Vascular System & Stroke - Acute Stroke Flashcards
Definition of stroke
Clinical syndrome characterised by rapidly developing clinical symptoms and/or signs of focal neurological deficit lasting more than 24 hrs and thought to be of vascular origin
Why is stroke important
3rd leading cause of death
Incidence 150,000
Lifetime risk of 1 in 6
Number one cause of long-term disability
Diagnosing stroke
Hx
Examination
Scans
ECG, bloods, CXR, 24 hr tape
Hx of stroke
PC - onset times (<6 hrs for thrombectomy) PMH - risk factors Drug hx Allergies Social hx
Consistency of symptoms
Handedness
What can’t you thrombolyse with on ACE inhibitors
Alteplase - can cause angiodema
Examination for stroke
HR, BP, oxygen sats, temp, BM CVS incl for carotid bruits - listening for whooshing with stethoscope on neck Resp Abdo Cranial nerves Speech PNS Gait if possible
Bloods for stroke investigations
FBC U&E LFTs Bone Clotting Blood sugar Cholesterol \+/- ESR, antiphospholipid screen, haemophilia screen, vasculitis screen
Investigations for stroke
Bloods ECG CT head CXR \+/- CT perfusion scan, MRI Carotid dopplers/ CT angiogram Echo + 24 hr tape +/- prolonged cardiac monitoring
CT perfusion scan
Injecting large quantities of dye and taking several CTs at once
Done when onset time is unknown and to see whether or not the pt can be thrombolysed (size of penumbra)
Types of stroke
Ischaemic
Haemorrhagic
Types of haemorrhagic stroke
Primary
Secondary
Primary haemorrhagic stroke causes
Amyloid angiopathy
Hypertensive
Secondary haemorrhagic stroke causes
AVM
Aneurysm
Coagulopathy
AVM
Arterial Venous Malformation
Cryptogenic
Idiopathic
Bamford (Oxford) Classification of strokes
Lacunar (LACS)
Partial anterior circulation (PACS)
Total anterior circulation (TACS)
Posterior circulation (POCS)
Signs of lacunar stroke
Motor or sensory impairments only
Sensorimotor
Ataxic hemiparesis
Signs of PACS
2 of following: motor or sensory; cortical; hemianopia
Signs of TACS
All of: motor or sensory; cortical; homonymous hemianopia
Cortical impairment
Aphasia, ataxias, weakness etc
Signs of POCS
Isolated hemianopia Brain stem signs Cerebellar - balance (ataxia) Dysarthria Hemiparesis Vertigo, vomiting Diplopia Facial weakness/ numbness Dysphagia
Hemianopia
Blindness over half the field of vision
Posterior circulation of brain
Posterior cerebral artery Posterior communicating artery Basilar artery Superior cerebellar artery Anterior inferior cerebellar artery Anterior spinal artery Vertebral artery
Anterior circulation of brain
Anterior cerebral artery Anterior communicating artery Middle cerebral artery External carotid artery Internal carotid artery Common carotid artery
Dysphasia
Partial loss of language due to brain disease
Diplopia
Double vision
% Dead at 1 year - PACS
20
% Dead at 1 year - TACS
60
% Dead at 1 year - POCS
20
% Dependent at 1 year - LACS
25
% Dependent at 1 year - PACS
30
% Dependent at 1 year - TACS
35
% Dependent at 1 year - POCS
20
ICH score
Score predicting 30-day mortality after stroke
From 1 - 6. Higher the score - higher mortality
Looks at GCS, ICH volume, Infrantentorial origin of ICH and age
TIA definition
Neurological signs that are consistent with a stroke that lasts for less than 24 hrs
Usually last «_space;24 hrs
No damage on CT, maybe on MRI
Importance of TIA’s
Opportunity to reduce stroke risk factors and prevent strokes
ABCD2 score
Predicts risk of stroke 7 days after TIA
Total out of 7
Stroke mimcs
Migraine Tumour Abscess Subarachnoid/ subdural Cerebral vein thrombosis Epilepsy and Todd's palsy MS Myasthenia gravis Bell's palsy Functional neurological disorder Metabolic disorder e.g. hypoglycaemia Sepsis
Least tolerant organ of ischaemia
Brain
Where is the highest metabolic demand in the brain
Closely packed neuronal cell bodies (metabolic centre of nerve cell)
Brain preferred energy substrate
Glucose, transported via glucose transporters or capillary endothelial cells, neurons and astrocytes
Key structural adaptations of brain to ensure constant blood supply
The Circle of Willis
The Microcirculation
Function of Circle of Willis
Helps safeguard oxygen supply from interruption by arterial blockage
Allows collateral circulation if theres an arterial blockage
Whats included in Circle of Willis
Anterior cerebral artery Anterior communicating artery Middle cerebral artery Posterior communicating artery Posterior cerebral artery Superior cerebellar artery
How does blood reach brain
Through 4 source arteries (2 internal carotid arteries and two vertebral arteries)
The microcirculation
A high capillary density optimises O2 transport in the brain
Red Cell Velocity is very high (1mm/sec) and heterogenous (0.3 to 3.2 mm/sec)
How does 1-3 week(s) of chronic hypoxia exposure affect brain capillaries
Density nearly doubles
How does HTN affects brain capillaries
Decreases no.
What does interruption of cerebral blood flow for a few seconds cause
Unconsciousness
What does persistent ischaemia for a few mins cause
Irreversible cellular damage
How does the brain regulate mean arterial pressure
Through a feedback loop
What does MAP play a role in
Determining CPP
MAP
Mean arterial pressure
CPP
Cerebral Perfusion Pressure
What happens when MAP is increased
Detected by baroreceptors
Increase in afferent pathways
Bradycardia and vasodilation counteracts
Physiological responses when MAP is decreased
Increased sympathetic outflow
Decreased sympathetic outflow
Vasoconstriction, tachycardia
Definition of CPP
Amount of pressure required to maintain blood flow to the brain
What is CPP regulated by
Two balanced opposed forces
- MAP - driving force that pushes blood into brain
- ICP - force keeping blood out
ICP
Intracranial pressure
CPP target
> 60 mmgh
CBF
Cerebral blood flow
Major determinant of CBF
CPP
What is ICP increased by
Intracranial bleeding
Cerebral oedema
Tumour
What does increased ICP leads to
Collapsed veins
Decreases effective CPP
Reduced blood flow
Calculating CPP
MAP - ICP
Regular range of CBF
Perfusion pressures of 50 and 150 mmHg
Ischaemic brain and CBF
Blood vessels become too dilated causing a reduction in CBF
HTN and CBF
Remains normal
Cerebral vascular resistance also increases
Calculating CBF
MAP / resistance
Cushing’s Reflex
An increase in ICP compresses blood vessel leading to brain
Increased ICP reduces CPP
Cerebral ischemia causes massive sympathetic activation –> increases systemic blood pressures
CBF regulation and metabolic requirements
Autoregulation ensures a basal
CBF can change in response to brain activity
Blood Brain Barrier
Cerebral capillaries form a tight BBB - protective mechanism
Stops most drugs from getting in CNS
What can freely cross BBB
Lipid soluble molecules e.g. O2, CO2 and general anaesthetic
D-glucose carried on GLUT1
Carriers for adenosine, metabolic acids (lactate), amino acids
Astrocytes regulation w/ capillaries in brain
Regulate CBF
Upregulate tight junction proteins
Contribute to ion and water homeostasis
Interface directly with neurons
Neurovascular unit
Component of BBB
Both astrocytes and neurons cooperate in neuromuscular coupling through glutamate signalling
What does the neuromuscular unit produce
An increase in local blood flow that is 4x higher than their consumption of oxygen and ATP of local neurons
What do neurons release in the neurovacsular unit
Glutamate –> increases intracellular Ca in astrocytes –> stimulates release of vasodilators.
Some release NO, PGE2, VIP - also vasodilators
When is neuromuscular unit defective
Stroke, HTN, SCI (spinal cord injury)
Metabolic changes causing changes in CBF
Neural activity leads to ATP breakdown - adenosine, lactate
Lowering of pO2, rising pCO2 trigger vasodilation
Fall in pH in blood extracellular fluid evokes pronounced dilation