Phillips B A, McConnell J W, Smith M D
Department of Medicine, University of Kentucky College of Medicine, Lexington.
Chest. 1988 Mar;93(3):471-5. doi: 10.1378/chest.93.3.471.
To establish a dose-response curve for the effects of isocapnic hypoxemia on cardiac output (CO), we studied 20 healthy men, aged 20 to 34 years, using a tight-fitting face mask and an isocapnic partial rebreathing system (a modified anesthesia machine). We blended oxygen and hypoxic gas to achieve arterial oxygen saturations (SaO2) of 80, 85, and 90 percent; subjects also breathed 100 percent oxygen and room air (RA). Target SaO2 and end-tidal carbon dioxide were continuously monitored using an ear oximeter and CO2 gas analyzer. Subjects experienced the five SaO2 measurements in random order. CO was measured noninvasively at approximately two-minute intervals, using continuous-wave Doppler echocardiography. Mean cardiac output increased with increasing hypoxemia from 6.84 L/min at FIo2 1.0 to 8.44 L/min at SaO2 80 percent (p less than 0.0005); the increase was entirely due to increased heart rate. We concluded that cardiac output increases significantly in a dose-response manner in response to acute isocapnic hypoxemia in normal persons.
为了建立等碳酸血症性低氧血症对心输出量（CO）影响的剂量反应曲线，我们使用紧密贴合的面罩和等碳酸血症部分再呼吸系统（改良麻醉机）对20名年龄在20至34岁的健康男性进行了研究。我们混合氧气和低氧气体以达到动脉血氧饱和度（SaO2）为80%、85%和90%；受试者还呼吸100%氧气和室内空气（RA）。使用耳式血氧计和二氧化碳气体分析仪持续监测目标SaO2和呼气末二氧化碳。受试者以随机顺序经历这五种SaO2测量。使用连续波多普勒超声心动图以大约两分钟的间隔无创测量CO。随着低氧血症加重，平均心输出量从吸入氧分数（FIo2）为1.0时的6.84 L/分钟增加到SaO2为80%时的8.44 L/分钟（p小于0.0005）；这种增加完全是由于心率增加所致。我们得出结论，在正常人中，急性等碳酸血症性低氧血症会以剂量反应方式使心输出量显著增加。
