Mean cerebral blood flow is about 55 ml/100 g/min and is maintained within a relatively narrow range compared with other organs. It varies between the anatomical structures of the brain with grey matter in general receiving more than twice (70 ml/100 g/min) the blood flow of white matter (30 ml/100 g/min).
The brain consumes about 3.5 ml/100 g/min oxygen leaving the jugular venous blood 65% saturated. Structures such as the colliculi and basal ganglia receive much greater blood flows than the brain stem and cerebellum. Cortical blood flow is dependent on activity and perfusion of specific areas reaches high levels (> 130 ml/100 g/min) when activated.
Cerebral blood flow can be estimated by:
• Kety method—an application of the Fick principle that determines the total cerebral blood flow in ml/100 g/min. Nitrous oxide is used as the transported substance because it has partition coefficient = 1, which ensures that the brain concentration becomes equal to the jugular venous concentration, after an equilibration time of 10 min. A subject breathes 15% nitrous oxide for 10 min. The total nitrous oxide transferred to 100 g brain tissue per min (Q) can be determined from the final nitrous oxide content of 100g of jugular venous blood divided by 10. The average arteriovenous difference (D) in nitrous oxide content per ml is determined from arterial and venous samples during equilibration. The blood flow can then be calculated from the ratio Q/D
• Scintillography—using radioactive tracers (xenon) to trace regional blood flow
• SPECT scanning—scintillography enhanced by CT or MRI scanning
• PET scanning—use of 2-deoxyglucose labelled with a positron emitter
• Doppler—crude but readily available for clinical use in ICU or operating theatre Regulation of Cerebral Blood Flow
Control of cerebral circulation is primarily through autoregulation due to local metabolic factors. Neural control is thought to play a minor role. Total cerebral blood flow is maintained constant over a range of mean arterial pressure and in the face of varying levels of PaCO2 and PaO2. This is achieved by control of total cerebrovascular resistance and cerebral perfusion pressure (Figure CR.35).
Regional cerebral blood flow on the other hand, is highly variable and varies according to activity and local metabolic factors. The factors affecting total cerebral blood flow include:
• Cerebral perfusion pressure—pressure across the cerebral vessels, given by the difference between the mean arterial pressure—(venous pressure + intracranial pressure). Raised intracranial pressure may reduce cerebral perfusion pressure
• PaCO2—arterial CO2 tensions have a marked influence over cerebral blood flow. Low PaCO2 vasoconstricts and raised PaCO2 vasodilates cerebral vessels. Hyperventilation reduces blood volume within the brain and is used to reduce raised intracranial pressure after head injury
• PaO2—low PaO2 vasodilates and high PaO2 vasoconstricts but the effect of oxygen tension on cerebral vessels occurs to a far lesser degree than with PaCO2
• pH—cerebral vessels are also sensitive to pH independently of PaCO2. A decreased pH causes vasodilatation
• Metabolites—adenosine and potassium have both been implicated in adjusting local cerebral perfusion. Any event causing decreased PaO2 or increased oxygen demand, produces raised local levels of adenosine in the brain, which are sustained throughout the event. A similar transient rise in potassium ion concentration is also produced. These substances are thought to be instrumental in linking regional blood flow to activity in the brain
Raised Intracranial Pressure (ICP)
The skull is a rigid bony enclosure that contains 1400 g brain tissue (80%), 75 ml blood (10%) and 75 ml cerebrospinal fluid (10%). These contents are effectively incompressible; therefore, any increase in one component produces a reciprocal decrease in the others (Monro-Kellie doctrine) and an increase in ICP. Cerebral oedema will, thus, be accompanied by a reduction in cerebral blood volume and compression of the ventricles. Brain injury secondary to raised ICP occurs when cerebral blood flow is compromised, or when the increase in ICP is asymmetrical and brain shift occurs. Normal ICP is 0-10 mmHg, while > 15 mmHg is considered significantly raised. As ICP continues to rise, cerebral blood flow is increasingly reduced and brain tissue becomes ischaemic. Vital centres respond by increasing systemic arterial blood pressure, slowing the heart rate and respiratory rate. The blood pressure response attempts to restore cerebral blood flow by restoring the cerebral perfusion pressure. Ultimately herniation of the cerebellar tonsils through the foremen magnum causes compression of the brainstem and death.
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