33. Cerebral Blood Flow Flashcards
Basic concepts >
What is global CBF
White matter flow
Grey Matter flow
Resting oxygenation comsumption
Global CBF: 50 mL/100 g brain tissue/minute.
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).
.
What does regional CVF depend on
What is the mechanism of blood flow control
what are the values
How do we calculate CPP
What is normal CPP
> 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)
Myogenic theory of cerebral autoregulation.
A change in perfusion pressure
results in a myogenic response in the
cerebral vascular smooth muscle
in order to maintain constant CBF.
Forexample,
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.
Metabolic theory of 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.
What are the effects of changes in PaO2 and PaCO2 on CBF?
Diagram pg 103
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.
Do anaesthetic drugs have any effect on CBF?
1. > Volatiles: all increase CBF and reduce Cerebral metabolic oxygen requirements (CMRO2), thus uncoupling CBF from CMRO2.
- > N2O:
increases CBF and
increases CMRO2.
3.
> NMBA: do not affect CBF.
4. > Induction drugs: With the exception of ketamine, all other induction agents reduce CMRO2, CBF and ICP.
Ketamine increases ICP.
How does temperature affect CBF?
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.
What effect does brain injury have on cerebral blood flow?
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.
What is the Monro–Kellie doctrine?
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.
What is the normal ICP?
> 10–15 mmHg – normal.
> Above 20 mmHg – elevated ICP.
What are the common causes
of raised ICP?
> CSF – hydrocephalus.
> Brain – tumours/oedema/contusions.
> Blood – haematoma/cerebral aneurysm.
Draw a graph to show how ICP
is related to intracranial volume
(ICV).
PAGE 104
ICP on Y
Volume on x
decompensation around 20mmHg
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
cascade?
In head-injured patients,
the vasodilatory cascade describes
the vicious 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
RISE IN MAP
=
RISE IN CPP
= =
FALL IN ICP VASOCONSTRICTION
=
REDUCED CEREBRAL BLOOD VOLUME
Describe the physiological management of the head-injured patient.
Applying the above physiological principles, the following goals are aimed for
when managing patients with head injuries:
ABC approach 1. 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.
3.
Ensure good venous drainage of the head by
a) positioning the patient at 30° head up tilt,
b) do not obstruct venous drainage with
endotracheal tube ties but use tape instead to secure the ETT.
c) 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 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.
9.
• 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 controlICP but cooling has not been shown to improve outcomes in head injured
patients.
10.
Prevent/treat seizures that cause a dramatic increase in CMRO2.
11. • Maintain normoglycaemia. Do not administer hypotonic fluids such as 5% dextrose, which will increase brain oedema as they cross the disrupted blood–brain barrier.
