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Background There are several advantages of low flow anesthesia including safety, economics, and eco-friendliness. However, oxygen concentration of fresh gas flow and inspired gas are large different in low flow anesthesia. This is a hurdle to access to low flow anesthesia. In this study, we aimed to investigate the change in inhaled oxygen concentration in low flow anesthesia using oxygen and medical air. Methods A total of 60 patients scheduled for elective surgery with an American Society of Anesthesiologist physical status I or II were enrolled and randomly allocated into two groups. Group H: Fresh gas flow rate (FGF) 4 L/min (FiO₂ 0.5). Group L: FGF 1 L/min (FiO₂ 0.5). FGF was applied 4 L/min in initial phase (10 min) after intubation. After initial phase FGF was adjusted according to groups. FGF continued at the end of surgery. Oxygen and inhalation anesthetic gas concentration were recorded for 180 min at 15 min interval. Results The inspired oxygen concentration decreased by 5.5% during the first 15 min in the group L. Inspired oxygen decreased by 1.5% during next 15 min. Inspired oxygen decreased by 1.4% for 30 to 60 min. The inspired oxygen of group L is 35.4 ± 4.0% in 180 min. The group H had little difference in inspired oxygen concentration over time and decreased by 1.8% for 180 min. Conclusions The inspired oxygen concentration is maintained at 30% or more for 180 min in patients under 90 kg. Despite some technical difficulties, low flow anesthesia may be considered.

Background Postoperative pain is affected by preoperative depression. If the risk of postoperative pain associated with depression can be predicted preoperatively, anesthesiologists and/or surgeons can better manage it with personalized care. The objective of this study was to determine the efficacy of Patient Health Questionnaire-2 (PHQ-2) depression screening tool as a predictor of postoperative pain. Methods A total of 50 patients scheduled for elective laparoscopic cholecystectomy with an American Society of Anesthesiologists physical status 1 or 2 were enrolled. They answered the PHQ-2, which consists of two questions, under the supervision of a researcher on the day before the surgery. The numerical rating scale (NRS) scores were assessed at post-anesthesia care unit (PACU), at 24, and 48 postoperative hours, and the amount of intravenous patient-controlled analgesia (IV-PCA) administered was documented at 24, 48, and 72 postoperative hours. At 72 h, the IV-PCA device was removed and the final dosage was recorded. Results The NRS score in PACU was not significantly associated with the PHQ-2 score (correlation coefficients: 0.13 [P = 0.367]). However, the use of analgesics after surgery was higher in patients with PHQ-2 score of 3 or more (correlation coefficients: 0.33 [P = 0.018]). Conclusions We observed a correlation between the PHQ-2 score and postoperative pain. Therefore, PHQ-2 could be useful as a screening test for preoperative depression. Particularly, when 3 points were used as the cut-off score, the PHQ-2 score was associated with the dosage of analgesics, and the analgesic demand could be expected to be high with higher PHQ-2 scores.

Background Sedation by dexmedetomidine, like natural sleep, often causes bradycardia. We explored the nature of heart rate (HR) changes as they occur during natural sleep versus those occurring during dexmedetomidine sedation. Methods The present study included 30 patients who were scheduled to undergo elective surgery with spinal anesthesia. To assess HR and sedation, a pulse oximeter and bispectral index (BIS) monitor were attached to the patient in the ward and the operating room. After measuring HR and BIS at baseline, as the patients slept and once their BIS was below 70, HR and BIS were measured at 5-minute intervals during sleep. Baseline HR and BIS were also recorded before spinal anesthesia measured at 5-minute intervals after dexmedetomidine injection. Results During natural sleep, HR changes ranged from 2 to 19 beats/min (13.4 ± 4.4 beats/min), while in dexmedetomidine sedation, HR ranged from 9 to 40 beats/min (25.4 ± 8.5 beats/min). Decrease in HR was significantly correlated between natural sleep and dexmedetomidine sedation (R2 = 0.41, P < 0.001). The lowest HR was reached in 66 min during natural sleep (59 beats/min) and in 13 min with dexmedetomidine sedation (55 beats/min). The time to reach minimum HR was significantly different (P < 0.001), but there was no difference in the lowest HR obtained (P = 0.09). Conclusions There was a correlation between the change in HR during natural sleep and dexmedetomidine sedation. The bradycardia that occurs when using dexmedetomidine may be a normal physiologic change, that can be monitored rather than corrected.