Running head: ADULT CEREBRAL VASCULAR ACCIDENT SURVIVORS

Adult Cerebral Vascular Accident Survivors

Tracy Terrones
University of Arizona
RN-MS Student 2016
Clinical Systems Leadership Immersion
NURS 660

Introduction to Population
This paper will focus on the pathophysiology of the adult cerebral vascular accident
(CVA) survivors. A CVA occurs when the blood flow to the brain is interrupted or significantly
reduced, resulting in a certain amount of permanent neurological deficits due to cellular death.
Nearly 795,000 individuals experience a new or repeated CVA annually. Typically every 40
seconds someone in the United States has a CVA while every 4 minutes mortality occurs from
this neurologic event. Generally CVAs occur more often in males than females, until the age of
55 where they equalize at risk. Incidences are higher in the African-American, Hispanic,

American Indians, Alaska Natives, and Asian-Pacific Islander populations. Of all CVAs that
occur, approximately 65% happen to people over the age of 65. Persons with family history of
CVAs and persons with diabetes are also at greater risk than those without. Geographically the
Southeastern United States has the highest death rates related to CVAs and nearly half of
Americans have at least one major risk factor for this fifth leading cause of death.
Risk Factors for Primary Diagnosis
The primary pathophysiology of a CVA is an underlying cardiac or blood vessel disorder
(Kanekar, Zacharia, & Roller, 2012). The secondary manifestations in the brain are the
consequence of one or more of these primary disorders or risk factors (Kanekar et al., 2012).
According to the National Stroke Association 87% of CVAs are ischemic, meaning blood flow to
brain is obscured, and they remaining CVAs are hemorrhagic implying bleeding from a blood
vessel in the brain. Many risk factors affect individuals likelihoods of having a CVA. Risk
factors that are uncontrollable include age, gender, ethnicity, family history, previous CVA,
transient ischemic attack (TIA), patent foramen ovale (PFO), and fibromuscular dysplasia
(FMD) (American Heart Association, 2016). Hypertension, atherosclerosis, dyslipidemia, atrial
fibrillation, diabetes mellitus, circulatory problems, and carotid artery stenosis are primary
medical pathologies with uncontrolled hypertension being the number one cause of a CVA
(American Stroke Association, n.d.). Daily living risk factors include poor eating habits;
resulting in excess weight, lack of physical activity, smoking; which doubles ones risk of having
a CVA, and overindulgence of alcohol consumption (American Stroke Association, n.d.).
Health Promotion and Risk Reduction Recommendations
Long-term disabilities resulting from a CVA cannot only be devastating to an individual
but also very costly. It is estimated that the cost of health care services, pharmaceuticals for CVA

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patients, and absence from work is 34 billion dollars annually (Mayoclinic.org, n.d.). Stroke
prevention is recommended and can be accomplished by reducing risk factors within ones
control. It is advocated to life a healthy lifestyle. Being physically active, eating a well nourished
diet low in saturated fat, and maintaining the Healthy Peoples 2020 goals and the Centers for
Disease Control and Prevention (CDC) recommendations endorsing maintaining a healthy
weight have great impact on achieving the objective to prevent a CVA (Mayoclinic.org, n.d.).
Smoking cessation and alcohol limitation are valuable risk reducers to aide in prevention of a
stroke or recurrent stroke (American Stroke Association, n.d.). According to the National Stroke
Association (2016) up to 80% of CVAs are preventable and can occur to a person at anytime
regardless of age. Education and materials on cerebral vascular accidents can be found on the
websites, National Stroke Association, American Heart Association (AHA), and the CDC to
increase the publics awareness on the importance of risk reduction, recognition of CVA
symptoms, and making healthy lifestyle choices.
Pathophysiology of Primary Diagnosis
Acute ischemic cerebral vascular accident is defined as abrupt neurologic dysfunction
due to focal brain ischemia, developing from a cascade of occurrences, from energy depletion to
cell death, ensuing in neurologic insufficiency (Kanekar et al., 2012). Two main cell types make
the brains structure, active neurons and supporting glial cells. A neuron consists of a cell body,
which encompasses a nucleus, and one or more extensions projecting from the cell body
(Kanekar et al., 2012). One single neuron typically will be connected with at least 1000 other
neurons allowing transmission of information by chemical and electrical signaling (Tasker &
Duncan, 2015). The neuron membranes are made by phospholipid bilayers that maintain ionic
gradients across the membrane from assistance of ion channels and ion pumps (Hisham &

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Bayraktutan, 2013). This is an extreme energy consuming process requiring a constant supply of
oxygen and glucose to the neuron (Alexander, 2013). Any disruption, especially reduction in
oxygen and glucose affects the upholding of electrical potentials and ion gradients eventually
affecting cerebral cell function (Alexander, 2013). Vascular occlusion causes an ischemic
cascade including energy and sodium-potassium pump failure across the cerebral membrane,
increased intracellular calcium, and a generation of free radicals, depolarization, blood-brain
barrier disruption, inflammation, and apoptosis (Kanekar et al., 2012). These complex
mechanisms lead to an accumulation of toxic metabolites causing cellular and structural damage
of cerebral parenchyma (Kanekar et al., 2012).
Pathophysiology of Primary Symptoms of Primary Illness
CVA occurs from thromboembolism or hemodynamic failure. According to the National
Stroke Association (2016) a person loses 1.9 million neurons each minute cerebral blood flow is
disrupted. CVA symptoms are sudden onsets including paralysis or numbness of ones face, arm
or leg, especially on one side; confusion, trouble speaking or understanding; difficulties with
vision in one or both eyes; dizziness, unsteady gait, loss of coordination or balance; a severe
headache with unknown cause (American Stroke Association, n.d.). Thromboembolism is mainly
seen in elderly patients due to atherosclerosis, where as hemorrhagic or hemodynamic failure is
seen in pediatric or young adults (Alexander, 2013). A thrombus or internal clot is formed due to
a coagulation process or activation of a clotting cascade (American Stroke Association, n.d.). The
coagulation cascade involves a complex set of reactions involving approximately 30 different
proteins and two separate initial pathways, intrinsic and extrinsic, which converge to become one
common pathway (American Stroke Association, n.d.). These pathways activate the precursor
protein prothrombin to the active enzyme thrombin (American Stroke Association, n.d.). These

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reactions convert fibrinogen, a soluble protein, to strands of fibrin, which together with platelets,
forms a stable thrombus (Kanekar et al., 2012). The area where the small thrombus has formed
can enlarge as blood flow slows around the thrombus depositing platelets, red blood cells and
clotting factors, producing an enlarging blood clot (American Stroke Association, n.d.). This
disruption of cerebral blood flow due to the thrombus, leads to energy depletion and cellular
death of the brain. The area where the thrombus is formed and the area where the blood supply is
altered will depict the infarct location and result in different symptoms or deficits (Alexander,
2013). Brain tissue death may result in long-term mild to severe functional and cognitive
shortfalls.
Paralysis
The brain is made up of multiple lobes, or sections, in two halves called hemispheres
(Kanekar et al., 2012). Right and left hemispheres are divided by the medial longitudinal fissure
and are connected by the corpus callosum, a bundle of axons that facilitate communication
between these hemispheres (Tasker & Duncan, 2015). The cerebral cellular damage and the
neurological effects of a CVA depend primarily on the location of the obstruction and the extent
of the brain tissue affected (Tasker & Duncan, 2015). As every CVA is unique, they tend to affect
people in similar fashions. The hemispheres control the opposite side of ones body, so a CVA
affecting one hemisphere will result in neurological complications affecting the contrasting side
(Kanekar et al., 2012). Right hemisphere CVAs could produce, paralysis on the left side of the
body, vision problems, and memory loss, while left hemisphere CVAs would involve paralysis
on the right side of the body, speech/ language problems, and also memory loss (Kanekar et al.,
2012).
Difficulty Speaking or Aphasia

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The temporal lobe and the neurons in this region of the brain form the primary auditory
cortex, which contains Wernickes area and is responsible for speech and hearing processing
(Kanekar et al., 2012). Cellular death by diminished blood flow, damaging the left hemisphere
portion of the brain, is responsible for patients developing aphasia (Kanekar et al., 2012).
Aphasia impairs the communication and understanding of language. According to the National
Aphasia Association (2016), nearly 80,000 persons develop aphasia each year from CVAs.
Currently about one million people in the United States have aphasia.
Severe Headache
A sudden severe headache with unknown cause is a symptom from a cerebral vascular
accident (Kanekar et al., 2012). The brain requires a near constant supply of oxygen and glucose
to maintain adequate energy for normal functioning (Hisham & Bayraktutan, 2013). Individual
cells within the central nervous system have a very limited capacity to store oxygen or glucose,
and demands are high (Alexander, 2013). Adequate energy is vital for neurons as it is the source
of energy used by the cell to maintain homeostasis of the cell membrane (Hisham &
Bayraktutan, 2013). As cerebral vascular occlusion inhibits oxygen and glucose supplies,
cellular-level energy failure ensues (Alexander, 2013). The location of a headache following the
lack of oxygen and glucose enriched blood may depend on the area where the blockage is
occurring (Alexander, 2013). CVAs arising from a carotid artery may produce a severe forehead
headache and CVAs in the vertebrobasilar system may cause a severe headache in the back of
the head (Tasker & Duncan, 2015). It is reported that stroke victims report some sort of headache
while experiencing a CVA.

Standard lab and diagnostic data

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CVA diagnosis is currently based mostly on non-laboratory testing; diagnosis includes a

physical and neurological exam and a variation of radiological imaging procedures. Laboratory
tests continue to be researched to find CVA biomarkers that could be used to screen, diagnosis,
treat, and manage stroke patients (Mayoclinic.org, n.d.). These test are currently not widely
available, and their uses are mainly on research studies. Laboratory blood tests such as complete
blood count (CBC), prothrombin time (PT)/INR, partial thromboplastin time (PTT), glucose,
electrolytes, HgA1c, and a lipid panel assist in evaluating and managing CVA patients
(Mayoclinic.org, n.d.). Bleeding times, clotting factors, and levels of glucose, being at
abnormally high or low levels need to be monitored and adjusted to limit neuronal damage after
ischemia ("National Stroke Association," 2016). Physical and neurological exams will include,
evaluation of symptoms, onset of symptoms, auscultation of carotid arteries to evaluate for the
presence of a bruit, and vital signs ("National Stroke Association," 2016). Computerized
tomography (CT) scan and magnetic resonance imaging (MRI) produce a three dimensional
image to diagnose an ischemic or hemorrhagic CVA in the acute phase (Mayoclinic.org, n.d.).
Carotid ultrasound, cerebral and carotid angiography, electroencephalogram (EEG), and a
transesophageal echocardiogram (TEE) are utilized to manage and prevent future cerebral
neurological events (Kanekar et al., 2012).
Nurse-Sensitive Outcomes
Cerebral vascular accidents are a major health issue in the United States Emergency
Departments (ED). ED nurses and paramedics are on the front lines, and must be able to
recognize the presentation of an ischemic stroke, and have the knowledge of the appropriate
intervention referring to the recommended guidelines published by the AHA (Traynelis, 2012).
Education for nurses of the current evidence-based practice guidelines for the management of

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patients suffering from a CVA will facilitate more efficient and more accurate recognition,
resulting in quicker treatments to foster enhanced patient outcomes (Traynelis, 2012). Recent
research has identified ways to minimize the effects of a CVA and reduce their recurrence.
Actions taken by the nurse following these evidenced based guidelines include, rapid assessment,
apply the NIH Stroke Scale, and provide rapid transportation to CT or MRI as ordered ("Elsevier
Nursing Solutions," 2011). Intervention and reperfusion by administration of tissue plasminogen
activator (tPA), thrombectomy, or hemicraniectomy offers the potential to reduce the extent of
ischemic injury (Mayoclinic.org, n.d.). Educating patients and families for recognizing CVA
symptoms can prevent a CVA or a recurring CVA. Information on antiplatelet agents and their
importance will help manage stroke prevention, as well as personalized risk factors to help
reduce chances of a second cerebral event (Traynelis, 2012). The term FAST, Facial drooping,
Arm weakness, Speech difficulty, and Time to call 911 by the Strokeassociation.org are valuable
indicators of a CVA and necessary for community awareness (American Stroke Association,
n.d.). Emotional support needs to be provided to the patient and family due to this devastating
lifestyle change. Follow up care for possible signs of depression and groups offering support for
CVA patients will need to be made available ("Elsevier Nursing Solutions," 2011). Stroke
nursing is a continuous process throughout the patients journey of care, wherever the setting.
The provider must have the comprehension, clinical proficiencies, self-assurance, and concern to
provide effective healing care and recuperation.
Collaborative Outcomes
The best CVA patient outcomes and prevention of recurrence are the results of the
merging of various healthcare professionals. Nurses, physicians, physiotherapists, occupational
therapists, speech therapists, social workers, psychologists, dieticians, orthoptists, and

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pharmacists are all key players for this patient population ("Elsevier Nursing Solutions," 2011).
The communication among this multidisciplinary team following the CVA patient and family
from admission to discharge is essential for success. The caring and support for patients and
families; setting and meeting appropriate goals; liaison with other professionals, educating staff,
patients, and relatives; attendance at collaborative health provider meetings and case
conferences; and networking with other health care professionals in the management of CVAs
are the responsibilities of this collaborative care management ("Elsevier Nursing Solutions,"
2011). In a personal interview with colleague Dr. Jonathon Man, (January 18, 2016) a cardiac
electrophysiologist who studies and treats the electrical pathways of the heart, he concurs it takes
a collaborative team to prevent cerebral vascular accidents (J. Man, personal communication,
January 18, 2016). Each consult he has involving atrial fibrillation (A Fib) or atrial flutter (A
Flutter) is either a consult following a CVA or to prevent a CVA from occurring (J. Man, personal
communication, January 18, 2016). The patients Dr. Man consults on are at a high risk for a CVA
as they have failed medical therapy and continue with atrial fibrillation requiring an ablation.
Atrial fibrillation ablation decreases this populations risk for stroke. The information and care
the patient has been provided from the interprofessional team eases this process. National
required performance measures for evidence based stroke care include venous thromboembolism
prophylaxis (VTE) initiated by day 2; discharged on antithrombotic therapy; anticoagulation
therapy for A Fib and A Flutter; thrombolytic therapy; antithrombotic therapy by end of hospital
day 2; discharged on statin medication; stroke education; and assessment for rehabilitation (J.
Man, personal communication, January 18, 2016). Assuring the use of these clinical practice
guidelines, providers will continue to decrease not only the deaths from CVAs but also the
serious long-term disabilities for adult CVA survivors.

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References
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(1st ed.). Hoboken, NJ: John Wiley & Sons, Inc.
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American Stroke Association. (n.d.). www.strokeassociation.org/STROKEORG/
Evidence-based practice: managing stroke. (2011). Retrieved from
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Hisham, N. F., & Bayraktutan, U. (2013, October). Epidimiology, pathophysiology, and
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Kanekar, S. G., Zacharia, T., & Roller, R. (2012, January). Image of Stroke: Part 2,
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http://dx.doi.org/10.1097/MOP.0000000000000287

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Traynelis, L. (2012, August). Emergency department nurses knowledge of evidenced-based
ischemic stroke care. Kaleidoscope: Vol. 10 article 44
What is a stroke? (2016). Retrieved from http://www.strokecenter.org

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