CVA Flashcards
CVA: S/Sx
- numbness/weakness face, arm, leg
- confusion
- dysphasia
- visual disturbance in one or both eyes
- ataxia
- dizziness
- severe headache
Face drooping
Arm weakness
Speech Difficulty
Time
Possible Hidden Causes of CVA
- a-fib
- heart structure problem
- heart atherosclerosis
- blood clotting disorders
Hemiplegia
paralysis of one side of the body
Hemiparesis
weakness of one side of the body
Dysphasia
speech disorders in which there was impairment of the power of expression by speech, writing, or signs or impairment of the power of comprehension of spoken or written language
Dysphagia
difficulty swallowing
impairment of cranial nerves 9 and 10
Expressive Aphasia (Broca’s area)
can understand
can’t speak or write
impairment of motor speech center in frontal lobe
Receptive Aphasia (Wernicke’s area)
can’t understand or follow commands
impairment of auditory association area in temporal lobe
Types of Strokes
thrombotic stroke: from plaque
embolic stroke: from embolus (blood clot, fat, air)
hemorrhagic stoke: burst blood vessel (usually aneurysm)
- intracerebral hemorrhage: bleeding w/in the brain
- subarachnoid hemorrhage: bleeding into the CSF-filled space between the arachnoid and the pia mater membranes on the surface of the brain
Penumbra
the area surrounding an ischemic event such as thrombotic or embolic stoke
salvageable brain area
immediately following the event, blood flow and therefore O2 is reduced locally > hypoxia of the cell near the location of the original insult
CVA: Risk Factors
- female = more deaths
- male = more likely to have 2nd CVA in 5 years
- african americans = 2x risk and mortality
- > 50YO
- women taking birth control pills
- young black w/ sickle cell disease
- diabetics w/ carotid artery disease
- hx of heart disease
- hx of HTN
- high cholesterol
- obesity
- smoking
- sedentary lifestyle
- heredity
- alcohol
Developmental Processes of Ischemic/Embolic Strokes
- TIA
- RIND (reversible ischemic neuro deficit)
- Stroke in evolution: recognized stroke and comes to hospital, can be treated
- Completed Stroke: stroke in sleep or unrecognized, doesn’t get tx until much later
*TIA and RIND are reversible on their own
TIA
- more likely to have CVA after TIA (like a warning sign)
- last seconds to 12 hours w/o residual effect (avg = 10-20 minutes and resolve in 1 hr)
- signifies advanced atherosclerosis
-will do carotid u/s in to r/o clots and plaques, if there is significant blockage > carotid endarterectomy to prevent future stroke
TIA and Cerebral Edema
cerebral edema peaks in 72 hours and remains for 2 weeks
need CT scan to look for further bleeding and cerebral edema
RIND
reversible ischemic neurological deficit
small stroke
reversible by itself in 48hrs to 3wks
may have multiple over years in the same are of the brain
usually d/t to carotid artery stenosis
Stroke in Evolution
progressive stroke
deficit occurs in steps
some over 24 hours, other 72 hours
Completed Stroke
stable deficits w/in 1 hour
can have secondary injury up to 72 hours as a result of stroke (do NIH stroke scale and CT scan to monitor for changes)
approximately 60% occur during sleep
Collaborative Care of Stroke
involve radiology, PT, OT, Speech ASAP
tPA Therapy
max time frame for use - 3 hours
dosage: 0.9mg/kg; max: 90mg
tPA Therapy: Complications
intracerebral hemorrhage:
- highest risk is w/in 24 after administration
- control BP to prevent (keep systolic less than 185, keep diastolic less than 105)
tPA Therapy: Exclusion Criteria
- evidence of hemorrhage on CT scan
- <18 YO
- minor or rapidly improving stroke symptoms (this indicates TIA or RIND and tPA isn’t needed)
- outside 3 hour time frame
- active bleeding or hx of recent surgery (less than 8 weeks ago)
- seizure activity w/ stroke symptoms
Mechanical Revascularization
used when:
- tPA therapy ineffective b/c the clot was a thrombosis (from plaque) not an embolus
- client is not a candidate for tPA
CVA and BP
maintain systolic BP at 150mm Hg to perfuse brain
CVA and Hypervolemic/hemodilution w/ NS and albumin
- maintain CPP
- lowers blood viscosity
- maintains slightly elevated BP
- Hct decreases from 35-33 d/t dilution of hematocrit and it’s a false reading
- vasodilates cerebral vessels = increased perfusion
- works well for subarachnoid bleeds and vasospasm
- not as well in ischemic/embolic strokes
How do you minimize disuse syndrome?
- minimize time on flaccid side
- use affected hand to wrist; wrist to elbow
- avoid excessive pull on affected shoulder (vulnerable to subluxation and adduction contractures)
- prevent external rotation of hip
- heels off mattress
- AROM and PROM as much as possible
- hi-top sneakers to prevent foot drop
- resting splint (assess skin under splint regularly)
- skin care - assess frequently (decrease skin pressure in chairs)
- place things on affected side to force pt to use this side
- use adaptive equipment to regain ADLs
- early ambulation
Dysphagia: Sx
facial droop
drooling
weak voice
Dysphagia: Silent Aspiration
silent aspiration = aspirate w/o choking (no reflexes)
Dysphagia: Standard of Care
- speech therapist will do barium swallow test
- evaluate swallowing before allowing PO fluids/food/meds
- quiet environment for eating to concentrate on swallowing
- HOB elevated
- aspiration precautions
- mouth care before meals (stimulate saliva flow)
- position food in visual field (if necessary)
- mechanical soft diet better than liquids (thickeners)
- small bites (on unaffected side of mouth)
- chew thoroughly
- sweep mouth after each bite for “pockets”
- mouth care after meals (clean out pockets w/ gauze)
- accurate I&O until sufficient intake achieved
- weekly weights to ensure nutritional status has not been impaired by stroke
Cerebral Aneurysm - Subarachnoid Hemorrhage
dilation of wall of cerebral artery usually at arterial junction (berry aneurysm)
80% occur in circle of willis
aneurysm ruptures and bleeds into subarachnoid space
can be d/t trauma
sx occur when aneurysm enlarges and exerts pressure on brain, or when ruptures
Predisposing Factors that Cause Rupture of Aneurysms
- valsalva maneuver
- sexual intercourse
- physical exertion
*if rupture occurred during activity, pt may be reluctant to do that activity again
Hemorrhagic Stroke: Sx
Prior to rupture:
- severe HA
- photophobia (look at shape of pupils, may be oval)
- intermittent nausea
After rupture:
- severe HA
- unequal pupils
- dysconjugate gaze
- seizures
- nuchal rigidity (b/c bleeding is going into CSF and causing rigidness and neck pain)
- hemiparesis
- loss of consciousness
- increased ICP
Hemorrhagic Stroke: Dx Tests
- lumbar puncture (blood in CSF = hemorrhage in brain)
- cerebral angiogram
- CT scan
Hemorrhagic Stroke: Tx
craniotomy to clip or coil aneurysm before rupture
meds:
- osmotic diuretics (Mannitol): to help decrease ICP
- anti-HTN
goal: prevent further increase in ICP and subsequent rupture
Craniotomy: Post-op
- immediate, strict bed rest
- prevent valsalva maneuver
- prevent anything that will increase ICP
- check swallowing
- HOB elevated
- quiet, dim, non-stimulating environment
- constant monitoring
- keep BP lower (to prevent risk of re-bleed)
- vasoactive meds: Ca channel blockers (vasodilators to ensure to perfusion to brain and help decrease vasospasms which will cause rebleeding)
- frequent checks on pt
Aneurysm: Complications
rebleed
hydrocephalus (which may require ventricular shunt)
vasospasm
