Department of Clinical Pharmacy, School of Pharmacy, University of Colorado Denver, Aurora, CO, USA.
Ann Pharmacother. 2011 Mar;45(3):e15. doi: 10.1345/aph.1P547. Epub 2011 Mar 8.
To report a case of neuromuscular blockade resistance to multiple agents during therapeutic hypothermia and discuss possible mechanisms of this resistance.
A 64-year-old man with stage IV non-small-cell lung cancer and respiratory distress developed cardiac arrest in the emergency department. The man was quickly resuscitated and treated with therapeutic hypothermia. A chest tube was inserted for pleural drainage of a large right-sided effusion that collapsed the right lung; this was unsuccessful in reinflating the lung. A bronchopleural fistula developed and independent lung ventilation was initiated due to persistent hypoxemia. Neuromuscular blockade was initiated after sedation and analgesia did not control shivering and was continued due to patient-ventilator dyssynchrony and persistent hypoxemia. Despite large doses of 3 different neuromuscular blocking agents and negligible response to train-of-four tests, clinical neuromuscular blockade, represented by ventilator synchrony, was not achieved until the patient was warmed.
Resistance to neuromuscular blocking agents has been reported in critically ill patients. Our case of neuromuscular blockade resistance occurred in a patient treated with therapeutic hypothermia, which generally requires a dose reduction of neuromuscular blocking agents. Resistance to neuromuscular blockade was quickly reversed upon warming of the patient as patient-ventilator synchrony was achieved at lower neuromuscular blocking agent doses.
Clinicians should be aware of a potential blunted response to neuromuscular blocking agents during therapeutic hypothermia and difficulty with paralysis monitoring since train-of-four response may correlate poorly with clinical neuromuscular blockade during hypothermia. Further research is needed to elucidate the mechanism of this interaction, identify patients at risk, and evaluate alternative strategies to neuromuscular blockade for controlling shivering in patients undergoing therapeutic hypothermia.
报告一例在治疗性低温期间对多种药物产生神经肌肉阻滞抵抗的病例,并讨论这种抵抗的可能机制。
一名 64 岁男性患有 IV 期非小细胞肺癌和呼吸窘迫,在急诊科发生心脏骤停。该男子迅速复苏并接受治疗性低温治疗。插入胸腔引流管以排出大量右侧胸腔积液,导致右肺塌陷;但未能重新充气。由于持续低氧血症,发生了支气管胸膜瘘,并开始进行独立的肺通气。镇静和镇痛未能控制寒战,因此开始使用神经肌肉阻滞剂,并因患者-呼吸机不同步和持续低氧血症而继续使用。尽管使用了 3 种不同的神经肌肉阻滞剂大剂量,但对肌松监测的 4 个成串刺激(train-of-four,TOF)测试反应几乎为零,直到患者体温升高,才达到临床神经肌肉阻滞(表现为呼吸机同步)。
在危重症患者中已报道存在神经肌肉阻滞剂抵抗。我们的神经肌肉阻滞剂抵抗病例发生在接受治疗性低温治疗的患者中,通常需要减少神经肌肉阻滞剂的剂量。随着患者体温升高,神经肌肉阻滞剂抵抗迅速逆转,因为在较低的神经肌肉阻滞剂剂量下实现了患者-呼吸机同步。
临床医生应意识到在治疗性低温期间可能对神经肌肉阻滞剂的反应减弱,并在进行神经肌肉阻滞监测时存在困难,因为在低温期间,TOF 反应可能与临床神经肌肉阻滞相关性较差。需要进一步研究以阐明这种相互作用的机制,确定有风险的患者,并评估替代策略以控制接受治疗性低温的患者的寒战。