Naguib Mohamed, Brewer Lara, LaPierre Cristen, Kopman Aaron F, Johnson Ken B
From the *Department of General Anesthesia, Anesthesiology Institute, Cleveland Clinic, Cleveland, Ohio; †Department of Anesthesiology, University of Utah, Salt Lake City, Utah; and ‡Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Boston, Massachusetts.
Anesth Analg. 2016 Jul;123(1):82-92. doi: 10.1213/ANE.0000000000001347.
An unanticipated difficult airway during induction of anesthesia can be a vexing problem. In the setting of can't intubate, can't ventilate (CICV), rapid recovery of spontaneous ventilation is a reasonable goal. The urgency of restoring ventilation is a function of how quickly a patient's hemoglobin oxygen saturation decreases versus how much time is required for the effects of induction drugs to dissipate, namely the duration of unresponsiveness, ventilatory depression, and neuromuscular blockade. It has been suggested that prompt reversal of rocuronium-induced neuromuscular blockade with sugammadex will allow respiratory activity to recover before significant arterial desaturation. Using pharmacologic simulation, we compared the duration of unresponsiveness, ventilatory depression, and neuromuscular blockade in normal, obese, and morbidly obese body sizes in this life-threatening CICV scenario. We hypothesized that although neuromuscular function could be rapidly restored with sugammadex, significant arterial desaturation will occur before the recovery from unresponsiveness and/or central ventilatory depression in obese and morbidly obese body sizes.
We used published models to simulate the duration of unresponsiveness and ventilatory depression using a common induction technique with predicted rates of oxygen desaturation in various size patients and explored to what degree rapid reversal of rocuronium-induced neuromuscular blockade with sugammadex might improve the return of spontaneous ventilation in CICV situations.
Our simulations showed that the duration of neuromuscular blockade was longer with 1.0 mg/kg succinylcholine than with 1.2 mg/kg rocuronium followed 3 minutes later by 16 mg/kg sugammadex (10.0 vs 4.5 minutes). Once rocuronium neuromuscular blockade was completely reversed with sugammadex, the duration of hemoglobin oxygen saturation >90%, loss of responsiveness, and intolerable ventilatory depression (a respiratory rate of ≤4 breaths/min) were dependent on the body habitus and duration of oxygen administration. There is a high probability of intolerable ventilatory depression that extends well beyond the time when oxygen saturation decreases <90%, especially in obese and morbidly obese patients. If ventilatory rescue is inadequate, oxygen desaturation will persist in the latter groups, despite full reversal of neuromuscular blockade. Depending on body habitus, the duration of intolerable ventilatory depression after sugammadex reversal may be as long as 15 minutes in 5% of individuals.
The clinical management of CICV should focus primarily on restoration of airway patency, oxygenation, and ventilation consistent with the American Society of Anesthesiologist's practice guidelines for management of the difficult airway. Pharmacologic intervention cannot be relied upon to rescue patients in a CICV crisis.
麻醉诱导期间意外出现的困难气道可能是一个棘手的问题。在无法插管且无法通气(CICV)的情况下,迅速恢复自主通气是一个合理的目标。恢复通气的紧迫性取决于患者血红蛋白氧饱和度下降的速度与诱导药物作用消散所需时间的对比,即无反应期、通气抑制期和神经肌肉阻滞期的时长。有人提出,使用舒更葡糖迅速逆转罗库溴铵诱导的神经肌肉阻滞将使呼吸活动在动脉血氧饱和度显著下降之前恢复。我们通过药理学模拟,比较了在这种危及生命的CICV情况下,正常体型、肥胖体型和病态肥胖体型患者的无反应期、通气抑制期和神经肌肉阻滞期的时长。我们假设,尽管舒更葡糖可迅速恢复神经肌肉功能,但在肥胖和病态肥胖体型患者从无反应和/或中枢性通气抑制中恢复之前,将发生显著的动脉血氧饱和度下降。
我们使用已发表的模型,采用常见的诱导技术模拟无反应期和通气抑制期的时长,并预测不同体型患者的氧饱和度下降速率,探讨舒更葡糖迅速逆转罗库溴铵诱导的神经肌肉阻滞在CICV情况下对自主通气恢复的改善程度。
我们的模拟显示,与先给予1.2mg/kg罗库溴铵、3分钟后再给予16mg/kg舒更葡糖相比,给予1.0mg/kg琥珀酰胆碱后的神经肌肉阻滞期更长(10.0分钟对4.5分钟)。一旦罗库溴铵的神经肌肉阻滞被舒更葡糖完全逆转,血红蛋白氧饱和度>90%的时长、无反应期和无法耐受的通气抑制(呼吸频率≤4次/分钟)取决于身体形态和吸氧时长。出现无法耐受的通气抑制且持续时间远超氧饱和度降至<90%的时间的可能性很高,尤其是在肥胖和病态肥胖患者中。如果通气救援不足,尽管神经肌肉阻滞已完全逆转,后两组患者的氧饱和度仍会持续下降。根据身体形态,在5%的个体中,舒更葡糖逆转后无法耐受的通气抑制期可能长达15分钟。
CICV的临床管理应主要侧重于按照美国麻醉医师协会困难气道管理实践指南恢复气道通畅、进行氧合和通气。在CICV危机中,不能依赖药物干预来挽救患者。