clinical aspects of cerebral perfusion Flashcards

1
Q

What % of cardiac output goes to the brain?

A

15%

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2
Q

How much blood per g of brain tissue in an average adult brain?
In white matter?
In grey matter?

A

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

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3
Q

When is brain tissue considered to be ischaemic vs permanent damage?

A

Ischeamia: when 20ml/100g

Permanent damage when 10ml/100g

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4
Q

Which factors control cerebral blood flow?

A
  • Cerebral perfusion pressure
  • Concentration of arterial CO2
  • Arterial P02
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5
Q

Which is most important factor in the control of CCF?

A

CPP
blood gradient across the brain
*CPP=MAP-ICP

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6
Q

What is cerebral auto regulation

A

The ability to maintain blood flow to the Brain over a wide range of pressure (50-150mm-Hg)

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7
Q

How does cerebral auto regulation work?

A

When CPP is low the arterioles dilate to allow increased flow at a lower pressure
When CPP is high the arterioles constrict

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8
Q

When the CPP considered to be hypertensive?

A

Over 150mmhg

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9
Q

List a few pathologies which can interfere with cerebral auto regulation and explain them?

A

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.

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10
Q

What is the blood brain barrier?

A

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

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11
Q

How do substances move to brain tissue?

A
  • Lipid soluble substances can move across the capillary endothelium passively
  • Water soluble substance tend to be transported actively
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12
Q

What is ICP derived from?

A

Pressure of:

  • Brain + ISF
  • blood
  • CSF
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13
Q

How is the ICP pressure split between its components

A
  • Brain + ISF: 80%
  • Blood: 10%
  • CSF: 10%
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14
Q

Volume of the brain

A

1700 ml

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15
Q

What does the mono-kelly doctrine state?

A

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

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16
Q

definition of compliance and elastance?

A

COMPLIANCE: change in volume related to change in pressure dV/dP
ELASTANCE: change in pressure per given change in volume dP/dV

17
Q

Which are the homeostatic mechanisms in place to maintain the equilibrium of the ICP?

A

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.

18
Q

What happens once the critical value has been reached

A

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

19
Q

Compliance at different ICP?

A

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

20
Q

What are Lundberg waves?

A

Wave patterns in the brain which are detected in response to a change in ICP following head trauma

A waves

B waves

C waves

21
Q

A waves

A

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

22
Q

B waves

A

Related to rhyme variations in breathing
From 0.5- 2 amplitude per minute
Not necessarily related to a decrease in CPP

23
Q

C waves

A

Related to waves of systemic blood waves

Small amplitude

24
Q

What is the gold standard for measuring ICP?

A

Using an external ventricular drain
Connected to external strain gauge
Catheter tip into foramen off Monro

25
Q

What is Cushing’s reflex and what does it lead to?

A
Neurological response to change in ICP 
Results in:
Increased blood pressure: hypertension 
Bradycardia 
Irregular breathing
26
Q

How does bushings reflex work?

A

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

27
Q

How to treat ICP?

A

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

28
Q

Different types of oedema

A

Vasogenic oedema
Cytotoxic oedema
Intersistial oedema

29
Q

Location of oedema

A

Vasogenic: white matter
Cytotoxic: grey and white
Intersistial: across membrane surrounding the ventricles in white matter of hydrocephalus

30
Q

Pathogenesis of oedema

A

Vasogenic: increased capillary permeability
Cytotoxic: cellular swelling
Intersistial: increased water in brain due to impaired absorption of CSF.

31
Q

Causes of oedema

A

Vasogenic: tumour, abbess, late stages of infarction, trauma
Intersistitial: obstructive/communicating hydrocephalus
Cytotoxic: infactio/intoxication

32
Q

Which oedema increases and which decreases ECF

A

Increase: vasogenic and intersistial
Decreases: cytotoxic