Westendorp R G, Blauw G J, Frölich M, Simons R
Department of Clinical Epidemiology, Leiden University Hospital, The Netherlands.
Aviat Space Environ Med. 1997 May;68(5):410-4.
Syncope at altitude of otherwise healthy individuals is a well-known phenomenon (22). We report on the cardiovascular effects observed in subjects exposed to hypoxia to illustrate the role of the sympathetic-adrenergic system in hypoxic syncope. This study describes unexpected episodes of (near) syncope during two crossover trials at simulated altitude in a low pressure chamber.
In study A, 30 healthy male volunteers underwent 4 exposures to short-term (20 min) acute severe hypoxia (20,000 ft or 6096 m) to assess psychological performance. In study B, five volunteers were studied during prolonged exposure (1 h) to moderate hypoxia (13,500 ft or 4115 m) with and without concomitant low dose infusion with atrial natriuretic peptide to investigate the effects on pulmonary gas exchange.
In study A (acute severe hypoxia), 6 out of 120 exposures (5%), in 5 subjects, were accompanied by lightheadedness, pallor, sweating, and bradycardia. Two subjects (2%) had syncope with cardiac asystole. In study B during moderate hypoxia without atrial natriuretic peptide, adverse reactions were absent and the (nor)epinephrine levels remained unchanged. Concomitant infusion with atrial natriuretic peptide resulted in near syncope (recumbent in 3, standing in 2) at an oxygen saturation of 82%. While the epinephrine level had eightfold increased, mean arterial pressure fell from 94 to 40 mm Hg and heart rate from 79 to 44 bpm. The norepinephrine level remained unchanged illustrating a dissociated sympathetic-adrenergic response. All subjects with syncope recovered spontaneously within few minutes in Trendelenburg's position with oxygen supplied. None suffered from prolonged side effects.
It is concluded that exposure to acute severe hypoxia is a sufficient cause for syncope in healthy individuals. Enhanced vasodilatation to epinephrine may contribute to the withdrawal of sympathetic and enhancement of parasympatic activity, leading to vascular collapse, bradycardia or asystole (Bezold-Jarisch reflex). Patients fully recover in Trendelenburg's position with supplemental oxygen and further clinical examinations are not necessary.
原本健康的个体在高原地区发生晕厥是一种众所周知的现象（22）。我们报告了在暴露于低氧环境的受试者中观察到的心血管效应，以说明交感 - 肾上腺素能系统在低氧性晕厥中的作用。本研究描述了在低压舱模拟高原的两项交叉试验中出现的意外（近乎）晕厥发作。
在研究A中，30名健康男性志愿者接受了4次短期（20分钟）急性重度低氧（20000英尺或6096米）暴露，以评估心理表现。在研究B中，5名志愿者在长时间暴露（1小时）于中度低氧（13500英尺或4115米）的情况下进行了研究，分别在有无同时输注低剂量心房利钠肽的情况下，以研究对肺气体交换的影响。
在研究A（急性重度低氧）中，120次暴露中有6次（5%），涉及5名受试者，伴有头晕、面色苍白、出汗和心动过缓。两名受试者（2%）发生了心脏停搏性晕厥。在研究B中，在中度低氧且未使用心房利钠肽的情况下，未出现不良反应，（去甲）肾上腺素水平保持不变。同时输注心房利钠肽导致在氧饱和度为82%时出现近乎晕厥（3人卧位，2人站立位）。虽然肾上腺素水平增加了八倍，但平均动脉压从94毫米汞柱降至40毫米汞柱，心率从79次/分钟降至44次/分钟。去甲肾上腺素水平保持不变，说明了交感 - 肾上腺素能反应的分离。所有晕厥受试者在给予氧气的情况下，采用头低脚高位，几分钟内自发恢复。无人出现长期副作用。
得出的结论是，暴露于急性重度低氧是健康个体发生晕厥的充分原因。对肾上腺素增强的血管舒张作用可能有助于交感神经的撤离和副交感神经活动的增强，导致血管塌陷、心动过缓或心脏停搏（贝佐尔德 - 雅里什反射）。患者采用头低脚高位并补充氧气后可完全恢复，无需进一步的临床检查。
