Galletly D C, Williams T B, Robinson B J
Section of Anaesthesia, Wellington School of Medicine, New Zealand.
Br J Anaesth. 1996 Apr;76(4):503-7. doi: 10.1093/bja/76.4.503.
We have examined the effects of sedation with midazolam 0.1 mg kg-1 and reversal with flumazenil 0.5 mg on beat-to-beat heart rate (HR) variability (HRV), systolic arterial pressure (SAP), finger photoplethysmograph amplitude (PLA) and impedence pneumography in eight volunteers. With the onset of sedation there was a small decrease in SAP and increase in HR (ns). Spectral analysis of the HR time series showed reductions in the proportion of power in the high (> 0.15 Hz) frequency "ventilatory" band consistent with midazolam causing vagolysis. During sedation, low frequency (< 0.05 Hz) oscillations of PLA, HR, SAP and ventilation were observed. These were thought to be secondary to activity of coupled cardiorespiratory neurones within the brain stem and the ventilatory periodicity appeared similar to that observed during the early stages of sleep. The diminished high frequency and increased low frequency oscillations induced by midazolam sedation were reversed by administration of flumazenil.
我们研究了0.1毫克/千克咪达唑仑镇静及0.5毫克氟马西尼逆转对8名志愿者逐搏心率(HR)变异性(HRV)、收缩压(SAP)、手指光电容积脉搏波幅度(PLA)和阻抗式肺量计的影响。随着镇静开始,SAP略有下降,HR升高(无统计学意义)。HR时间序列的频谱分析显示,高频(>0.15赫兹)“通气”频段的功率比例降低,这与咪达唑仑导致迷走神经解逸一致。在镇静期间,观察到PLA、HR、SAP和通气的低频(<0.05赫兹)振荡。这些被认为是脑干内耦合心肺神经元活动的继发表现,且通气周期性似乎与睡眠早期观察到的相似。咪达唑仑镇静引起的高频振荡减弱和低频振荡增加通过给予氟马西尼得以逆转。