CVA - 1a Intro to CVAs Flashcards
what is a CVA
cerebral vascular accident
sudden loss of neurologic function d/t lack of blood flow to brain
what is the path of a CVA in 1 word
vascular
what flag is a CVA
red - medical emergency
call 911!
what is the differential b/w CVA and TIA
sx of a CVA persist for >24hrs
what is the usual duration of TIAs
5min
what is a TIA
transient ischemic attack
sx are same as CVA, but resolve w/i 24hrs
what flag is a TIA and why
red - medical emergency, call 911!
can’t distinguish TIA from stroke-in-evolution
what is the CVA morbidity post TIA
50% of all CVA occur in first few days after TIA
almost 1/2 (40%) of people will have stroke w/i 5yrs after a TIA
what are the main sx of a CVA
BE FAST
Balance - loss of balance?
Eyes - visual disturbances?
Face - symmetry?
Arms - raise for 10sec?
Speech - slurred? difficulty swallowing/speaking?
Time = brain
what sx are more common in post circulation strokes
5Ds
Dizziness
Drowsiness
Dysarthria
Diplopia
Dysphasia
how does a higher education influence the CVAs
people w higher education are more aware of early stroke sx
where does almost 3/4 of strokes occur in the world
low and middle income countries
how does race factor into CVAs
black people are 50% more likely to have a stroke than white people
what are non modifiable risk factors for CVAs(4)
age
family history
african americans
sex
how is age a risk factor for CVAs
risk 2x every 10yrs after 55yo
- 70% occur in >65yo
why is being african american a risk factor for CVAs
AAs have congenital inc risk for sickle cell anemia
- inc risk factor for blood clots
how is sex a risk factor for CVAs
men > women
ovarian estrogen dec risk of stroke = dec risk in women
what are 5 modifiable risk factors for CVAs
smoking
HTN
DM type 2
CVD
SDOH
what is the greatest modifiable risk factor for CVAs
HTN
what are modifiable risk factors that contribute to HTN (5)
hypercholesterolemia
hyperlipidemia
obesity
heavy EtOH
sedentary lifestyle
what CVD is a significant risk for CVAs
a-fib
- inc risk for CVAs 5fold
- inc risk of embolus -> embolic stroke
what is 1 SDOH that inc risk of CVA
health inequities
what are 5 races/ethnicities that have and inc risk of CVAs
african americans
mexican americans
hispanics
native americans
native alaskans
what type of CVA is most common
ischemic > hemorrhagic
where in the meninges should be filled w CSF in a normal/healthy human
sub arachnoid space
where in the meninges are blood vessels contained in a normal/healthy human
arachnoid mater
what are 5 etiologies for an ischemic CVA
thrombotic
embolic
vasospasm
low perfusion
coagulopathy
what happens during an ischemic stroke
blood flow to corresponding brain territory is blocked
- leading to ischemia and infarction
what is infarction
obstruction of blood supply to brain d/t clot and causes cell death
what is ischemia
inadequate blood flow to brain, doesn’t necessarily mean cell death
- could just mean dec perfusion and oxygenation
what is mortality rate of ischemic CVAs
low
what is a thrombus
blood clot commonly caused by atherosclerotic plaques in cerebral blood vessels
what is an embolus
travelling clot from outside cerebral circulation
what is a common origin of an embolus and why
heart
- d/t afib
what result does an embolic stroke has on disability
results in greater disability
- clots tend to be bigger
- get to smaller vessels of brain
- more ischemia and dec O2 perfusion bc bigger blockage
what are 3 reasons for low perfusion leading to an ischemic stroke
cardiac failure
HoTN
blood loss
how can atherosclerotic plaques lead to a thrombus
atherosclerosis
- artery wall thickens d/t chronic inflammation and WBCs -> dec elasticity of artery walls
plaque formation = accumulation of lipids, fibrin, calcium deposits on walls
-> narrowing of walls -> dec blood flow
what could global low perfusion indicate
anoxic brain injury
what are vasospasms
blood vessels continuously contract
what are 3 etiologies for vasospasms in the brain
SE to drugs
SE from hemorrhagic stroke
Raynauds dz
what is coagulopathy as it relates to causing an ischemic stroke
RBCs get sticky and block blood flow
what role does HTN play in the etiology of ischemic strokes
HTN damages arterial linings
HTN can push thru build up of cells and lipids large enough to block blood flow
how quickly can cell death happen in the brain
w/i 5-6min
describe the ischemic stroke pathophysiological process after there is a lack of blood flow
- lack of blood flow = loss of O2 and glucose
- neuronal cell death in ischemic core w/i minutes
- ischemic cascade = impaired energy production and further neural damage/death
- ischemic penumbra forms in areas adjacent to ischemic core
- cerebral edema leads to inc ICP (frequent cause of death in large strokes)
describe the ischemic cascade in detail
- changes in neural cell permeability
- release of excess transmitters
- inability of brain cells to produce energy
- influx of Na+ and output of K+
- open Ca- channels and allow influx of Ca-
- RESULTS IN FREE RADICAL DAMAGED CELLS
describe the movement of fluid in ischemic strokes and a possible result
movement of fluid from blood into brain tissues and redistribution of CSF on ipsilateral side
- bc of edema from one side to other, can have midline shift
what is a hemorrhagic CVA
rupture of blood vessel -> bleeding into extravascular spaces of brain
what occurs after the initial bleeding in a hemorrhagic CVA (3)
edema
ischemia
infarction
when do you see edema in hemorrhagic strokes and what is the accompanying risk w edema
get edema/swelling if bleed into area that is restricted by skull
risk factor for brainstem herniation (life threatening)
what happens to the blood cells once they bleed out of the broken vessel in a hemorrhagic stroke
blood is a neurotoxin
- blood cells die, swell, and burst -> releasing toxins that further damage brain cells in areas surrounding the hematoma
infarction and necrosis in hemorrhagic vs ischemic strokes
much more infarction (tissue death) and necrosis in hemorrhagic
- in ischemic, blood reperfusion is possible
mortality of hemorrhagic CVAs
higher than ischemic
what are 2 types of hemorrhagic strokes
intracerebral hemorrhage (ICH)
subarachnoid hemorrhage (SAH)
what is an intracerebral hemorrhage (ICH)
rupture of cerebral blood vessel w bleeding into brain
what is a subarachnoid hemorrage (SAH)
rupture of vessel on brain surface w bleeding into subarachnoid space
what is the problem w SAH and what does this result in
not much space b/w pia and arachnoid, and dura maters
- causes swelling throughout whole brain and can be very damaging
what is the most common cause of a SAH
aneurysm (80% of time)
what does it mean if a SAH is caused by trauma
this is a TBI not a stroke
- not vascular in nature, secondary to trauma
why are both ICH and SAH dangerous in nature
both can cause brainstem herniation and cell death
- blood accumulates and presses on surrounding tissues
- restriction of blood flow to areas
what is a subdural hematoma/hemorrhage (SDH)
bleeding usually caused by head trauma b/w dura and arachnoid layers
- TBI not a stroke
what are 4 causes of hemorrhagic stroke
HTN
cocaine use
aneurysm
arteriovenous malformation (AVM)
trauma - but TBI not a stroke
how can HTN lead to a hemorrhagic stroke
overstretching internal elastic membrane of blood vessels
-> aneurysm -> stroke
how can cocaine use lead to a hemorrhagic stroke
vasoconstriction -> HTN -> overstretching internal elastic membrane of blood vessels
-> aneurysm -> stroke
what is an aneurysm
bulge in wall of blood vessel, that over time can weaken wall and burst
can be congenital or d/t atherosclerosis
what is an arteriovenous malformation (AVM)
abnormal connection of blood vessels
tangle of blood vessels in brain that bypasses normal brain tissues and directly diverts blood from arteries to veins
do AVM change? how?
don’t grow or change much
- vessels might grow, dilate, or shrink d/t clots
what will AVMs most likely lead to
ICH
- bleeding caused by weakened vessels that burst d/t high pressure of blood flow in arteries
how can AVMs be dx
CAT scan
MRI
cerebral angiogram
treatment for AVMS?
typically treated if accessible and not too large
if can’t be treated:
- avoid activities that elevate BP
- avoid blood thinners
etiology of AVMs
congenital
how common are each of the etiologies of non-traumatic ICHs
HTN = aneurysm
AVM (less than either)
what is the MAIN difference in sx b/w SAH and ICH
SAH will come in saying worst HA of their life
- “thunderclap headache”
what are the 3 main different sx of SAH compared to ICH
thunderclap HA
diplopia
stiff neck, LBP
why do you see stiff neck and LBP in SAH
accumulation of blood in CSF
-> meningeal irritation that travels down SC
how is ICP impacted in ICH vs SAH
elevated ICP in both
describe 7 sx seen in ICH
severe HA
difficulty speaking
confusion
impaired vision
large pupils
n/v, sz
LOC
describe 8 sx seen in SAH
*thunderclap HA
facial/eye pain
*diplopia
impaired peripheral vision
confused, difficulty to arouse
restless
*stiff neck, LBP
vomitting, dizziness
edema in ischemic vs hemorrhagic strokes
edema local in ischemic
- global in hemorrhagic
what is the pathophys of a hemorrhagic stroke
- release of blood causes destruction of brain tissue
- toxins in released blood cause edema in response to inflammatory brain processes from these cellular changes
- inc ICP from added volume of blood being released
- severe edema restricts blood flow to remote areas and leads to global anoxia
- greater risk of brainstem herniation and death
how can SAH lead to hydrocephalus
blood enters CSF pathway or the CSF pathway is obstructed
-> potentially blocking sites of CSF absorption -> restricts CSF flow -> hydrocephalus
what is hydrocephalus
abnormal accumulation of CSF w/i cavities in brain -> pressure inc -> ventricles enlarge -> inc ICP
what is a consideration of blood in the CSF other than causing a secondary sequelae of hydrocephalus
blood in CSF irritates meninges -> LE pain
what are 2 concerns with hydrocephalus
can lead to herniation and death
treatment for hydrocephalus
EVDs - tube placed into ventricles to drain some of fluid and dec ICP
