Neurophysiology - Cerebral Blood Flow Flashcards
Name the main arteries that supply the brain and state the approximate proportion of the brain supplied by these vessels
Internal carotid arteries x 2 –> supply 80% (40% x 2)
Vertebral arteries x 2 –> supply 20% (10% x 2)
(the two vertebral arteries fuse to form the basilar artery)
What are ‘watershed areas’
Watershed locations are those border-zone regions in the brain supplied by the major cerebral arteries where blood supply is decreased –> these overlapping areas determine the severity of focal ischaemia following systemic hypotension, focal vasospasm and major vessel occlusion.
What is mean cerebral blood flow and state the CBF at which neurons can survive
Cerebral blood flow ± 50 ml/100g/minute
CBF 18 -25 ml/100g/minute –> nerves survive but don’t function
CBF < 18 ml/100g/minute –> nerves die
In which settings is venous drainage to the brain relevant to the anaesthetist
- Jugular venous bulb SaO2 monitoring
2. Ensuring venous drainage in RICP to optimise CPP
Which sinuses form the internal jugular
Transverse Sinuses
Inferior Petrosal Sinuses
What proportion of blood in the internal jugular comes from the ipsilateral and contralateral sides of the brain
Right internal jugular: 70% ipsilateral and 30% contralateral
What percentage of the blood in the jugular veins is from extracranial sources?
3%
What percentage of adults have unilateral transverse sinus drainage?
5 - 12%
What are normal jugular venous SaO2 and what is implied if this is lower or higher than this?
65%
Higher –> Hyperemia or failure of utilization
Lower –> indicative of ischaemia and are an indication for increasing CPP and assessing the effect on further jugular venous saturations.
Draw the graph representing the effect of PaCO2 and PaO2 on Cerebral blood flow
See Page 1 of FCA workbook notes
What effect do systemic vasodilators have on cerebral blood flow
Unchanged or increased CBF due to cerebral vasodilation
What effects to alpha 1 blockers have on CBF
Minimal
What effects do beta agonists have on CBF
Low dose - no effect
High dose - Increase CBF and CMR
What effects do beta blockers have on CBF
Minimal
What effects does dopamine have on CBF
Probable vasodilation. high dose –> vasoconstriction
Which anaesthetic agents decrease CMR/CBF
- Barbiturates
- Propofol
- Etomidate
- Benzodiazepines (decrease CMR and increase CBF)
Which anaesthetic agents increase CMR/CBF
Ketamine
Which anaesthetic agents uncouple CMR
Inhaled agents –> luxury perfusion with POORLY MAINTAINED Autoregulation
Which anaesthetic agents have minimal effect on CMR/CBF/Autoregulation
- Morphine
- Fentanil
- Alfentanil
- Sufentanil
- Remifentanil
Which anaesthetic agents change the effect of CO2 on CBF
None
What specific effect do alfentanil, sufentanil and remifentanil have on the CNS and why
Increase ICP briefly if given as a stat dose. IVI infusion does not cause increase ICP. Sudden MAP change –> Cerebral VC as part of autoreg response. If given slowly no change to MAP.
Compare the brain’s relative weight to its proportion of cardiac output and O2 consumption
2% of the body weight
15% of Cardiac output
- CBF = 50 ml/100g/min - 40ml to grey and 10ml to white matter
20% of total O2 consumption
What is the O2 consumption of the brain
3 - 3.8 ml/100g/minute = 35 - 70 ml/minute
- 75% by neurons
- 10% by glial cells
Wide range is due to different activation states of the CNS
List the normal values for the following:
- CBF
- CMRO2
- CO to brain
- Brain glucose utilization
- ICP
- CPP
- CBF –> 50 ml/100g/minute
- CMRO2 –> 50ml/100g/minute
- CO to brain –> 20% (2% TBW)
- Brain glucose utilization –> 5g/100g/minute
- ICP –> 8 - 12 mmHg
- CPP –> 80 - 100mmHg
Describe the levels of CBF and CPP at which reduced and isoelectric activity occur. Include also the CBF and CPP at which irreversible brain death occurs
CBF Normal: 50 ml/100g/minute Slow EEG: 20 - 25 ml/100g/minute Isolelectric EEG: 15 - 20 ml/100g/minute Irreversible brain death: < 15 ml/100g/minute
CPP Normal: 80 - 100 mmHg Slow EEG: 40 - 50 mmHg Isoelectric EEG: 25 - 40 mmHg Irreversible brain death: < 25 mmHg
What is the optimal viscosity for O2 blood delivery to the brain and how does viscosity affect CBF
Increased viscosity reduces cerebral blood flow. But O2 delivery depends on Hct.
Hct of 30 - 34 % is optimal viscosity for O2 delivery to the brain.
How does noradrenalin affect cerebral autoregulation - draw the graph
It extends the plateau phase leading to a prolonged interval of stable CBF over a greater range of MAP. See page 4 FCA workbook.
How does the administration of vasodilators such as hydralazine/captopril affect cerebral autoregulation
These agents shorten the plateau phase leading to a diminished range of MAP for which CBF remains stable. Page 4 FCA workbook
What factors impair cerebral autoregulation
- Sepsis
- Acidosis
- Hypoxia
- Intracranial disease (TBI/SAH)
- Epilepsy
- Anaesthesia (But autoreg maintained with MAC < 1 for isoflurane and less than 1.5 for sevoflurane)
What is the “paradoxical CBF effect’ or ‘steal effect’ related to changes in CBF with PaCO2
High PaCO2 –> No increase CBF to diseased vessel. Increased CBF to non-diseased vessels. Therefore stealing blood from already relatively ischaemic areas.
How is CBF influenced by hypoxia?
Hypoxia does not impact CBF significantly until the PaO2 drops below 8 kPa at which point CBF rises exponentially. FCA work book page 3.
How does temperature affect CMRO2
For each drop of 1 degree C –> 5 - 7% decrease CMRO2
At 20 deg C –> Isoelectric EEG
Tb 37 - 42 deg C –> increased CBF
Tb > 42 deg C –> dramatic decrease CBF (protein degradation)
What role does the autonomic nervous system play in cerebral autoregulation
About 10% of the VD/VC
Apparently protects BBB under conditions of very high MAP.
