Peter H Hackett

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Travel to a high altitude requires that the human body acclimatize to hypobaric hypoxia. Failure to acclimatize results in three common but preventable maladies known collectively as high-altitude illness: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). Capillary leakage in the brain (AMS/HACE)(More)
Acute mountain sickness (A.M.S.) and its severe complications, high-altitude pulmonary oedema (H.A.P.O.) and cerebral oedema (C.O.), were studied in 278 unacclimatised hikers at 4243 m altitude at Pheriche in the Himalayas of Nepal. The overall incidence of A.M.S. was 53%, the incidence being increased in the young and in those who flew to 2800 m, climbed(More)
CONTEXT Because of its onset in generally remote environments, high-altitude cerebral edema (HACE) has received little scientific attention. Understanding the pathophysiology might have implications for prevention and treatment of both this disorder and the much more common acute mountain sickness. OBJECTIVES To identify a clinical imaging correlate for(More)
Traditionally, scientists and clinicians have explored peripheral physiological responses to acute hypoxia to explain the pathophysiological processes that lead to acute mountain sickness (AMS) and high-altitude cerebral edema (HACE). After more than 100 years of investigation, little is yet known about the fundamental causes of the headache and nausea that(More)
This is an international consensus statement of an ad hoc committee formed by the International Society for Mountain Medicine (ISMM) at the VI World Congress on Mountain Medicine and High Altitude Physiology (Xining, China; 2004) and represents the committee's interpretation of the current knowledge with regard to the most common chronic and subacute high(More)
BACKGROUND Acute mountain sickness (AMS) is a usually self-limiting syndrome encompassing headache, nausea and dizziness. AMS is seen in those that go from low to high altitudes too quickly, without allowing sufficient time to acclimatize. At present, susceptibility to AMS cannot be predicted. One feature of AMS noted in some studies is impaired gas(More)
The presence of pulmonary, cerebral, and/or peripheral edema in acute mountain sickness (AMS) implies a derangement in the body's handling of water. Previously, we demonstrated water retention and increased symptoms of AMS when hypocapnia was prevented in subjects exposed to simulated high altitude. This led us to the hypothesis that upon ascent to high(More)
To assess the ventilatory adaptation during gradual ascent to extreme altitude, we studied seven healthy males as part of the 40 d simulated ascent of Mt. Everest in a hypobaric chamber. We measured resting ventilation (VE, l.min-1), arterial oxygen saturation (SaO2%), the ventilatory response to oxygen breathing, isocapnic hypoxic ventilatory response(More)
Pulmonary gas exchange was studied on members of the American Medical Research Expedition to Everest at altitudes of 8,050 m (barometric pressure 284 Torr), 8,400 m (267 Torr) and 8,848 m (summit of Mt. Everest, 253 Torr). Thirty-four valid alveolar gas samples were taken using a special automatic sampler including 4 samples on the summit. Venous blood was(More)
Maximal exercise at extreme altitudes was studied during the course of the American Medical Research Expedition to Everest. Measurements were carried out at sea level [inspired O2 partial pressure (PO2) 147 Torr], 6,300 m during air breathing (inspired PO2 64 Torr), 6,300 m during 16% O2 breathing (inspired PO2 49 Torr), and 6,300 m during 14% O2 breathing(More)