Effects of spinal anesthesia and sedation with dexmedetomidine or propofol on cerebral regional oxygen saturation and systemic oxygenation a period after spinal injection

• Published in: Journal of anesthesia Vol. 34; no. 6; pp. 806 - 813
• Main Authors: Kumakura, Yasutomo, Ishiyama, Tadahiko, Matsuoka, Toru, Iijima, Tetsuya, Matsukawa, Takashi
• Format: Journal Article
• Language: English
• Published: Singapore Springer Singapore 01.12.2020; Springer
• Subjects: Analysis; Anesthesia; Anesthesia, Spinal; Anesthesiology; Critical Care Medicine; Dexmedetomidine; Emergency Medicine; Evaluation; Heart beat; Humans; Hypnotics and Sedatives; Infrared spectroscopy; Injections, Spinal; Intensive; Medicine; Medicine & Public Health; Original Article; Oximetry; Oxygen; Pain Medicine; Phenols; Propofol; Sensors; Japan; Propofol; Dexmedetomidine; Near-infrared spectroscopy; Spinal anesthesia
• ISSN: 0913-8668; 1438-8359
• DOI: 10.1007/s00540-020-02816-5

Purpose To evaluate changes in cerebral regional oxygen saturation (rSO 2 ) after spinal anesthesia and compare the changes in rSO 2 and systemic oxygenation between dexmedetomidine sedation and propofol sedation. Methods Thirty-six patients scheduled to undergo transurethral surgery under spinal anesthesia were randomly assigned to the dexmedetomidine ( n = 18) and propofol groups ( n = 18). We used near-infrared spectroscopy sensors to measure rSO 2 , and obtained data from each side were averaged. After oxygen insufflation, baseline measurements of mean arterial blood pressure (MAP), heart rate, rSO 2 , pulse oximetry saturation (SpO 2 ), bispectral index, and body temperature were made. After spinal anesthesia, we measured these parameters every 5 min. Twenty minutes after spinal injection, dexmedetomidine or propofol administration was started. We measured each parameter at 10, 25, and 40 min after the administration of dexmedetomidine or propofol. Results The baseline rSO 2 in the dexmedetomidine group was 71.3 ± 7.3%, and that in the propofol group was 71.8 ± 5.6%. After spinal anesthesia, rSO 2 in both groups decreased significantly (dexmedetomidine group: 65.4 ± 6.9%; propofol group: 64.3 ± 7.4%). After administering sedatives, rSO 2 was equivalent after spinal anesthesia. rSO 2 was comparable between the two groups. MAP and SpO 2 were significantly higher in the dexmedetomidine group than in the propofol group. Conclusion Spinal anesthesia decreased rSO 2 ; however, the decline was not severe. Dexmedetomidine and propofol did not compromise cerebral oxygenation under spinal anesthesia. Nevertheless, MAP and SpO 2 were more stable in dexmedetomidine sedation than in propofol sedation. Dexmedetomidine may be suitable for spinal anesthesia.