Linko K, Wirtavuori K, Tammisto T
Eur J Anaesthesiol. 1984 Jun;1(2):105-12.
The effects of progressive curarization on spontaneous ventilation were studied in 23 patients during light halothane-nitrous oxide-oxygen anaesthesia. In 11 patients, in whom the end-expiratory CO2 concentration and evoked mechanical response were recorded, increasing curarization caused first a slow CO2 accumulation and later an abrupt ventilatory impairment at a twitch tension of between 5 and 50% of original muscle strength. In 12 patients, in whom the evoked integrated hypothenar EMG, spontaneous frontal EMG and mean frequency and amplitude of the EEG were recorded, the spontaneous frontal EMG and ventilation diminished within 3 min, following the first 5 mg dose of tubocurarine. At this stage muscle strength, indicated by the amplitude of the evoked EMG and the train-of-four ratio, was unchanged. Repeated 5 mg doses of tubocurarine caused an almost linear decrease in ventilation and an increase in end-tidal CO2 concentration without affecting the rate of breathing until the sudden impairment of ventilation that occurred usually after the fourth dose of tubocurarine. The EEG changes during curarization were minimal and no common trend was seen. The results suggest that tubocurarine may be given to anaesthetized patients in a dose which is too small to produce, using the evoked EMG, a detectable neuromuscular block, but is sufficient to cause ventilatory depression without a compensatory increase in the rate of breathing.
在23例接受氟烷-氧化亚氮-氧气浅麻醉的患者中,研究了递增性箭毒化对自主通气的影响。对11例记录了呼气末二氧化碳浓度和诱发机械反应的患者,箭毒化程度增加首先导致二氧化碳缓慢蓄积,随后在肌肉抽搐张力降至原来肌力的5%至50%时,通气突然受损。对12例记录了诱发的小鱼际肌肌电图、自发的额部肌电图以及脑电图平均频率和波幅的患者,首次静脉注射5mg筒箭毒碱后3分钟内,自发的额部肌电图和通气量即减少。此时,由诱发肌电图波幅和四个成串刺激比值所表示的肌力并无变化。重复注射5mg筒箭毒碱几乎使通气量呈线性下降,呼气末二氧化碳浓度升高,且在通常于第四次注射筒箭毒碱后发生通气突然受损之前,呼吸频率未受影响。箭毒化过程中脑电图变化极小,未发现共同趋势。结果提示,可给麻醉患者使用小剂量筒箭毒碱,该剂量用诱发肌电图检测时,不足以产生可察觉的神经肌肉阻滞,但足以引起通气抑制且无呼吸频率的代偿性增加。