01 PHYSIOLOGY

33. Cerebral blood

flow
Cerebral function is dependent upon cerebral blood flow (CBF) and oxygenation. An understanding of the
physiology of CBF regulation is essential in order to manage patients who may have decompensated intracranial
pathology or injuries.

Basic concepts > Global CBF: 50 mL/100 g brain tissue/minute.

Myogenic theory of cerebral
autoregulation.
> White matter blood flow: 20 mL/100 g/minute.
> Grey matter blood flow: 70 mL/100 g/minute.
> Resting oxygen consumption of the brain: 50 mL/minute (20% of total
body oxygen requirements).
> Regional CBF varies depending on metabolic rates of local areas of brain.
> CBF exhibits autoregulation – the maintenance of constant blood flow
despite changes in cerebral perfusion pressure (CPP).
> CPP = mean arterial pressure (MAP) – [Intracranial Pressure (ICP) + CVP].
N.B. CVP is often omitted from this equation.
> Normal CPP is approximately 70–80 mmHg.
> Cerebral blood flow: myogenic theory vs. local metabolites.
> CBF is autoregulated between an MAP range of 50 and 150 mmHg
(curve is shifted to the right in hypertensive patients).
A change in perfusion pressure results in a myogenic response in the
cerebral vascular smooth muscle in order to maintain constant CBF. For
example, a hypertensive response during exercise with an increase in MAP
results in cerebral vasoconstriction thus keeping CBF constant. Conversely,
a fall in MAP will result in cerebral vascular smooth muscle relaxation causing
vasodilatation thus maintaining CBF.
100

CBF 50
(mL/100 g/min)

0
50 150
MAP (mmHg)

Fig. 33.1  Autoregulation of cerebral blood flow

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Metabolic theory of cerebral
blood flow.
What are the effects of changes
in PaO2 and PaCO2 on CBF?
Do anaesthetic drugs have any
effect on CBF?
How does temperature affect
CBF?
What effect does brain injury
have on cerebral blood flow?
What is the Monro–Kellie
doctrine?
What is the normal ICP?
What are the common causes
of raised ICP?
9781785230981_text.indb 103
CEREBRAL BLOOD FLOW
CBF and cerebral metabolism are coupled. Thus, regional CBF varies with
metabolic activity. Products of metabolism (H+/K+/adenosine/nitric oxide)
cause vasodilatation. Thus, CBF matches metabolic requirements.
100
PCO2
CBF
(mL/100 g/min) 50 PO2
0 5 10 15 20
Gas Tension (kPa)
Fig. 33.2  Physiological control of cerebral blood flow
CBF increases linearly between a PaCO2 range of 3 and 10 kPa. Outside this
range CO2 reactivity is lost. This has clinical implications: hypocapnia can
result in intense cerebral vasoconstriction and ischaemia; hypercapnia can
result in increased intracranial blood volume, which may result in a rise in ICP.
CBF increases below a PaO2 of 8 kPa due to hypoxic vasodilatation. Clinical
implication: in patients with head injuries hypoxia may lead to further rises in
ICP and result in brain ischaemia.
> Volatiles: all increase CBF and reduce Cerebral metabolic oxygen
requirements (CMRO2), thus uncoupling CBF from CMRO2.
> N2O: increases CBF and increases CMRO2.
> NMBA: do not affect CBF.
> Induction drugs: With the exception of ketamine, all other induction
agents reduce CMRO2, CBF and ICP. Ketamine increases ICP.
Cerebral metabolic requirement for oxygen (CMRO2) falls by 7% per 1 °C
decrease in core body temperature. As a result, CBF parallels this reduction
in CMRO2.
Brain injury can lead to loss of cerebral autoregulation in injury-affected areas
of the brain, resulting in the development of a pressure-dependent perfusion
area. Thus, a fall in CPP may lead to secondary ischaemic brain injury.
The skull is a rigid box containing brain tissue (80%), blood (12%) and CSF
(8%). The volume of the box is constant, so an increase in volume of any one
of the intracranial constituents must be accompanied by a parallel reduction
in the volume of another constituent if ICP is to remain constant.
> 10–15 mmHg – normal.
> Above 20 mmHg – elevated ICP.
> CSF – hydrocephalus.
> Brain – tumours/oedema/contusions.
> Blood – haematoma/cerebral aneurysm.
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 01 PHYSIOLOGY
Draw a graph to show how ICP
is related to intracranial volume 100
(ICV).

Intracranial
Pressure
(mmHg) Decompensation

10

Intracranial volume

Fig. 33.3  Effect of intracranial volume on intracranial pressure

As intracranial volume increases (e.g. cerebral oedema secondary to

a traumatic brain injury) there is no initial rise in ICP as compensatory
mechanisms occur such as a reduction in intracranial venous blood volume
and an increase in CSF absorption combined with CSF movement into the
spinal compartment. When these mechanisms are exhausted any further
small increase in intracranial volume results in a large increase in ICP, i.e.
decompensation has occurred.
What is the vasodilatory In head-injured patients, the vasodilatory cascade describes the vicious
cascade? cycle that develops if there is a reduction in cerebral perfusion pressure.
Conversely, the vasoconstriction cascade describes the treatment of the
above situation.

FALL IN MAP

FALL IN CPP

RISE IN ICP VASODILATATION

INCREASE CEREBRAL BLOOD VOLUME

Fig. 33.4  Vasodilatory cascade

RISE IN MAP

RISE IN CPP

FALL IN ICP VASOCONSTRICTION

REDUCED CEREBRAL BLOOD VOLUME

Fig. 33.5  Vasoconstriction cascade

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Describe the physiological
management of the head-injured
patient.
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CEREBRAL BLOOD FLOW
Applying the above physiological principles, the following goals are aimed for
when managing patients with head injuries:
ABC approach
Maintain oxygenation: Keep PaO2 >10 kPa as hypoxia will cause cellular
ischaemia and raise ICP through vasodilatation
Maintain CPP >70–80 mmHg to ensure adequate CBF and to prevent
the vasodilatory cascade (CPP = MAP − ICP). The ICP in an unconscious
patient can be presumed to be >20 mmHg; therefore, MAP should
be maintained at around 90 mmHg. This may require fluids and/or
vasopressors. Ensure good venous drainage of the head by positioning
the patient at 30° head up tilt, do not obstruct venous drainage with
endotracheal tube ties but use tape instead to secure the ETT. Ideally, ICP
should be monitored, but this is monitoring usually available in specialist
centres only.
Reduce ICP: Maintain normocapnia and normoxia. Hypercapnia and
hypoxia will both increase cerebral blood volume and, therefore, ICP,
according to the Monroe–Kellie doctrine.
• Sedate adequately and paralyse the patient to avoid straining.
• Consider the use of furosemide (0.25–1.0 mg/kg) or mannitol
(0.25–1.0 g/kg) or hypertonic saline to decrease ICP by reducing
cerebral oedema.
Reduce CMRO2: Consider infusions of propofol or midazolam to reduce
cerebral metabolism, or in certain situations thiopentone to induce a
‘thiopentone coma’.
• Treat pyrexia.
• Therapeutic hypothermia: CMRO2 decreases by 7% for every 1 °C fall
in temperature and is paralleled by a fall in CBF. This may help to control
ICP but cooling has not been shown to improve outcomes in head-
injured patients.
• Prevent/treat seizures that cause a dramatic increase in CMRO2.
• Maintain normoglycaemia.
Do not administer hypotonic fluids such as 5% dextrose, which will increase
brain oedema as they cross the disrupted blood–brain barrier.
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