You can't manage what you don't measure.

Abstract

‘‘You can’t manage what you don’t measure’’. This quote is an old management adage that perfectly suits clinical anesthesia as well. Nowadays, anesthesiologists do have a variety of monitoring tools to assist with the care of their patients, however, many aspects of the impact of anesthetic agents on human physiology remain largely unknown. Although it has to be acknowledged that new measurements undoubtedly involve new forms of errors, the measurements (and their errors) have the potential to lead to a more comprehensive understanding of human physiology and to shed some light on previously unknown territory [1]. One of these ‘‘black boxes’’ is cerebral autoregulation. In a landmark paper published in 1959 [2], Lassen described an autoregulatory plateau between mean arterial pressures (MAP) of 50 and 150 mmHg, over which cerebral perfusion is maintained by alterations in vascular resistance. This classic description of autoregulation is widely accepted and has been propagated in many textbooks, and so most anesthesiologists aim for a MAP within this range during surgery. However, already in 1997, Drummond expressed concerns regarding the validity of this concept [3]. Several diseases have been shown to impair cerebral autoregulation [3–5], and recent data suggest that intact cerebral autoregulation actually consists of a series of different responses and that the classical concept of autoregulation might represent only part of the picture [6, 7]. Moreover, wide inter-individual variations in the lower limits of autoregulation (LLA) have been demonstrated [8]. Agents with cerebral vasodilating properties, including carbon dioxide (CO2) and anesthetic agents, affect the limits of autoregulation [9–12]. It is thus not reasonable to accept an empirically chosen LLA for every anesthetized patient in every situation [13]. If we are uncertain of the limits of autoregulation in any individual patient, how can we be sure that the blood pressure at any moment is sufficient for adequate cerebral blood flow (CBF)? Do we have any alternative methods to guide our clinical management? Over the last two decades, the development of new methods for continuous monitoring of cerebral autoregulation, and the clinical application of these methods, has become an area of intense investigation. It has been demonstrated that real-time autoregulation monitoring can be accomplished by the continuous calculation of the correlation coefficient between CBF and MAP, generating an index of autoregulatory vasoreactivity [14]. Blood pressure in the autoregulation range is indicated by an index that approaches zero, while an index approaching 1 indicates either impaired autoregulation or MAP beyond the limits of autoregulation. However, it has to be acknowledged that the lack of a quantitative gold-standard measure of cerebral autoregulation makes it challenging to advance our knowledge in this field. In this issue of JCMC, Goettel et al. [15] describe the results of a study in which concurrent measurements of MAP and middle cerebral artery flow velocity (by transcranial doppler ultrasonography, TCD) were used to calculate the autoregulation index. Hereby, they were able to evaluate the effect of sevoflurane anesthesia on the shape of the cerebral autoregulation curve in two age groups (18–40 years and C65 years). They conclude that the width & Annelies Moerman annelies.moerman@UGent.be