Hohenhaus E, Paul A, McCullough R E, Kücherer H, Bärtsch P
Dept of Sports Medicine, University of Heidelberg, Germany.
Eur Respir J. 1995 Nov;8(11):1825-33. doi: 10.1183/09031936.95.08111825.
Reduced tolerance to high altitude may be associated with a low ventilatory and an increased pulmonary vascular response to hypoxia. We therefore, examined whether individuals susceptible to acute mountain sickness (AMS) or high altitude pulmonary oedema (HAPE) could be identified by noninvasive measurements of these parameters at low altitude. Ventilatory response to hypoxia (HVR) and hypercapnia (HCVR) at rest and during exercise, as well as hypoxic pulmonary vascular response (HPVR) at rest, were examined in 30 mountaineers whose susceptibility was known from previous identical exposures to high altitude. Isocapnic HVR expressed as difference in minute ventilation related to difference in arterial oxygen saturation (delta V'E/ delta Sa,O2) (L.min-1/%) was significantly lower in subjects susceptible to HAPE (mean +/- SEM 0.8 +/- 0.1; n = 10) compared to nonsusceptible controls (1.5 +/- 0.2; n = 10), but was not significantly different from subjects susceptible to AMS (1.2 +/- 0.2; n = 10). Hypercapnic ventilatory response was not significantly different between the three groups. Discrimination between groups could not be improved by measurements of HVR during exercise (50% maximum oxygen consumption (V'O2,max)), or by assessing ventilation and oxygen saturation during a 15 min steady-state exercise (35% V'O2,max) at fractional inspiratory oxygen (FI,O2) of 0.14. Pulmonary artery pressure (Ppa) estimated by Doppler measurements of tricuspid valve pressure at an FI,O2 of 0.21 and 0.12 (10 min) did not lead to a further discrimination between subjects susceptible to HAPE and AMS with the exception of three subjects susceptible to HAPE who showed an exaggerated HPVR. It is concluded that a low ventilatory response to hypoxia is associated with an increased risk for high altitude pulmonary oedema, whilst susceptibility to acute mountain sickness may be associated with a high or low ventilatory response to hypoxia. A reliable discrimination between subjects susceptible to high altitude pulmonary oedema and acute mountain sickness with a low ventilatory response to hypoxia is not possible by Doppler echocardiographic estimations of hypoxic pulmonary vascular response.
对高海拔的耐受性降低可能与通气功能低下以及对低氧的肺血管反应增强有关。因此，我们研究了是否可以通过在低海拔地区对这些参数进行无创测量来识别易患急性高原病（AMS）或高原肺水肿（HAPE）的个体。在30名登山者中，检测了静息和运动时对低氧（HVR）和高碳酸血症（HCVR）的通气反应，以及静息时的低氧肺血管反应（HPVR），这些登山者的易感性可从之前相同的高海拔暴露情况得知。与不易感的对照组（1.5±0.2；n = 10）相比，易患HAPE的受试者（平均±标准误0.8±0.1；n = 10）以分钟通气量差异与动脉血氧饱和度差异的比值表示的等碳酸血症HVR（δV'E/δSa,O2）（L·min-1/%）显著更低，但与易患AMS的受试者（1.2±0.2；n = 10）无显著差异。三组之间的高碳酸血症通气反应无显著差异。通过运动时（最大耗氧量（V'O2,max）的50%）的HVR测量，或在吸入氧分数（FI,O2）为0.14的15分钟稳态运动（V'O2,max的35%）期间评估通气和血氧饱和度，均无法改善组间的区分。在FI,O2为0.21和0.12（10分钟）时，通过多普勒测量三尖瓣压力估算的肺动脉压（Ppa），除了三名易患HAPE且表现出过度HPVR的受试者外，并未进一步区分易患HAPE和AMS的受试者。结论是，对低氧的通气反应低下与高原肺水肿风险增加有关，而对急性高原病的易感性可能与对低氧的通气反应高或低有关。通过多普勒超声心动图估算低氧肺血管反应，无法可靠地区分对低氧通气反应低下的高原肺水肿和急性高原病易感个体。
