Swinburn C R, Wakefield J M, Jones P W
Clin Sci (Lond). 1984 Nov;67(5):515-9. doi: 10.1042/cs0670515.
We have examined the hypothesis that hypoxaemia contributes to breathlessness by a mechanism distinct from its action as a ventilatory stimulant. Five patients who developed arterial oxygen desaturation during incremental exercise were studied. Exercise tests were performed on a cycle-ergometer. Breathlessness was measured by using a visual analogue scale technique. All five patients had considerable previous experience of these procedures. Two identical exercise tests were performed by each patient, breathing either room air or 60% oxygen in a blind randomized study. Breathing air, arterial saturation at rest was 93% and fell by 7% during exercise. Breathing 60% oxygen, resting saturation was 98% and there was no fall during exercise. Breathing oxygen, ventilation for a given work load was reduced and exercise duration was increased when compared with air breathing. In each of the five patients the relationship between breathlessness and minute ventilation was the same whether breathing air or 60% oxygen, despite the reduction in ventilation for a given work rate.
我们检验了这样一种假说,即低氧血症通过一种与其作为通气刺激物的作用不同的机制导致呼吸急促。对5名在递增运动过程中出现动脉血氧饱和度下降的患者进行了研究。运动测试在自行车测力计上进行。使用视觉模拟量表技术测量呼吸急促程度。所有5名患者此前都对这些程序有相当丰富的经验。在一项盲法随机研究中,每位患者进行了两次相同的运动测试,分别呼吸室内空气或60%的氧气。呼吸空气时,静息时动脉血氧饱和度为93%,运动期间下降了7%。呼吸60%的氧气时,静息饱和度为98%,运动期间没有下降。与呼吸空气相比,呼吸氧气时,给定工作负荷下的通气量减少,运动持续时间增加。在这5名患者中,无论呼吸空气还是60%的氧气,呼吸急促与分钟通气量之间的关系都是相同的,尽管给定工作率下的通气量有所减少。