Domej W, Tilz G P, Dimai H P, Friedl K, Berghold F, Lang J K, Schwaberger G
Department of Internal Medicine, Karl-Franzens-University, Graz, Austria.
Wien Klin Wochenschr. 2001 Feb 15;113(3-4):130-3.
High-altitude pulmonary edema (HAPE), a potentially life-threatening altitude adaptation disorder, is considered to be caused by an exaggerated increase in pulmonary blood pressure and a non-cardiogenic rise in pulmonary vascular permeability subsequent to alveolar hypoxia. A 40-year-old male mountaineer was affected by an advanced stage of HAPE at high altitude (Monte Rosa plateau, 4000 m). The symptoms abated immediately after the patient descended from the altitude. However, six hours after the symptoms had resolved, radiographic signs of pulmonary edema, confined to the right lung, were seen. This rarely described unilateral radiological pattern of HAPE resolved completely within two days. We suggest that aspiration events of nasal secretion, the right sleeping position at night and an elevated right diaphragm reduced the patient's compensatory hyperventilation capacity of the right lung. The resulting increased alveolar hypoxia in the right lung was responsible for unilateral edema. The pathophysiological mechanism underlying unilateral HAPE is discussed.
高原肺水肿(HAPE)是一种潜在的危及生命的高原适应障碍,被认为是由肺泡缺氧后肺血压过度升高和肺血管通透性非心源性升高引起的。一名40岁的男性登山者在高海拔地区(罗莎峰高原,4000米)患上了晚期高原肺水肿。患者从高海拔地区下降后症状立即减轻。然而,症状缓解六小时后,出现了仅局限于右肺的肺水肿影像学征象。这种很少被描述的高原肺水肿单侧放射学模式在两天内完全消退。我们认为,夜间右侧卧位、右膈肌抬高以及鼻分泌物吸入事件降低了患者右肺的代偿性过度通气能力。由此导致的右肺肺泡缺氧增加是单侧水肿的原因。本文讨论了单侧高原肺水肿的病理生理机制。