Nursing Case Study On Stroke



Cerebrovascular AccidentCerebrovascular Accident is a sudden loss of function resulting from disruption of the blood supply to a part of the brain. Stroke, also called brain attack or ischemicstroke, happens when the arteries leading to the brain are blocked or ruptured. Whenthe brain does not receive the needed oxygen supply, the brain cells begin to die, astroke can cause paralysis, inability to talk, inability to understand, and other conditionsbrought on by brain damage.Four types of stoke:


Cerebral Thrombosis- caused by blood clots.


Cerebral Embolism- caused by blood clots.


Cerebral Hemorrhage- caused by bleeding inside the brain.4.Subarachnoid Hemorrhage- caused by bleeding inside the brain.Cerebral Thrombosis

 The most common type of brain attack.

Occurs when a blood clot (thrombus) forms and blocks blood flow in an arteryleading to the brain arteries primarily affected by atherosclerosis and moresusceptible to blood clots.

Most often occurs at night or in the morning when blood pressure in low.

Often preceded by a transient ischemic attack (TIA) or “mini-stroke”.Cerebral Embolism

Occurs when a wondering clot (embolus) or some other particle forms in a bloodvessel away from the brain, usually in the heart. The clot then travels and lodges inan artery leading on the brain.Cerebral Hemorrhage

Occurs when a defective artery in the brain busts.Subarachnoid Hemorrhage

Occurs when a blood vessel on the surface of the brain ruptures and bleeds intothe space between the brain and the skull. The World Health Organization (WHO) definition of stroke is “rapidly developingclinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting24 hours or longer or leading to death, with no apparent cause other than of (1) Non-communicable disease. WHO Geneva (2) vascular origin” (3) By applying this definitiontransient ischemic attack (TIA), which is defined to less than 24 hours, and patients withstroke symptoms caused by subdural hemorrhage, tumors, poisoning, or trauma, areexcluded.Based from the data gathered from TCGPH records section, there were 10 reportedcases of CVA as of January 2009 until December 2009 comprises of 2 mortality cases and8 morbidity cases.

Why this case?

We have chosen this case as our topic during the case presentation because wewould like that we, student-nurses, to be aware about CVA and also to broaden ourknowledge about the management and treatment of this disease.

Having awareness and gaining more knowledge about CVA would enhance ourskills and attitudes in handling patients suffering from this disease.

Cardioembolic Stroke: A Case Study

  1. Lisa A. Babkair, RN, MSN⇑
  1. Lisa A. Babkair holds an academic appointment at King AbdulAziz University, College of Nursing, Jeddah, Saudi Arabia, and is currently a doctoral candidate at New York University, New York, New York.
  1. Corresponding author: Lisa A. Babkair, rn, msn, 433 First Ave, New York, NY 10010. (e-mail: lab720{at}


Cardioembolic stroke is a critical health condition that requires immediate intervention. Cardiac emboli are the most common type of embolism and account for 14% to 30% of all ischemic strokes. Atrial fibrillation is the most common cause of cardioembolic strokes, and its prevalence increases substantially with age. Other factors that increase the risk for cardioembolic stroke include hypertension, diabetes mellitus, hyperlipidemia, cardiac disease, and lifestyle choices. General supportive care and treatment of the acute phase and subsequent complications should be started immediately. Nurses must play an active role in screening patients for stroke subtypes, using appropriate diagnostic tools, and providing medical and nursing interventions. Nurses also play a crucial role in prevention by providing education to patients and patients’ families on how to recognize stroke signs and symptoms. This case study discusses the course of illness, treatment, and prevention strategies for patients who have suffered cardioembolic stroke due to atrial fibrillation.

Stroke is a rapid-onset medical emergency that can cause neurological damage and disability. Each year about 795 000 persons in the United States experience new or recurrent strokes, accounting for approximately 1 of every 20 deaths.1 About 610 000 of these strokes are first occurrences; 185 000 are recurrent.1 The overall age-adjusted prevalence of stroke was 2.7% in 2006 and 2.6% in 2010 in the United States.2 Of all strokes, 87% are ischemic, 10% are intracerebral hemorrhages, and 3% are subarachnoid hemorrhages.1 Embolism is a leading cause of ischemic stroke. Embolic stroke occurs when blood clots, or emboli formed from other materials such as bacteria or fat, travel and lodge in an artery (or arteries) and prevent normal blood flow to a particular region of the brain.3 These emboli often originate from a source in the heart, aorta, or large blood vessels.

Cardiac emboli are the most common type of embolism and account for 14% to 30% of all ischemic strokes.3 The risk for cardioembolic stroke increases with several cardiac conditions, including atrial fibrillation, myocardial infarction, presence of mechanical prosthetic valves, dilated myocardiopathy, and mitral rheumatic stenosis.3 The prevalence of atrial fibrillation, the most common cause of cardioembolic stroke, increases substantially with age. The risk for stroke due to atrial fibrillation increases from 1.5% at the age of 50 years to 24% at the age of 80 years.3

Whereas atrial fibrillation increases the risk for cardio embolic stroke, a number of additional factors increase the risk for ischemic stroke. Risk factors have been classified as modifiable and nonmodifiable1,3–5 (Table 1). Race and ethnic factors play a role in the incidence of ischemic stroke. The risk of having a first stroke is nearly twice as high for African Americans compared with whites, and African Americans are more likely to die after a stroke than are whites.1 The risk for stroke in Hispanics is between the risk for whites and the risk for African Americans.1 Furthermore, women have a higher lifetime risk of stroke than do men. According to research,1,6 among patients 55 to 75 years old, the lifetime risk of stroke is 1 in 5 for women (20%–21%) and about 1 in 6 for men (14%–17%). Among patients who previously had taken warfarin, women were at greater risk for thromboembolism than were men (3.5% vs 1.8%).5 Therefore, identifying the risk factors for cardioembolic stroke will help nurses provide early preventive measures, such as using anticoagulant therapy as a secondary prevention for stroke recurrence, in patients who are at risk for cardioembolic stroke.

The underlying mechanism of cardioembolic stroke is occlusion of cerebral vessels with debris of cardiac origin. The pathophysiology and natural history of cardioembolic stroke depend on the underlying cardiac disease, and each source of debris must be considered individually. Emboli from abnormalities of the cardiac chamber such as atrial fibrillation and myocardial infarction are induced by stasis, whereas emboli associated with valves are due to endothelial abnormalities with attachment of material.7 Emboli from the heart get distributed throughout the body via cardiac output. About 80% of these emboli involve the brain. Once the emboli reach the cerebral circulation, they occlude the blood flow in the brain-supplying arteries, resulting in cerebral ischemia.7 Because emboli are loosely attached to vessels walls, the emboli migrate distally. Reperfusion of the damaged capillaries and arterioles allows blood to leak into the surrounding infarcted tissue. Termed hemorrhagic transformation, this process occurs in up to 71% of cardioembolic strokes.3 Hemorrhagic transformation might be petechial hemorrhage or intracerebral hematoma. Hemorrhagic transformation of a brain infarct is a common event that occurs spontaneously after thrombolytic therapy.3

The course of severe illness and death associated with acute ischemic stroke varies greatly depending on the severity of the stroke and the patient’s premorbid conditions, age, and complications that occur after a stroke.8 Some common complications of ischemic stroke include hemorrhagic transformation, cardiac dysfunction, and arrhythmia.3 Cardiogenic emboli have been associated with the highest first-month mortality rates among the subtypes of ischemic infarcts.1,3 The in-hospital mortality rate is 27.3% for cardiogenic emboli, 0.8% for lacunar infarcts, and 21.7% for atherothrombotic stroke.1,3

Early diagnosis and treatment are crucial for patients with cardioembolic stroke to improve stroke outcomes. Nurses caring for such patients must be aware of various signs and symptoms associated with ischemic stroke (Table 2) and with the diagnostic measurements and treatment options for cardioembolic stroke and its complications.3,9,10 The ability of stroke patients to access a high level of care in the shortest amount time possible is the key element in improving patient outcomes. In the following case study, I describe the course of illness and treatment for a patient who had a cardioembolic stroke and provide a comprehensive advanced medical and nursing care plan during an inpatient hospital stay.

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Case Study

Patient H was a 69-year-old white man with a history of atrial fibrillation, coronary artery disease, coronary artery bypass grafting, and aortic valve replacement. Because of his coronary artery disease and risk for formation of emboli, he was taking daily doses of simvastatin and clopidogrel. He had a history of smoking 1 pack of cigarettes per day but no history of use of alcohol or illicit drugs. His family history was significant for diabetes, hypertension, and hyperlipidemia. Patient H lived with his wife and 2 sons. He was retired and independent in his activities of daily living. He spoke English fluently. He appeared well nourished but was obese with a body mass index of 31.6 (calculated as weight in kilograms divided by height in meters squared).

On the day of admission, a neighbor saw patient H collapse while gardening at approximately 9:30 am. Emergency services were called, and patient H was immediately brought to the hospital’s emergency department by air ambulance. The hospital’s “stroke alert” was initiated at 11:30 am while the patient was still in transit to the hospital. Patient H arrived at 11:40 am. The emergency medical personnel reported that he had left-sided weakness and slurred speech.

Upon arrival, patient H was alert and oriented to person, time, and place. A quick examination revealed left-sided weakness that included the face and the upper and lower extremities. Left-sided facial droop and lack of sensation on the left side of the face were also noted. Slurred speech and mild dysarthria were detected during the examination. The National Institutes of Health Stroke Scale was completed to evaluate and document the patient’s neurological status (Table 3). The score was 17, which correlates with a “severe stroke.”10–12 Initial vital signs were a heart rate of 79/min, blood pressure of 127/72 mm Hg, respirations of 20/min, oxygen saturation of 99% on room air, and body temperature of 36.8°C. A 12-lead electrocardiogram revealed an irregular rhythm with atrial fibrillation. An urgent computed tomography (CT) angiogram of the head and neck revealed an occlusion of the right middle cerebral artery (MCA) with no evidence of midline shift or intracranial hemorrhage. On the basis of these results, the radiologist suggested that embolic occlusion be considered. Figure 1 was the first image obtained before medical interventions. The angiogram also showed minimal atherosclerotic calcifications involving the aortic arch, a bilateral carotid bulb, and the right intracranial internal carotid artery.

Figure 1

Computed tomography scan of head shows no midline shift or intracranial hemorrhage.

Patient H was brought to the hospital within 3 hours of the onset of signs and symptoms, his blood pressure was less than 185/110 mm Hg, and he had an international normalized ratio of 1.2 and normal prothrombin time, all of which satisfy criteria for eligibility for thrombolysis treatment with recombinant tissue plasminogen activator.10 Other laboratory tests performed before thrombolysis treatment included arterial blood gas analysis, determination of blood glucose level, a coagulation profile, complete blood cell counts, measurement of electrolyte levels, and a renal profile (Table 4).13

After patient H’s wife granted consent for the procedures, he received thrombolytic medication followed by mechanical thrombectomy for recanalization. Mechanical thrombectomy devices have thrombus retrieval tools that directly disrupt the clot and prevent the emboli from travelling distally.14,15 Several clinical trials have indicated that mechanical thrombectomy is appropriate for patients with large, proximal intracranial artery occlusions due to emboli of cardiac or arterial origin.16 However, this procedure is associated with some adverse effects, including intracerebral hemorrhage, subarachnoid hemorrhage, and new embolism from fragmentation of the target thrombus.16

Early diagnosis and treatment are crucial for patients with cardioembolic stroke to improve stroke outcomes.

Another CT scan of the head obtained to evaluate the results of the interventions showed an improvement in perfusion in the right MCA. Complete loss of the insular ribbon and sulcal effacement of the right frontal lobe were also evident (Figure 2). The loss of the insular ribbon is the loss of definition of the gray-white interface in the lateral margins of the insula.17 The insular segment and the claustral branches of the MCA supply the insular ribbon. With interruption of the MCA flow, the insular ribbon becomes the region most distal from the anterior and posterior cerebral collateral circulations.17 Therefore, the insular ribbon effectively becomes a watershed arterial zone. Another frequent and reliable finding in acute MCA infarction is sulcal effacement, in which brain swelling leads to loss of definition of the sulci and subsequent parenchymal hypodensity.18

Figure 2

Computed tomography scan of the head shows loss of the insular ribbon (loss of definition of the gray-white interface in the lateral margins of the insula) and sulcal effacement (result of increasing mass effect over the cerebral hemisphere) of the right frontal lobe.

Patient H was admitted to the neurology intensive care unit at 5 pm for monitoring. Supportive care and treatment of acute complications were established immediately. The patient’s score on the Glasgow Coma Scale was 10 of 15; he had spontaneous eye opening and was able to follow simple commands but was confused, and at times his speech was incomprehensible. He continued to have left-sided weakness and was unable to move his left extremities against gravity. His gag reflex was weak, and he had difficulty swallowing.

In order to prevent complications associated with stroke, patient H was given 2% hypertonic saline at a rate of 75 mL/h, titrated to a target serum sodium level of 145 to 150 mEq/L, to minimize formation of cerebral edema before the edema produced major increases in intracranial pressure. The head of the bed was elevated at 20° to 30° to promote venous drainage.10,19 In addition, administration of intravenous metoprolol was started to control heart rate and prevent dysrhythmia. Systolic blood pressure was continuously monitored, and the addition of nicardipine was considered for pressure greater than 180 mm Hg to prevent cerebral hemorrhage.10,20 According to the guidelines10,20 of the American Heart Association/American Stroke Association, blood pressure during and after treatment with recombinant tissue plasminogen activator or other acute reperfusion therapy should be maintained at or less than 180/105 mm Hg. Labetalol 10 mg intravenously followed by a continuous intravenous infusion at 2 to 8 mg/min or nicardipine 5 mg/h intravenously, titrated up to desired effect by 2.5 mg/h every 5 to 15 minutes (maximum 15 mg/h), are the recommended medications to control blood pressure.10,20 Acetaminophen was also prescribed as needed for its antipyretic effect. Hyperthermia results in poor neurological outcomes if left untreated and might increase metabolic demands and enhance the release of neurotransmitters.10,21,22 Approximately one-third of patients admitted with stroke are hyperthermic (temperature > 37.6°C) within the first hours after the onset of the stroke.10,21,22

Blood glucose level was controlled by using a quick-acting insulin on a sliding scale. Hyperglycemia is common during the acute phase of stroke and worsens outcomes.10,23 Other health providers included in the care of patient H throughout his hospital stay were occupational therapists, physical therapists, speech language pathologists, and physical medicine and rehabilitation physicians.

On hospital day 2, patient H’s vital signs were within reference limits: heart rate 77/min, blood pressure 130/76 mm Hg, and respirations 18 breaths/min with an oxygen saturation maintained at greater than 95% while receiving 4 L of supplemental oxygen via a nasal cannula. His speech improved markedly compared with the day before, and he was once again fluent. He was able to answer questions verbally and follow commands but was still unable to move his left side. Magnetic resonance imaging was performed 24 hours after the thrombolysis intervention. The findings were comparable with the findings of the previous head CT of a large infarction in the distribution of the right MCA.

Patient H was examined by a cardiologist for evaluation of atrial fibrillation and abnormal levels of troponin I, brain-type natriuretic peptide, and d-dimer (Table 4). Thyroid function tests were performed to ensure that the atrial fibrillation was unrelated to a thyroid disorder. A transesophageal echocardiogram showed biatrial enlargement and tricuspid regurgitation but no evidence of left atrial appendage thrombi. Because patient H had enlargement of the upper chamber of the heart, the risk for emboli was increased.3 However, the medical team remained aware of the risk for subsequent emboli, and administration of aspirin 325 mg and simvastatin 40 mg were started after insertion of a feeding tube on hospital day 3. Oral administration of aspirin (initial dose 325 mg/d) within 24 to 48 hours after the onset of stroke is recommended for treatment of most stroke patients and for prevention of recurrent stroke.10,24 Furthermore, 5000 U of subcutaneous heparin was administered every 8 hours to prevent deep venous thrombosis (DVT).24,25 In seriously ill patients, anticoagulants are given to prevent DVT and pulmonary embolism.10,25 Complications after stroke, which usually develop during the first 4 days, are associated with stroke severity.26 Although most patients stay in bed, in order to prevent DVT, mobilization usually begins as soon as the patient’s condition is considered stable enough.26

On hospital day 4, patient H’s clinical status worsened somewhat: he experienced somnolence, followed commands more slowly than before, had no spontaneous eye opening, and was difficult to arouse. An urgent head CT scan showed an evolving right MCA infarct producing a mass effect and consequent midline shift of 11 mm. The CT scan also revealed a subarachnoid hemorrhage in the Sylvian fissure, which might have been due to thrombolytic therapy (Figures 3A and 3B). The patient’s intravenous fluids were changed from 2% to 3% hypertonic saline with a target serum level of sodium of 150 to 155 mEq/L to minimize formation of cerebral edema. However, intracranial pressure was not measured.10

Figure 3

Computed tomography scans of the head show a subarachnoid hemorrhage in the Sylvian fissure (A) and a midline shift of about 11 mm (B).

On the same day, patient H continued to have somnolence and decreased responsiveness. Electroencephalography was performed to rule out current seizure activity. The results indicated an abnormal awake and drowsy wave but did not show current seizure activity. Clinicians administered a 50-g dose of mannitol for cerebral edema.10

By the following day, patient H showed slight improvement by opening his eyes and responding to commands, but he was still unable to move his left side. The follow-up head CT scan showed an 8-mm midline shift without hemorrhagic transformation or marked edema (Figure 4). In order to prevent further complications, Doppler ultrasound studies of the upper and lower extremities were done to determine if patient H had DVT; no evidence of DVT was detected. Blood, sputum, and urine specimens were also obtained for microbial cultures. None of the cultures was positive for bacterial infection.

Figure 4

Computed tomography scan of the head shows a midline shift of about 8 mm.

On the night of hospital day 7, results of arterial blood gas analysis indicated mild hypoxia (Table 4), which most likely was related to the atelectasis and pulmonary edema evident on chest radiographs. Patient H was unable to clear his oral secretions because of impaired oropharyngeal mobility and loss of protective reflexes, situations that increased his risk for aspiration pneumonia.10 Albuterol and ipratropium nebulizer treatments were prescribed, the amount of supplemental oxygen was increased, and chest physiotherapy with incentive spirometry was continued.10 The health care team suspected that patient H had already aspirated material into his lungs and continued to order that he receive nothing by mouth until swallowing tests were obtained and showed swallowing function adequate enough to prevent aspiration.

On hospital day 8, patient H had a heart rate of up to 150/min despite being treated with metoprolol to control heart rate. He was given a digoxin loading dose (0.25 mg) to further control the heart rate. Patient H’s blood pressure decreased to 90/69 mm Hg, but the heart rate returned to less than 100/min after the dose of digoxin and a fluid bolus of 500 mL of physiological saline were administered.10 An arterial catheter was inserted for continuous blood pressure monitoring and frequent sampling for arterial blood gas studies. A speech evaluation indicated that patient H was at high risk for aspiration.

On hospital day 11, patient H became febrile with an elevated white blood cell count (Table 4). This response was attributed to the development of a urinary tract infection with Proteus bacteria, and sputum cultures revealed pneumonia caused by Haemophilus influenzae. Treatment with cefotaxime was started to treat these infections.10

Patient H had a second episode of rapid heart rate (164/min), which was refractory to a second dose of intravenous digoxin 0.125 mg, diltiazem 39 mg, and metoprolol 5 mg. Therefore, the medical team decided to start an amiodarone infusion after administering a loading dose of 150 mg.27 Because of the increased risk for embolic events with pharmacological cardioversion, the cardiology team decided to discontinue amiodarone on the next day and instead increased metoprolol to 100 mg every 8 hours.27 During this time, patient H also had an elevation in serum troponin I levels, which was thought to be mostly associated with demand ischemia from the atrial fibrillation and rapid ventricular rate. An electrocardiogram showed T-wave inversion and ST-segment elevation in leads AVF and II—findings consistent with cardiac ischemia.

By hospital day 13, patient H was able to feel light touch on his left upper and lower extremities. Therapy with hypertonic saline was changed to administration of physiological saline at a rate of 75 mL/h, with a target serum level of sodium of 145 to 150 mEq/L. During physical examination, the nursing staff noticed swelling of the patient’s left arm and redness between the elbow and the wrist area; ultrasound revealed DVT in the left upper extremity. The team ordered a repeat head CT scan before starting full anticoagulation treatment. The scan showed an improvement in the right MCA infarct with decreasing mass effect and an interval decrease in the leftward midline shift. No hemorrhagic transformation was evident (Figure 5). Consequently, subcutaneous heparin was increased to a therapeutic dose of 7500 U every 8 hours.10,25

Figure 5

Computed tomography scan of the head shows decreasing mass effect and an interval decrease in the leftward midline shift.

Two days later, follow-up ultrasound of the left upper extremity showed nonocclusive thrombi in the mid and distal left subclavian vein, but the distal thrombus appeared to be extending into the left cephalic vein and occluding the vein at its origin. Furthermore, because of his persistent inability to pass a swallowing test, patient H had a percutaneous endoscopic gastrostomy tube inserted to aid in providing adequate nutrition.

On hospital day 17, patient H was alert, oriented, answering questions, and following commands. He was still unable to move his left extremities. His target serum level of sodium was decreased to the reference level, and his heart rate ranged from 75/min to 83/min with treatment of metoprolol alone.

Evaluation and treatment by physical and occupational therapists and speech and language pathologists were started once patient H was medically able to tolerate these interventions. Patient H was evaluated by personnel from rehabilitation medicine; they recommended transferring him to a skilled nursing facility for special care when he was discharged from the hospital. Patient H’s condition became stable enough for him to be transferred to a telemetry unit on hospital day 20, where he stayed until he was ready for discharge on day 24.

Upon discharge, patient H was admitted to a skilled nursing facility because of his continued need for assistance with activities of daily living and for additional physical, occupational, and speech therapies. He was able to use his left leg and hand with assistance. The consensus of the medical team was that patient H needed long-term anticoagulation to prevent further emboli formation. Therefore, warfarin was prescribed as part of his home medications, and a goal international normalized ratio of 2 to 3 was set.28

Approximately 1 month after discharge from the hospital, patient H returned for a follow-up appointment with the neurology department. Although he was not back to his baseline, patient H had improved; he was consistently able to follow commands in answering questions and moving his extremities per request. He was able to touch his nose with his left hand and raise his left foot. He was safely ambulating with assistance of a wheelchair. He continued therapy at the nursing facility.

Table 3

Scores on National Institutes of Health Stroke Scale for patient Ha

Table 4

Selected laboratory results for patient H during 20-day stay

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Atrial fibrillation and atrial flutter are the most important modifiable risk factors frequently associated with cardioembolic stroke.29 Patients with comorbid heart disease such as atrial fibrillation and mitral valve stenosis are at great risk for future embolism.3,29 However, up to 80% of stroke in people with atrial fibrillation can be prevented.3,29 Stroke in patients with atrial fibrillation tends to be more severe than in stroke patients without atrial fibrillation and is accompanied by a marked reduction in quality of life.3 Atrial fibrillation is associated with poor outcomes and an increase in hospital mortality. Several predictors of mortality among consecutive patients with cardioembolic stroke have been identified.3,29,30 Decreased consciousness, limb weakness, presence of congestive heart failure, male sex, and age appear to be associated with in-hospital mortality.30

The American Heart Association/American Stroke Association has published guidelines10 for the early management of patients with acute ischemic stroke. General supportive care and treatment of the acute phase and subsequent complications should be started immediately. Medical care and nursing interventions for patient H are discussed in Table 5. The most important part of stroke treatment is recognizing that time plays a crucial role in the patient’s outcome.10 In order to achieve the best outcomes, stroke patients must receive medical interventions as soon as the signs and symptoms of stroke are identified. For patient H, both the helicopter and medical teams were able to provide quick assessments and begin treatment in a timely manner, ultimately playing a large part in his overall clinical success.

General supportive care and treatment of the acute phase and subsequent complications should be started immediately for patients with acute ischemic stroke.

The neurological examination should be brief but thorough. The examination can be enhanced by using a formal stroke scale, such as the National Institutes of Health Stroke Scale.10–12 The stroke scale not only helps quantify the degree of neurological deficit but also facilitates communication between health care professionals, identifies the possible locations of vessel occlusion, provides early prognosis, helps determine patient eligibility for various interventions, and indicates the potential for complications.10–12

Noncontrast CT of the head is universally considered a first-line neurodiagnostic tool for stroke.10 Although noncontrast CT scans will not visualize an acute ischemic stroke in the stroke’s earliest stages, they will show the presence of blood, which provides quick information about a patient’s eligibility for thrombolysis treatment.3,10 Patient H had a head CT scan immediately after he arrived in the emergency department to determine the stroke subtype. Then, he received thrombolytic therapy. In addition, laboratory tests, especially measurements of levels of troponin I and brain-type natriuretic peptide, help health care providers identify stroke subtypes.31 Darki et al31 found elevated levels of cardiac biomarkers during the acute period of ischemic stroke, with a significant correlation with abnormality in cardiac wall motion.

An interprofessional team provided advanced medical treatment for patient H to begin early management and prevent complications. Patient H experienced cerebral edema, a respiratory infection, cardiac dysrhythmia, DVT, dysphagia, and a urinary tract infection. All of his complications were diagnosed and treated with the appropriate interventions. Moreover, a feeding tube was inserted to provide continual nutrition because dehydration and malnourishment may delay recovery after stroke.32 Because patient H had a history of atrial fibrillation and he had a prosthetic valve, the health care team was aware of the high risk for emboli. The team recognized that the patient’s previous anticoagulation regimen of clopidogrel did not protect him from cardiac emboli, and this knowledge led them to consider having patient H change to warfarin therapy with a targeted international normalized ratio after discharge from the hospital.25 Patient H was also appropriately discharged to a skilled nursing facility to continue the special care required by stroke patients with complications.

Although patient H survived this instance of acute stroke with minor disabilities, he remains at risk for stroke recurrence. Prevention measures should now focus on his risk factors. Nurses need to provide both stroke patients and the patients’ family members with basic information about stroke pathophysiology, risk factors, strategies for modification of risk factors, emergency action during stroke, and management and rehabilitation for stroke.10 Nurses must consider the patient’s education ability and barriers such as limitations in recording and giving return information.10,33 Therefore, evaluations of the knowledge of stroke survivors before and after education are recommended.33

Nursing care should focus on treating risk factors such as diabetes mellitus, hypertension, and cardiac disease. Lifestyle changes must be evaluated and included in the education about secondary stroke prevention.10,33 Strong evidence indicates that smoking is an independent risk factor for ischemic stroke.34 Therefore, health care providers should advise every stroke survivor who has smoked in the past to quit. They should also encourage patients who are heavy drinkers to reduce consumption of alcohol.34 Moreover, physical activity can have an effect in lowering blood pressure and body weight, improving vasodilatation, enhancing glucose tolerance, and improving cardiovascular health.34 Active persons have a 20% lower risk for stroke than do persons who are inactive, and persons who are highly active have a 27% lower risk.35 Because of patient H’s physical disability, supervision by a physiotherapist or rehabilitation professional was encouraged at least at the beginning of the exercise regimen.34

Patient H has a great risk for stroke recurrence because of his history of atrial fibrillation and valvular disease. The key element in avoiding stroke recurrence among patients with atrial fibrillation is the use of anticoagulants. Selection of appropriate anticoagulants depends on knowledge of the underlying causes of cardioembolic stroke, the risk for ischemic stroke risk, and the risk for hemorrhage.36 Anticoagulant therapy including aspirin, warfarin, or clopidogrel are the recommended medications for prevention. Patient H was prescribed warfarin because of his history of atrial fibrillation and valvular disease. Patient H must follow up regularly with a cardiologist for cardiac monitoring, screening for thrombus, and obtaining blood samples for determining his international normalized ratio.

Table 5

Nursing interventions for patient H

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This case study illustrates the course of illness and treatment of a patient who had cardioembolic stroke due to atrial fibrillation. Cardioembolic stroke is a serious condition that requires immediate intervention. Prehospital evaluation and supportive care must be provided quickly to prevent further neurological damage. Nurses must remain alert to the signs and symptoms of potentially deadly cardioembolic stroke while understanding the associated diagnostic tools, causes, pathophysiology, treatment, and prevention. Patient H required a multitude of nursing interventions to optimize his outcomes and manage his complications. Nurses should educate stroke patients and the patients’ family members about risk factors and modification of risk factors to minimize the recurrence of strokes. Furthermore, nurses are in a critical position to affect the outcomes of these patients through meticulous observation and monitoring, coordination of interprofessional care, and the application of evidence-based practices.

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With heartfelt acknowledgments to Chery Lehman, rn, phd, cns-bc, rn-bc, crrn, Augusto Parra, md, mph, faha, Deborah A. Chyun, rn, phd, faha, faan, and Neesha Ramchandani, pnp, cde.

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  • See also

    To learn more about caring for patients who have experienced a stroke, read “Functional Status and Disability in Patients After Acute Stroke: A Longitudinal Study” by López-Espuela et al in the American Journal of Critical Care, March 2016;25:144–151. Available at

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  1. Centers for Disease Control and Prevention. Prevalence of stroke—United States, 2006–2010. MMWR Morb Mortal Wkly Rep. 2012; 61(20):379–382. . Accessed November 8, 2016.

Table 1

Risk factors for ischemic strokea

Table 2

Signs and symptoms associated with ischemic strokea

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