Silverman Andrew, Petersen Nils H.
Yale University
Cerebral autoregulation is the ability of the cerebral vasculature to maintain stable blood flow despite changes in blood pressure (or, more accurately, cerebral perfusion pressure). Under normal circumstances, cerebral blood flow is regulated through changes in arteriolar diameter, which, in turn, drive changes in cerebrovascular resistance following the Hagen-Poiseuille equation. Although decades of research have illuminated some underpinning mechanisms, the exact molecular means underlying autoregulation remain elusive. Various processes, including myogenic, neurogenic, endothelial, and metabolic responses, have mediated cerebral vasomotor reactions. See Physiology of Cerebral Autoregulation. Still, it is essential to differentiate carbon dioxide reactivity and flow-metabolism coupling from cerebral autoregulation. Carbon dioxide reactivity describes vascular reactions in response to changes in the partial pressure of arterial carbon dioxide (PaCO) but does not consider reactions to pressure changes. Flow-metabolism coupling, in comparison, involves regulating cerebral blood flow relative to local cellular demand, for example, as a consequence of neural activation during cognitive tasks. Similar to PaCO reactivity, flow-metabolism coupling, and the neurovascular unit function irrespective of fluctuations in cerebral perfusion pressure. With a working definition of autoregulation and an understanding of what it is not, researchers have developed technology that now boasts the ability to measure autoregulatory function in real-time, which may lead to fine-tuning long-established guidelines. Updated guidelines may ameliorate clinical and functional outcomes after acute brain injury by individualizing cerebral perfusion pressure targets based on patients' unique hemodynamic physiology. Autoregulation is assessable by examining changes in cerebral blood flow, or its surrogates, in response to changes in cerebral perfusion pressure or mean arterial pressure as its surrogate. Individualization of autoregulatory pressure ranges and the developing concept of an optimum mean arterial pressure landscape for the injured brain represent a novel and innovative application of autoregulation neuromonitoring. This topic is further discussed in the concluding section of this review.
脑自动调节是指脑血管系统在血压(或更准确地说,脑灌注压)发生变化时维持稳定血流的能力。在正常情况下,脑血流通过小动脉直径的变化进行调节,而小动脉直径的变化又会根据哈根 - 泊肃叶方程驱动脑血管阻力的变化。尽管数十年的研究揭示了一些潜在机制,但脑自动调节的确切分子机制仍然难以捉摸。包括肌源性、神经源性、内皮和代谢反应在内的各种过程介导了脑血管舒缩反应。见《脑自动调节的生理学》。不过,区分二氧化碳反应性和血流 - 代谢耦联与脑自动调节至关重要。二氧化碳反应性描述的是血管对动脉血二氧化碳分压(PaCO₂)变化的反应,但不考虑对压力变化的反应。相比之下,血流 - 代谢耦联涉及根据局部细胞需求调节脑血流,例如,在认知任务期间神经激活的结果。与PaCO₂反应性类似,血流 - 代谢耦联以及神经血管单元功能不受脑灌注压波动的影响。有了自动调节的有效定义并了解了它不是什么之后,研究人员开发出了现在能够实时测量自动调节功能的技术,这可能会导致对长期既定指南进行微调。更新后的指南可能通过根据患者独特的血流动力学生理特性个体化脑灌注压目标,改善急性脑损伤后的临床和功能结局。通过检查脑血流或其替代指标在脑灌注压或作为其替代指标的平均动脉压变化时的变化,可以评估自动调节功能。自动调节压力范围的个体化以及针对受伤大脑的最佳平均动脉压格局这一不断发展的概念代表了自动调节神经监测的一种新颖创新应用。本综述的结论部分将进一步讨论这个话题。