CEREBROVASCULAR

DISORDERS
By: Esperancita A Ferrer RN MD
 Definition
 Umbrela term that refers to a functional
abnormality of the CNS that occurs when the
normal blood supply is interrupted.
 Two major categories
 Ischemic stroke- caused by thrombus and
embolus
 Hemorrhagic stroke- caused commonly by

hypertensive bleeding
 Etiology
 Atherosclerotic Plaque or thrombosis
 Cardiac causes of emboli include: AF, Mitral
valve prolapse, infectious endocarditis, &
prosthetic heart valve
 Risk Factors
MEDICAL CONDITION
 Hypertension

 Cardiac Disorders – CHD, Valvular conditions,

endocarditis
 Atrial Fibrillation

 Diabetes Mellitus

 Hyperlipidemia

 Carotid Stenosis

 Prior Hx of TIA or Stroke

MODIFIABLE
 Cigarette Smoking

 Alcohol Abuse

 Physical Inactivity

 Cocaine Use

NONMODIFIABLE
 Age

 Gender

 Heredity

 Ethnic Background
CEREBROVASCULAR
ACCIDENT
ISCHEMIC STROKE
 Sudden loss of function
resulting from
disruption of the blood
supply to part of the
brain.
 Types:
 Cerebral thrombosis
 Cerebral Embolism
 Cerebral Thrombosis
 Formation & development of a blood clot or
thrombus in a cerebral vessel primarily the arteries
 Highly associated w/ Atherosclerosis & Hypertension

 Plaques – narrowing & stenosis

 Sites:

LARGE ARTERY THROMBOTIC STROKES

SMALL PENETRATING ARTERY THROMBOTIC
STROKE – Most common (Lacunar Stroke)
 Cerebral Embolism
 Occlusion of a vessel when blood clots, tumor,
fat, bacteria, or air are dislodged from site of
formation & carried by the bloodstream to
occlude small, distal cerebral arteries
 CARDIOGENIC EMBOLIC STROKE
 Associated w/ cardiac dysrhythmia, AF
CRYPTOGENIC STROKE
(unknown)

OTHERS:
Illicit drug use, spontaneous dissection of carotid
or vertebral arteries
 Pathophysiology
Cerebral blood flow less < 25ml/100
g/min
Anaerobic
metabolism
Nueron incapable of
Produce lactic acid producing enough ATP

Acidosis Ion imbalance

↑ intracellular Ca Release of glutamate

Cell membranes and proteins

breakdown
Formation of free radicals
Protein production decreased

Cell injury and death

 Penumbra region – an area of low cerebral
blood flow early in the cascade
 The brain requires a constant supply of
glucose and oxygen
 No reserve oxygen
 Normal cerebral function can continue only 8
to 10 seconds after ischemia
 Irreversible damage occurs after 6 to 8 minutes
 Transient Ischemic Attack
 Temporary episode of focal neurological
dysfunction presumed to be vascular in origin
 Begins rapidly & resolves completely
 Caused by occlusions in either carotid artery
system or the vertebrobasilar system
 Duration: 2-15min less than 24h
 Stroke in evolution
 A progressive or continuous neurological
impairment over a period of sveral hours or
days.
 Extension of growth of thrombus or multiple
emboli that causes a gradual stepwise
impairment in cerebral blood flow &
neurologic deficit
 Diagnostic Evaluation
 CT Scan
 MRI
 PET Scan
 Angiography
 12 Lead ECG
 Carotid ultrasound
Neurologic Deficits
Visual Field Deficits
 HOMONYMOUS
HEMIANOPSIA
Loss of half of visual field
Neglect of one side of the
body
 LOSS OF
PERIPHERAL
VISION
Difficulty seeing at night
Unaware of borders of
object
DIPLOPIA
Double Vision
 Motor Deficits
 HEMIPARESIS
Weakness of face, arm, & leg on the same side (due to a
lesion in the opposite hemisphere
 HEMIPLEGIA

Paralysis of face, arm, & leg on the same side (due to a

lesion in the opposite hemisphere
 ATAXIA

Staggering unsteady gait

 DYSARTHRIA

Difficulty in forming words

 Dysphagia

Difficulty in swallowing
 MOTOR LOSS
UPPER MOTOR LOWER MOTOR
NEURON LESION NEURON LESION
 Loss of voluntary  Loss of voluntary

control control
 Increased ms tone  Decreased muscle tone

 Muscle spasticity  Flaccid ms paralysis

 No muscle atrophy  Muscle atrophy

 Hyperactive abnormal  Absent or decreased

reflexes reflexes
 Early:
Flaccid paralysis loss of DTR
 48h:

Increased tone & spasticity

 SENSORY DEFICITS
PARESTHESIA
Numbness & tingling of extremity
Difficulty with proprioception (position sense)
Agnosia- deficit in recognition previously
familiar objects
 VERBAL DEFICITS
 Expressive Aphasia BROCA’S APHASIA
Unable to form words that are understandable
 Receptive Aphasia WERNICKE’S APHASIA

Unable to comprehend the spoken word; can speak but

makes no sense
 Global Aphasia (mixed)

Combination
 Dysarthria

Difficulty speaking
 Apraxia

Inabilty to perform a previously learned action

a. EXPRESSIVE APHASIA

BROCA’S APHASIA

DOMINANT FRONTAL LOBE

REMEMBER: BROCA’S IS
BROKEN SPEECH

INTACT COMPREHENSION
 b. RECEPTIVE APHASIA
WERNICKE’S APHASIA
DOMINANT TEMPORAL LOBE

REMEMBER: WERNICKE’S IS WORDY

BUT MAKES NO SENSE

No comprehension but can hear will answer wrong

 COGNITIVE DEFICIT
 Short or long term memory loss
 ↓attention span
 Impaired ability to concentrate
 Poor abstract reasoning
 Altered judgment

Frontal Lobe affected- learning capacity, memory

impaired
 EMOTIONAL DEFICIT
 Loss of self-control
 ↓tolerance to stressful situations
 Emotional lability
 depression
 Withdrawal
 Fear, hostility and anger
 Feelings of isolation
 Comparison of Left & Right Hemispheric
Stroke
Right Hemisphere Left Hemisphere
LANGUAGE Intact Receptive &
Expressive Aphasia
SPEECH Dysarthria Dysarthria
SENSATION Left sensory loss Right sensory loss
PERCEPTION Decreased awareness Normal awareness of
of left side of the body the right side of the
Loss of Depth perception body
Disoriented TPP

VISION Left Visual Field Deficit Right Visual Field Deficit

BEHAVIOR Impulsive Behavior & Poor Slow cautious behavior
Judgment

MOVEMENT Left sided paralysis or Right sided paralysis

paresis or paresis
Apraxia Apraxia less common
 Medical Management
 Anticoagulant
warfarin (Coumadin)
 Antiplatelet aggregators
aspirin, clopidrogel (Plavix), ticlopidine
(Ticlid)
 Statins
symvastatin
 Antihypertensive
ACE inhibitors, Thiazide diuretics, Ca channel
blockers, Vassopressors
 Thrombolytic Therapy
eg. recombinant t-PA
 Binds w/ fibrin converts plasminogen into plasmin
w/c stimulate fibrinolysis of atherosclerotic lesion
 Leads to decrease in size & improvement in
functional outcome
Complication: Bleeding
 Inclusion Criteria
 Onset of Sx:
 Within 3h IV tPA
 Within 6h IA tPA
 Ischemic Stroke
 No hemorrhage noted on CT scan of the brain
 Clearly defined time of onset
 Exclusion Criteria
 CT demonstrates early signs of infarction or
hemorrhage
 Uncontrolled HPN unresponsive to IV or oral agent
(Sys. >185 Dias. >110 mmHg)
 Glucose level >400 mg/dl
 Coagulopathy
 Heparin w/in past 48h
 On Warfarin
 Elevated PTT or PT
 Platelet Count <100,000
 Hx of previous ICH, Head Trauma or stroke
within the last 3 months
 GI or GUT hemorrhage in the past 3 wks
 Hx of major Surgery in the past 2 wks
REMEMBER!

ANTICOAGULANTS
ANTIPLATELET

THROMBOLYTICS

ARE CONTRAINDICATED
IN HEMORRHAGIC STROKE
 Osmotic Diuretics
Mannitol
Decrease ICP. Establishes osmotic gradient
across BBB that deplete IC & EC Fluid
volume
 Corticosteroids
Dexamethasone
Decrease inflammation & Vasogenic Cerebral
edema
Surgical Management

 Carotid Endarterectomy
Nursing Assessment
 Voluntary or involuntary movements, tone of
muscles, presence of DTR (reflex return signals
end of flaccid period & return of ms tone)
 Mental status, cranial nerve function, sensation &
proprioception
 Monitor bowel & bladder function/control
 Monitor Effectiveness of anticoagulant therapy
 Level Function
 Skin breakdown, contractures & other
complications of immobility
Skin Break Down
Contracture
 FOOT DROP
 Nursing Diagnosis
 Impaired Physical Mobility
 Acute Pain
 Self Care Deficit: Bathing Dresssing Toileting
 Disturbed sensory perception
 Imbalanced Nutrition: Less than Body
requirements r/t impaired swallowing
 Impaired Urinary Elimination
 Impaired Verbal Communication
 Risk for Impaired Skin Integrity
Nursing Interventions
Acute Phase
 Ensure patent airway
 Keep patient in lateral position

 Monitor VS, GCS, pupil size

 IVF therapy with caution as not to increase

ICP
 NGT inserted

 Supplemental O
2
 Medications: Steroids, Mannitol, Diazepam
 Improve Mobility and prevent joint
deformities
 Functional position of all extremities to prevent
contractures
 Trochanter roll from crest of ilium to the midthigh
(external rotation of hip)
 Place pillow under axilla of affected side (adduction of
affected shoulder)
 Hand is placed in slight supination- “C”
 Distal joints should be higher than proximal joints
(edema & fibrosis)
 Avoid excessive pressure on ball of foot after spasticity
develops
 Turn every 2 hours
 Place in prone position 15-30 minutes daily & avoid sitting up
in chair for long periods (knee &`hip flexion contractures)
 Splints & Braces support flaccid extremities/spastic extremities
 Volar splint (wrist)
 Sling (shoulder subluxation)
 High top sneaker (ankle/foot support)
 Passive ROM 4 – 5x/day
 Use unaffected extremity to move affected one
 Assist w/ Ambulation (done only when sitting balance & standing
balance achieved), have client wear walking shoes or tennis shoes
Transfer / Ambulation Assisting Belt
 Preventing shoulder pain
 Never lift by the flaccid shoulder
 Proper movement & positioning
 Flaccid arm is positioned on a table or w/
pillows while px is seated
 Use arm sling, when ambulating
 ROM exercises
 Medications:
 Amitriptyline hcl (Elavil)
 Lamotrigine (Lamictal)
 Enhance self-care
 Done when can sit alone
 Encourage use of assistive devices chart 62-3 p2219
 Carry out ADL’s on the unaffected side but not to
neglect affected side
 Encourage to look toward the affected side
 Adjust environment (call light, tray) to side of
awareness; visual field defect approach univolved
side
 Clothing is placed on the affected side first, 1 size
larger, Use large mirror – client aware what is put on
 Personal care items, urinal & commode are nearby
Manage sensory-perceptual difficulties
 Approach patient on the unaffected side
 Place all visual stimuli on the unaffected side
 Use natural or artificial lighting
 Homonymous Hemianopsia – turns away from
affected side of the body & tends to neglect that side
(Amorphosynthesis)
 Encourage to turn the head to the affected side to
compensate for visual loss
 Loss of peripheral vision
 Place objects in the center field of vision
 Diplopia: double vision
 Patching one eye alternate
Assisting w/ nutrition
 Test for pharyngeal reflexes before feeding
 Place food on the UNAFFECTED side
 Provide smaller bolus of food
 May start with thick liquid or pureed diet
 Position sitting during feeding, maintain position 30-
45 minutes after meals
 Instruct client to tuck chin towards chest when
swallowing
 Chew on unaffected side
 Manage tube feedings if prescribed
 Check for residual volume
 Raise bed at least 30 degrees
 Check for tube placement
Help patient attain bowel and bladder
control
 Intermittent catheterization is done in the acute
stage
 Offer bedpan on a regular schedule
 High fiber diet and prescribed fluid intake (prevent
straining)
 Establish regular time for toileting (usually after
breakfast)
Improve communication
 Anticipate the needs of the patient
 Offer support

 Provide time to complete the sentence

 Provide a written copy of scheduled

activities
 Use of communication board

 Give one instruction at a time

 Provide consistent schedules, routines

 If aphasic
 Face the patient and establish eye contact
 Speak in normal manner and tone

 Use short phrases and pause between phrases

 Limit conversation to practical and concrete

matters
 As the patient uses and handles an object, say

what the object is

 Be consistent in using same words and gestures

each time you give instructions or asks questions

 Keep extraneous noises and sounds to a minimum
Maintain skin integrity
 Regular turning and positioning
 Keep pressure off bony prominences
 Proper Hygiene, avoid use of hot water, exposure to
cold & low humidity- increase dryness prone to
irritation
 Use of moisturizing lotion
 Kept clean & dry from urine, feces sweat
 Avoid massage over bony prominences
 Provide adequate nutrition (calories, CHON,
Vitamins, Iron)
 Avoid skin trauma
 Smooth firm wrinkle free linen to lie & sit on
 Mechanical devices for reducing pressure on body parts:
Sheep skin. Heel protector, egg crate mattress,
Mechanical Devices
 Heel protector made of
sheep skin

 Egg crate mattress

HEMORRHAGIC
STROKE


cover
DAP
Meninges: protective triple layer

 Dura mater = outer layer

Arachnoid = middle layer

 Pia mater = inner layer

 Cerebral spinal fluid circulates

within the Arachnoid
  Caused by bleeding into the brain tissue, ventricles or the
subarachnoid space
Types:
 PRIMARY

INTRACEREBRAL
HEMORRHAGE (80%)
 Spontaneous rupture of small
blood vessels
 Cause: HPN
 SECONDARY
INTRACEREBRAL
HEMORRHAGE
 Cause: Arterial Venous
Malformation, intracranial
aneurysm, intracranial
neoplasm, medications
(anticoagulants,
amphetamines)
Intracranial Cerebral Aneurysm
 Dilatation of the walls
of a cerebral artery
 Usually occur at
bifurcations of the large
arteries
 Arteriovenous Malformations
 Abnormality in the
embryonal development
that leads to a tangle of
arteries & veins in the
brain that lacks a
capillary bed w/c leads
to dilatations of a. & v.
& eventual rupture.
 Common in young
people
LOCATION: Cerebral
lobes, basal ganglia,
thalamus, brainstem
(pons), cerebellum
 SUBARACHNOID HEMORRHAGE
 Cause
 AVM Most common
 Intracranial aneurysm
 Trauma
 HPN
 Pathophysiology
Causes: AVM, Aneurysm,
subarachnoid space

Bleedin
g
Brain exposed to ↑ICP Entry of blood
blood into subarachnoid
space
Disrupted brain
Compress and
metabolism
injure brain
injury
↓ cerebral perfusion Vasospas
m
Secondary ischemia
 Clinical Manifestations
 Neurological Deficits
 Vomiting

 Sudden change in LOC

 Focal Seizure

Leaking Aneurysm or AVM

 Sudden onset severe headache assoc. N/V, no neurologic deficit

Subarachnoid Hemorrhage
 Sudden severe headache, meningeal signs (nuchal rigidity,

photophobia, irritability), neurologic dysfunction

 Diagnostic Evaluation
 CT Scan
 Cerebral Angiography
 Lumbar Puncture ( if no increase in ICP)
 Medical Management
 Goals:
 To allow brain to recover from initial bleeding
 To prevent or minimize the risk for rebleeding
 To prevent or treat complications
 Manage vasospasm
 Calcium-channel blockers
 Nimodipine, Verapamil, Nifedipine
 Manage ↑ICP
 Antihypertensive

 Stool softeners
 Surgical Management
 Craniotomy – to
evacuate clot
(>3cm and GCS
below 14)
 Clipping &

ligation of
aneurysm
 Complications
 Cerebral Hypoxia & Decreased Blood Flow
 Vasospasm - ↑ Vascular resistance, impedes
CBF causes Brain Ischemia & Infarction
 Occur 4-14d after initial bleed
 Increased ICP
 Systemic HPN
 Nursing Diagnosis
 Risk for Injury r/t potential rebleeding,
vasospasm, hydrocephalus
 Ineffective Tisssue Perfusion r/t disease
process ans vasospasm
 Acute Pain secondary to cerebral hemorrhage,
meningeal irritation, surgical procedure
Nursing Interventions
 To prevent or minimize the risk for
rebleeding & control BP
 Bed rest, HOB elevated, ↓ environmental
stimuli, avoidance of neck flexion & Valsalva
maneuver, no caffeine
 Management of HPN w/ nitroprusside
(Nipride) close monitoring to prevent
precipitous drop in BP aggravating ischemia
 Prevention of Vasospasm w/ Ca channel
blockers such as Nimodipine
 Prophylactic seizure management contoversial.
Phenytoin (Dilantin), fosphenytoin (Cerebyx)
phenobarbital (Luminal)
 Modify activity to prevent complications
 PRECAUTIONS: reduce envt. stimuli, limit
stress, & ↓ risk of rebleed or ↑ in ICP
 CBR HOB elevated 30 degrees
 Maintain quiet envt, restrict visitors
 Avoid activities that ↑ ICP: straining, sneezing,
acute flexion/rotation of neck, cigarette smoking,
Valsalva maneuver
 Administer Mannitol monitor for Hyponatremia
 Administer stool softeners prevent straining, avoid
rectal temp, enemas, suppositories, teach to exhale
thru mouth during defacation
 Avoid caffeinated beverages & extremes of Temp
 Provide for self care activities: Bathing, Feeding
 SEIZURE PRECAUTIONS: padded side rails,
suction equipment, & oral airway at bedside
 Assess for signs of ↑ ICP: Cushings Triad-

slow irregular respiration (Cheyne’s Stoke

pattern, apneustic, ataxic), Bradycardia,
Elevated BP
 Maintain BP parameters: treated SBP 160-180

Untreated: SBP 120 – 140

 Thigh high elastic compression stockings to ↓

incidence of DVT resulting from immobility.

S/Sx DVT: tenderness, redness, swelling,
warmth & edema
TED hose stockings
 Maintaining Cerebral Perfusion
 Monitor neurologic status: LOC pupillary
reaction, motor & sensory fxn, CN fxn,
speech, presence of HA
 Assess for subj neurologic complaints specific
to ↓ perfusion (diplopia, HA, blurred vision) &
recognize peak time for vasospasm occurrence
4-12 days after bleed
 Assess for S/Sx of vasospasm: insidious onset
of confusion, disorientation, ↓ LOC or focal
deficit
 Document findings: subtle changes-pronator
drift 1st sign of deterioration
 Adequate O2
 Hgb & Hct acceptable levels
 Adequate hydration to reduce blood viscosity
& improve blood flow
 Observe for seizure activity (compromise
blood flow)
 Reducing Pain
 Assess level of pain
 Analgesics, Opiod check CNS depression ↓
RR ↓ PR
 Distraction & relaxation techniques
 Elevate HOB
 Cool compress head
 Provide quiet dark environment
 Assess for unrelieved or ↑ pain, neurologic
signs: nuchal rigidity, photophobia, changes in
vision- signal hemorrhage, meningeal irritation
THANK YOU