Department of Anesthesiology and Intensive Care, Uppsala University, ANIVA ing 70 1tr, University hospital, S 75185 Uppsala, Sweden.
Crit Care. 2010;14(3):R93. doi: 10.1186/cc9027. Epub 2010 May 24.
Endotracheal intubation in critically ill patients is associated with severe life-threatening complications in about 20%, mainly due to hypoxemia. We hypothesized that apneic oxygenation via a pharyngeal catheter during the endotracheal intubation procedure would prevent or increase the time to life-threatening hypoxemia and tested this hypothesis in an acute lung injury animal model.
Eight anesthetized piglets with collapse-prone lungs induced by lung lavage were ventilated with a fraction of inspired oxygen of 1.0 and a positive end-expiratory pressure of 5 cmH2O. The shunt fraction was calculated after obtaining arterial and mixed venous blood gases. The trachea was extubated, and in randomized order each animal received either 10 L oxygen per minute or no oxygen via a pharyngeal catheter, and the time to desaturation to pulse oximeter saturation (SpO2) 60% was measured. If SpO2 was maintained at over 60%, the experiment ended when 10 minutes had elapsed.
Without pharyngeal oxygen, the animals desaturated after 103 (88-111) seconds (median and interquartile range), whereas with pharyngeal oxygen five animals had a SpO2 > 60% for the 10-minute experimental period, one animal desaturated after 7 minutes, and two animals desaturated within 90 seconds (P < 0.016, Wilcoxon signed rank test). The time to desaturation was related to shunt fraction (R2 = 0.81, P = 0.002, linear regression); the animals that desaturated within 90 seconds had shunt fractions >40%, whereas the others had shunt fractions <25%.
In this experimental acute lung injury model, pharyngeal oxygen administration markedly prolonged the time to severe desaturation during apnea, suggesting that this technique might be useful when intubating critically ill patients with acute respiratory failure.
在危重病患者中进行气管插管与约 20%的严重危及生命的并发症相关,主要是由于低氧血症引起的。我们假设在气管插管过程中通过咽导管进行无通气给氧可以预防或延长危及生命的低氧血症发生的时间,并在急性肺损伤动物模型中对此假设进行了测试。
8 只通过肺灌洗诱发易塌陷肺的麻醉小猪以 1.0 的吸入氧分数和 5cmH2O 的呼气末正压通气。在获得动脉和混合静脉血气后计算分流量。气管拔管后,每只动物随机接受 10L/min 的氧气或通过咽导管接受无氧气,并测量至脉搏血氧饱和度(SpO2)降至 60%的时间。如果 SpO2 保持在 60%以上,则在 10 分钟后实验结束。
在没有咽氧的情况下,动物在 103(88-111)秒后(中位数和四分位间距)发生低氧血症,而在有咽氧的情况下,5 只动物在 10 分钟的实验期间 SpO2>60%,1 只动物在 7 分钟后发生低氧血症,2 只动物在 90 秒内发生低氧血症(P<0.016,Wilcoxon 符号秩检验)。低氧血症发生的时间与分流量有关(R2=0.81,P=0.002,线性回归);在 90 秒内发生低氧血症的动物分流量>40%,而其他动物的分流量<25%。
在这个实验性急性肺损伤模型中,咽氧的给予显著延长了无通气时严重低氧血症发生的时间,提示在急性呼吸衰竭的危重病患者进行气管插管时,该技术可能有用。