A 53-year-old man (161 cm, 83.6 kg) who had severe aortic valve stenosis and regurgitation due to a bicuspid aortic valve was scheduled for aortic valve replacement and ascending aortic replacement. He had no history and was not taking any medication.
Baseline blood pressure (BP) and heart rate (HR) were 143/90 mmHg and 74 bpm with sinus rhythm, respectively. General anesthesia was induced by 6 mg/kg/h remimazolam, 100 μg fentanyl, and 0.15 μg/kg/min remifentanil. After loss of consciousness, the dose of remimazolam was decreased to 1 mg/kg/h and rocuronium (0.8 mg/kg) was administered. Although manual mask ventilation was performed without difficulty and BIS value was 46 to 62 during ventilation, HR gradually increased from 72 to 103 bpm, and BP also increased from 115/59 mmHg to 157/86 mmHg (Fig. 1). At that time, end-tidal carbon dioxide concentration was 35–40 mmHg, and there was no problem with the intravenous line for administration of remimazolam (e.g., occlusion, formation of a precipitation, extravasation). We discontinued remimazolam and started administration of sevoflurane, suspecting that remimazolam was responsible for adrenergic responses. After the end-tidal sevoflurane concentration reached 1.5%, HR and BP decreased to 84 bpm and 115/61 mmHg, respectively, and the BIS value was 46. The patient was intubated about 7 min after administration of rocuronium. After the anesthetic agent had been changed from remimazolam to sevoflurane during anesthetic induction and propofol was administered during cardiopulmonary bypass, there were no unexpected hemodynamic changes throughout the anesthetic period. Surgical procedures were completed successfully. There was no peri-anesthetic awareness and/or recall that could have induced adrenergic responses.