Personalized intraoperative arterial pressure management and mitochondrial oxygen tension in patients having major non-cardiac surgery: a pilot substudy of the IMPROVE trial

The "Cellular Oxygen METabolism" (COMET) system (Photonics Healthcare, Utrecht, The Netherlands) non-invasively measures mitochondrial oxygen tension (mitoPO₂) in the skin. The effects of general anesthesia and major non-cardiac surgery on mitoPO₂ remain unknown. In this pre-planned pilot substudy of the "Intraoperative blood pressure Management based on the individual blood PRessure profile: impact on postOperatiVE organ function" (IMPROVE) trial, we measured mitoPO₂ from induction of general anesthesia until the end of surgery in 19 major non-cardiac surgery patients (10 assigned to personalized and 9 to routine intraoperative arterial pressure management). In the overall cohort, the median (25th to 75th percentile) preoperative awake mitoPO₂ was 63 (53 to 82) mmHg and mitoPO₂ after induction of general anesthesia was 42 (35 to 59) mmHg. The intraoperative average mitoPO₂ was 39 (30 to 50) mmHg. Thirteen patients (68%) had intraoperative mitoPO₂ values below 20 mmHg and the median percentage of surgical time with mitoPO₂ < 20 mmHg was 17 (0 to 31)%. MitoPO₂ was weakly correlated with mean arterial pressure (repeated measures correlation (r_rm(n); r_rm(984) = 0.26, 95% confidence interval 0.20 to 0.32; P < 0.001), but not meaningfully with heart rate (r_rm(984) = -0.05, 95% confidence interval -0.11 to 0.01; P = 0.117). There was no important difference in intraoperative average mitoPO₂ between patients assigned to personalized or to routine intraoperative arterial pressure management (P = 0.653). MitoPO₂ under general anesthesia was about a quarter lower than preoperative awake mitoPO₂, substantially fluctuated during major non-cardiac surgery, and transiently decreased below 20 mmHg in about two-thirds of the patients. Personalized - compared to routine - intraoperative arterial pressure management did not increase intraoperative mitoPO₂. Whether intraoperative decreases in mitoPO₂ are clinically meaningful warrants further investigation.