Central Nervous System
Cerebral Blood Flow
Blood flow to the brain is via the internal carotid (anterior) and vertebral (posterior) arteries. They anastomose to form the Circle of Willis.
The control of blood flow is regulated within strict limits. Our brain is very sensitive to ischaemia/hypoxia – you will lose conciousness within 5 seconds of cerebral blood flow disruption! If this disruption – either by a blood clot, haemorrhage, metabolic conditions or sepsis is prolonged to 2-3 minutes, there could be irreversible brain damage.
The brain receives up to 15% of cardiac output.
Here we will look at the three systems that regulate cerebral blood flow: autoregulation, local control and neural control.
Autoregulation is the condition in which the brain maintains its blood flow over a wide range of blood pressures.
The brain achieves autoregulation via myogenic or metabolic pathways.
First you need to understand the concept of Cerebral Perfusion Pressure (CPP). CPP is the net pressure gradient that drives oxygen delivery to cerebral tissue. It is the difference between the mean arterial pressure (MAP) and the Intracranial Pressure (ICP), measured in millimeters of mercury (mm Hg).
CPP = MAP – ICP
(Remember this equation. This may be asked in your exam!)
Myogenic autoregulation occurs when the cerebral blood vessels constrict or dilate based on the blood pressure. When the BP rises the blood vessels constrict to decrease blood flow; when BP decreases the blood vessels dilate to increase flow. Our brain does this every few seconds and is very good at compensating for variation of blood pressures.
However, this mechanism has a limit at which it can compensate:
- If CPP falls below 50mmHg, dilatation of blood vessels fail to maintain flow and causes cerebral ischaemia. If it falls further below 30mmHg – death occurs.
- If CPP rises too high at 150-160 mmHg, constriction fails and the vessels may become abnormally permeable, leading to cerebral oedema.
Myogenic autoregulation may be disrupted by:
- cerebral haemorrhage
Metabolic autoregulation depends on which parts of the brain is actively functioning. If a task is performed by a specific area of the brain, it will have increased activity leading to decrease in PaO2 and increase in PaCO2 and [H].
These changes result in local vasodilation of cerebral blood vessels therefore increasing perfusion.
Local Control of Cerebral Blood Flow
As mentioned above, cerebral blood flow (CBF) is also very sensitive to changes in arterial PaO2 and PaCO2.
Increase in PaCO2 causes vasodilatation, fall in PaCO2 will then cause vasoconstriction.
This is an important concept to consider in head injury patients. Maintaining low-normal PaCO2 will prevent increase in ICP by restricting vasodilatation. At the same time, if the PaCO2 falls too low it will cause vasoconstriction and brain ischaemia will ensue!
The effects of hypoxia is not as marked. It causes significant changes when PaO2 falls below 8kPa. If it falls below this CBF may fall dramatically.
Increase in PaCO2 will cause mild cerebral vasoconstriction – hyperbaric oxygen therapy can reduce CBF by up to 30%.
Neural Control of Cerebral Blood Flow
The CBF also receives some sympathetic vasoconstriction and parasympathetic vasodilatation. However their effect is weak and their role unclear. Remember this to earn brownie points in your viva exam!