Abstract
In the adult, cerebral blood flow (CBF) is typically 15% of the resting cardiac output (approximately 750 mL/min). CBF is commonly expressed in terms of the weight of brain parenchyma – normal CBF is 50 mL/100 g brain tissue/min. It is determined by the ratio of the cerebral perfusion pressure (CPP) and cerebral vascular resistance (CVR).
What proportion of the cardiac output is directed to the brain?
In the adult, cerebral blood flow (CBF) is typically 15% of the resting cardiac output (approximately 750 mL/min). CBF is commonly expressed in terms of the weight of brain parenchyma – normal CBF is 50 mL/100 g brain tissue/min. It is determined by the ratio of the cerebral perfusion pressure (CPP) and cerebral vascular resistance (CVR).
What is CPP?
CPP is the net pressure gradient driving blood flow through the cerebral circulation, resulting in the CBF. It is dependent upon both the mean arterial pressure (MAP) and the intracranial pressure (ICP). It is related to the remaining key parameters as follows:
In relation to ICP:
CPP = MAP – ICP
In relation to CVR:
CPP = CBF × CVR
What is cerebral autoregulation?
CBF is remarkably constant, remaining close to 50 mL/100 g/min across a wide range of cerebral perfusion pressures, ranging from 50 to 150 mmHg (Figure 48.1). This property of the brain is known as autoregulation.
Figure 48.1 Cerebral autoregulation.
Autoregulation is thought to take place through a myogenic mechanism in which the cerebral arterioles vasoconstrict in response to an increase in wall tension, and they vasodilate in response to a decrease in wall tension, thereby increasing or decreasing CVR (see Chapter 34).
Outside the autoregulatory range:
When CPP is greater than 150 mmHg, CBF becomes directly proportional to CPP.
When CPP falls below 50 mmHg, CBF falls below the ‘normal’ value of 50 mL/100 g/min, resulting in brain ischaemia.
The autoregulation curve (Figure 48.1) is shifted to the right in patients with chronic hypertension and to the left in neonates.
What happens to neurons when CBF falls below 50 mL/100 g/min?
The brain is more sensitive to even short periods of ischaemia than any other organ in the body. For example, a reduction in CBF to 30 mL/100 g/min for just 5 s, as may occur during a vasovagal episode, results in loss of consciousness. As CBF decreases, there is a corresponding reduction in cerebral O2 delivery, which leads to cellular ischaemia:
CBF < 50 mL/100 g/min results in cellular acidosis.
CBF < 40 mL/100 g/min results in impaired protein synthesis.
CBF < 30 mL/100 g/min results in cellular oedema.
CBF < 20 mL/100 g/min leads to failure of cell membrane ion pumps, with loss of transmembrane electrochemical gradients.
CBF < 10 mL/100 g/min results in cellular death.
What is meant by the term ‘flow–metabolism coupling’?
Although the overall CBF remains close to 50 mL/100 g/min, blood is preferentially routed to the most metabolically active brain regions. For example, CBF to grey matter is 70 mL/100 g/min, whereas CBF to white matter is only 20 mL/100 g/min. Areas of metabolically active brain have higher concentrations of vasodilatory metabolites (e.g. CO2, H+, K+ and adenosine), thereby increasing local blood flow and O2 delivery.