Вы находитесь на странице: 1из 5

Brain attack: Treating acute ischemic CVA

Mower, Donna M
"Time is brain" when your patient suffers a CVA. Here's how to make the first fast moves to give him the best
chance for recovery.
BRAIN ATTACK. YOU MAY NOT BE familiar with the term, but it's the third leading cause of death and the
leading cause of disability in the United States. Better known as cerebrovascular accident (CVA) or stroke,
brain attack strikes approximately 550,000 people in the United States each year, claiming the life of about
150,000 of its victims. But perhaps more significantly, 3 million people are currently CVA survivors, many
with permanent disability.
To help reduce death and disability, early treatment is vital. You have an essential role in getting treatment
to the stroke victim in time (see Sending A New Message). In this article, I'll discuss how to minimize
damage from a CVA. But before I discuss CVA treatment, let's review some terms.
Defining our terms
Cerebrovascular accident or stroke is the sudden interruption of blood flow to a part of the brain, killing brain
cells and destroying or impairing body functions controlled by that part of the brain. An ischemic CVA occurs
when an embolism or thrombus obstructs a cerebral artery, blocking the flow of blood to the brain. In
contrast, a hemorrhagic CVA strikes when a vessel in the brain suddenly ruptures, allowing blood to
permeate the brain tissue.
Most strokes-over 80%-are ischemic; the remainder are hemorrhagic. Because the acute management of
hemorrhagic and ischemic stroke differs and ischemic strokes predominate, I'll focus on ischemic CVA in this
article.
Ischemic CVA can be divided into two subtypes-embolic and thrombotic-based on the underlying cause. An
embolic CVA results from an embolus that travels to a cerebral artery from a distant site, most commonly the
heart or neck. Atrial fibrillation, an arrhythmia that allows blood to pool in the atria, is often an underlying
cause. When the embolus reaches a cerebral artery that's too narrow to pass, it lodges, blocking blood flow
to part of the brain. Embolic CVA causes a sudden deficit (within seconds to minutes) and usually occurs later
in the day when the person is active.
Unlike embolic CVA, thrombotic CVA results from a gradual process. Atherosclerosis is the main risk factor:
As atherosclerotic plaque slowly accumulates in a cerebral artery, the potential for thrombotic stroke builds.
If the plaque isn't treated, a thrombus, or clot, may form, further occluding the artery and causing ischemia
and neurologic deficits that evolve over hours to days. Symptoms usually begin when the person's blood
pressure (BP) is relatively low (for example, in the early morning or during rest).
One or more transient ischemic attacks (TIAs) may precede a thrombotic (but not an embolic) CVA. A TIA is
a temporary interruption of blood supply to an area of the brain. The person experiences a sudden onset of
stroke symptoms that last for a few minutes to as long as 24 hours before they disappear. The TIA
symptoms correlate to the portion of the brain that isn't receiving sufficient perfusion. A TIA sounds a
warning that treatment is essential to avert a CVA-one-third of persons who experience a TIA suffer a CVA.
Like a CVA, a TIA is a medical emergency.
When a stroke strikes
George Teller, a 68-year-old obese, black, retired accountant with insulindependent diabetes mellitus,
awakes one morning with garbled speech and a weak right arm. His wife, a retired LPN, knows to treat his
symptoms as an emergency and calls 911. Emergency medical services personnel alert the emergency
department (ED) where you work that they're transporting a patient with a possible CVA.
Mr. Teller presents at the ED with a headache, slurred speech, and right-arm weakness. He reports no
history of CVA, heart disease, or hypertension. But he has several risk factors for stroke: male sex, black
race, advanced age, diabetes, and obesity (see Understanding Ischemic CVA Risks).
What do you do first?
After you address Mr. Teller's ABCs (airway, breathing, and circulation), obtain a 12-lead electrocardiogram
(ECG) and place him on a cardiac monitor. You'll want to know his cardiac status right away for two reasons.
First, atrial fibrillation is a specific risk factor for embolic stroke, so its presence can help focus your
diagnosis. Second, events caused by the stroke itself (seizure activity, increased intracranial pressure [ICP],
and neurologic injury) can cause arrhythmias such as bradycardia, premature ventricular contractions,
supraventricular tachycardia, and atrioventricular block. So getting a baseline ECG is essential.
Your initial goals are to stabilize the patient and restore circulation to the affected area of the brain. You'll
also need to take measures to prevent or manage increased ICP (see Keeping the Pressure Down).
Understanding ischemic CVA risks
Your patient's risk of suffering an ischemic stroke escalates if he has any of the following risk factorsand the
more he has, the greater his risk.
Controllable risk factors
Hypertension
Heart disease (especially atrial fibrillation)
Cigarette smoking
Excessive alcohol intake
High cholesterol level Obesity
Uncontrollable risk factors
Increasing age
Male sex
Black race
Personal history of diabetes (even if controlled, diabetes itself is a risk factor)
Previous stroke or transient ischemic attack (TIA)
Family history of stroke or TIA
Closely monitor his vital signs (including temperature) and neurologic status and initiate pulse oximetry and
oxygen therapy, as ordered. Also obtain a chest X-ray and stat lab blood tests, such as an arterial blood gas
analysis, a complete blood cell count with differential, electrolytes, blood glucose, creatinine, blood urea
nitrogen, prothrombin time, and activated partial thromboplastin time (aPTT). If a myocardial infarction (MI)
also is suspected, add to your list creatine kinase with isoenzymes as well as a cardiology consult.
Getting the scoop
The patient's risk factors and the onset of symptoms provide important clues that can help speed a
diagnosis, so get a complete, accurate history from the patient or a family member. A good history along
with a complete physical examination focusing on neurologic deficits will help you plan appropriate
treatment.
Mr. Teller's symptoms began early in the day; your physical examination shows that his signs and symptoms
have worsened since he arrived in the ED. This information, along with Mr. Teller's risk factors, point toward
a thrombotic ischemic stroke.
Scanning aids
As soon as you suspect that a patient is having a CVA, arrange for a stat computed tomography (CT) scan of
the head. This test is used to rule out tumor, abscess, or intracerebral hemorrhage caused by hemorrhagic
CVA, large embolic CVA, or hypertensive intracranial hemorrhage.
The physician may also request a magnetic resonance imaging (MRI) scan if the CT scan is inconclusive or
she feels an MRI scan can add important clinical information. An MRI scan doesn't show acute bleeding as
well as a CT scan, but it provides a better picture of the brain stem and related structures. An MRI scan also
reveals evidence of ischemic stroke much sooner than a CT scan does. On the other hand, CT scans can be
performed faster (an important consideration in acute stroke treatment), are less expensive, and are
available at more facilities.
Within 45 minutes of admission, Mr. Teller is rushed for an emergency nonenhanced CT scan. The CT scan
shows edema in the left parietal-temporal lobe, which is an early indication of a CVA. Not surprisingly, no
infarction is found; infarction may not be visualized on a CT scan for 48 to 96 hours. A repeat CT scan will be
done in 2 or 3 days, or earlier if symptoms warrant.
Checking Mr. Teller's other results, you find that his chest X-ray is normal and his lab tests are within normal
limits except for an elevated blood glucose level of 289 mg/dl. Diabetic patients like Mr. Teller have an
increased risk of stroke because of progressive changes to the vascular endothelium. Also, elevated blood
glucose levels can cause more severe brain damage: During the ischemic episode, increases in cerebral
glucose may lead to increased glycolysis. An increase in lactic acid, which is neurotoxic, results. So you need
to bring down Mr. Teller's blood glucose level as soon as possible by implementing the insulin sliding scale
that the physician orders.
Begin an isotonic intravenous (I.V) infusion of 0.9% sodium chloride solution, as ordered, to maintain
hydration. Unless the patient is hypoglycemic, solutions containing dextrose are rarely indicated; because
they're hypotonic, these solutions can increase cerebral edema and raise ICP.
Perform frequent neurologic assessments to gauge any changes in deficit. Report even subtle changes: A
slight decrease in Mr. Teller's level of consciousness may indicate worsening ischemia from hypotension,
hypoxia, or cerebral edema. Carefully monitor his respiratory status and Spo2 while maintaining
supplementary oxygen, as ordered. Adequate ventilation is needed to prevent hypoxia, another factor that
can increase ICP.
Be on the lookout for seizuresthey occur in about 15% of patients with CVA and can adversely affect
cardiovascular function and acidbase metabolism. To be on the safe side, pad the side rails and place Mr.
Teller on seizure precautions. If he does have a seizure, protect the airway, give oxygen, and administer an
anticonvulsant drug (for example, phenytoin [Dilantin]), as ordered. But don't administer anticonvulsant
drugs prophylactically if seizures aren't present-most anticonvulsant agents can cause hypotension.
Blood pressure considerations
Besides neurologic factors, carefully monitor Mr. Teller's BP. Most patients with acute stroke are
hypertensive, but the BP usually decreases without treatment during the first few days. Correcting hypoxia,
vomiting, and other distressing symptoms helps to reduce BP, so be sure to treat the causes of hypertension
first. During the acute management of a CVA, you'll need to treat only severe hypertension-a mean arterial
pressure of greater than 140 mm Hg or a systolic BP of greater than 200 mm Hg-to prevent loss of
autoregulation. Medications used to reduce BP in stroke include beta-blockers and nitroprusside. You'll
administer these drugs in dosages designed to gradually decrease the BP. A sudden drop in BP can further
damage the ischemic area surrounding the infarcted area of the brain, called the penumbra, which is
sensitive to changes in oxygen tension and BP.
Mr. Teller's BP is 168/92. As ordered, you monitor and document it carefully but don't treat it. You need to
maintain a delicate balance, providing sufficient perfusion to the penumbra in order to limit the region of cell
death without increasing ICP.
Treating with t-PA
Mr. Teller's history, risk factors, clinical examination, and lack of hemorrhage on the imaging study confirm
the diagnosis of an ischemic CVA. After carefully reviewing the data and the time from onset of symptoms,
the physician decides to treat Mr. Teller's CVA with tissue plasminogen activator (t-PA).
Although the thrombolytic agent t-PA has been used to treat MIs for many years, it's only recently been
approved for use in CVAs. And because this drug is contraindicated in hemorrhagic stroke and in many other
clinical situations, it must be used with great care and only if the CVA is clearly not hemorrhagic in origin.
"Time is brain" when administering t-PA. Given within 3 hours of the onset of symptoms, t-PA can limit
neurologic deficit in patients with an evolving ischemic CVA. But research shows that when administered
after more than 3 hours, t-PA may worsen the patient's condition by increasing the risk of hemorrhage.
Now that the decision has been made to give t-PA, time becomes even more vital. While the physician
discusses with Mr. Teller and his wife the risks and benefits of using t-PA, you carefully review the drug's
indications, contraindications, and adverse effects. You also doublecheck several points about Mr. Teller's
medical history with his wife.
Mr. Teller weighs 220 pounds (100 kg), and the physician prescribes the maximum dose of 90 mg (0.9
mg/kg; maximum dose, 90 mg). You reconstitute the t-PA with sterile water injection to create a 1 mg/1 ml
solution. As ordered, you administer 9 mg (10%) as an I.V. bolus over 1 minute, timing it carefully. Then you
infuse the remaining 81 mg (90%) in 0.9% sodium chloride solution over 60 minutes. During the infusion,
monitor Mr. Teller's vital signs and neurologic, cardiovascular, and respiratory status and check carefully for
signs and symptoms of bleeding.
When does heparin help?
Anticoagulation therapy with heparin (and later with warfarin [Coumadin]) allows the body's natural
fibrinolytic processes to dissolve the existing clot and prevents new clots from forming. In this way, heparin
may halt or reverse the progression of neurologic deficits. Remember these two special rules when using
heparin in a patient with a CVA:
Administer heparin only to patients with TIAs or evolving ischemic CVA-never to patients with hemorrhagic
CVA.
Don't administer any anticoagulant or antiplatelet agent within 24 hours of thrombolytic therapy.
About 48 hours after the onset of symptoms in embolic stroke, the embolus may dissolve or collateral blood
flow around the blockage may develop. This may result in hemorrhagic transformation, in which bleeding
occurs spontaneously because vessels that have been damaged during the CVA begin to leak. When you
administer heparin to a patient with an embolic stroke, realize that heparin may increase the risk of
hemorrhagic transformation. Monitor vigilantly for any indication of severe bleeding. If he has an acute
change in neurologic status, immediately discontinue the heparin and obtain an order for a stat CT scan to
rule out hemorrhage.
In most cases, you'll want to maintain the patient's aPTT from one and a half to two times his baseline.
Anticipate a physician's order for frequent aPTT determinations (usually every 6 to 8 hours until the desired
level is reached and then daily). Initiate long-term warfarin therapy, as ordered. The two types of
anticoagulant therapy must overlap; you'll need to continue heparin therapy until a therapeutic international
normalized ratio of warfarin of 2.0 to 3.0 is achieved-about 2 days.
Teaming up
Whenever you're caring for a patient with a CVA, you need to work closely with a multidisciplinary team. You
may find yourself acting as the "point" person, coordinating the many facets of care that your patient will
need to help him recover.
Early consults should include social services, physical medicine, and rehabilitation to help coordinate
discharge planning and continuing care. Get the occupational therapy and physical therapy departments
involved right away. That way, as soon as Mr. Teller is hemodynamically stable, he can begin a program of
appropriately increased activity.
Supporting the family
The sudden onset of CVA and disability in a loved one can prove devastating to family members. You need to
provide careful and caring explanations and ongoing support to help Mr. Teller's family cope with these
extraordinary changes.
Make a point of meeting with family members of any stroke patient as soon as possible after the patient has
been stabilized. But realize that emotional upheaval may limit their ability to process information at first-you
may need to reinforce material frequently in the period following the patient's CVA.
Also anticipate that additional questions and possible denial may surface as family members absorb the
enormity of both the patient's disability and their own new responsibilities. Always remember that family
members are integral components of the team helping the patient recover; include them as much as possible
in all aspects of care and decisions.
Other problems
Patients with CVA (especially elderly persons) sometimes experience environmental disorientation. If Mr.
Teller appears confused, orient him frequently and ask his wife to bring in a calendar and clock as well as
family pictures and other familiar items. Institute safety precautions for all CVA patients according to hospital
policy.
Postural hypotension may develop from prolonged bed rest or neurologic damage, so exercise caution as Mr.
Teller increases his activity level. As soon as possible, encourage him to participate in activities of daily
living. Doing so will not only increase his strength and range of motion, but also will give him an increased
sense of control that may help stave off clinical depression, which often follows CVA.
Along with problems that directly result from the CVA, patients can experience a wide range of problems
associated with immobility, such as deep vein thrombosis, pulmonary embolism, and skin breakdown. Many
of these complications can be averted by instituting commonsense precautions and mobilizing the patient as
soon as possible.
Planning for a smooth transition
Successful discharge planning for a CVA patient begins at admission. You've already played a major role in
optimizing Mr. Teller's recovery by responding quickly and appropriately during the acute phase of his CVA.
Now-like most first-time CVA survivors-he's scheduled to be discharged home. There, he's going to need
home health care and outpatient rehabilitation services to continue regaining his functional abilities. The
postdischarge supports you've set up will help smooth the transition to the rehabilitation phase of his
recovery.
For selected World Wide Web sites related to this article, see our Web site http://www.springnet.com. On our
home page, select Continuing Education; links to the sites are embedded within each CE article.
SELECTED REFERENCES
American Heart Association: What You Should Know about Stroke. Dallas, American Heart Association, 1994.
Barker, E.: Neuroscience Nursing. St. Louis, MosbyYear Book, Inc., 1994.
Hacke, W., et al.: "Intravenous Thrombolysis with Recombinant Tissue Plasminogen Activator for Acute
Hemispheric Stroke: The European Cooperative Acute Stroke Study (ECASS)," JAMA. 274(13): 1017-1025,
October 1995.
Wojner, A.: "Optimizing Ischemic Stroke Outcomes: An Interdisciplinary Approach to Poststroke
Rehabilitation in Acute Care," Critical Care Nursing Quarterly. 19(2):47-61, August 1996.
BY DONNA M. MOWER, RN, CNRN, CS, MS Neurosurgical Clinical Nurse Specialist Medical Center of Delaware
Stanton, Del.
Copyright Springhouse Corporation Mar 1997
Provided by ProQuest Information and Learning Company. All rights Reserved

Вам также может понравиться