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58 Cards in this Set

  • Front
  • Back
Describe what happens in the brain during a CVA "brain attack"
Disruption in the nml blood supply to the brain
What is Cerebral Autoregulation? How is it characterized?
1000ml/min blood flow
Dilation/constriction prn
Lack of perfusion
Name the 2 types of strokes and their subsets.
Ischemic (occlusive)
Thrombolic stroke
Embolic stroke
Describe the etiology of an embolic stroke.
Embolus/emboli travel to cerebral arteries via carotid artery
Sources of emboli are cardiac
Can be TIA's, RIND's or permanent
Accounts for 1/3d of all strokes
Describe the etiology of a Thrombolic Stroke. Acounts for 1/2 of all strokes
Associated with atherosclerosis, plaques build up and occlude vessels
slow onset of s/s
occurs at bifurcations of the common carotid and vertebral arteries at juncture with basilar artery
What types of medications will be given for the eschimic stroke?
Heparin initially until INR's are therapeutic then concurrent Coumadin for a few days before d/cing Heparin.
inablility to use/ comprehend
expressive/ receptive
reading difficulty
writing difficulty
paralysis, one sided
weakness, one sided
flaccidity (hypotonia)
nurse notes a fall to one side
what is the etiology of an Hemorragic stroke?
weakened vessel walls cause a rupture and brain bleed
Saccular or Berry aneurysm
What is a TIA
What is a RIND
how are they the same and how are they different.
what type of stoke are they associated with?
TIA = few minutes, <24 hours
–Weakness/gait disturbance
–Numbness (transient)
–Aphasia/dysarthria (slurred speech)
RIND = > 24 hours <week
what are some physical assessments of an eschimic stroke
Cognitive changes:
LOC may vary
Spatial/ proprioceptive dysfx
memory impairment
Prolem solving/decision-malking issues
What types of manifestations are seen with the Left sided brain injury/stroke?
Aphasia, alexia, agraphia. This is the speech/language center
What clinical manifestations are associated with Right sided brain injury/stroke?
Neglect syndrome
visual field deficitsamaurosis fugax/brief blindness
may be impulsive
emotional lability if frotal lobe is involved.
Causes of Hemorrhagic Stroke?
HTN--stretches and thins vessel wall
genetic/traumatic weakening of the vessel walls
Rupture usually occurs with activity
Risk Factors for hemoragic stroke
HTN, diabetis mellitus
heart disease
nonvalvular a-fib
smoking/substance abuse
sedentary lifestyle
WOMEN--high Hgb (>14)
what kind of Hx is gathered for stroke pts.
• Accurate history
• Important to affected area
• s/sx?
• When did it start? (ischemic = sleep; hemorrhagic = activity…usually)
• How the s/sx progressed?
• Onset important (embolic/hemo = abrupt; thrombolytic = gradual…usually)
• S/Sx come and go? (TIA, RIND)
• Observe LOC during interview
• Monitor speech pattern/body posture, etc
• Medical hx?
• Family hx?
• Diet?
interventions for stroke pts
•Stabilize patient, reduce further injury
•Determined by type/extent of injury
•Nonsurgical management
Patient may be at risk for increased ICP
Glasgow Coma Scale (GCS)
What are key features of increased ICP
Decreases LOC sensorimotor ^
Behavioral^s pupillary^
HA cranial nerve involve
N/V ataxia
Speech ? sz
Aphasia Cushings' Triad
Slurred speech Posturing
What is Cushings Triad/ cuushings reflex?
Bradycardia, hypertension, widening pulse pressure
Nursing interventions for ICP increase
•Frequent nursing assessments
First 72 hours critical
•Elevate HOB
•Maintain head position ¨ drainage
•Avoid extreme flexion (ª ITP)
•Avoid clustering of activities
Drug Therapy for increased ICP
Thrombolytic therapy - dissolves occlusion
•Rt-PA (recomb tissue plasminogen act)
What labs for drug therapy
• Endarterectomy
• Extracranial-intracranial bypass
• AVM management
• Craniotomy
Remove clots
Nursing interventions FOR SURGERY of stroke pts
• Self-Care Deficit
Facilitate increased muscle strength/function
Positioning important
•Splinting Avoid contractures
DVTs are a risk to develop
• Antiembolism stockings
• Compression boots
• Frequent position changes
• Mobilization of the client
Disturbed Sensory Perception interventions (r-sided)
visual/perceptual or spatial impairments depth erception/discrimination (up/down) thus ADLs
•Provide frequent cues
•Break down tasks into simple steps
•Approach from UNAFFECTED side
•UNAFFECTED side: should FACE the door
•Teach patient to scan environment
•Diplopia: use patch
•Remove clutter
interventions for L sided repercussions?
Memory deficits, simple tasks difficult
Reorient to month, day, year
Establish routine schedule
Structured environment
Familiar objects
Step by step teaching
Unilateral Neglect
•Goal: compensate for affected side
•Most common with R-sided stroke
•increased risk for injury
Teach patient to touch/use both sides
Affected side first
Turn head for full vision fields
"scanning" technique
Impaired Verbal Communication l-sided
•Goal: effective communication
Language/speech (dominant hemisphere)
Expressive (Broca's; motor) frontal
Receptive (Wernicke's; sensory) Temporal/Parietal area: may talk but language is meaningless
Global (mixed)
Describe Broca's
1. Motor speech problem
2. Understands but unable to communicate
3. Difficulty with writing
4. Frustration and anger
describe Wernicke's
Receptive /sensory
1. Unable to understand spoken and written word
2. Neologisms
3. Global or mixed aphasia
4. Reading and writing equally affected
Waht are foods that facilitate salivary production and aid is swollowing. What interventions for cliet iwth difficulty swallowing?
Beef broth, sweek, sour, salty

Place food on the unaffected side
reduce distratctions
observe for s/s of fatigue
Health Teaching for stroke pt and their families
Medication schedule (s/s bleeding, electric razor, avoid Vit.K etc.)
•Communication (patience, shortcommands)
•Dietary (fat reduction diet with thrombotic stoke)
•Activity/self-care skills
•Psychosocial intervention (lability) (depression precautions)
•Families encouraged to permit individual to do as much as possible
•Families - take and plan for extra time to do things
•Care givers may need respite/time to relax
what age grou[ is most affected by TBIs
18-34•year olds
MVA, most common cause
•Summer, spring, pm, noc, weekends
•3X more in males
TBI: Glascow Coma Scale
Mild :13-15 gait altered
Mod: decreasing LOC GCS 9-12¨ 24 h observation
Severe: GCS <9 ¨ critical care
What is the problem with increased ICP
increased ICP = decresed cerebral blood flow = tissue hypoxia = ¯decreased serum pH and ­ increased CO2 = cerebral vasodilation = edema = increased ICP = brain hernation = irreversible brain damage = death (uncal herniation)
when there is an increase in ICP, what happens to the cerebral blood flow
what happens with increase ICP and decreased cerebral blood flow?
tissue hypoxia, decrease in pH
increase in CO2 (causing cerebral vasodilation, edema, further increaseing iCP
brain my herniate into brainstem (uncal)
Cytotoxic, cellular edema
From hypoxia
Disturbance in cellular metabolism
Sodium pump Active ion transport
Brain depleted of O2, CHO, glycogen
Na+ pump fails, Na+ enters the cells and pulls H2O
Simultaneous decrease Na+ serum (<120 mEq/L)
Interstitial edema:
Acute brain swelling
Assoc with HTN,increased ICP
Three types of cerebral hemorrhage
Epidural Hematoma
Subdural Hematoma (SDH)
Intracrebral Hemorrhage
Epidural Hematoma
Arterial bleeding
Space: skull and dura mater
Frequent site: temporal lobe injury
"lucid" interval leading to unconsciousness
May proceed to coma and death
Subdural Hematoma (SDH)
Space: dura mater and arachnoid
Common: laceration of brain tissue
Bleed is slower
•Acute - preseents with 48 hourse after impact
•Subacute - between 48 hours and 2 weeks
•Chronic - form 2 weeks to several months following the injury
Intracrebral Hemorrhage
Intracrebral Hemorrhage
Accumulation of blood within tissue
Abnormal increase CSF volume
Caused dilation of ventricles
May lead to increased ICP
Uncal: life threatening
Shift of one/both temporal lobes (uncus)
Pressure on 3rd cranial nerve
S/Sx: dilated/fixed pupils
Rapid? in conciousness
Downward shift of brainstem
S/Sx: Cheyne-Stokes respirations
Pinpoint, fixed, nonreactive pupils
Traumatic Brain Injury-Interventions
Prevention of increased ICP
•Fluid and electrolyte balance
•Induction of barbiturate coma/drug therapy (mannitol)
•Strategies for sensory/perceptual alterations
•Pulmonary management/behavioral management
•Strategies for preventing complications of immobility
•Nutrition management
Surgical management for TBI's
Intracranial pressure monitoring
Brain Tumors-Complications
Cerebral (vasogenic) edema/ „^ ICP
Herniation of brain tissue/ischemia of affected area
Rupture/hemorrhage into brain tissue
Seizure activity/hydrocephalus
Pituitary dysfunction/SIADH/diabetes insipidusFluid and electrolyte imbalances
Brain Tumors-Classification
„PƒnMalignant or benign
Gliomas (malignant)
Meningiomas (benign)
Pituitary gland (benign)
Acoustic neuromas
Brain Tumors-Symptoms
Headache (severe on awakening in the AM)
Nausea and vomiting
Visual symptoms
Changes in mentation or personality
Papilledema (swelling of the optic disk)
Brain Tumors-Interventions
Nonsurgical management
ƒnBlood brain barrier disruption
Recombinant DN
Monoclonal antibodies„PƒnAntineoplastic drugs
Surgical management
Brain Tumors-Postoperative Complications
Increased ICP
Hydrocephalus accumulation of the fluid
Respiratory problems
Neurogenic pulmonary edema
Would infection
Fluid/electrolyte imbalance