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首页> 外文期刊>Journal of clinical monitoring and computing >Effects of inspiratory oxygen concentration on endtidal carbon monoxide concentration.
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Effects of inspiratory oxygen concentration on endtidal carbon monoxide concentration.

机译:吸氧浓度对潮气中一氧化碳浓度的影响。

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Objective. Carbon monoxide (CO) is eliminated mainly via the lungs so that exhaled carbon monoxide concentration reflects endogenous production. In this context, we studied the effects of inspiratory oxygen concentration and endotracheal intubation on endtidal CO concentrations. Methods. In patients undergoing general anaesthesia, endtidal CO concentrations were measured while breathing room air, oxygen as well as after induction of general anaesthesia and endotracheal intubation. To exclude time-dependent effects, patients were assigned to two groups. Patients in group 1 (n = 20) were preoxygenated for 5 minutes, whereas patients in group 2 (n = 20) were preoxygenated for 10 minutes. We also studied the effects of different inspiratory oxygen concentrations in volunteers (n = 20) breathing room air, 50% and 100% oxygen. Results. Breathing oxygen for 5 minutes increased endtidal carbon monoxide concentrations in all patients (in group 1 from 7.6+/-4.9 to 12.6+/- 5.0 ppm, p < 0.001; in group 2 from 7.1+/-6.1 to 16.4 +/- 8.6 ppm, p < 0.001). No further change of CO concentration was detected after 10 minutes of preoxygenation (16.4 +/- 9.0 vs. 16.4 +/- 8.6 ppm, p > 0.05). Endtidal CO values however significantly increased with induction of anaesthesia and endotracheal intubation (in group 1 to 21.5 +/- 6.3 ppm, p < 0.001, in group 2 to 26.1 +/- 13.1 ppm, p < 0.001). In volunteers, mean endtidal CO values increased from 10.7 +/-5.9 to 14.8+/-7.3 ppm after breathing 50% oxygen for 3 minutes (p < 0.001). Breathing pure oxygen had no additional effect on endtidal CO values (16.0 +/- 6.0 ppm, p > 0.05). Conclusions. Endtidal carbon monoxide levels are influenced by inspiratory oxygen concentrations. Induction of anaesthesia and endotracheal intubation further increases endtidal CO concentrations beyond the effects attributable to preoxygenation alone.
机译:目的。一氧化碳(CO)主要通过肺部清除,因此呼出的一氧化碳浓度反映了内源性产生。在这种情况下,我们研究了吸氧浓度和气管内插管对潮气中一氧化碳浓度的影响。方法。在接受全身麻醉的患者中,在呼吸室内空气,氧气以及进行全身麻醉和气管内插管后,测量潮气中的CO浓度。为了排除时间依赖性的影响,将患者分为两组。第一组(n = 20)的患者被预充氧5分钟,而第二组(n = 20)的患者被预充氧10分钟。我们还研究了不同的吸氧浓度对志愿者(n = 20)呼吸室内空气,50%和100%的氧气的影响。结果。呼吸氧气5分钟可使所有患者的潮气中一氧化碳浓度增加(第1组从7.6 +/- 4.9增至12.6 +/- 5.0 ppm,p <0.001;第2组从7.1 +/- 6.1增至16.4 +/- 8.6 ppm,p <0.001)。预氧化10分钟后未检测到CO浓度的进一步变化(16.4 +/- 9.0对16.4 +/- 8.6 ppm,p> 0.05)。然而,随着麻醉的诱导和气管插管,潮气中CO值显着增加(第1组至21.5 +/- 6.3 ppm,p <0.001,第2组至26.1 +/- 13.1 ppm,p <0.001)。在志愿者中,呼吸50%的氧气3分钟后,平均内陆CO值从10.7 +/- 5.9增加到14.8 +/- 7.3 ppm(p <0.001)。呼吸纯氧对潮气中的CO值没有其他影响(16.0 +/- 6.0 ppm,p> 0.05)。结论。潮气中一氧化碳水平受吸氧浓度的影响。麻醉诱导和气管插管进一步增加了潮气中的CO浓度,超出了仅因预加氧引起的影响。

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