Cerebral Oximetry and Mean Arterial Pressure: Not a Straight Relationship, the Flow Between?

To the Editor We read with great interest the substudy by Holmgaard et al1 that analyzed data from their original trial published in Circulation (Perfusion Pressure Cerebral Infarct Trial),2 with a new focus on the relationship between regional cerebral tissue oxygenation (rScO2) and the level of mean arterial pressure (MAP) during cardiopulmonary bypass (CPB).1 The study gives us new insights regarding the target MAP that would be optimal during CPB. The authors showed that increasing MAP led to a decrease in rScO2 and concluded that (1) vasoconstrictors should not be used to optimize rScO2 and (2) the decrease of rScO2 might have been due to a cutaneous vasoconstriction contamination. We think that these conclusions, while potentially true, are debatable. Pump flow used in the original study2 was 2.69 L/min/m2, a high value as mentioned by the authors. Because rScO2 is primary impacted by flow rather than pressure,3 it could partly explain why rScO2 was high in both groups. Indeed, studies aiming at improving rScO2 per se showed much more desaturations wherein 12%–33% of the treated patients presented a cerebral desaturation load (CDL) upper than 20% of the baseline (CDL20), contrary to this study, where 0% of the patients presented a CDL20. As noted by the authors, rScO2 has been proposed as an acceptable surrogate of cerebral blood flow (CBF) to detect the lower and upper pressure limit of autoregulation.4 Then increasing MAP when rScO2 is already in the acceptable range (as CDL20 was 0) might be potentially harmful if the patient exceeds the upper limit pressure of autoregulation. Hence, another hypothesis than a contamination by cutaneous tissue of the small decrease of the rScO2 in the high MAP group could be that a cerebral arteriolar vasoconstriction might have occurred to limit a cerebral luxury perfusion in this state of high pump flow, as already experienced by Moerman et al.3 Making the distinction between cutaneous and cerebral vasoconstriction to explain the decrease of rScO2 would have needed a continuous measurement CBF, such as transcranial Doppler. On the other hand, using a vasoconstrictor when the MAP is below the lower limit of CBF autoregulation would increase the CBF and then the rScO2. Vasoconstrictors will have consequently different effects on rScO2 depending on the individual’s upper and lower limit of CBF autoregulation. Finally, this study highlights the importance of flow when optimizing cerebral perfusion. Working with higher pump flow may shift the CBF autoregulation plateau to the left and allow lower MAP during CPB. We totally agree with the authors that increasing MAP to increase rScO2 should not be the first step when a cerebral desaturation occurs, but we might consider a greater pump flow. Olivier Desebbe, MDDepartments of Anesthesiology and Intensive CareClinique de la SauvegardeLyon, FranceAlexandre Joosten, MD, PhDDepartment of Anesthesiology and Intensive CareHôpitaux Universitaires Paris-SudUniversité Paris-SudUniversité Paris-SaclayHôpital De BicêtreAssistance Publique Hôpitaux de Paris (AP-HP)Le Kremlin-Bicêtre, France[email protected]; [email protected]Andre Denault, MD, PhDDepartment of Anesthesia & Critical Care DivisionMontreal Heart InstituteUniversity of MontrealMontreal, Quebec, Canada

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