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Background: An unintentional large dose of dexmedetomidine during sedation can lead to increased side effects such as bradycardia and hypotension. We investigated whether the frequency of bradycardia in patients undergoing surgery under spinal anesthesia and sedation with dexmedetomidine was effected if bispectral index (BIS) was used to monitor the sedation. Methodology: Fifty patients between 20 and 60 y of age, who underwent spinal anesthesia, were included in this study. The patients were divided into two groups (control and BIS groups). Patients in the control group were administered a loading dose of 1 μg/kg dexmedetomidine for the first 10 min without BIS monitoring, followed by a maintenance dose of 0.2 μg/kg/h. Patients in the BIS group received a loading dose of 1 μg/kg dexmedetomidine for the first 10 min. The maintenance dose in this group was administered at the discretion of the anesthesiologist to maintain the BIS score between 50 and 70. The baseline heart rate (HR), lowest HR, and the difference between baseline and the lowest HR were calculated. Results: The baseline HR was 74.4 ± 11.0 beats per minute (bpm) and 80.9 ± 16.0 bpm, in the control and BIS groups respectively (p = 0.098). The difference between the baseline and lowest HR in the control and BIS groups was 19.4 ± 7.6 bpm and 25.5 ± 8.8 bpm, respectively (p = 0.011). Low baseline HR was positively correlated with a reduced lowest HR. Conclusions: The frequency of bradycardia during sedation with dexmedetomidine decreased with BIS monitoring. Patients with a low baseline HR were more likely to develop bradycardia during sedation with dexmedetomidine. Therefore, BIS monitoring may be helpful in patients with low baseline HR. Key words: Bispectral index monitor; Dexmedetomidine; heart rate; spinal anesthesia Citation: Kim J, Kim HY, Yun M, Lee J, Kim JD, Kang D. Bispectral index monitoring during sedation with dexmedetomidine in spinal anesthesia prevents bradycardia: a randomized clinical trial. Anaesth. pain intensive care 2021;26(1):14-19 ; DOI: 10.35975/apic.v26i1.1760

Background: The STOP-BANG questionnaire is a simple screening tool with high sensitivity for the detection of severe obstructive sleep apnea (OSA). Predicting airway obstruction would allow the safe management of sedative patients to prevent intraoperative hypoxia. This study was designed to check the correlation between the STOP-BANG score and oxygen saturation (SpO2) during sedation and confirm the availability of the STOP-BANG questionnaire as a preoperative exam for predicting the incidence of hypoxia in sedative patient management.Methods: This study included 56 patients who received spinal anesthesia. The pre-anesthesia evaluation was conducted using the STOP-Bang questionnaire. The patients were under spinal anesthesia with an average block level of T10. Dexmedetomidine was infused with a loading dose of 1 μg/kg over 10 min and a maintenance dose of 0.5 μg/kg/h until the end of the procedure. The SpO2 of the patients was recorded every 5 min.Results: The STOP-Bang score was negatively correlated with the lowest SpO2 (coefficient = –0.774, 95% confidence interval [CI]: –0.855 to –0.649, standard error [SE] = 0.054, P < 0.001). The item of “observed apnea” was the most correlated one with hypoxic events (odds ratio = 6.00, 95% CI: 1.086 to 33.145).Conclusions: The STOP-BANG score was significantly correlated with the lowest SpO2 during spinal anesthesia, which enabled the prediction of meaningful hypoxia before it occurred in the sedated patients.

Although the physiological function of receptor-interacting protein kinase (RIPK) 3 has emerged as a critical mediator of programmed necrosis/necroptosis, the intracellular role it plays as an attenuator in human lungs and human bronchial epithelia remains unclear. Here, we show that the expression of RIPK3 dramatically decreased in the inflamed tissues of human lungs, and moved from the nucleus to the cytoplasm. The overexpression of RIPK3 dramatically increased F-actin formation and decreased the expression of genes for pro-inflammatory cytokines (IL-6 and IL-1β), but not siRNA-RIPK3. Interestingly, whereas RIPK3 was bound to histone 1b without LPS stimulation, the interaction between them was disrupted after 15 min of LPS treatment. Histone methylation could not maintain the binding of RIPK3 and activated movement towards the cytoplasm. In the cytoplasm, overexpressed RIPK3 continuously attenuated pro-inflammatory cytokine gene expression by inhibiting NF-κB activation, preventing the progression of inflammation during Pseudomonas aeruginosa infection. Our data indicated that RIPK3 is critical for the regulation of the LPS-induced inflammatory microenvironment. Therefore, we suggest that RIPK3 is a potential therapeutic candidate for bacterial infection-induced pulmonary inflammation.