DPG] concentrations at altitude.     

Everest 1953, first ascent: a clinical record

No mountaineering expedition to Mt. Everest mounted by the Royal Geographical Society and the Alpine Club from 1921 onward reached the summit, despite the mountaineering difficulties being of a similar order to those found on the ascent of Mont Blanc (15,800 ft), the highest peak in Europe, which was first climbed in 1786. The reason for their lack of success was their inability to solve the medical and physiological problems imposed by the altitude and cold of the last thousand feet, between 28,000 and 29,028 ft. It was the solution of these problems by the Medical Research Council, backed by the Royal Society, in London, in early 1951 through 1952 that made the breakthrough leading to success in 1953. During the first ascent, in order to assess the effectiveness of these solutions, accounts were taken immediately on their descent from every climber who had been as high as the South Col (26,000 ft) or higher, including the two who had reached the summit (29,028 ft). These accounts provided a unique record and illustrated, for the first time in 30 years of Everest expeditions, how the use of adequate flow rates of supplementary oxygen when climbing, adequate supplementary oxygen when sleeping, adequate daily fluid intake, and adequate protection from the cold could transform the performance of climbers at extreme altitude from "sick men climbing in a dream" to those capable of overcoming all climatic and mountaineering obstacles. None of these advantages had been available to mountaineers of British parties of the 1920s and 1930s, nor to the Swiss expeditions in the spring and autumn of 1952, with the result that none of them was successful in reaching the summit.     

Ludolph Brauer, German aeromedical pioneer

Ludolph Brauer (1865-1951) played an influential role in the history of aviation medicine in Germany. The Treaty of Versailles had put a stop to the development of German aviation and associated medical activities at the end of World War I. Brauer deserves credit for restarting civilian aviation medicine in Germany in the 1920s, paving the way for it to flourish in the 1930s. As Medical Director of the Hamburg-Eppendorf General Hospital, Brauer established the first German Institute of Aviation Medicine (GIAM) in 1927 in affiliation with the Tuberculosis Research Institute with its two large pneumatic chambers. The GIAM was active in altitude research and the selection of pilots, as well as educating medical students in aviation medicine, training Aviation Medical Examiners, and exploring clinical applications of hypobaric and climatic therapy. Brauer was forced to retire in 1934 for political reasons as the GIAM came under the influence of the military; in 1939 it was made part of the Aeromedical Research Institute of the "Reichsluftfahrt" Ministry. Brauer was a co-editor of the journal Luftfahrtmedizin in the 1930s and 1940s. He died in Munich on November 25th, 1951.     

A tale of two climbers: hypothermia, death, and survival on Mount Everest

Hypothermia is an acknowledged risk for those who venture into high altitude regions. There is however little quantitative information on this risk that can be used to implement mitigation strategies. Here we provide an analysis of the meteorological and hypothermic risk parameters, wind chill temperature, and facial frostbite time, during the spring 2006 Mount Everest climbing season. This season was marked by two high profile events where a solo climber was forced to spend the night in highly exposed conditions near the summit. One climber survived, while the other did not. Although this retrospective examination of two individual cases has admittedly a small sample size, and there are other factors that undoubtedly contributed to the difference in outcomes, we show that wind chill temperature and facial frostbite time experienced by the two climbers were dramatically different. In particular, the climber who did not survive experienced conditions that were approximately one standard deviation more severe that usual for that time of the year; while the climber who survived experienced conditions that were approximately one standard deviation less severe then usual. This suggests that the environmental conditions associated with hypothermia played an important role in the outcomes. This report confirms the importance of providing quantitative guidance to climbers as the risk of hypothermia on high mountains.     

Transient neurological disorders during a simulated ascent of Mount Everest

BACKGROUND: Transient neurological disorders are often observed at high altitude but are poorly documented under field conditions. The mechanism usually invoked is a hypocapnic vasoconstriction due to severe hypoxic hyperventilation. During a simulated ascent of Mount Everest in a hypobaric chamber by eight volunteer alpinists (Operation Everest III, Comex '97), three subjects presented neurological symptoms. We report here on the clinical observations and testing to detect mechanisms in addition to hypocapnic vasoconstriction. METHODS: The experiment was designed to investigate factors limiting physiological performance at altitude and the pathophysiology of acute mountain sickness. A retrospective analysis was made comparing the three cases of transient neurological disorder at high altitude (TNDHA) with the five subjects who had no neurological symptoms. RESULTS: Analysis of clinical and blood parameters showed no difference between cases and controls. The cases showed no neurological sequelae following the experiment and were normal on cardiac imaging. However, one case had a history of migraine in his youth, leading us to hypothesize that segmental vasoconstriction was a factor. In another case, gas bubbles were detected in the pulmonary artery by transthoracic echocardiography when he was symptomatic, suggesting that gas emboli may have played a role. All three cases shared a possible triggering factor in that each experienced hyperventilation alternating with straining against a closed glottis shortly before the onset of symptoms. CONCLUSION: Mechanisms other than hypocapnic vasoconstriction in hypoxia may be causal factors of TNDHA. The existence of triggering factors and evidence of a possible embolic mechanism should be further explored.     

Theodor Benzinger, German pioneer in high altitude physiology research and altitude protection

Theodore Benzinger was a pilot-physician who performed pioneering research-often involving self-experimentation-in areas related to flight at high altitude during World War II. Of greatest historical interest to those of us in aerospace medicine is his work on the effects of rapid decompression and related oxygen equipment. Benzinger was born in Stuttgart, Germany, on 28th August 1905. He studied medicine and natural sciences at the universities of Tuebingen, Munich, and Berlin. From 1934 to 1944, Benzinger headed the aeromedical laboratory "EMed" in Rechlin, where he was instrumental in conducting studies related to stratospheric flight, including self-experimentation with rapid decompression up to 19,000 m (62,320 ft). His Rechlin experiments made an important contribution to understanding the physiology and life-support requirements for high-altitude aviation and later work under space-equivalent conditions. Following World War II, Benzinger joined the staff of the U.S. Army Air Force Aeromedical Center in Heidelberg. In 1947 he was recruited by "Operation Paperclip" to work at the U.S. Naval Medical Research Institute (NMRI) in Bethesda, MD, where he worked on various aspects of human physiology. He died as a U.S. citizen in Bethesda, MD, on 26th October 1999.