Cerebral blood flow

Introduction The brain has both a high demand for energy and an inability to store important substrates for metabolism. This means that it is highly dependent on a constant supply of oxygen and glucose, provided to the tissues by capillary perfusion. Even brief interruptions in flow will trigger loss of cerebral function within seconds (e.g. syncope during cardiac arrhythmias). Cerebral blood flow (CBF), a measure of brain perfusion, is therefore a vital parameter in assessing the adequacy of substrate delivery and viability of the brain, especially in cerebrovascular disease states where flow may be impaired. It is expressed as the volume of blood reaching a defined mass of brain tissue in a given period of time (typically ml per 100 g/min). Regional reductions in CBF, usually related to mechanical obstruction (thrombosis, stenosis, vasospasm), may lead to neurological deficits and, if prolonged, focal areas of irreversible cerebral infarction. Normal whole-brain CBF is approx. 50 ml/100 g/min [1]. This averages the more metabolically active gray matter (CBF approx. 80 ml/100 g/min), and the white matter (20ml/100g/min) [2]. Flow must be adequate to deliver oxygen to meet the metabolic demands of the tissue. To ensure this, flow and metabolism usually remain tightly coupled, whereas increases in cerebral metabolic demand (expressed as CMRO₂, or cerebral metabolic rate of oxygen) are matched by increases in CBF and oxygen delivery (DO₂). Considerable reserve is maintained, such that CBF normally delivers 2–3 times the required oxygen (e.g. DO₂ of approx. 8 ml of oxygen per 100 g/min compared to a metabolic requirement of 3 ml of oxygen/100g/min). Therefore, the proportion of oxygen extracted (OEF) should remain constant (normally ~ 30–35%), rising only if DO₂ falls out of proportion to CMRO₂. The Fick principle describes the relationship between metabolism, delivery and extraction of oxygen:Where DO₂ = CBF × CaO₂ (arterial oxygen content in ml O₂ per ml blood)