 It is a sudden loss of function resulting from disruption of the blood supply to a

part of the brain. It is a result of long standing cerebrovascular disease.

(Smeltzer)
 It is an acute focal neurologic deficit caused by a vascular disorder that
injures brain tissue. It is caused by cerebrovascular obstruction by thrombosis
or emboli. (Porth)
 5 types according to cause
 Large artery thrombotic strokes-due to atherosclerotic
plaques in the large blood vessels of the brain.
 Small Penetrating Artery Thrombotic Strokes-affects
one or more vessels and are the most common type of
ischemic stroke.
 Lacunar Strokes-due to the cavity that is created once
the infracted brain tissue disintegrate
 Cardiogenic Embolic Strokes-associated with cardiac
dysrythmias usually atrial fibrillation.
 Cryptogenic-no known cause
 Causes of Ischemic Stroke

 D,E - Large Artery Stroke

 F - Small Artery Stroke

 A,B,C - Embolic Stroke
 CLINICAL MANIFESTATIONS
 visual field
 hemianopia
 loss of peripheral vision
 diplopia
 motor deficits
 hemiparesis
 hemiplegia
 ataxia
 dysarthria
 dysphagia
 sensory deficits
 paresthesia
 verbal deficits
 expressive aphasia
 receptive aphasia
 global aphasia
 cognitive deficits
 short and long term memory loss
 decreased attention span
 impaired ability to concentrate
 poor abstract reasoning
 altered judgment
 Patophysiology of Ischemic Stroke
etiology: Risk Factors:
Idiopathic HPN advanced age cocaine use
CAD heart dse cigarette TID hx of stroke
smoking
DM polycythemia vera
sedentary lifesyle
hypercholesterolemia

Arterial wall injury

Atherogenesis

Non-infectious inflammation

Adhesion of circulating monocytes

Release of chemical mediators

 … from non infectious inflammation

Release of molecular factors

Platelet derived eleosanoids cytokines nitric oxide
growth factors

Proliferation and migration of smooth muscle cells

In the tunica intima during atherogenesis

Thickening of blood vessel

Decreased lumen size

 .. From release of chemical mediators

Leukotrienes, histamine, prostaglandin interleukin-6

vascular permeability liver

Na, Ca, H2O, CHON and humural production of intracellular

Substance deposition adhesion mol. 1 & vascular adhesion
mol. 1
Thickening of blood vessel
attraction & binding of more mono-decreased lumen size cytes to
endothelial cells & enter the
subendothelial space

monocytes: transformed into a phagocytic stage

(macrphage)

ingestion of LDL by macrophage

oxidation of LDL
 Oxidation of LDL’s

Formation of foam cells atherogenesis progression

Becomes of the primary compmonent of fatty streak

Molding up of plaques in the vessel wall

Plaque destabilization thickening of the blood vessel

Has cytotoxic properties chemoattractant inhibits ingestion by

That promotes endothelial macrophages
Injury
increased accumulation of plaque
Plaque destabilization thickening of blood vessels

Rupture of atherosclerotic plaques decreased cerebral bld flow

Exposure of endothelial collagen to bloodstream

Platelet: activated with platelet adhesion

Zymogen: converted into an activated coagulation factor

Factor X: converts prothrombin to thrombin

Thrombin: leaves fibrinopeptides from fibrinogen

Fibrin monomeres, polymerizes & converts factor XIII & XIIIa

Thrombus formation

Production of enlarging thrombosis

Atherotrombotic occlusion cerebral-arterial primary small vessel
Of larger thrombosis atherothrombosis cardiovascular
adhesion
breaking-off of embolus

Embolus reaches an arterythat is too narrow to pass through

And becomes dislodged

Blood flow to arteries becomes occluded

A B C
 A
Signs and symptoms of CVA by involved cerebral artery

a.1 a.2 a.3 a.4

Ant. Cerebral artery

Infarction of the medial aspects

Paralysis of contralateral legs

Impaired gait
Paresis of contralateral arms
Aphasia
Decision-making problems
Urinary incontinence
Cognitive and affective d/o
Easily distraction
Slowness of thought
Vasomotor paresis
Lack of spontaneity
 a.2
Middle cerebral artery

Infarction of the left hemisphere and deeper structures of the frontal,

parietal, and temporal lobes

Contralateral hemiplegia
Aphasia
Hemonopia
Altered LOC
Vasomotor paresis and irritability
Hemiattention
Sensory impairment
 a.3
Post. Cerebral artery

Occipital lobe thalamus cerebral peduncle

Hemianopia loss of sensory modalities abn. Oculomotor

Perseveration spontaneous pain nerve impulse
Memory def. Aphasia
(temp. lobe) hemiparesis
 a.4
Basilar vein
Infarction on the following:

Cerebellum pons med.oblongata midbrain

Loss of bal. Loss of loss of reflexes visual and

ataxia respi. Control auditory impairment
Intention tremor
 B
central core of hypoxia

Oxy. Depletion glucose depletion cell-ATP exhaustion

In seconds (2-4 mins.) (4-6 mins.)

anaerobic metabolism lactic acid & fatty acid

accumulation

cell death
 C
Ischemia penumbra region

Failure of cellular ionic gradients

Efflux of K influx of NaCl & H2O influx of Ca

inc. EC K dec. EC Na cellular cytotoxic Ca toxicity

edema

Neuron depolarization glutamate receptor cell break-

stimulation down

Further Ca reflux through voltage release of glutamate

Gated channel & accumulation of
free radicals

excitotoxicity
Ca toxicity further inc. in NaCl into the cell

Activation of cellular subs. Cellular edema

Severe cellular damage

Cell death
BBB breakdown

Vasogenic edema

Inc. ICP

Brain herniation

Neurons, nerve tracts, and cerebral arteries compression

Persistent ischemia
 Irreversible brain damage

Failure of CNS auto-regulation

Multiple organ failure

DEATH
 ASSESSMENT AND
DIAGNOSTIC FINDINGS
 Airway patency
 cardiovascular Status (BP, HR, PR)
 CT Scan-to determine if it is ischemic or hemorrhagic
 12 lead ECG and carotid ultrasound – to identify the source of thrombi
or emboli
 MEDICAL MANAGEMENT
Thrombolytic Therapy
 thrombolytic agent
 dissolving the blood clot that is blocking blood flow to the brain.
 t-PA ( tissue-Plasminogen activator)
 thrombolytic substance made naturally by the body
 it works by binding to fibrin and converting plasminogen to plasmin which
stimulates fibrinolysis of the antherosclerotic lesion.
Initial Management:
 CT Scanning
 determination of wether the patient,s meets all he criteria of t-PA
Contraindications:
 symptoms onset greater than 3 hors PTA
 a patient who is anticoagulated
 a patient who has had recent MI
 a patient who has had any type of intracranial pathology (stroke, head
injury, trauma)
Assessments before the use of t-
PA (National Health Stroke Scale)
 the patient is weighed to determine the dose of t-PA
 minimum dose: 0.9mg/kg
 maximum dose: 90 mg
 loading dose: 10% of the calculated dose and administered over 1
minute
 remaining dose is administered over via infusion pump
 after it is completed, the line is flushed with 20 ml of Normal
Saline
 Management for t-PA

 vital Signs are Obtained (every 15 mins for the first 2

hours and every 30 mins for the next 6 hours0
 BP should be maintained with systolic pressure of 180
mmHg and diastolic pressure of 100 mmHg
 common side effect: bleeding
Therapy for patient with ischemic stroke not receiving t-PA
Management:
 anticoagulant administration
 careful maintenance of cerebral hemodynamics to maintain cerebral
perfusion
 if ICP occur: to reduce, administer osmotic diuretic
 maintain PaCO2 within normal range of 30-35 mmHg
 position patient to avoid hypoxia
 elevate the head of the bed to promote venous drainage and to lower ICP
 Endarterectomy for Prevention of Ischemic Stroke
 Carotid Endarterectomy
 management for TIA
 removal of an atherosclerotic plaque or thrombus from the carotid artery to
ptevent stroke
 Management

 maintain adequate blood pressure levels immediately after

operating period
 hypotension is avoided to prevent cerebral ischemia and
thrombosis
 Na Nitroprusside-used to reduce the blood pressure to the
previous level of stroke.
NURSING DIAGNOSES and
their INTERVENTIONS
 Impaired Physical Mobility r/t
hemiparesis, loss of balance and
coordination, spasticity and brain injury
 correct positioning to prevent contractures
 maintain good alignment by assisting the
patient
 change position every 2 hours
 Place patient in a side lying position. A
pillow is placed between the legs before the
patient is turned to promote venous return
and prevent edema
 patient is placed in prone position for 15-30
minutes at several times.
 Acute pain r/t hemiplegia

 never lift the patient by the flaccid shoulder

 flaccid arm is positioned with pillows while the
patient is seated
 encourage ROM exercises
 avoid strenuous movements
 instruct to interlace the fingers, place the
palms together and push and clasp hands slowly
forward to bring the scapulae forward
 instruct patient to flex the affected wrist at
intervals and move all joints of the affected
fingers
 elevate hand and arm to prevent edema in the
hand
 Self Care deficits r/t stroke sequence

 encourage self care

 personal hygiene is encouraged
 Disturbed Sensory Perception r/t altered
sensory perception

 patient with decreased field of vision should be

approached on the side where visual is intact
 all visual stimuli should be placed placed on
unaffected side
 make an eye contact with the patient and draw
attention to the affected side by encouraging to
move the head
 increase the natural lighting in the room
 provide eye glasses
 Impaired Swallowing

 observe patient for coughing, food dribbling and

food retained for long periods in the mouth
 provide soft diet
 use total parenteral nutririon
 if patient is unable to reume oral intake by mouth,
NGT is inserted as ordered
 Incontinence r/t flaccid
bladder
 ensure elimination
 monitor bowel movements
 monitor I and O
 provide indwelling catheter care
Disturbed thought process r/t
brain damage
 nurse must be supportive
 observe patient performance and progress
 give positive feedback
 convey an attitude of confidence and hope
Disturbed thought process r/t
brain damage
 be sensitive to the patient’s reactions and need and
respond to them in an appropriate manner
 always treat them in a polite manner
 provide strong and moral support and understanding
to allay anxiety
 eatablish means of anxiety
 use simple commands
 speak slowly
 explain all care that are to be done
 risk for impaired skin integrity r/t
hemiparesis

 regular turning and positioning to minimize pressure

and skin break down
 patient’s skin must be kept clean and dry
Interrupted family process r/t
caregiving burdens

 provide support to the family

 love and interest must be present in the therapy
 Sexual dysfunction r/t neurologic
deficit on fear of failure
 provide relevant information, education, reassurance, and
adjustment of medications
 counsel regarding coping skills
 suggest for alternative position
A hemorrhagic stroke is damage to brain
tissue resulting from bleeding inside the
skull.
There are two main types of hemorrhagic
strokes:
1.intracerebral hemorrhage- occurs within
the brain.
2.subarachnoid hemorrhage - between the
inner layer (pia mater) and middle layer
(arachnoid mater) of the tissue covering the
brain (meninges).
Sites of Brain Hemorrhage
PATHOPHYSIOLOGY

ETIOLOGY PREDISPOSING FACTORS

>idiopathic >AVM

>aneurysm

>HPN

>head trauma

>atherosclerosis

spontaneous rupture of vessels

leakage of blood

Intracerebral hemorrhage Subarachnoid hemorrhage

Resistance of Irritation of Imbalance of barain

the brain tissue brain tissues components in the cranial
to expansion of vault
bleeding

hematoma swelling

Increased
ICP
 spasms edema herniation hydrocephalus

decreased cerebral blood flow

decreased perfusion

ischemia

altered neurological function affectation of cranial nerves

coma

death
>SUBARACHNOID HEMORRHAGE
A subarachnoid hemorrhage is sudden bleeding into the space (subarachnoid space)
between the inner layer (pia mater) and middle layer (arachnoid mater) of the
tissue covering the brain (meninges).

>INTRACEREBRAL HEMORRHAGE
An intracerebral hemorrhage is bleeding within the brain.

>ATRIOVENOUS MALFORMATION(AVM)
is an abnormal collection of blood vessels. Normally, oxygenated blood is
pumped by the heart through branching tubes called arteries to the brain,
where it enters a fine network of tiny vessels called capillaries. It is in these
capillary beds where the blood nourishes the tissues. Arterial-Venous
Malformations are areas that lack the tiny capillaries.

>ANEURYSM
is localized, blood-filled dilation (bulge) of a blood vessel caused by disease or
weakening of the vessel wall. Aneurysms most commonly occur in arteries at the base
of the brain (the circle of Willis) and in the aorta (the main artery coming out of the
heart), a so-called aortic aneurysm. The bulge in a blood vessel can burst and lead to
death at any time, much like a bulge in an over-inflated inner tube. The larger an
aneurysm becomes, the more likely it is to burst.
A.ANEURYMS B.AVM
CLINICAL MANIFESTATIONS
(Intracerebral)
 severe headache
 weakness
 paralysis
 numbness
 loss of speech or vision
 confusion
 Nausea
 vomiting
 Seizures
 loss of consciousness
ASSESSMENT AND DIAGNOSTIC FINDINGS
 CTscan
-determine the size and location of hematoma
-presence or absence of venrticular blood
-hydrocepalus
 magnetic resonance imaging (MRI)
-the procedures can also detect how much brain tissue has been damaged
and whether pressure is increased in other areas of the brain.
 Spinal tap (lumbar puncture)
-can detect any blood in the cerebrospinal fluid.
-is not usually performed in intracerebral hemorrhge, it can cause
herniation of the brain
 Cerebral angiography
-usually performed within 72 hours to confirm the diagnosis and to identify
the site of the aneurysm or arteriovenous malformation
Hunt-Hess classification system
MEDICAL MANAGEMENT

•Bed rest with sedation

•Analgesics (codeine, acetaminophen)
•Elastic compression stockings

Managing Complications;
•cerebral hypoxia and decreased blood flow
-provide adequate oxygenation (supplemental oxygen)
-IV fluids for adequate hydration
•Vasospasm
-administering calcium channel blockers nimodipine
•Increased ICP
-ventricular catheter drainage
-mannitol
-lumbar puncture
•Systemic Hypertension
-antihypertensive therapy (labetalol ,nicardipine,
nitroprusside)
SURGICAL MANAGEMENT

 extracranial-intracranial arterial bypass

-establish collateral blood supply to allow surgery in the aneurysm
 Endovascular treatment
-occlusion of the patent artery
 Aneurysm coiling
-obstruction of the aneurysm site with a coil
ASSESSMENT
-Altered level of consciousness
-Sluggish papillary reaction
-Motor and sensory dysfunction
-Cranial nerves
deficits(extraoccular eye
movements, facial droop,
presence of ptosis)
-Speech difficulties and visual
disturbance
-Head ache and nuchal rigidity
NURSING DIAGNOSIS
Ineffective cerebral tissue
perfusion R/T bleeding
Disturbed sensory perception R/T
medically imposed
restrictions(aneurysm precaution)
Anxiety R/T illness and/or
medically imposed
restrictions(aneurysm precaution)
PLANNING
Improved cerebral perfusion
Relief of sensory and
perceptual deprivation
Relief of anxiety and the
absence of complications
INTERVENTION EVALUATION
-Monitor for neurologic -Demonstrates intact
deterioration occurring from neurologic status and normal
recurrent bleeding ,increased vital signs and respiratory
ICP or vasospasm, patterns
-V/S monitoring -Demonstrates normal sensory
-Papillary response and motor perception
function are checked hourly -Exhibits reduced anxiety level
-Exhibits absence of
complications
-Providing non stimulating
environment
-Prevent increases of ICP
elevation of head 15 - 30
-bed rest
-avoid activity that requires
exertion
-Prevent further bleeding
-Keeping patient well informed
of the plan of care appropriate
reassurance