clinical aspects of cerebral perfusion Flashcards
What % of cardiac output goes to the brain?
15%
How much blood per g of brain tissue in an average adult brain?
In white matter?
In grey matter?
About 55ml-60m/ 100g of brain tissue per minute in an average adult
Blood flow in grey matter tends to be 75 ml/100g
Blood flow through white matter tends to be 45l/100g
When is brain tissue considered to be ischaemic vs permanent damage?
Ischeamia: when 20ml/100g
Permanent damage when 10ml/100g
Which factors control cerebral blood flow?
- Cerebral perfusion pressure
- Concentration of arterial CO2
- Arterial P02
Which is most important factor in the control of CCF?
CPP
blood gradient across the brain
*CPP=MAP-ICP
What is cerebral auto regulation
The ability to maintain blood flow to the Brain over a wide range of pressure (50-150mm-Hg)
How does cerebral auto regulation work?
When CPP is low the arterioles dilate to allow increased flow at a lower pressure
When CPP is high the arterioles constrict
When the CPP considered to be hypertensive?
Over 150mmhg
List a few pathologies which can interfere with cerebral auto regulation and explain them?
Cerebrovascular dilatation
Due to the presence of toxins in the blood such as CO2
Causes improper auto regulation
Head trauma
Can experience improper auto regulation within the first 4-5 days
Cerebral edema
Often a cause for intracranial hypertension to the swelling of the cranium due to increase water content.
What is the blood brain barrier?
Barrier made up of astrocytes feet wrapping around capillary endothelium (which is made up of tight junctions)
Prevents toxic materials in the blood from reaching the neural tissue passively
How do substances move to brain tissue?
- Lipid soluble substances can move across the capillary endothelium passively
- Water soluble substance tend to be transported actively
What is ICP derived from?
Pressure of:
- Brain + ISF
- blood
- CSF
How is the ICP pressure split between its components
- Brain + ISF: 80%
- Blood: 10%
- CSF: 10%
Volume of the brain
1700 ml
What does the mono-kelly doctrine state?
The cranium is a rigid structure so: when an new intracranial mass is inserted in the cranium there must be a compensatory change in volume through a reduction venous blood or CSF in order to maintain the intracranial pressure constant
definition of compliance and elastance?
COMPLIANCE: change in volume related to change in pressure dV/dP
ELASTANCE: change in pressure per given change in volume dP/dV
Which are the homeostatic mechanisms in place to maintain the equilibrium of the ICP?
Volume of venous system can be decreased quickly: venous system collapses and blood is squeezed out into the jugular or emissary/ scalp veins.
CSF volume can be decreased through ventricular ssystem through the Lusaka (lateral) and Magendie (medial) from the 4th ventricle into the subarachnoid space.
What happens once the critical value has been reached
Once these homeostatic mechanisms have been exhausted a small change in volume results in a massive change in pressure
Once the critical measure has been reached then there is a high chance that intracranial hypertension
Compliance at different ICP?
Up to 15mmHg- HIGH COMPLIANCE= big change in volume per small change in pressure
Up to 25mmHg- LOW COMPLIANCE= small change in volume per high change in pressure
Over 25mmgh- NO COMPLIANCE= small to no change in volume per BIG change in pressure
What are Lundberg waves?
Wave patterns in the brain which are detected in response to a change in ICP following head trauma
A waves
B waves
C waves
A waves
When sudden increase in ICP for 5-20 mins followed by return to normal
Amplitude as high 50-100 mmhm
Result from increase in cerebrovascular volume and CPP decrease
B waves
Related to rhyme variations in breathing
From 0.5- 2 amplitude per minute
Not necessarily related to a decrease in CPP
C waves
Related to waves of systemic blood waves
Small amplitude
What is the gold standard for measuring ICP?
Using an external ventricular drain
Connected to external strain gauge
Catheter tip into foramen off Monro
What is Cushing’s reflex and what does it lead to?
Neurological response to change in ICP Results in: Increased blood pressure: hypertension Bradycardia Irregular breathing
How does bushings reflex work?
ICP > MAP
Compression of cerebral arterioles
This leads to decreased Cerebral blood flow
Decreased CBF causes activation of autonomic nervous system
Sympathetic response: alpha-1 adrenergic receptors lead to hypertension and tachycardia
Aorto baro-receptors stimulate vagus nerve= bradycardia
Bradycardia can also result from mechanical distortion of the medulla
How to treat ICP?
Elevate the head= facilitates venous return
Mannitol/ hypertonic saline solution
Hyperventilation: decreases CBF
Barbituate coma: decreases cerebral metabolism and CBF
Surgical decompression
Brain tissue oxygenation monitoring: probe to detect and treat areas of low oxygenation
Micro-dialysis: investigation of brain metabolism- insertion of small catheters to detect areas of higher metabolism
Different types of oedema
Vasogenic oedema
Cytotoxic oedema
Intersistial oedema
Location of oedema
Vasogenic: white matter
Cytotoxic: grey and white
Intersistial: across membrane surrounding the ventricles in white matter of hydrocephalus
Pathogenesis of oedema
Vasogenic: increased capillary permeability
Cytotoxic: cellular swelling
Intersistial: increased water in brain due to impaired absorption of CSF.
Causes of oedema
Vasogenic: tumour, abbess, late stages of infarction, trauma
Intersistitial: obstructive/communicating hydrocephalus
Cytotoxic: infactio/intoxication
Which oedema increases and which decreases ECF
Increase: vasogenic and intersistial
Decreases: cytotoxic
