CEREBROVASCULAR ACCIDENT

(STROKE)
Ns. Frengki Apryanto, S.Kep.,M.Kep
• A cerebrovascular accident, or stroke, is a
prolonged interruption in the flow of blood
through one of the arteries supplying the
brain.
• Stroke is the third leading cause of death
among adult Americans.
• Each year, approximately 780,000 Americans
have a new or recurrent stroke (American
Heart Association/American Stroke
Association, 2008).
• Brain and cerebral nerve cells are extremely
sensitive to a lack of oxygen; if the brain is
deprived of oxygenated blood for 3 to 7 minutes
during stroke, both the brain and nerve cells
begin to die.
• Once these cells are destroyed, the outcome is
irreversible. Although the site of the cellular
damage is located in the brain, the consequences
are widespread.
• About one third of stroke victims die; most
survivors have permanent disabilities.
• Permanent neurologic deficits have a profound
physical, emotional, and financial effect on the
client and the family.
 Pathophysiology and Etiology
• There are two main types of stroke: ischemic
strokes and hemorrhagic strokes.
• Ischemic strokes occur when a thrombus or
embolus obstructs an artery carrying blood to
the brain (Fig. 1); about 80% of strokes are the
ischemic variety.
• Hemorrhagic strokes occur when a cerebral
blood vessel ruptures and blood is released in
brain tissue (Fig. 2).
 FIGURE 1. In ischemic stroke, arterial blood flow to part of the
brain is blocked by a clot that forms in a cerebral artery (thrombotic
stroke) or by a clot that travels to and lodges in a cerebral artery from
another location (embolic stroke). (From the Anatomical Chart
Company.)
 FIGURE 2. Cerebral hemorrhage. A postmortem specimen
shows bleeding into the basal ganglia. (From Rubin, R., & Strayer, D. S.,
eds. [2008]. Pathology: Clinicopathologic foundations of medicine
[5th ed.]. Baltimore: Lippincott Williams & Wilkins.)
• When ischemic strokes occur, glucose and oxygen
to brain cells are reduced.
• The reduced glucose quickly depletes the stores
of adenosine triphosphate (ATP), resulting in
anaerobic cellular metabolism and the
accumulation of toxic by-products such as lactic
acid.
• Although some brain cells die from anoxia, the
lack of oxygen destroys additional brain cells by a
secondary mechanism.
• Oxygen depletion triggers the release of glutamate, an
excitatory neurotransmitter that activates neuronal
receptors known as N-methyl-D-aspartate (NMDA)
receptors.
• The receptors allow large amounts of calcium followed
by glutamate to enter the cells.
• Once glutamate is inside the brain cells, it literally
overexcites them, causing disordered enzyme activities
that release toxic free radicals, which destroy the cells .
• This secondary assault extends the zone of cerebral
infarction (death of brain tissue).
 FIGURE 3. During a stroke, oxygen is depleted, which causes release of glutamate. Glutamate
activates NMDA receptors and overexcites brain cells, leading to the release of toxic free radicals,
which destroy the cells.
• When a hemorrhagic stroke occurs, blood leaks
from intracerebral arteries.
• The collection of blood adds volume to the
intracranial contents, resulting in elevated
pressure.
• Hemorrhagic strokes are more common in
particular areas of the brain such as the
cerebellum, the structure that facilitates balance
and coordination, and brain stem, which controls
breathing, BP, and heart rate.
• Various factors increase the risk for a CVA.
• Some are controllable and some are
uncontrollable.
• Atherosclerosis and arteriosclerosis are major
contributors to the formation of thromboemboli
and subsequent CVAs.
• Common causes of cerebral hemorrhage are
rupture of cerebral vessels, hemorrhagic
disorders such as leukemia and aplastic anemia,
severe hypertension, and brain tumors.
 Assessment Findings
Signs and Symptoms
• In some instances, clients experience one or
more TIAs days, weeks, or years before a CVA,
or there may be no warning and the
symptoms develop suddenly.
Signs of an impending stroke include the
following:
• Numbness or weakness of one side of the
face, an arm, or leg
• Mental confusion
• Difficulty speaking or understanding
• Impaired walking or coordination
• Severe headache
• Immediately after a large cerebral hemorrhage,
the client is unconscious.
• Breathing is noisy and labored.
• The cheek on the side of the CVA blows out on
exhalation.
• The eyes deviate toward the affected side of the
brain.
• The pulse is slow, full, and bounding. Initially, BP
is elevated.
• Temperature is elevated during the acute
phase and persists for several days.
• The level of consciousness (LOC) ranges from
lethargy and mental confusion to deep coma,
which can persist for days or even weeks.
• The longer the coma, the poorer the prognosis
and the less likely that consciousness will
return.
Diagnostic Findings
• MRI
• CT scan
• A lumbar puncture often is performed. If
subarachnoid bleeding has occurred, the
cerebrospinal fluid will be bloody.
• Cerebral angiography shows displacement or
blockage of cerebral vessels.
Medical and Surgical Management
• thrombolytic agent (It is contraindicated in
hemorrhagic CVAs, as is anticoagulant
therapy).
• Several neuroprotective agents, such as
NMDA receptor blockers, calcium and
glutamate antagonists,
 Nursing Management
Client and family teaching also is essential and focuses on the
following points:
• Administer medications as directed and understand the
potential side and adverse effects.
• Implement eating and swallowing techniques that reduce
the potential for aspiration .
• Perform the Heimlich maneuver to clear the airway if the
client cannot speak or breathe after swallowing food
• Continue follow-up care with the speech pathologist and
dietitian.
• Contact community resources such as medical supply
companies that rent or sell special care devices such as a
hospital bed, bedside commode, walker, or tripod cane.