Critical Thresholds for Cerebrovascular Reactivity: Facts, No Fiction!
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LETTER TO THE EDITOR
Critical Thresholds for Cerebrovascular Reactivity: Facts, No Fiction! Jennifer Diedler • Enrico Sorrentino • Magdalen Kasprowicz Peter Smielewski • Karol Budohoski • Marek Czosnyka
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Published online: 14 June 2012 Springer Science+Business Media, LLC 2012
We are grateful for the letter [1], which gives us an opportunity to reiterate some important points regarding continuous monitoring of cerebrovascular reactivity. Nordstrom and Nielsen are correct about the definition of autoregulation. However, pressure-reactivity index (PRx) is not an index of cerebral autoregulation, as noted before [2]. There is a link between vascular reactivity and autoregulation, but the overall correlation coefficient between PRx and autoregulation derived from Transcranial Doppler (TCD) or other CBF monitors (direct or indirect) is far from +1 (average values range from 0.4 to 0.7, depending on computational details, pathology studied, and so forth [2, 3]). Another point is that the limits of vascular reactivity extend beyond the limits of autoregulation. Obviously, non-reactive vessels cannot autoregulate, but in reactive arterioles, too weak response of cerebrovascular resistance to a change in cerebral perfusion pressure may still make CBF pressure passive. PRx is a robust measure of vascular reactivity, which:
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Concurrently, it has disadvantages: •
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• J. Diedler Department of Neurology, University of Heidelberg, Heidelberg, Germany E. Sorrentino Department of Anaesthetics and Intensive Care, Western Sussex Hospitals NHS Trust, Worthing, UK M. Kasprowicz Institute of Biomedical Engineering and Instrumentation, Wroclaw University of Technology, Wroclaw, Poland P. Smielewski K. Budohoski M. Czosnyka (&) Neurosurgical Unit, Department of Clinical Neurosciences, Addenbrooke’s Hospital, Cambridge, UK e-mail: [email protected]
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Independently from ICP, CPP, and GCS correlates with outcome after TBI. Particularly it shows steep difference between patients who die or survive after TBI [4]. Averaged in time (minimum period is from 0.5 to 1 h) gives an impression of how reactivity fluctuates during brain monitoring period [5]. Averaged across various CPP levels, allows establishing ‘‘optimal CPP’’ which is an individual timedependent target CPP during the acute phase of management after TBI [6].
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It is noisy, and depends on how much change in arterial pressure may affect change in ICP. Signal-to-noise ratio is particularly poor if arterial pressure fluctuates very little. At high ICP, when a Cushing response is observed, it becomes close to +1 (probably, vascular reactivity is deranged at this point anyway) In patients where pressure–volume curve is not steep enough (e.g., after decompressive craniectomy) it does not work [7]. PRx may be affected by local or global changes in cerebral metabolism [8]. The impact of this phenomenon has not been determined, however, it seems to be more pronounced at states of decreased cerebral metabolism suggesting that this relationship may represent severit
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