Measurement of arterial blood gases at the transition from exercise to rest.
Measurement of arterial blood gases at the transition from exercise to rest.
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从运动到休息过渡时测量动脉血气。
DOI：
10.1152/jappl.1983.54.5.1340
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Lewis,BM
中科院分区：
文献类型：
--
作者：
Lewis,BM
对137名受试者进行了爬楼梯运动后5-20 s的动脉血气分析，并与最后30 s的动脉血气分析进行了比较。动脉CO2分压（PaCO 2）没有显著变化，在110例受试者中，两个样本均在分析变异范围内（+/- 2 Torr），支持呼吸调节的心脏动力学假设。10名受试者在运动期间过度通气（PaCO 2小于34），15名受试者患有重度阻塞[1秒用力呼气量（FEV 1）小于70%用力肺活量（FVC），FVC小于70%预测值]，其中PaCO 2显著增加。总体而言，动脉血氧分压（PaO 2）平均增加3.49 Torr（P <0.001）。在PaCO 2升高的两组中，运动后PaO 2没有升高。此外，运动持续时间影响PaO 2反应。PaO 2在短时间（小于2分钟）运动后比长时间（4-6分钟）运动后显著增加，并且这种差异仅在分析正常或临界呼吸功能的受试者时增加。在13名受试者中，在运动后30-45秒采集了第二份样本，PaO 2的增加是渐进的，短期和长期运动之间的差异再次明显。调节呼吸以维持PaCO 2和O2-CO2动力学变化，导致运动-休息过渡时气体交换率增加，是这些数据的最可能解释，这些数据确定了正常受试者和大多数患者停止运动的通常反应是PaCO 2不变和PaO 2可变增加。
Arterial blood gas samples obtained 5–20 s after stair-climbing exercise were compared with samples taken during the last 30 s of exercise in 137 subjects. Arterial partial pressure of CO2 (PaCO2) did not change significantly, and in 110 subjects the two samples were within the analytical variation (+/- 2 Torr), supporting the cardiodynamic hypothesis of respiratory regulation. Exceptions to this response were 10 subjects who hyperventilated (PaCO2 less than 34) during exercise and 15 with severe obstruction [forced expiratory volume in 1 s (FEV1) less than 70% forced vital capacity (FVC), and FVC less than 70% of predicted] in whom PaCO2 increased significantly. Overall, arterial partial pressure of O2 (PaO2) increased an average of 3.49 Torr (P less than 0.001). In the two groups in which PaCO2 increased, postexercise PaO2 did not rise. In addition, duration of exercise affected PaO2 response. PaO2 increased significantly more after brief (less than 2 min) periods than after longer (4–6 min) exercise, and this difference increased only when subjects with normal or borderline ventilatory function were analyzed. In 13 subjects in whom a second sample was taken 30–45 s after exercise, the increase in PaO2 was progressive and again the difference between short and long exercise was evident. Regulation of respiration to maintain PaCO2 and changes in O2-CO2 kinetics, leading to an increase in the gas exchange ratio at the exercise-rest transition, are the most likely explanations of these data which establish that the usual response to stopping exercise in normal subjects and most patients is an unchanged PaCO2 and a variable increase in PaO2.
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