Regulation of Cerebral Circulation Flashcards
Why does grey matter neural damage occur so quickly?
How is the brain adapted to prevent this?
What are the 3 structural adaptations of the brain?
- It no energy reserves; only uses oxygen
- o High, constant oxygen consumption and supply
o High blood flow with constant changes in regions of the brain
o Receives a large proportion of the CO relative to its small size - • Circle of Willis; anastomosis achieves constant blood flow
• High Capillary density; high oxygen extraction
• BBB; formed by continuous capillaries
Functional adaptations:
What does the brain modulate to maintain cerebral perfusion?
Which receptors detect changes in cerebral perfusion?
What is the benefit of there being autoregulation?
What causes Regional Hyperaemia in the brain?
→ What will occur if there’s a very large ↑K+?
- Sympathetic vasoconstriction
- Carotid sinus Baroreceptors
- Cerebral blood flow will remain constant with changes in arterial BP
- Active neurons; Lots of K+ efflux = Hyperpolarisation = VGCCs switch off = ↓Ca2+ influx = Vasodilation
→ Vasospasm
What is the pattern of artery innervation for the brain?
What are arterioles not involved in?
What do Perivascular nerves release?
What do Perivascular sensory C-fibres do? How?
Based on this, what can be given for migraines? How do they work?
- Cerebral arteries outside brain receive dense innervation from sympathetic nerves, Arterioles inside brain receive little innervation
- Baroreflex vasoconstriction
- Serotonin/5-HT
- Mediate the pain of vascular headaches in strokes and the later phase of Migraine; They release dilators (Sub P) and reduce constrictors (5-HT)
- Sumatriptan; 5-HT1B agonist which causes vasoconstriction, reduces inflammation-induced vasodilation
BBB:
What are the properties of its wall?
Which molecule types does it allow through?
What does it keep in and out?
Where is the BBB defective? What does this allow? Give 3 areas
- Has tight junctions (poor filtration), Little vesicle transport system, Carrier-mediated transport (e.g. for Glucose, AA)
- Lipid soluble molecules (e.g. O2, CO2, General anaesthetics)
- o Keeps out Neuro-active chemicals that would interfere with neuronal signalling (e.g. Catecholamines)
o Keeps in Neurotransmitters - Defective to allow access of circulating signalling molecules;
o Area Postrema; emetic molecules → vomiting centre
o Subfornicular organ of Hypothalamus; Ang II → Thirst sensation
o Periventricular Osmoreceptors in Hypothalamus; Osmolarity → ADH secretion
Postural Hypotension:
What is the venous blood distribution when supine? How does this affect SV?
How does the venous blood distribution change on Orthostasis? How does this cause the symptoms of Cerebral Underperfusion?
What exacerbated postural hypotension?
How does the baroreflex work to counter postural hypotension?
- Lying down, there is EVEN venous blood distribution; High Filling pressure = High SV
- Venous blood ‘pools’ in the legs; ↓CVP = ↓SV = ↓BP = ↓Cerebral blood flow = Dizziness, Visual fade
- Warmth (venodilation), Bed rest, Zero gravity, Medication
- Unloading; ↓BP switches off Baroreceptor afferents, causing Disinhibition of CVLM-RVLM inhibitory pathway, therefore causing ↑Sympathetic activity = ↑SV = ↑BPQ
Cerebral Artery Vasospasm:
What event can cause vasospasm?
What can vasospasm lead to?
What is the vasospasm due to?
How is this treated?
Space-occupying Lesions (SOL) & Cushing’s Reflex:
What does it cause?
How does brain herniation lead to an increase in BP?
Why does a patient with an SOL also present with Bradycardia?
- SA/IC Haemorrhage
- Stroke, due to infarction
- Vasoconstrictor agents; Serotonin, NPY, ET-1, ↑↑↑K+ from damaged cells
- CCBs, ETA receptor blockers
- ↑ICP = Herniation of brain through Foramen Magnum
- Pressure onto RVLM = Chronic ↑Sympathetic vasoconstrictor activity = ↑BP
- Baroreflex causes Bradycardia to try and counter these effects but isn’t able to due to the chronic pressure on RVLM
