Division of Anesthesiology and Pain Medicine, Children's National Medical Center, 111 Michigan Ave., NW, Washington, DC 20010, USA.
Anesth Analg. 2010 Mar 1;110(3):747-53. doi: 10.1213/ANE.0b013e3181cc4b9f.
Carbon monoxide (CO) can be produced in the anesthesia circuit when inhaled anesthetics are degraded by dried carbon dioxide absorbent and exhaled CO can potentially be rebreathed during low-flow anesthesia. Exposure to low concentrations of CO (12.5 ppm) can cause neurotoxicity in the developing brain and may lead to neurodevelopmental impairment. In this study, we aimed to quantify the amount of CO present within a circle system breathing circuit during general endotracheal anesthesia in infants and children with fresh strong metal alkali carbon dioxide absorbent and define the variables associated with the levels detected.
Fifteen infants and children (aged 4 months to 8 years) undergoing mask induction followed by general endotracheal anesthesia were evaluated in this observational study. CO was measured in real time from the inspiratory limb of the anesthesia circuit every 5 minutes for 1 hour during general anesthesia. Carboxyhemoglobin (COHb) levels were measured at the 1-hour time point and compared with baseline.
CO was detected in all patients older than 2 years (0-18 ppm, mean 3.7 +/- 4.8 ppm) and rarely detected in patients younger than 2 years (0-2 ppm, mean 0.2 +/- 0.6 ppm). Only the relationship between CO concentration and fresh gas flow to minute ventilation ratio (FGF:(.)VE) remained significant after adjustment in longitudinal regression analysis (P < 0.001). Although not powered to determine such a relationship, CO levels were weakly associated with the use of desflurane and female sex. There was no significant association between CO concentration and anesthetic concentration. Baseline COHb levels were higher in children younger than 2 years and decreased significantly at the 1-hour time point compared with baseline and children older than 2 years. However, COHb levels increased significantly from baseline in a predictable manner consistent with CO exposure in children older than 2 years. FGF:(.)VE correlated significantly with change in COHb using simple linear regression (r = 0.62; P < 0.02).
CO was detected routinely during general anesthesia in infants and children when FGF:(.)VE was <1. Peak CO levels measured in the anesthesia breathing circuit were in the range thought to impair the developing brain. Further study is required to identify the source of CO detected (CO produced by degradation of volatile anesthetic versus rebreathing CO from endogenous sources or both). However, these findings suggest that avoidance of low-flow anesthesia will prevent rebreathing of exhaled CO, and use of carbon dioxide absorbents that lack strong metal hydroxide could limit inspired CO if detection was attributable to degradation of volatile anesthetic.
当吸入麻醉剂被干燥的二氧化碳吸收剂降解时,麻醉回路中会产生一氧化碳(CO),并且在低流量麻醉期间呼出的 CO 可能会被再次吸入。暴露于低浓度的 CO(12.5ppm)可导致发育中的大脑神经毒性,并可能导致神经发育障碍。在这项研究中,我们旨在量化新鲜强碱金属碱式碳酸吸收剂在婴儿和儿童全身气管内麻醉期间,圆形系统呼吸回路中存在的 CO 量,并确定与检测到的水平相关的变量。
本观察性研究评估了 15 名接受面罩诱导后行全身气管内麻醉的婴儿和儿童。在全身麻醉期间,每隔 5 分钟从麻醉回路的吸气支实时测量 CO,共 1 小时。在 1 小时时间点测量碳氧血红蛋白(COHb)水平,并与基线水平进行比较。
所有年龄大于 2 岁的患者(0-18ppm,平均 3.7+/-4.8ppm)均检测到 CO,而年龄小于 2 岁的患者很少检测到 CO(0-2ppm,平均 0.2+/-0.6ppm)。只有在纵向回归分析中调整了新鲜气体流量与分钟通气量比(FGF:VE)的关系后,CO 浓度仍然具有显著意义(P<0.001)。虽然没有足够的力量来确定这种关系,但 CO 水平与使用地氟烷和女性性别呈弱相关。CO 浓度与麻醉浓度之间无显著相关性。与基线相比,年龄小于 2 岁的儿童在 1 小时时间点的基线 COHb 水平显著升高,而年龄大于 2 岁的儿童则显著降低。然而,年龄大于 2 岁的儿童 COHb 水平以可预测的方式显著升高,与 CO 暴露一致。简单线性回归显示,FGF:VE 与 COHb 的变化显著相关(r=0.62;P<0.02)。
当 FGF:VE<1 时,在婴儿和儿童全身麻醉期间常规检测到 CO。在麻醉呼吸回路中测量到的 CO 峰值水平处于被认为会损害发育中大脑的范围内。需要进一步研究以确定检测到的 CO 的来源(是挥发性麻醉剂降解产生的 CO,还是源自内源性来源的再呼吸 CO,或是两者兼而有之)。然而,这些发现表明,避免低流量麻醉将防止呼出 CO 的再呼吸,而使用缺乏强碱金属氢氧化物的二氧化碳吸收剂如果归因于挥发性麻醉剂的降解,则可限制吸入 CO。