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Academic Neurosurgery, Addenbrooke’s Hospital, University of Cambridge, United Kingdom
To the Editor:
We have read with interest the publication by Endoh et al. (1). We would like to comment on two methodological issues concerning the assessment of autoregulation based on the index of autoregulation that has been used by the authors and that is also known as the static rate of autoregulation (SRoR) (2).
SRoR is a percentage change in cerebrovascular resistance divided by percentage change in cerebral perfusion pressure. When patients are supposed to have normal intracranial pressure, arterial pressure may be used instead. However, this is an uncertain assumption. With a phenylephrine-induced increase in arterial pressure of substantial magnitude (around 20 mmHg), intracranial pressure may rise even in patients without obvious intracranial volume expansion (3).
Secondly, SRoR is a linear index, which is not ideal to describe the non-linear behavior of cerebral blood flow to changes in cerebral perfusion pressure. This index has been introduced to describe only a fragment of the autoregulatory curve—namely the autoregulatory plateau. To make a statement on the extent to which a drug affects autoregulation, ideally the autoregulatory curve (including upper and lower thresholds of autoregulation and the slope of the autoregulatory plateau before and after administration of the study drug) need to be known. With drug-induced hypotension, two possible phenomena may occur: the slope of the plateau may change or the lower limit of autoregulation can be exceeded. A change in SRoR does not allow distinguishing between these two scenarios. From this point of view, judging drug effects by comparing SRoR measured in two different ranges of arterial pressure (from 60 to 80 and from 80 to 100) is problematic.
References
Department of Emergency & Critical Care Medicine, Niigata University Faculty of Medicine, Asahimachi, Niigata, Japan
In Response:
Thank you for the valuable comments regarding our article (1). We would like to reply to the comments concerning methodological issues.
As criticized, a moderate increase in mean arterial pressure (MAP) (20mmHg) induced with phenylephrine may cause an increase in intracranial pressure (ICP), even in patients without intracranial pathology. However, Strebel et al. have shown that phenylephrine does not directly affect intracranial hemodynamics in anesthetized patients, but rather that hemodynamic changes caused with phenylephrine reflect the effect of the background anesthetic agents on cerebral pressure autoregulation (2). Propofol, which is known to produce a "hyper-regulated" state of cerebral vessels (3), was used in our study as background anesthesia. Thus, in our study, the influence of phenylephrine on ICP seems to be minimal, supporting our methodology based on MAP, not cerebral perfusion pressure. On the other hand, we evaluated the influence of nitroglycerin in this study (1). Nitroglycerin is known to possess potent venous dilating properties, presumably resulting in an increased ICP. However, our previous study showed that, during nitroglycerin-induced hypotension, critical closing pressure, representing effective downstream pressure rather than ICP, was not significantly changed from baseline (4), which also may support our methodology based on MAP.
Essentially, the index of static rate of regulation (SRoR) only assesses the gradient of the autoregulatory plateau, because SRoR is calculated from the percentage change in cerebral vascular resistance per percentage change in MAP. Furthermore, because the changes induced in MAP are only moderate (20mmHg), SRoR cannot assess changes in the width of the plateau (5). Ideally, as criticized, cerebral pressure autoregulation should be assessed from the entire autoregulatory curve: the upper and lower thresholds, the slope, and the width of plateau. However, such assessment needs a large change in MAP, which seems ethically unacceptable, and to ensure that assessment at the upper threshold is not a clinical concern during induced hypotension. Indeed, SRoR cannot distinguish between the change of slope and the upward shift of lower threshold. However, in a broader sense, both scenarios mean impaired cerebral pressure autoregulation. Thus, our findings still remain clinically relevant.
Thank you again for your valuable comments.
References
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