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JOURNAL ARTICLE
RANDOMIZED CONTROLLED TRIAL
Effect of lung-protective ventilation-induced respiratory acidosis on the duration of neuromuscular blockade by rocuronium.
Journal of Anesthesia 2016 December
PURPOSE: The purpose of this study was to elucidate whether lung-protective ventilation-induced respiratory acidosis increased the duration of neuromuscular blockade by rocuronium.
METHODS: A total of 72 patients were enrolled. After the induction of general anesthesia, rocuronium 0.6 mg/kg real body weight was administered. Tidal volume and positive end-expiratory pressure were randomly assigned as either 10 ml/kg predicted body weight and 0 cmH2 O (group S) or 6 ml/kg and 5 cmH2 O (group L), respectively. Respiratory rate was started at 10/min. Neuromuscular blockade was monitored by acceleromyography at the adductor pollicis with train-of-four stimulation. The time from the initial bolus injection of rocuronium to first recovery of the first twitch was defined as DUR1. Immediately, rocuronium 0.15 mg/kg was administered. The time from first recovery of the first twitch to second recovery of the first twitch was defined as DUR2. We also measured arterial pH (pH1 and pH2, respectively).
RESULTS: Data from 66 patients (33 each in groups L and S) were eventually available. pH1 and pH2 were significantly lower in group L compared with group S [pH1: 7.308 (7.288-7.334) vs. 7.439 (7.423-7.466); p < 0.01, pH2: 7.306 (7.285-7.330) vs. 7.453 (7.436-7.476); p < 0.01]. DUR1 and DUR2 were significantly prolonged in group L compared with group S [DUR1: 31 (24-36) vs. 24 (20-30) min; p = 0.029, DUR2: 19 (15-22) vs. 15 (12-17) min; p = 0.020].
CONCLUSIONS: Lung-protective ventilation-induced respiratory acidosis increased the duration of neuromuscular blockade by rocuronium.
METHODS: A total of 72 patients were enrolled. After the induction of general anesthesia, rocuronium 0.6 mg/kg real body weight was administered. Tidal volume and positive end-expiratory pressure were randomly assigned as either 10 ml/kg predicted body weight and 0 cmH2 O (group S) or 6 ml/kg and 5 cmH2 O (group L), respectively. Respiratory rate was started at 10/min. Neuromuscular blockade was monitored by acceleromyography at the adductor pollicis with train-of-four stimulation. The time from the initial bolus injection of rocuronium to first recovery of the first twitch was defined as DUR1. Immediately, rocuronium 0.15 mg/kg was administered. The time from first recovery of the first twitch to second recovery of the first twitch was defined as DUR2. We also measured arterial pH (pH1 and pH2, respectively).
RESULTS: Data from 66 patients (33 each in groups L and S) were eventually available. pH1 and pH2 were significantly lower in group L compared with group S [pH1: 7.308 (7.288-7.334) vs. 7.439 (7.423-7.466); p < 0.01, pH2: 7.306 (7.285-7.330) vs. 7.453 (7.436-7.476); p < 0.01]. DUR1 and DUR2 were significantly prolonged in group L compared with group S [DUR1: 31 (24-36) vs. 24 (20-30) min; p = 0.029, DUR2: 19 (15-22) vs. 15 (12-17) min; p = 0.020].
CONCLUSIONS: Lung-protective ventilation-induced respiratory acidosis increased the duration of neuromuscular blockade by rocuronium.
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