acute stroke Flashcards
what does timely out of bed activities prevent
- DVT
- pulmonary emboli
- pneumonia
- falls
why is orthostatic hypertension so bad for CVA pts
- because it decrease blood perfusion and O2 to the brain
- do not avocate for high intensity in acute care only rehab
types of stokes
- embolic
- lacunar
- athero-thrombotic
what does the lacunal strokes affect
- motor due to lack of O2 during stroke to internal capsule
- usually involves the posterior limb of the internal capsule
- no sensory, aphasia, or visual field abnormalities
- dysarthria might be present
lacunar stroke or lacunar infarct pathology
- most common type of ischemic stroke
- resulting from the osculation of small penetrating arteries the provide blood to the brains deep structures (internal capsule)
- etiology of chronic hypertension
signs and symptoms to review prior to out of bed activities
- nausea
- vomiting
- dizziness
- light-headedness
- loss of alertness
- confusion
- headache
- ringing in ears
- sweating
location of the internal capsule
- subcortical structures that include: internal capsule, caudate, putamen, globus pallidus, thalamus, brainstem
- anterior limb separates the caudate nucleus and lenticular nucleus
- the posterior limb separates the thalamus and lenticular nucleus
type of fibers in the internal capsule
- anterior limb: frontopontine fibers, thalamocortical fibers
- genu: corticobulbar fibers
- posterior limb: corticospinal fibers (cortex to spine), sensory fibers
blood supply to the internal capsule
- anterior limb: lenticulostriate branches of MCA and ACA
- Genu: lenticulostriate branches of MCA
- posterior limb: lenticulostriate branches of MCA and anterior choroidal artery
clinical findings in internal capsular stroke
- weakness of the face, arm and or leg (test CN 7 and 2)
- UMN signs: hyperreflexia, babinski sign, hoffman present, clonus, spasticity
watershed infarctions
- infarcts in areas where this is reduced profusion due to blockage of the ACA, MCA, or PCA.
- occurs with internal carotid artery blockage or a carotid artery blockage
Transient Ischemic Attacks (TIA)
- typically less then 10 minutes
- longer then 10 minutes tissue cells will start to die
- TIA lasting longer then an hour will cause small infarcts
- requires an ER visit
- Early warning sign for a larger stroke
Etiology of TIA
- thrombus emerging
- vasospasm
- small emboli: dissolves
signs and symptoms of a TIA
- high BP
- weakness on one side of the body
- vision problems
- slurred speech
treatment of TIA
medication, surgery, and healthy lifestyle changes
cerebral edema
- internal pressure within the cortex from hemorrhage or inflammation
- fluid can push the brain contents to the other side
- serious consequence of stroke that can lead to early mortality
cerebral perfusion pressure (CPP)
the net pressure gradient that drives oxygen delivery to cerebral tissue
intracranial pressure (ICP)
- measured invasively though an intracranial pressure transduction device (intraventricular monitor)
- mean arterial pressure - ICP = cerebral perfusion pressure
normal CPP
55 to 60
normal ICP
5 to 15
ICP values of 20 to 30 represent intracranial hypertension
hemorrhagic stroke
leads to increased pressure in teh brain and reduces cerebral perfusion
tumors in the brain
create cortical pressure and reduce brain perfusion
infection of the brain
changes in the regulation of cerebral perfusion may occur
CARE for individual with CVA
stage 1: hospital and acute care
stage 2: inpt rehab or SNF
stage 3: At home health care
stage 4: outpt care
stage 5: after discharge
goldilocks : u shaped curve
make sure the ex is an appropriate level of intensity so the BP does not get too high or too low
tissue plasminogen activator (tPA)
- clot buster and timely management of high BP
- when administered 3 hrs after a sroke it helps to restore blood flow to brain regions affected by a stroke, thereby limited the risk of damage and functional impairment
what is tPA associated with
- more frequent independent ambulation at discharge
- discharge to home
- reduced mortality and symptomatic intracerebreal hemorrhage
not a candidate for IV tPA or IAT
BP up to 220/120 may be permitted to allow for maximal perfusion unless otherwise contraindicated
candidate for IV tPA or IAT
lower BP to less them 185/110 prior to giving tPA or in preperation for the angiography suite
hypotension in the intial setting of stroke care
no formal guidelines exist for a lower limit of BP, hypotension is associated with worse outcomes. ensure that it is not related to volume depletion, cardiac abnormalities or shock
during IAT
maintain systolic BP at 140-180
incomplete reperfusion after tPA
maintain BP of greater then 180/105 consider induces hypertension
successful reperfusion of tPA
- consider a lower threshold of systolic less then 140-160
- monitor closely for changes in neurologic examination which can suggest reperfusion injury
mobility after acute ischemic stroke
pt should receive mobility 13-24 hours after receiving tPA
SBP should be between 140-160
what is the recommendation for out of bed activities
Early lower- dose out of bed activities
first day: 10-20 minutes
Preparing for out of bed activities
- receive orders from MD
- review the chart (look for type of stroke, location and meds)
PT area if assessment and decision making
- skin integrity: ER and one floor
- Mobility: out of bed with PT
- Caregiver availability (education)
- spasticity
- durable medical equipment
- recommendation regarding transition to appropriate level of care
rapid large falls in BP can reduce
cerebral blood flow leading to extension of the cerebral infarction or perihematomal ischemia
what is the general goal for CVA patients BP
less then 180. 20 point role fro systolic
deterioration
change in orientation
- symptoms: new headache, acute hypertension, nausea or vomiting, changes in pulse ox or 02 sat, SOB, syncope
when should BP start to return back to nomal after tPA
48 hrs after given
outcome measures for stroke
- 6 minute walk
- TUG
- 5 TSTS
- 10 MWT
