Nordahl SteinHelgeGlad, Aasen Torbjørn, Risberg Jan, Owe Jan Ove, Molvaer Otto Inge
Department of Otolaryngology/Head and Neck Surgery, Haukeland University Hospital, Bergen, Norway.
Aviat Space Environ Med. 2002 Mar;73(3):184-90.
Earlier studies have shown that acute hypoxia at simulated altitudes up to 18,000 ft affects postural control. The main objective of this study was to investigate whether this is caused by hypoxia or by other effects of reduced barometric pressure. Doppler monitoring was included to rule out venous gas emboli (VGE) as a possible cause of disturbed postural control. A secondary objective was to evaluate two conventional altitude chamber training profiles regarding release of VGE.
Chamber flights up to 18,000 ft affect postural control due to acute hypoxia or other effects of reduced barometric pressure such as bubble formation. VGE probably will not be formed at the altitude chamber flight profiles and procedures selected for this study.
Repeated registrations of postural control and Doppler monitoring for detection of possible VGE were performed on 12 subjects before, during, and after exposure to two different altitude chamber flight profiles. In chamber flight profile 1 the subjects were first preoxygenated for 45 min and then exposed to a normoxic environment at altitudes of 25,000, 18,000, 14,000, and 8000 ft. Chamber flight profile 2 consisted of an 80 min exposure to 14,000 ft without preoxygenation or supplemental oxygen for the first 60 min.
In chamber flight profile 1, where normoxic conditions were achieved during all balance testing, no significant changes in postural control were found. No VGE were observed and no subjective dizziness was reported during this exposure. In chamber flight profile 2, a significant influence on postural control was reported for the eyes-open condition, when breathing air at 14,000 ft. These changes normalized when reaching ground level. VGE were observed in one of the 12 subjects after 75 min at 14,000 ft. Another subject complained of severe dizziness during the initial part of the decompression to 14,000 ft, and was excluded from further experiments.
Changes in postural control at altitudes up to 18,000 ft is probably due to acute hypoxia. VGE may form during acute altitude exposure to 14,000 ft.
早期研究表明，在模拟海拔高达18000英尺的急性低氧环境会影响姿势控制。本研究的主要目的是调查这是由低氧引起的，还是由气压降低的其他影响导致的。采用多普勒监测以排除静脉气体栓塞（VGE）作为姿势控制紊乱的可能原因。次要目的是评估两种传统的高空舱训练方案对VGE释放的影响。
高达18000英尺的舱内飞行由于急性低氧或气压降低的其他影响（如气泡形成）而影响姿势控制。在本研究选择的高空舱飞行方案和程序中，可能不会形成VGE。
对12名受试者在暴露于两种不同的高空舱飞行方案之前、期间和之后，重复记录姿势控制情况并进行多普勒监测以检测可能的VGE。在舱内飞行方案1中，受试者首先进行45分钟的预充氧，然后暴露于25000英尺、18000英尺、14000英尺和8000英尺高度的常氧环境中。舱内飞行方案2包括在不进行预充氧或在前60分钟不补充氧气的情况下暴露于14000英尺80分钟。
在舱内飞行方案1中，在所有平衡测试期间均达到常氧条件，未发现姿势控制有显著变化。在此暴露期间未观察到VGE，也未报告主观头晕。在舱内飞行方案2中，当在14000英尺呼吸空气时，睁眼条件下姿势控制受到显著影响。到达地面水平时，这些变化恢复正常。在12名受试者中的一名在14000英尺75分钟后观察到VGE。另一名受试者在减压至14000英尺的初始阶段抱怨严重头晕，并被排除在进一步实验之外。
高达18000英尺海拔高度时姿势控制的变化可能是由于急性低氧。在急性海拔暴露于14000英尺时可能会形成VGE。
