Normal Brain Protection

Brain blood supply:

Internal carotid arteries anteriorly
Vertebral arteries posteriorly
Circle of Willis
Local auto-regulation of normal brain blood flow
by:
(a) Metabolism - Increased blood flow when
CO2 increases, H+increases, and/or O2 decreased
(b) Pressure - resists changes in
systemic arterial pressure (example-with exercise)

CVA
Cerebrovascular Accidents
TIA
Transient Ischemic Attack

Stroke - Brain Attack

Cerebrovascular Accident
CVA
Stroke(Brain Attack)

Cerebrovascular Accident
Stroke-sudden loss of brain function accompanied by
neurological deficit due to loss of cerebral circulation caused
by partial or complete blockage in one or more cerebral
vessels leading to cerebral infarction (death of brain tissue)
from lack of oxygen.
Stroke -is a disruption in the normal blood supply to the brain
resulting from disruption of the blood supply to a part of the
brain. It often occurs suddenly and produces focal neurologic
deficits.
Inadequate blood supply to brain with accompanying
ischemic cell destruction occurs within 5 minutes
s/s depends on location & size of infarct

Decreased blood supply to a part of the brain

Caused by rupture,occlusion, or stenosis of the blood vessels
Onset may be sudden or gradual
Symptoms and patient problems depend on location and size of
area of brain with reduced or absent blood supply

Right CVA results in Left side involvement often associated with

safety/ judgment
Left CVA results in Right side involvement often associated with
speech problems

Cerebrovascular Accident
CVA
Stroke(Bran Attack)

Etiology
--Ischemia from a thrombus, embolus,
severe vasospasm, or hemmorhage ---neurological deficits of sensation,
movement, thought, memory, speech---temporarily or permanently--

Symptoms related to location and size of brain area

affected
Approximately 50% of survivors permanently disabled
High proportion experiencing recurrence within weeks to
years
Chances for complete recovery depending an circulation
returning to normal soon after the initial stroke
Third most common cause of neurological disability

Cerebrovascular Accident
Pathophysiology

CVA - Patho continued

The brain must receive a constant flow of blood for normal

function, because it is unable to store oxygen or glucose.
Blood flow is important for the removal of metabolic waste,
CO2, & lactic acid. If deprived of its blood flow, the brain can
be damaged irreparable within a few minutes

These processes then cause infarction or death of the

neurons, the glia, and the vasculature of the involved
area of the brain. In addition, brain metabolism after
stroke is affected in the involved area as well as in the
contralateral(opposite side) hemisphere.

Through the process of cerebral autoregulation, blood flow to

the brain is maintained at a fairly constant rate of 750L/min.
In response to BP changes r changes in CO2 tension, the
cerebral arteries dilate or constrict.

Small lacunar infarcts may also occur. Lacunae are

small, deep cavities within the brain that result from
occlusion of a small vessel.

In the event of a CVA, ischemia occurs in the brain tissue

supplied by the affected artery, leads to hypoxia or anoxia and
hypoglycemia.

Types of CVA
Thrombotic (Ischemic Stroke)
Embolic (Ischemic Stroke) & Hemorrhagic
Thrombosis: (ischemic-caused by occlusion of cerebral
artery by thrombus or embolus)

CVA
Sudden loss of brain functioning from lack of blood
supply
3rd leading cause of death

TIAs
Stroke in Evolution
RIND (reversible ischemic neurological deficit)
Lacunar(pertaining to or characterized by the presence
of pits, depressions, hollows, or spaces)

Embolic (ischemic)
Hemorrhagic

of survivors 40% need help with ADL

Causes
Thrombosis-formation, development, or existence of a blood
clot or thrombus(blood clot that obstructs a blood vessel or a
cavity of the heart) within the vascular system
Embolism-obstruction of blood vessel by foreign substances
(such as valve replacement, cardiac stents) or blood clot
Ischemia-insufficient blood supply due to obstruction of the
circulation to a part
Hemorrhage-abnormal internal or external discharge of blood

CVA Causes (1) Cerebral Thrombosis

(2) Cerebral Embolism (3) Cerebral Hemorrhage
Cerebral Thrombosis
Thombosis - a blood clot within
a blood vessel of brain or neck
Arteriosclerosis, HTN, and
slowing of circulation main
cause CVA
Most common cause of stroke
Cerebral Embolism
A blood clot or other material
carried to the brain from
another part of the body. Most
cerebral emboli are caused by
thrombi from the heart, Assoc
with heart disease, Atrial Fib

Cerebral embolism
Treat with anticoagulants
before Sx
Sudden onset of hemiparesis or
hemiplegia
With or without aphasia or LOC
in cardiac & pulmonary pt
Assoc with heart disease
Sites where emboli can
originate (most from heart):

Infective endocarditis
Rheumatic heart disease
MI
Pulmonary infection

CVA Causes (1) Cerebral Thrombosis

(2) Cerebral Embolism (3) Cerebral Hemorrhage
Cerebral Hemorrhage
Rupture of a cerebral
blood vessel with bleeding
into the brain tissue or
spaces surrounding the
brain

Most common cause of death

due to CVA, high fatality rate
Results in most extensive
neurologic deficits & slowest
recovery

Most often secondary to

arteriosclerosis & HTN
after age 50

CVA Causes (1) Cerebral Thrombosis

(2) Cerebral Embolism (3) Cerebral Hemorrhage
Cerebral Hemorrhage
(1) Extradural
Outside the dura, emergency
usually follows skull fracture,
tear of artery
(2)Subdural
Same as extradural except a
vein is torn
(3)Subarachnoid
From trauma or HTN, most
common leaking aneurysm in
circle of Willis

(4) Intercerebral
Bleeding into brain substance
common with HTN &
Atherosclerosis
Onset abrupt with severe HA
Prevent HTN
If bleed is suspected
Reduce BP, not too low or too
rapidly

Activity

Bed Flat
for
Embolic or
thrombolic
strokes
to increase
cerebral perfusion

Cerebrovascular Accident
Classifications
CVAs are generally classified as ischemic (occlusive) or
hemorrhagic.
Ischemic strokes are further divided into thrombotic strokes
and embolic strokes.
Ischemic Stroke caused by occlusion of a cerebral artery
by either a thrombus or an embolus.
Hemorrhagic Stroke - integrity of the vessel is interrupted.
Hemorrhage into the brain tissue generally results from a
ruptured saccular (berry) aneurysm, rupture of an AV
malformation or, hypertension. A ruptured cerebral aneurysm
is another cause of hemorrhagic stroke.

Stroke (Brain Attack)

HOB elevated

for
hemorrhagic stroke

to decrease
cerebral perfusion

Ischemic stroke (most common -75%)

=TIA, thrombic, embolic
Hemorrhagic stroke=bleeding into brain tissue
(often fatal)
Risk factors:
Increased age, heart disease (atrial fibrillation)
alcohol, hypertension, artherosclerosis

Ischemic Stroke - continued

Ischemic Stroke
Cerebrovascular obstruction by thrombosis or
emboli
1. TIA=focal ischemic neurologic deficits for
15mins - 24 hrs
Cause: Cerebral atherosclerosis, emboli
Effect depends on artery: weakness of forearm,
hand, mouth (middle cerebral);
Lost vision (posterior cerebral artery)

2. Thrombic stroke - most common

Develops in atherosclerotic vessels at branches of
larger arteries, risk atherosclerosis & HTN
Gradual development slowly over hours/days/weeks,
may occur at rest, variable recovery
Intermittent or stepwise improvement between
episodes of worsening until complete stroke

3. Cardiogenic Embolic Stroke

Moving blood clot --small cerebral vessels
Originate as thrombus in Left heart, or carotid

Epidemiology
Acute Brain Infarct (ABI)
75% of all strokes
Risk increases with age

Intracerebral Hemorrhage
15% of all strokes
Mortality high

Pathophysiology - Acute Brain Infarct

Thrombotic: occlusion of blood flow
atherosclerosis
Embolic: 1-2 TIAs before true embolic stroke
Stroke develops over 24-hour period
Common sources of emboli

Subarachnoid Hemorrhage
10% of all strokes
25% of all stroke deaths

Heart after MI
Atrial fib
Common carotid artery
Aorta

Pathophysiology Intracerebral
Hemorrhage
Brain vessel breaks ischemia & hypoxia
Contributing factors

Vascular malformation or angiomas

Trauma from blood ejected into brain tissue
Mechanical compression of surrounding tissue
ICP CBF

Aneurysmal Subarachnoid Hemorrhage

Due to berry aneurism (ex Circle of Willis)
Hypertension cause
Bleeding into CSF --severe headache, meningeal
irritation
May be preceded by small leaks
consequences: rebleeding, vasospasm,
hydrocephalus (>ICP) due to obstruction of
arachnoid ville
Treatment: surgery where possible

Pathophysiology
Subarachnoid Hemorrhage
Bleeding in Subarachnoid space
Contributing factors
Ruptured congenital saccular aneurysms
Extravasation of blood
CSF outflow obstruction
Hydrocephalus ICP
Delayed vasospasm

Evolution

Ischemic
Thrombotic

Ischemic
Embolic

Hemorrhagic

Onset

Gradual dev
Intermittent or
stepwise
improvement
between episodes of
worsening
Completed stroke
Preserved
Pt awake

Abrupt dev of
completed stroke
Steady progression

Usually abrupt onset

Preserved
Pt awake

Deepening stupor or
coma

HTN
Atherosclerosis

Cardiac disease
Atrial Fibrilltion

HTN
Vessel disorders

Deficits during 1st

few wk
Slight HA
Speech deficits
Visual problems
confusion

Max deficit at onset

Paralysis
Expressive aphasia

Focal deficits
Severe frequent

LOC
Assoc
Factors
Neuro deficits

Ischemic vs Hemorrhatic
Ischemic Stroke

Hemorrhagic Stroke

Results from lack of blood

reaching a certain part of
the brain
Caused by blood clot or
narrowing of the arteries

results from bleeding in

the brain
Blood will not reach areas
past the site of bleeding
Accumulation of blood
caused increased pressure
in the skull

Predisposing factors-CVA

History TIAs
Hypertension
Arrhythmias
Atherosclerosis
Rheumatic Heart
Disease
MI
DM

CVA Causes

CVA -Uncontrolled Risk Factors

Increasing age
Male gender
Black race
Hx of diabetes, even if controlled
Prior stroke or TIA
Family hx of stroke or TIA

Incidence increased with aging

Atherosclerosis
Embolism
Thrombosis
Hemorrhage from ruptured cerebral aneurysm
hypertension

CVA
Signs and Symptoms

Clinical Manifestations
CVA
Mentation and emotion changes
Speech & vision affected
Movement affected
Most changes are irreversible
Severe HA & loss of consciousness
(Hemorrhagic)

High serum
triglyceride levels
Lack of exercise
Cigarette smoking
Family history

Altered LOC
Change in mental status
Decreased attention span
Decreased ability to think and reason
Difficulty following simple directions
Communication; motor and sensory aphasia
difficulty with reading ,writing, speaking, or
understanding
Bowel and bladder dysfunction retention
impaction or incontinence

Left vs Right CVA

Signs & Symptoms

CVA
Signs and Symptoms
Seizures
Limited motor function; paralysis, dysphgia, weakness ,
hemiplegia, loss of function or contractures
Loss of sensation/ perception
Headaches and syncope
Loss of temp regulation elevated TPR and BP
Absent of gag reflex ( aspiration). Check reflex, feed on
unaffected side of mouth, diet-soft, chopped, thickener
added
Unusual emotional responses; depression, anxiety, anger,
verbal outburst, and crying: emotional lability
Problems related with immobility

Left CVA

Left sided CVA causes

right sided hemi

Right sided CVA causes

left sided hemi

Communication deficits
Aphasia, global, expressive &
receptive
Memory deficits
Loss of problem solving skills
Right visual field deficits
Right sided hemiplegia

Left sided paralysis

Left visual field deficits
Agnosia-inability to recognize
familiar objects (keys, pen, etc.)
or persons
Poor judgement
Impulsive behavior
Anosognosia-denial of deficits
Easily distracted
Unilateral neglect

Right CVA

Rt hemiplegia/hemiparesis
Left hemiplegia/paresis
Language - Aphasia, Agraphia Language-Impaired sense of

Alexia(inability to comprehend
written words)
Memory -Deficit may be
present
Vision-Unable to discriminate
words & letters. Read problems.
Deficits in right visual field
Behavior-slow, cautious,
anxious when attempting new
task, depression or catastrophic
response to illness, sense of
guilt, feeling of worthlessness,
worries over future, quick anger
& frustration
Hearing-no deficit

humor
Memory-Disoriented to time,
place, person. Cannot
recognized faces
Visual spatial deficits.
Neglect of left visual field.
Loss of depth perception
Behavior-Impulsive.Not
aware of neuro deficits.
Confabulates. Euphoric.
Constant smile Denies ill,
Poor judgement. Over
estimates abilities (risk for
injury)
HearingCannot hear tonal variations

CVA Assessment

CVA Residual Problems

Left CVA with Rt hemi

Usually dominant
Aphasia
Right hemiplegia
Cautious behavior

Right CVA with Left hemi

Left Hemiplegia
Spatial/Perceptual Deficits
(Provide safety)
Impulsive Behavior
Neglect Affected Side
(provide safety)

Functional Deficits After Stroke

Usually Contralateral (Opposite side hemisphere)
1. Motor - weakness

General Signs
HA
HTN
LOC

Focal Signs
Hemiparesis(weakness)
Hemiplegia(paralysis of
the left or right half of
the body)
Language disorders

Flaccid --spastic (hypertonia->resistance to stretching

of extremities)
Absence of muscle tone (Hypotonia)

2. Language (aphasia)
Middle cerebral artery of dominant hemisphere (usually
left)
Speech disorders (motor)
Language disorders - receptive and/or expressive
(frustrating)
Bleeding into the left side of brain causes aphasia & right
hemiplegia

Functional Deficits After Stroke

Usually Contralateral (opposite side hemisphere)
3. Apraxia - cortical integrative impairment (motor
association areas) Impairment in ability to perform purposeful
acts or to manipulate objects in the absence or loss of motor power
sensation or coordination

4. Agnosia - unable to recognize significance of sensory

stimuli (exVisual, auditory, olfactory, tactile). Total or
partial loss of ability to recognize familiar objects (keys, pencils,
etc) or persons

5. Hemi attention or denial - in non-dominant hemisphere

-- neglect of left side of body and its environment

CVA
Fever
Headache Memory impairment
Mental changes-confusion,
Emotional lability
disorientation
Visual defects -Homonymous
Conjugate Deviation of eyesHemianopsia-pt sees only 1/2
eyes slowly wander or move
of normal vision on same side
around
of each eye
Decrease cough/swallow reflex
Heart abnormalities
Aphasia (Left CVA)
Vomiting
Resp problems-decrease
Perceptual defects (Left CVA)
neuromuscular control
HTN
Incontinence
Apraxia -decreased learned
+Brudzinskis-neck flexion
movement-moves affected part
causes flex of thighs, hips &
but not for specific purposes
knees +Kernigs sign with
Focal neuro S/S-Paralysis,
hemorrhage-pain in hamstring
sensory loss, language disorder,
muscles after flexing thigh
reflex changes

Neuro Deficits of Stroke

Motor Deficits

Neuro Deficits of Stroke

Visual Field Deficits
Neuro Deficit
1) Homonymous hemianopsia
(loss of 1/2 visual field)

2) Loss of Peripheral Vision

3) Diplopia

Manifestation
1) Unaware of person or
objects on side of visual loss
Neglect of one side of body
Diff judging distances
Have pt turn head side to side
2) Difficulty seeing at night
Unaware of objects at the
borders of objects

Motor Deficit

Manifestation

1)Hemiparesis

1)Weakness of face, arm, leg on

same side (due to a lesion in the
opposite hemisphere)

2)Hemiplegia

2) Paralysis of face, arm, & leg

on the same side (due to a
lesion in opposite hemisphere)
3) Staggering, unsteady gait
Unable to keep feet together,
needs a broad base to stand

3)ataxia

3) Double vision

Neuro Deficits of Stroke

Motor & Sensory Deficits

Neuro Deficits of Stroke

Verbal Deficits

Manifestation

Verbal Deficit

Manifestation

4)Dyarthria

4) Difficulty in forming words

1) Expressive aphasia
Brocas Area-

5)Dysphagia

5) Difficulty in swallowing

1) Unable to form words that

are understandable; may be able
to speak in single-word
responses
nonfluent speech

Motor Deficit

Sensory Deficits
1) Paresthesia (occurs on the
side opposite the lesion)

1) Numbness & tingling of body

parts
Difficulty with proprioception

Nurse to exhibit patience & wait

for pt to finish sentence. Dont
anticipate what pt is trying to say &
finish sentence for pt

hesitant
agrammatic speech re: Order &
arrangement of words
characterized by abundant
nouns & verbs

Neuro Deficits of Stroke

Verbal Deficits

Neuro Deficits of Stroke

Verbal Deficits

Verbal Deficit

Manifestation

Verbal Deficit

Manifestation

2) Receptive aphasia
Wernickes Area-

2) Unable to comprehend the

spoken word; is able to speak
but may not make sense

3)Global aphasia

3) Combination of both
receptive & expressive aphasia

Pt may articulate normally,

speech is incoherent, malformed
or substitue words & errors in
grammer

Aphasia with impairment in

Comprehension of written &
spoken words, caused by lesion
in Wernickes center.

Loss of ability to use any forms

of written or spoken language,
involves both sensory & motor
nerve tracts.
Communicatin attempted thru

GESTURES of use of

Example-Mother in law calls

you & talks on & on for 30min
about nothing conversation makes
no sense

Neuro Deficits of Stroke

Neuro Deficits
Cognitive Deficits

Emotional Deficits

automatic words & phrases

Comparison of Hemispheric Stroke

Left-Sided
Right-Sided

Manifestation

Left Hemispheric Stroke

Right Hemispheric Stroke

Paralysis on right side of body

Paralysis on left side of body

Right visual field defects

Left visual field defects

Aphasia (expressive, receptive,

or global)

Spacial-perceptual deficits

1) Short & Long term memory loss

2) Decreased attention span
3) Impaired ability to concentrate
4) Poor abstract reasoning
5) Altered judgement

1) Loss of self-control
2) Emotional lability
3) < tolerance to stressful situations
4) Depression
5) Withdrawal 6) Fear, hostility, & anger
7) Feelings of isolation

Altered intellectual ability

Increased distractibility
Impulsive behavior & poor
judgement

Slow, cautious behavior

Lack of awareness of deficits

CVA

Homonymous Hemianopsia - loss of half of the visual field

Amorphosynthesis - turns away from the affected side
Disturbances in vision- spatial relationship.
Perceptual Disturbances - Pupil abnormalities: Frequently

CVA Assessment
General Signs
Headache, HTN, LOC

there is inequality of pupils, typically larger pupil is on the side

opposite the cerebral lesion

Sensory loss
Loss of proprioception
Aphasia
Brocas Area - speech center (expressive aphasia)
Wernickes Area - near temporal lobe
(receptive aphasia) Speech comprehension

Focal signs
Hemiparesis
Hemiplegia
Language disorders

Change in LOC
Presence of voluntary
movements
Neck stiffness
Pupils, V/S, ability to
speak
Color of face &
extremities, temp of skin,
volume of fluids

CVA - Diagnosis
Based on History & Physical Assessment, important to identify
underlying cause since treatment protocols differ based on cause
Angiography-detects vessel abnormalities. Definitive in
identifying occlusion or narrowing
Doppler Studies-Used to evaluate blood flow as well as help
pinpoint the cause of a stroke. Shows size of intracranial vessels
& direction of blood flow & locates obstructed cerebral vessel.
Info about cerebral vasculature. Useful for dx of blocked arteries
Lumbar puncture-looks at CSF contents
Thrombotic/Embolic CVA: CSF is clear, pressure is
increased. Hemorrhagic CVA: Blood usually present, pressure
is increased
EEG-looks for decreased electrical activity, focal slowing in
presence of stroke as well as other neuro diseases

Diagnostic Tools

CVA Diagnosis
Cerebral angiogram-xray visualization of internal anatomy of
heart & blood vessels after the intravascular introduction of
radiopaque contrast medium. (Iodine can cause allergic reaction,
test for hypersensitivity before radiopaque substance is used)
Carotid ultrasonogram-info about cerebral vasculature. Useful for
dx of blocked arteries
Lab Values-Serum cholesterol & Triglycerides are elevated

CT scans (also known as CAT scans)

CT or MRI differentiates CVA from other brain disorders

A series of x-rays taken at different angles

CT scan

Effectively notes intracerebral bleed better than an MRI

Shows necrotic areas in a few days
Highly sensitive to hemorrhage
Readily accessible

x-ray tube & detector spin around axis, hence

Computerized axial tomography (CAT scan)
Computer reconstructs 2 dimensional slices

MRI
Reveals evidence of ischemic stroke much earlier than CT
More sensitive to identify early brain damage
Slower than CT

Each slice like slice from loaf of bread

Slices can be stacked to form 3 dimensional images

Used after CT

Common 1st assessment of stroke (blockage or bleed)

CT Scans
Neurological uses
Stroke - Cerebrovascular Accident
Blockage or bleed hemorrhagic CVA from
Ischemic CVA
Brain tumors (larger than 2-4mm)
Enhanced with contrast material Hydrocephalus

MRI - Magnetic Resonance Imaging

Does not expose individual to x-rays
Must make sure pt does not have metal implants
(old aneurysm clip, pacemaker)
Powerful magnetic field
Atoms align with field
Radio pulses flip hydrogen atoms
Different tissues have different times to realign

Subdural hematoma
Evaluation of traumatic head injury

MRI Clinical uses for Neurology

Management in Acute Phase of CVA

Lateral or semiprone position HOB slightly elevated

AV malformationAnteriovenous malformation
Hydrocephalus
Aubacute suble hemorrhagic
CVA
Ischemic CVA with 48 hr of
symptom onset
Cerebral Contusion
Shearing injury

Dementia
Brain tumor
Cerebral atrophy
Multiple Sclerosis
Pituitary disease
Congenital anomalies

Maintain airway
Monitor for pulmonary complications-most common
cause of deaths is pneumonia
Heart abnormalities or CHF
Acute phase 48-72 hr

Management of CVA
Diuretics to decrease cerebral edema
Cerebral edema Maxes in 3-5 days. Deficits begin to
resolve as edema decreases. Gradual progression to
normal function in various areas from proximal to distal
for 1-2 years

Drug Therapy
aims to improve & restore circulation
to the brain
1. Diuretics - to <cerebral edema. Edema reaches
maximum levels 3-5 days after cerebral infarction

2. Anticoagulants-to prevent further development or

propagation of the thrombosis or embolization elsewhere
in the cardiovascular system

Anticoagulant therapy- heparin

3. Antiplatelets-platelets play a major role in thrombus

Complications
Cerebral hypoxia, cerebral blood flow
dependent on BP, cardiac output, & integrity of
cerebral blood vessels, cerebral embolism

4. Antihypertensives-reduce pressure on cerebral blood

formation and embolization

vessels. Must use caution not to decrease BP too quickly or
too low

CVA Treatments - continued

CVA Treatments
(1) Maintain airway & cerebral perfusion
(2) Prevent cerebral edema (3) Regulate temp
Remove cause, prevent complications, and
maintain function, rehabilitation to restore
function
Meds
Antihypertensives
Anticoagulants
Stool softners

As appropriate-steriods,
anticonvulsants,
diuretics

Surgical removal of clot, repair of aneurysm,

carotid endarterectomy or balloon agioplasty
(see next slide)

Surgical Management-depends on the cause of stroke

Ischemic Strokes- (1) Carotid endartectomy (2) Superior
temporal artery-middle cerebral artery (STA-MCA)
Endarterectomy-removes artherosclerotic plaque from the inner
lining of the artery, usually the carotid artery. This will open the artery
enough to re-establish blood flow
Complication-cranial nerve dysfunction-monitor for difficulty
swallowing
Balloon Angioplasty-dilate or open an obstructed blood vessel by
threading a small balloon tipped catheter into vessel. Balloon inflated
to widen blood vessel by compressing foreign material against the
walls, leaving a larger lumen, thru which blood can pass

10

CVA Treatments - Surgery continued

CVA Treatments - continued

Surgical Management-depends on the cause of stroke

Carotid endartectomy- removal of intimal lining of an artery,

done to clear major artery that may be blocked by plaque
accumulation
Complication-cranial nerve dysfunction-monitor of difficulty in
swallowing

Superior temporal artery-middle cerebral artery

(STA-MCA)
STA-MCA Anastomosis-Surgeon performs a craniotomy &
bypasses the blocked artery by making a graft or a bypass from
the superior temporal artery to the middle cerebral artery. The
procedure establishes blood flow around the blocked artery &
re-established blood flow to the involved areas. Procedure used
in only selected pt in whom it is believed that more conservative
therapy would not be beneficial

Embolectomy-surgical incision into an artery for removal or

embolus or clot

Craniotomy-surgical opening into the skull done to (1) relieve

intracranial pressure (2) control bleeding (3) remove a tumor

Complications of CVA
1. Cerebral Hypoxia
Is minimized by providing adequate oxygenation of blood to
the brain. <02 can >cerebral damage
Oxygen delivery to the tissues- > 02 to < cerebral damage
Maintaining H&H

2. Cerebral Blood Flow

Is dependent upon the BP, cardiac output, & integrity of
cerebral blood vessels
Adequate hydration (to improve blood flow)

3. Cerebral Embolism
May occur after MI, Atrial Fib, or prosthetic heart valve
The embolus will decrease blood flow into the brain & further
compromise cerebral blood flow
Correct dysrhythmias

Nursing Interventions
Improve mobility & prevent
deformities
Correct positioning & proper
bed position
Position on unaffected side with
short periods on the affected
side & back
Ex-left side hemiplegiaplace on right side more often,
short periods on left side &
back
Prevent shoulder adduction pillow under arm
Prevent hip rotation - trochanter
roll

CVA
Nursing Interventions

Patent airway
Maintain bedrest
Provide complete care
Use turn sheet
Anticipate needs
Place items within reach
Place in chair ASAP
ROM passive and active
Skin assessment-prevent
decubiti
Reposition q2h

Mattress- Flotation, firm, gel, etc.,

turn & position q2h, provide
sheepskin, massage bony
prominences
Maintain proper body alignment
Pillow and external rotation of
affected hip with trochanter rolls
Footboard or high top sneakers to
maintain proper position of feet at
right angles to legs
Use of pillows for positioning,
supporting extremities

Hand & finger position

Keep palms faced upward
Change position q2h Passive
ROM 4-5 qd
Ambulation ASAP
Achieve self care
Goal of rehab
Attain bladder control
Improve thought processes
Achieve communication &
maintain skin integrity
Sexual dysfunction

CVA
Nursing Interventions

O2 with humidity
C,T, DB q2h
Suction PRN
Keep head turned to side
Place in semi- fowlers

Assess nutrition daily with I&O,

WT, %diet, calorie count
Provide N/G or PEG feedings if
needed. Check residual q4haspiration precautions

Maintain IV fluids
Progress to soft diet prn
TPN as ordered
Aspiration precautions
Dietary consult & Speech for
swallowing

11

CVA
Nursing interventions
Establish means of
communication
Call bell pad and pencil
Nonverbal gestures
Use simple commands
Speak slowly
Explain all care
Speech therapy

Be nonjudgmental about
personality changes
Encourage family
participation
Provide diversional
activities
Praise accomplishments
Be realistic

CVA
Nursing Interventions

Assess LOC
Maintain safety
Use side rails
Restrain only as necessary
Observe for ICP
V/S &
Neuro Checks q 4 h
Seizure precautions

CVA
Nursing interventions
Family support
Begin discharge teaching
early
Physical therapy
Speech therapy
Occupational therapy
Prevent complications of
decubiti-turn & position q2h,
massage bony prominences,
render incontinent skin care,
special mattress, etc.

Prevent complications of
immobility Position to prevent
deformity
Extremities extended to
prevent flexion/contractures.
Use of pillows for
positioning
Footboard to prevent
footdrop or high top sneakers to
promote proper positioning of
feet at right angles to lets

Ensure elimination
Assess bowel sounds
Monitor bowel movements
I&O
Indwelling catheter prn
Bowel and bladder training-pt
history 1st-What was the pt
normal B/B habits?

CVA Implementation

Life Support
Positioning
Skin Integrity
ADLs
Safety Needs esp
(R)CVA secondary to
spacial perception

Nutrition
Hydration
Elimination
Emotional support esp
(L)CVA secondary to
depression, cries easily
Rehab

ADLs

CVA - Nsg Dx
*Altered (Cerebral) Tissue Perfusion R/T interruption of arterial
blood flow & possible increase in ICP
Impaired Physical Mobility & Self Care Deficit R/T hemiparesis
or hemiplegia, decreased LOC, or cognitive dysfunction
Sensory/Perceptual Alterations R/T decreased sensation, neglect,
or visual impairment
Unilateral Neglect R/T right cerebral hemisphere dysfunction
Impaired Verbal Communication R/T decreased circulation in the
brain
Impaired Swallowing R/T weakness of the muscles necessary for
swallowing and a decreased gag reflex
Total (Urinary) Incontinence & Bowel Incontinence R/T
neurologic dysfunction, decreased sensation, cognitive dysfunction,
immobility, or expressive aphasia(knows what to say but cannot
articulate the words)

Transient Ischemic Attacks -TIA

Referred to as Mini Stroke It is not a stroke at all & doesnt
typically cause permanent brain damage. It is a warning sign that a
stroke may occur in the future
Altered cerebral tissue perfusion related to a temporary neurologic
disturbance
Manifested by sudden loss of motor or sensory function
Lasts for a few minutes to a few hours
Caused by temporarily diminished blood supply to an area of the
brain
High risk for stroke

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Transient Ischemic Attack

Transient Ischemic Attack

Etiology
Strokes are caused by an
occlusion in an artery from a
thrombus or an embolus,
also caused from hypertension.

African-Americans affected more frequently as a

result of high frequency of diabetes and HTN in this
group.
Prevalence Estimated million stroke survivors in
U.S.
The number of strokes occurring in the younger
population is increasing as a result of IV drug abuse.
Those using crack cocaine experience increased
incidence of stroke due to changes in clotting
mechanism caused by the drugs or sudden increase
in systolic BP.

Risk factors include:

smoking
substance abuse (esp. cocaine)
obesity
sedentary lifestyle
high
stress levels
Sudden discontinuation of
elevated cholesterol, lipoprotein,
antihypertensive medications
triglycerides
can cause hemorrhagic stroke.
previous CVA or TIA
heavy alcohol use.

Clinical Manifestations - TIA

TIA
Visual Deficits

Sensory Deficits

Blurred vision
Diplopia
Blindness in one
eye
Tunnel vision
Motor Deficits
Transient
weakness (arm,
hand, or leg)
Gait disturbance

Transient
numbness (face,
arm, or hand)
Vertigo
Speech Deficits
Aphasia
Dysarthria
(slurred speech)

TIA
Temporary numbness face
or limbs
Slurring of words
Confusion, dizziness
Changes or blackouts in
vision
Mental Confusion
Drowsiness
Dizziness
Headache

As a general rule When S&S last longer than 24 hr, it

means than an infarction has occurred.
In most cases, the patient is left with
irreversible sensory, motor, or cognitive
deficits

Blindness in ONE eye

Diplopia
Visual field defects
Transcient loss of speech
Hemiplegia
Facial paralysis

**S&S last 10 mintues to

hours, then disappear
=TIA

TIA
Treatment

TIA
S&S last 10 minutes to hours, then
disappear

Control hypertension
Low sodium diet
Possible anticoagulant therapy
Stop smoking

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Treatment of Ischemic Stroke

Treatment of a TIA

Warning - treat to prevent stroke

Antiplatelet drugs - ex aspirin
Anticoagulant drugs - ex warfarin
avoid dehydration, hypotension
Endarterectomy for carotid plaque
Emphasis on saving brain tissue by use of thrombolytic
agents (<disability) Ex-streptokinase
Use CT scan to exclude hemorrhagic stroke (also
anticoagulant drugs, >BP)
Begin therapy within 3 hr of onset of symptoms

CVA
Permanent brain injury
Usually residual neuro
deficit
Damage of CVA ranges
from minimal to
devasting

Treatment
Ischemic
Thrombolytic agents (TPA)

Hemorrhagic
Stop bleeding and prevention of another
Surgery

All strokes
Bedrest
external stimuli
intracranial edema & pressure

TIA
Neuro deficits last less than
24 hours
Symptoms can last for a
few minutes or go on for
hours
If symptoms occur over 24
hours, it is considered a
CVA
TIA is considered a wake
up call to be alert for risk
factors toward possible
CVA

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