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, PaCO₂), 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.

脑血流量 (CBF) 的控制对于神经危重症患者的管理至关重要。检验心输出量 (CO) 作为 CBF 决定因素的作用的小型研究不一致地证明了心脑耦合的证据。支撑这种耦合的假定生理机制包括动脉血压搏动的变化，这将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作用产生血管舒张，以及可能改善脑灌注压的静脉背压变化。我们试图总结和背景化有关 CO 和 CBF 之间关系的文献，并讨论心脑耦合对神经重症监护的影响。对文献的系统回顾产生了 41 项研究；所有这些都是低质量和高偏倚风险。结果是异质的，有证据表明在正常和异常脑血管状态下 CO 和 CBF 之间的关系得到证实和反驳。研究的共同局限性是缺乏瞬时 CBF 测量，依赖经颅多普勒衍生的血流速度作为替代指标，无法控制已确定的 CBF 决定因素（例如，PaCO₂），以及用于改变 CO 的干预措施对 CBF 的直接影响。目前，文献不足以证实 CO 和 CBF 之间的独立关系。假设，心脑耦合的存在将对临床实践产生重要影响。CBF 的操作可以在没有与极端动脉压相关的风险的情况下发生，从而可能改善对各种病因的脑缺血患者的治疗。然而，目前的文献不足以证实 CO 和 CBF 之间的独立关系，在治疗干预可以基于心脑耦合之前，需要进一步研究改进方法。