• Fabio Silvio Taccone, Diego Castanares-Zapatero, Daliana Peres-Bota, Jean-Louis Vincent, Jacques Berre', and Christian Melot.
• Department of Intensive Care, Erasme University Hospital, Université Libre de Bruxelles (ULB), Route de Lennik, 808, 1070, Brussels, Belgium. ftaccone@ulb.ac.be
• Neurocrit Care. 2010 Feb 1;12(1):35-42.

BackgroundAltered brain perfusion may play an important role in the development of sepsis-associated encephalopathy. However, whether or not cerebral autoregulation (CA) is preserved in such condition has been debated. CA is dependent on cerebral vascular tone, the main determinant of which is the concentration of carbon dioxide (CO2). The purpose of this study was to evaluate the influence of PaCO2 on the cerebral autoregulatory capacity in patients with septic shock.MethodsUsing transcranial Doppler sonography recordings from the middle cerebral artery (MCA), we evaluated the static cerebral autoregulatory responses within the first 3 days of septic shock. Changes in cerebrovascular resistance (CVR) were calculated from the changes in the mean velocity in the MCA (VMCA, cm/s), in response to an increase in mean arterial pressure (MAP, mmHg) induced by vasopressors. The cerebral autoregulation index (CAI) was calculated as the ratio of the relative changes in CVR and MAP (CAI = DeltaMAP%/DeltaCVR%), with normal values ranging between 0 and 2.ResultsWe studied 21 mechanically ventilated patients, with a baseline MAP of 65 +/- 6 mmHg, a mean VMCA of 60 +/- 20 cm/s and a median PaCO(2) of 35 [28-49] mmHg. Fourteen of the 21 patients had impaired CA, including 7 of the 14 patients with a PaCO2 <40 mmHg and all 7 patients with a PaCO2 >40 mmHg (Fisher's exact test, P = 0.046).ConclusionsAccording to these data, CA is impaired in the majority of patients with septic shock, especially in the presence of hypercapnia.

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