Understanding cerebral autoregulation and cerebrovascular reactivity: mechanistic perspectives and clinical insights from TBI
摘要
Cerebrovascular reactivity and cerebral blood flow autoregulation are critical determinants of brain homeostasis but are often conflated in clinical practice. Although these constructs are closely related and arise from vascular responses to vasoactive stimuli, they reflect distinct physiological responses and measurement approaches: autoregulation is assessed through changes in cerebral blood flow, and pressure reactivity through changes in cerebral blood volume. A fundamental clinical challenge is that the full autoregulatory curve is rarely observable in an individual patient at a single point in time; consequently, isolated measurements from classical assessments or continuous indices such as the pressure reactivity index (PRx), mean flow index (Mx), and arterial mean flow index (Mxa) are each associated with different components of cerebrovascular physiology, providing only partial views of cerebrovascular function and frequently yielding apparently conflicting results. This Review addresses a central clinical question: can multimodal neuromonitoring help determine where a patient is operating on the autoregulatory curve? We synthesise current understanding of the physiological relationships among cerebral perfusion pressure, cerebral blood flow, and cerebral blood volume, and examine the mechanisms underlying divergent autoregulatory index behaviour. By integrating mechanistic physiological schematics and representative clinical cases, we propose an objective educational framework that links classical cerebrovascular physiology with contemporary bedside monitoring. Within this framework, six conceptual physiological zones are delineated. These zones demonstrate how variations in vascular tone, intracranial compliance, and critical closing pressure shape autoregulatory responses generate differing patterns in PRx, Mx, and Mxa. Fully defining a patient’s complex cerebrovascular state requires looking beyond any single parameter. Together, PRx, Mx, and Mxa provide complementary information, where discordant findings may represent distinct physiological mechanisms rather than measurement error. Interpreting these indices together within a mechanistic framework may improve identification of a patient’s position along the autoregulatory curve, support more consistent bedside interpretation, and ultimately facilitate personalised cerebral perfusion pressure management.