Continuous Assessment of Cerebral Autoregulation in Subarachnoid Hemorrhage Martin Soehle, MD*†, Marek Czosnyka, PhD†, John D. Pickard, MCh, FRCS†, and Peter J. Kirkpatrick, FRCS(SN)† *Department of Anaesthesiology and Intensive Care Medicine, University of Bonn, Bonn, Germany; and †Academic Neurosurgery Unit, Addenbrooke’s Hospital, University of Cambridge, Cambridge, United Kingdom Cerebral vasospasm remains a leading cause of morbidity and mortality after subarachnoid hemorrhage (SAH). Ce- rebral ischemia may ensue when autoregulation fails to compensate for spasm. We examined how autoregulation is affected by vasospasm by using transcranial Doppler. The moving correlation coefficient between slow changes of arterial blood pressure and mean or systolic flow veloc- ity (FV), termed “Mx” and “Sx,” respectively, was used to characterize cerebral autoregulation. Vasospasm was de- clared when the mean FV increased to more than 120 cm/s and the Lindegaard ratio was more than 3. This oc- curred in 15 of 32 SAH patients. On the basis of the bilat- eral transcranial Doppler recordings of the middle cere- bral artery in vasospastic patients, Mx and Sx were calculated for baseline and vasospasm. Mx increased dur- ing vasospasm (0.46  0.32; mean  sd) and was signifi- cantly higher (P = 0.021) than at baseline (0.21  0.24). Sx was also increased (0.22  0.26 vs 0.05  0.21 at baseline; P = 0.03). Mx correlated with mean FV (r = 0.577; P = 0.025) and the Lindegaard ratio (r = 0.672; P  0.006). Mx (P = 0.006) and Sx (P = 0.044) were higher on the vasospastic side (Mx, 0.44  0.27; Sx, 0.24  0.23) when compared with the contralateral side (Mx, 0.34  0.29; Sx, 0.16  0.25). The increased Mx and Sx during cerebral vasospasm demon- strate impaired cerebral autoregulation. Mx and Sx pro- vide additional information on changes in autoregulation in SAH patients. (Anesth Analg 2004;98:1133–9) C erebral autoregulation refers to the intrinsic ca- pacity of the brain to maintain constant cerebral blood flow (CBF) despite changes in perfusion pressure (1,2). After subarachnoid hemorrhage (SAH), when cerebral autoregulation is frequently impaired (3–5), reductions in perfusion may contribute to de- layed ischemic deficits (DID). Indeed, impaired cere- bral autoregulation itself is a predictor of DID (5– 8). Cerebral vasospasm is often seen after SAH and is associated with DID (9,10). Initial studies suggest that patients with initially preserved autoregulation may be at less risk or even no risk of subsequently devel- oping DID as compared with patients with an initial autoregulation disturbance (11,12), but evaluation with a large number of patients is desirable. When vasospasm joins preexisting autoregulation impair- ment, the risk of DID increases (11). To identify patients at risk for DID, vasospasm and impaired autoregulation should be recognized early. Transcranial Doppler (TCD) sonography is a suitable technique for assessing vasospasm of the middle cere- bral artery (MCA) (10,13–15) and impaired autoregula- tion by using methods such as the cuff deflation test (16) or the transient hyperemic response test (17). Autoregu- lation tests are often performed by manipulating arterial blood pressure (ABP) by using external stimuli and ob- serving the related changes in CBF or blood flow velocity. A less invasive method based on spontaneous changes in ABP has been introduced (18). The indices of autoreg- ulation are calculated as moving correlation coefficients between spontaneous slow changes in ABP and slow changes in systolic (systolic index; Sx) or mean (mean index; Mx) flow velocities (FV). Sx and Mx have been shown to be indicators of autoregulation (19) and pre- dictors for outcome in head injury (18). However, Sx and Mx have not yet been applied to SAH patients. Mx can be interpreted as an indicator of autoregu- lation: a positive correlation between ABP and FV, as expressed by positive values of Mx, indicates passive dependence of blood flow on ABP (impaired autoreg- ulation). Negative or zero values suggest active cere- brovascular responses to changes in ABP (preserved Supported by Technology Foresight Challenge Award FCA234/ 95; G4200005 and Medical Research Council Programme Grant G9439390 (JDP). Accepted for publication November 13, 2003. Address correspondence and reprint requests to Martin Soehle, MD, Klinik fu ¨ r Ana ¨ sthesiologie und Spezielle Intensivmedizin, Uni- versita ¨t Bonn, Sigmund-Freud-Strae 25, 53105 Bonn, Germany. Address e-mail to martin.soehle@ukb.uni-bonn.de. DOI: 10.1213/01.ANE.0000111101.41190.99 ©2004 by the International Anesthesia Research Society 0003-2999/04 Anesth Analg 2004;98:1133–9 1133