Ischemic CVA -Lecture 11 Flashcards
ischemic CVA are
most common type of CVA
80%
what is an ischemic CVA
complete loss of blood flow to the cerebral tissue
what do ischemic strokes result in
decreased O2 and metabolites (glucose)
results in neuronal dysfunction and cell death
energy requirements for the brain
high
25% of all O2 supply
the brain has almost no
metabolic reserves
dependent on rich supply of O2 and glucose to fxn
what triggers the onset of neurologic deficits
stores of O2 and glucose are used quickly
what happens w/o blood flow
there is a toxic build up of metabolic waste –> additional damage
secondary damage
occurs in the aftermath of the acute infarct
damaged or dying neurons release excessive amounts of glutamate
what occurs to cells that normally take up glutamate
compromised
what occurs d/t the compromising of the cells that take up glutamate
inability to produce ATP
facilitates entry of Ca2+ into cells
area of apoptosis and tissue death beyond the infarction usually w/in 3-4 hours
facilitates entry of Ca2+ into cells
activates catabolic enzymes that further degrade neural structures
mechanisms of injury that occur in ischemia CVA
local hypoxia
local hypoglycemia
build-up of toxic metabolic waste
medical intervention
ischemia is reversible if it lasts for less than first 3 hrs
meds
meds
remove embolus
prevent secondary neuronal death
ex: t-PA
most common cause
thrombic and embolic occlusion of major vessels
80%
damage can be
cerebral infarction involving
–>all NS cells in a wide area
–>selective neuronal necrosis
selective neuronal necrosis
refers to structures that are most susceptible to ischemia
neurologic symptoms due to thrombic ischemia may be seen in these regions first
ischemic penumbra
transitional area surrounding the core
in the core zone of the ischemic penumbra
decrease of O2 and glucose –> rapid depletion of energy stores
severe ischemia –>
necrosis of neurons and supporting cellular elements (glial cells)
how long may the penumbra remain viable
several hours
how does the penumbra remain viable
collateral arteries anastomosing w/ branches of the occluded vascular tree
when is ischemic CVA fatal
rarely
ischemic cascade is
potentially fatal
ischemic cascade
decreased vascular perfusion into the brain
osmolarity increased during ischemia
influx of fluid into the brain to restore normal osmotic pressure
edema
when does ischemic cascade begin
minutes after occlusion
peaks in 3-4 days
what can ischemic cascade cause
increased ICP
severe secondary structural damage
what is the most frequent cause of death seen in large infarcts involving MCA and ICA
ischemic cascade
thrombic ischemia
development or existence of a blood clot within the cerebral vascular system
most common type of all CVAs
thrombic
40%
where does thrombic ischemia occur
already partially occluded vessel
partially occluded by atherosclerosis
where do thombic occlusions occur
at sites of turbulent flow
bifurcations and curvatures
thrombic occlusions are most common in
internal carotid and vertebral a
basilar a and middle cerebral a
atherosclerosis
most common form of vascular dz
what is atherosclerosis associated with
accumulation of lipids, fibrous tissue and calcium deposits on arterial walls
what do the accumulations on the arterial walls form
plaques
narrow the lumen
what aggregte around the plaques
platelets
produce clots
onset of thrombic CVA
slow or fast
frequently preceded by several TIAs
often manifests as a focal neurologic deficit that evolves over several hours or days
thrombus in evolution
symptoms occur over days
when do thrombic CVA occur
in sleep
what are thrombic CVA associated w/
atherosclerotic vessel dz
DM
HTN
deterioration from thrombic CVA
may continue first 2 days secondary to cerebral edema
prognosis –> thrombic CVA
poorer compared to emobolic
embolism
obstruction of blood secondary to a blood clot that is not inherent to the cerebral vascular system
most common form of cerebral emboli
fragments from a thrombus within the heart can dislodge and enter the cerebral circulation
75% of cardiac emboli lodge in the brain
someone w/ cardiac dz is 2-5x more likely to sustain a CVA
most common origins of emboli
a-fib
MI
a-fib
blood flow is stagnant in the L atrium
MI
damaged myocardium
other origins of emboli
intra-arterial thrombus
dislodged plaque
where is the progression of an emboli halted
bifurcation
where the lumen is narrowed and the ischemic infarction occurs
focal deficits correspond to
anatomic region supplied by the occluded vessel
what may there be during the onset of embolic CVA
“stuttering” onset of symptoms appearing & clearing as the emoblism moves along the blood stream
what are embolic CVA more frequently associated w/
TIA
what are embolic CVA associated w/
seizures
precipitating headache
transient confusion and/or loss of conciousness
where to emboli tend to terminally lodge in
smaller vesserls
producing more discrete, focal deficits
systemic cause of ischemic CVA
low systemic perfusion secondary to cardiac failure or significant blood loss
widespread hypoperfusion and ischemia
neurological deficits are global and bilateral in nature
anoxic brain injuries
ischemia can cause a hypoxic or an anoxic event within minutes of oxygen deprivation to the brain
areas most prone to anoxic brain injury
hippocampus –> memory deficits
purkinje fibers of the cerebellum –> ataxia
basal gangila –> increased muscle tone
what could lead to cerebral hypoperfusion
systemic hypertension
anoxic brain injuries can lead to
watershed lesions
watershed lesions
certain areas of the brain do not get sufficient blood supply
anterior watershed zone
ACA meets MCA
often causes bilateral UE weakness
posterior watershed zone
PCA meets MCA
often causes cortical blindness and aphasia
trombic/embolic CVA syndromes focal deficits
dictated by the location of the blockage of the cerebral vasculature
syndromes may be
partial or complete
where are more hypoxic damages found
proximal
greater collateral circulation results in
less extensive damage
less complete syndromes
circle of willis
what occurs with cerebellar edema
death from brainstem compression or herniation
medical treatment of ischemic CVA
blood pressure management
anticoagulation therapy
thrombolytic agents
nimodepine
corticosteroids
blood pressure management
pt is kept horizontal for the 1st few days post CVA
limited to bedside PROM
anticoagulation therapy
coumadin –> those w/ a-fib
used acutely with ischemic stroke to decrease occurrence
risk of conversion –> turning an ischemic stroke into a hemorrhagic CVA
prothombin time are –> closely monitored
thrombolytic agents
t-PA
given within 3-6 hours to break up thrombus to restore normal circulation
could you use t-PA for hemorrhagic strokes
no
t-pa gives
a chance of recovery and minimize disability
nimodepine
ca2+ channel antagonist
corticosteroids
decreased cerebral edema or in extreme cases
surgical management
carotid endarterectomy
posterior fossa decompression
carotid endarterectomy
removing the atherosclerotic deposits from the lining of the carotid artery
can dislodge a clot and cause more sx**
posterior fossa decompression
performed for potentially fatal brainstem compression
can be life saving**
