Effects of sevoflurane and propofol anaesthesia on cerebral oxygenation during normocapnia and mild hypercapnia: a pilot study

Abstract

Editor—In clinical practice, patients undergoing laparoscopic surgery are at risk of mild-to-moderate hypercapnia and CO2-mediated cerebral haemodynamic effects.1Murdock CM Wolff AJ Van Geem T Risk factors for hypercarbia, subcutaneous emphysema, pneumothorax, and pneumomediastinum during laparoscopy.Obstet Gynecol. 2000; 95: 704-709Crossref PubMed Scopus (125) Google Scholar, 2Nguyen NT Wolfe BM The physiologic effects of pneumoperitoneum in the morbidly obese.Ann Surg. 2005; 241: 219-226Crossref PubMed Scopus (249) Google Scholar, 3de Waal EE de Vries JW Kruitwagen CL Kalkman CJ The effects of low-pressure carbon dioxide pneumoperitoneum on cerebral oxygenation and cerebral blood volume in children.Anesth Analg. 2002; 94: 500-505Crossref PubMed Scopus (28) Google Scholar Regional cerebral oxygen saturation (rSO2) has also been used to monitor disturbances of cerebral perfusion, which may reflect tissue oxygen use.4Senanayake E Komber M Nassef A Massey N Cooper G Effective cerebral protection using near-infrared spectroscopy monitoring with antegrade cerebral perfusion during aortic surgery.J Card Surg. 2012; 27: 211-216Crossref PubMed Scopus (14) Google Scholar Sevoflurane and propofol have been widely used as anaesthetic agents for this surgery. Recent evidence has suggested that the effect of these anaesthetics on cerebral oxygenation may differ.5Yamada N Nagata H Sato Y Tomoyasu M Effects of propofol or sevoflurane on cerebral regional oxygen saturation (rSO2) during one-lung ventilation.Masui. 2008; 57: 1388-1397PubMed Google Scholar 6Kim SJ Kwon JY Cho AR Kim HK Kim TK The effects of sevoflurane and propofol anesthesia on cerebral oxygenation in gynecological laparoscopic surgery.Korean J Anesthesiol. 2011; 61: 225-232Crossref PubMed Scopus (19) Google Scholar However, their effects on cerebral oxygenation have not been investigated in the mild hypercapnia period well enough yet. Therefore, we examined the effects of propofol and sevoflurane anaesthesia on rSO2 during normocapnia and mild hypercapnia period on patients undergoing laparoscopic cholecystectomy. With Ethics Committee approval and informed consent, 60 patients, ASA I–II, 18–65 yr were recruited. They received a remifentanil infusion at a rate of 0.3 µg kg−1 min−1, and were randomized into two equal groups. Haemoglobin concentrations did not differ between the groups. For the induction and the maintenance of anaesthesia, sevoflurane (vital capacity breathing with 8% sevoflurane 6 litre min−1 airflow of 100% oxygen induction) and propofol (2 mg kg−1, 3 µg ml−1 target plasma concentration) were used in Group SR and in Group PR, respectively. Rocuronium 0.6 mg kg–1 was administered to facilitate tracheal intubation. For the maintenance of anaesthesia, sevoflurane concentration was changed by 0.2% and the target plasma concentration of propofol was changed by 0.5 µg ml−1 to maintain BIS values at 40–50. Vital signs (Datex Ohmeda S5) and rSO2 (INVOS 5100) were measured before (baseline) and after anaesthesia induction, immediately after low pressure (8 mm Hg) and high pressure (15 mm Hg) CO2 pneumoperitoneum, every 5 min during CO2 insufflation, and every 1 min during the hypercapnia period (end-tidal carbon dioxide tension 6–7.3 kPa). The lungs were mechanically ventilated with a mixture of oxygen and air. When hypercapnia occurred, minute ventilation was increased to maintain normocapnia. Parametric data were analysed by repeated-measures analysis of variance and the Student's t-test for multiple comparisons where appropriate. Non-parametric data were analysed by the Mann–Whitney U-test. There were no statistically significant differences in patient characteristic variables between the groups. After intubation and skin incision, right and left rSO2 values were found to be significantly higher in Group PR than in Group SR (P<0.05). When intra-abdominal pressure was 8 mm Hg, the increase in the right and left rSO2 values was significant in Group PR, when compared with Group SR (P<0.05). Haemodynamic parameters and SpO2 values were not associated with these changes because they did not differ between the groups at all time periods (P>0.05). The incidence of cerebral desaturation (more than 20% decreases from baseline) was not observed. In addition, no significant difference was observed between the groups in terms of haemodynamic parameters and rSO2 values during hypercarbia (P>0.05). In conclusion, the effects of equipotent BIS doses of propofol and sevoflurane are associated with similar rSO2 values during normocapnia and mild hypercapnia. However, in the periods in which stimulus is intense, propofol anaesthesia increased the rSO2 values when compared with sevoflurane anaesthesia likely caused by decreased cerebral metabolic rate of oxygen consumption and therefore reduced oxygen requirements. None declared.