Departments of Neurosurgery.
Intensive Care, Monash Health.
J Neurosurg Anesthesiol. 2022 Oct 1;34(4):352-363. doi: 10.1097/ANA.0000000000000768. Epub 2021 Mar 29.
Control of cerebral blood flow (CBF) is crucial to the management of neurocritically ill patients. Small studies which have examined the role of cardiac output (CO) as a determinant of CBF have inconsistently demonstrated evidence of cardio-cerebral coupling. Putative physiological mechanisms underpinning such coupling include changes in arterial blood pressure pulsatility, which would produce vasodilation through increased oscillatory wall-shear-stress and baroreceptor mediated reflex sympatholysis, and changes in venous backpressure which may improve cerebral perfusion pressure. We sought to summarize and contextualize the literature on the relationship between CO and CBF and discuss the implications of cardio-cerebral coupling for neurocritical care. A systematic review of the literature yielded 41 studies; all were of low-quality and at high-risk of bias. Results were heterogenous, with evidence for both corroboration and confutation of a relationship between CO and CBF in both normal and abnormal cerebrovascular states. Common limitations of studies were lack of instantaneous CBF measures with reliance on transcranial Doppler-derived blood flow velocity as a surrogate, inability to control for fluctuations in established determinants of CBF (eg, PaCO 2 ), and direct effects on CBF by the interventions used to alter CO. Currently, the literature is insufficiently robust to confirm an independent relationship between CO and CBF. Hypothetically, the presence of cardio-cerebral coupling would have important implications for clinical practice. Manipulation of CBF could occur without the risks associated with extremes of arterial pressure, potentially improving therapy for those with cerebral ischemia of various etiologies. However, current literature is insufficiently robust to confirm an independent relationship between CO and CBF, and further studies with improved methodology are required before therapeutic interventions can be based on cardio-cerebral coupling.
控制脑血流（CBF）对于神经危重症患者的管理至关重要。一些小型研究已经探讨了心输出量（CO）作为 CBF 决定因素的作用，但结果不一致，无法证明心脑耦合的存在。支持这种耦合的潜在生理机制包括动脉血压脉动性的变化，这会通过增加振荡壁剪切应力和压力感受器介导的反射性交感神经松弛来产生血管扩张，以及静脉后负荷的变化，这可能会改善脑灌注压。我们旨在总结和阐述 CO 与 CBF 之间关系的文献，并讨论心脑耦合对神经危重症护理的影响。对文献进行系统回顾，共得到 41 项研究；所有研究的质量都较低，存在较高的偏倚风险。结果存在异质性，有证据表明在正常和异常脑血管状态下，CO 与 CBF 之间存在关系的佐证和反驳。研究的常见局限性包括缺乏即时的 CBF 测量，依赖经颅多普勒衍生的血流速度作为替代指标，无法控制 CBF 的既定决定因素（例如 PaCO 2 ）的波动，以及干预措施对 CO 的直接影响。目前，文献还不够强大，无法确认 CO 和 CBF 之间存在独立关系。从理论上讲，心脑耦合的存在将对临床实践产生重要影响。在不引起动脉压极端波动的情况下，通过改变 CO 来操纵 CBF，可能会改善各种病因引起的脑缺血患者的治疗效果。然而，目前的文献还不足以确认 CO 和 CBF 之间存在独立关系，需要进一步进行改进方法的研究，然后才能根据心脑耦合来进行治疗干预。
