Cerebral Perfusion and Intracranial Pressure Flashcards
(35 cards)
What is the normal perfusion of cerebral blood flow?
55 to 60 mL/100g brain tissue per minute
What is the perfusion of cerebral blood flow in ischaemia?
20 mL/100 g/minute
At what perfusion does permanent damage occur?
When it drops below 10mL/100 g/minute
What is the cerebral perfusion pressure (CPP)?
It is the blood pressure gradient across the brain which determines cerebral blood flow
How do you work out the CPP?
CPP = MAP - ICP
This represents the pressure gradient driving cerebral blood flow (CBF) and hence oxygen and metabolite delivery.
How do you work out MAP?
MAP = DP + 1/3PP
MAP = 2/3DP + 1/3SP
DP - diastolic pressure
PP - pulse pressure
SP - systolic pressure
What is the effect of increased ICP on the CPP?
Increase ICP = decrease in CPP
Name three factors which regulate cerebral blood flow
- CPP
- Concentration of arterial CO2
- Arterial PO2
What is cerebral autoregulation?
The ability to maintain constant blood flow to the brain over a wide range of CPP (50-150 mm Hg)
What is the cerebral autoregulation when the CPP is low?
The cerebral arterioles dilate to allow adequate flow at the decreased pressure
What is the cerebral autoregulation when the CPP is high?
The cerebral arterioles constrict
In what pathological conditions can the cerebral blood flow not be autoregulated?
CPP exceeds 150 mm Hg, such as in hypertensive crisis, the autoregulatory system fails
- Exudation of fluid from the vascular system with resultant vasgoenic oedema
- Toxins like CO2 can cause diffuse cerebrovascular dilatation and inhibit proper autoregulation
- During the first 4-5 days of head trauma, many patients can experience disruption
What is cerebral oedema and what can it cause?
Increased brain volume as a result of an increase in water content
Prominent cause of subacute to chronic intracranial hypertension
What are the two different types of cerebral oedema?
Vasogenic oedema (extracellular) and cytotoxic oedema (intracellular)
Describe vasogenic oedema
- Increased capillary permeability
- Mainly white matter
- Extracellular fluid increased
- Plasma filtrate containing plasma protein
Describe cytotoxic oedema
- Cellular swelling (neuronal, glial and endothelial cells)
- Grey and white matter
- Increased intracellular after and sodium due to failure of membrane transport
- Extracellular fluid decreases
What is the blood brain barrier?
Endothelial tight junctions are the barrier to the passive movement of many substances in order to protect the sensitive neural tissue from toxic materials
It is composed of astrocytic foot processes wrapping around a capillary endothelium which contains tight junctions
How are materials transported across the endothelial cells?
- Lipid-soluble substances can penetrate all capillary endothelial cell membranes in a passive manner
- Amino acids and sugars are transported across the capillary endothelium by specific carrier-mediated mechanisms
What is the Monro-Kelly Doctrine?
It is the homeostatic intracerebral volume regulation, which stipulates that the total volume of the brain tissue, cerebrospinal fluid, and blood remains constant
When a new intracranial mass is introduced, a compensatory change in volume must occur through a reciprocal decrease in venous blood or CSF to keep the total intracranial volume constant
Describe the mechanisms for maintaining constant intracranial volume
Compliance vs elastance
Describe the elastance mechanism in maintaining constants intracranial volume
- Inverse of compliance
- Change in pressure for a given change in volume
- dP / dV
- Represents the accommodation to outward expansion of an intracranial mass
Describe compliance mechanism in maintaining constant intracranial volume
Change in volume observed for a given change in pressure
Describe how the venous system drains blood from the brain
It collapses easily and squeezes blood out through the jugular veins or through the emissary and scalp veins
Describe CSF exits the ventricles
Displaced from the ventricular system through the foramina of Luschka and Magendie into the spinal subarachnoid space