Fig. 1

Regulation of the cerebral circulation. CBF at the level of the microvasculature is directly proportional to CPP (difference between ABP and ICP) and inversely proportional to CVR. ICP exerts its effect on CBF through changes in CPP; compression of the venous vasculature where the bridging veins enter the sagittal sinus ensures that the bridging vein and post-capillary intravascular pressure is always above ICP. CBF is modulated by the cardiovascular system in terms of the regulation of SV, HR, and TPR (red). Control of TPR with vasopressors forms an integral part of many CBF protective strategies (even when TPR is not the primary cause of CBF disturbance). CVR is regulated at the level of the arterioles (purple) by variations in vascular tone in response to metabolic, neural, or myogenic inputs. In ischaemic stroke or vasospasm, CVR is dramatically increased, usually at the level of large intracranial arteries. ICP (blue) modulates CBF through its coupling with cerebral venous pressure. ICP increases can be caused by increases in cerebral blood volume (arterial or venous), increased CSF volume or increase in parenchyma (oedema), or abnormal material volume (mass lesion). All therapies that modulate CBF do so via one (or more) of these pathways. There is typically significant interdependence between the therapies, determinants, and influences of CBF. For example, a drop in ABP would be expected to result in a drop in CBF but this is short lived due to the baroreflex (HR increase in response to drop in ABP) and cerebral autoregulation (decrease in vascular tone in response to drop in ABP). ABP arterial blood pressure, CBF cerebral blood flow, CBV cerebral blood volume, CSF V cerebrospinal fluid volume, CVR cerebrovascular resistance, EVD external ventricular drainage, HR heart rate, ICP intracranial pressure, IIH idiopathic intracranial hypertension, SV stroke volume, TPR total peripheral resistance