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It was interesting to read the paper by Ko et al. [1] regarding cerebral oxygen saturation monitoring in patients undergoing an arthroscopic shoulder surgery in beach chair position (BCP). While mostly agreeing with their conclusion, one may also raise a few concerns, such as the timely determination of baseline values and the proper use of vasopressors.  As to whether blood pressure should be corrected to account for the level difference between the site of measurement (most commonly a non-invasive cuff on the non-operative arm) and the brain in BCP is under debate [2]. They indeed evaluated whether MAP measured at the level of the brain or at the level of the heart correlated with regional cerebral oxygen saturation (rSO2) in patients undergoing BCP surgery, and found that MAP measured at the brain, but not at the heart level, correlated with rSO2. Nevertheless, they stated in the conclusion that "Monitoring cerebral rSO2 and MAP at the level of brain can be helpful to detect the possibility of cerebral deoxygenation earlier" [1]. To admit their observation, it would be proper to state that "MAP measured at the brain but not at the heart level reflects rSO2 in patients undergoing surgery in BCP".  They also mentioned that "Baseline mean arterial pressure, ---, BIS, and left and right rSO2 were recorded while the patient's condition was stable over 5 minutes before induction." However, the induction of anesthesia and the use of high inspired oxygen fraction per se may significantly decrease BIS and increase rSO2 values [3]. As such, we believe that these parameters measured after (i.e., immediately before patients were raised into BCP) the induction of anesthesia better represents the baseline values.  Phenylephrine, an α-agonist, and ephedrine, an α- and β-agonist, are both commonly used to maintain MAP and thus, cerebral perfusion pressure in neurosurgical patients who develop hypotension. However, in healthy anesthetized subjects with intact cerebral autoregulation, a bolus administration of phenylephrine reduced the rSO2 measured by a near-infrared spectroscopy device under intravenous anesthesia with propofol/remifentanil, whereas ephedrine maintained it [4,5]. In this context, phenylephrine and ephedrine may have differentially affected rSO2 in their study. Moreover, they did not use equipotent dosages of the two vasopressors. Would it not be better for them to have included it as one of the limitations of the study?

Blood pressure management and regional cerebral oxygen saturation during surgery in beach chair position