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Hemodilution impairs cerebral autoregulation, demonstrating the complexity of integrative physiology.

J. Kevin Shoemaker, PhD Reflex adjustments to physical and orthostatic stress include a complex series of neurogenic, cardiac, and vascular reactions that defend cardiac output and systemic vascular resistance, so that arterial blood pressure and cerebral perfusion are sustained and near normal levels. In addition, an array of metabolic, circulating, endothelial, and local pressure-dependent regulatory mechanisms contribute to changes in cerebrovascular resistance. The ability of cerebral blood vessels to adjust their caliber and sustain blood flow over a wide range of perfusion pressure is termed autoregulation and has been the focus of research for many decades (1–3). Without such systemic and cerebrovascular responses, hypotension and cerebral hypoperfusion would occur. During surgery in anesthetized patients where normal physiology may be compromised, it is the role of anesthesiologists to sustain arterial blood pressure and cerebral perfusion at levels that are optimal for the circumstances. This objective often requires the enhancement of circulating blood volume with methods that dilute oxygen-carrying capacity. Yet the very practice of maintaining blood volume and cardiac output by hemodilution may be detrimental to cerebral function through reductions in oxygen delivery. The dangers of excessive hemodilution include poor neurologic (4,5) and other life-threatening outcomes after surgery (6). Several large observational (7–9) and experimental (10) studies have identified an association between very low intraoperative hematocrit levels ( 30%), altered cerebral metabolism, risk of in-hospital mortality, or adverse neurological outcomes. Hemodilution challenges cerebrovascular perfusion. Complex physiology is not regulated completely by simplistic strategies. The mechanism by which hemodilution affects cerebral blood flow (CBF) is perhaps as complex as the means by which CBF itself is sustained. One important question is the impact of hemodilution on cerebral autoregulation (CA). Further, if hemodilution impairs autoregulation, does it really matter under conditions where cardiac output is sustained under reflexive control? In the current issue of Anesthesia & Analgesia, Ogawa et al. (11) test the hypothesis that changes in circulating blood volume with hemodilution affect CA in conscious humans. This was accomplished by (a) reducing central blood volume with two levels of lower body suction (a simulated orthostatic stress), and (b) infusing normal saline at two rates to achieve up to approximately 5% reduction in hematocrit. With the saline infusion, there was a concurrent increase in circulating blood volume, cardiac filling pressure, and cardiac output. Examination of CA was accomplished using the transfer function gain approach (12–14), whereby spontaneous fluctuations in arterial blood pressure are correlated to concurrent variations in CBF velocity at various oscillating frequencies. With this comprehensive approach, analysis of static and dynamic autoregulation can be investigated along with questions regarding the relationship of cardiac output to CBF and oxygen delivery. This study offers a comprehensive approach in studying CA within the context of central and cerebral hemodynamics. Moreover, it offers opportunities for discussion of several points that are From the Neurovascular Research Laboratory, School of Kinesiology, The University of Western Ontario, London, Ontario. Accepted for publication July 17, 2007. Address correspondence and reprint requests to J. Kevin Shoemaker, PhD, Neurovascular Research Laboratory, School of Kinesiology, Room 3110 Thames Hall, The University of Western Ontario, London, ON N6A 3K7, Canada. Address e-mail to kshoemak@uwo.ca. Copyright © 2007 International Anesthesia Research Society DOI: 10.1213/01.ane.0000282825.13842.02