Measuring Cerebral Autoregulation in Stroke Patients

Stroke Patients To the Editor: We have read with interest the article by Georgiadis et al in the December 2002 issue of Stroke.1 The authors have attempted to examine the integrity of cerebral autoregulation in hypothermic stroke patients. We would like to raise 2 methodological issues. Despite measuring intracranial pressure, the authors have used mean arterial pressure rather than cerebral perfusion pressure to calculate the static rate of autoregulation in their patients. In patients with disturbed autoregulation, intracranial pressure will rise in response to an increase in mean arterial pressure and cerebral perfusion pressure will therefore change less than mean arterial pressure; this phenomenon is known as “false autoregulation” and has been recently reported as occurring frequently, at least in head-injured patients.2 Using mean arterial pressure instead of cerebral perfusion pressure may therefore lead to an overestimation of the static rate of autoregulation, ie, the patient seems to have better autoregulation than she or he really does. This is even more important when large increases in mean arterial blood pressure (.20 mm Hg) are used to test autoregulation, as in this study. Such large increases may lead to an increase in intracranial pressure even in subjects without intracranial pathology.3 The authors use a somewhat arbitrary cut-off of 40% in static rate of autoregulation to define abnormal autoregulation. This contrasts with previous work showing that healthy normal volunteers typically have a static rate of autoregulation .85%.4–6 Admittedly these studies were performed under propofol anesthesia, whereas the patients in the authors’ study were sedated with midazolam. However, both of these drugs have cerebral vasoconstricting properties7 and it is unlikely that there are large differences between them in terms of their effects on autoregulation. Autoregulation should probably be graded, rather than treated as a yes-or-no phenomenon; therefore, comparison to a control group of “normals” is perhaps more appropriate than defining dysautoregulation in terms of an arbitrary threshold. It is unclear why the authors expect autoregulation to fail in hypothermia. Theoretically, hypothermia should lead to an increase in the static rate of autoregulation as vasoconstriction results, even more so when alpha-stat management is used and PaCO2 is kept constant.8 We have attempted to use the data given in the table to calculate the influence of hypothermia on static rate of autoregulation. However, the number of typographical mistakes made this methodologically impossible; for example, the calculated percentage changes in mean arterial pressure did not always tally with the mean arterial pressure measurements (this was especially so for patients 12 and 13). There were also discrepancies in the article over the vasoactive agent being used to increase mean arterial pressure, with both norepinephrine and epinephrine being mentioned. As these agents have varying adrenergic receptor efficacy and therefore potentially differing effects on cerebral blood flow and metabolism, it is important that they were not used interchangeably.