Dynamic cerebral autoregulation and monitoring cerebral perfusion.

Cerebral autoregulation (CA) describes the capability of the brain to maintain its flow as relatively stable over a wide rage of mean arterial pressures (MAPs), for example, from 60 to 150 mm Hg. Because the brain is encompassed in the skull, CA is vital for preventing cerebral edema and hemorrhage, as illustrated in some patients experiencing acute liver failure.1 Also, CA counteracts the effect on cerebral blood flow (CBF) of a reduction in MAP in response to, for example, hemorrhage or a change in body position. Yet, when rising from a supine or seated position, one sometimes experiences symptoms indicative of a reduced CBF, like blurred vision.2 Thus, CA is of general clinical interest. For example, diabetic patients have increased risk of developing ischemic or hemorrhagic stroke, and in some diabetic patients CA is affected. Evidence for CA was provided in the 1930s when Fog,3 through a cranial window, observed the pial artery reaction to manipulation of MAP. For humans, CBF was measured with introduction of the method of Kety-Schmidt in 1948,4 and it was used in 1954 by Finnerty et al5 to determine cerebral hemodynamics of the ischemic brain after an acute reduction in MAP in attempt to define what now would be considered the lower limit of CA. However, it was the review by Lassen6 that introduced the concept of CA by plotting CBF against MAP to illustrate the relative stability of CBF over a wide range of blood pressure. Also, the lower and upper limits of CA were identified by a decrease in CBF at a low MAP and an increase in CBF when MAP was at a high level. A different approach to CA became available when Aaslid et al7 introduced the transcranial Doppler method for determination of mean flow velocity (Vmean) in basal cerebral arteries. Because transcranial Doppler reports a continuous (middle cerebral artery) Vmean, cerebral perfusion could be followed during the drop in MAP that follows release of thigh cuffs. It took 3 seconds for Vmean to recover from the sudden drop in MAP that followed the release of the thigh cuffs, and, accordingly, the acute response of cerebral perfusion to a change in MAP was referred to as the dynamic CA. Dynamic CA, or the instability of CBF during a sudden change in MAP, is important because it explains blurred vision sometimes experienced in response to a change in body position.2 The study by Tzeng et al8 takes advantage of the drop in blood pressure that manifests from a seated to an upright position to characterize dynamic CA. Conversely, the marked increase in MAP that develops in response to a Valsalva maneuver may be used to characterize CA during a sudden increase in MAP (Figure).9 Some scepticism may remain as to whether the classic (static) and dynamic CA describe the same physiological phenomenon, but supporting evidence was provided by Tiecks et al.10 These authors determined static and dynamic CA from monitoring Vmean during elective surgical procedures using propofol and high-dose isoflurane anesthesia. During propofol anesthesia, both static and dynamic CA (the Vmean response to administration of phenylephrine versus thigh-cuff release) remained intact, whereas the 2 expressions of CA became similarly affected when general anesthesia was shifted to isoflurane. Taken together, such observations indicate that CA can be described in terms of a high-pass filter for the transfer function from MAP to Vmean. Thus, CA is specified with regard to its gain and the phase angle for which Vmean leads blood pressure. In this issue of Hypertension, Tzeng et al8 renew the evaluation of dynamic CA. The Vmean response to a lowering of MAP, either by rising from a seated position or in response to the administration of nitroprusside, is supplemented by an evaluation of the Vmean response to an elevation of MAP by phenylephrine in volunteers. Surprisingly, they found that the ability of CA to respond (damp) to a rise in MAP is approximately twice as well developed as the ability to withstand a reduction in MAP, as suggested previously by Ogoh et al11 during exercise. If CA is much more capable of damping an increase than a decrease in blood pressure, it implicates that a simple correlation analysis is not ideal for characterization of the transfer function from blood pressure to Vmean. On the other hand, the pharmacological approach to CA introduced by Tzeng et al8 is both clinical relevant and feasible and definitely much easier to apply to patients than the invasive procedures needed for the determination of static CA based on CBF. We consider also that, in a clinical setting, it would be more straightforward to administer 2 drugs after each other than to use the thigh-cuff release method of Aaslid et al7 for the evaluation of (dynamic) CA. The question, however, remains regarding whether an evaluation of CA provides enough information to verify that CBF remains stable. We think not. We agree that it is relevant The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. From the Department of Anesthesia (N.H.S.), Rigshospitalet, Copenhagen Muscle Research Center, University of Copenhagen, Copenhagen, Denmark; Department of Internal Medicine (J.J.v.L.) and Laboratory for Clinical Cardiovascular Physiology (J.J.v.L.), Academic Medical Center Center for Heart Failure Research, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. Correspondence to Niels H. Secher, Department of Anesthesia, Rigshospitalet 2041, Blegdamsvej 9, DK-2100 Copenhagen Ø, Denmark. E-mail [email protected] (Hypertension. 2010;56:189-190.) © 2010 American Heart Association, Inc.