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GENERAL OBJECTIVE: After an hour and 30 minutes of teaching-learning process, the target audience will be able to acquire positive attitude, adequate knowledge and beginning skills towards the CEREBROVASCULAR DISEASE. SPECIFIC OBJECTIVES I. INTRODUCTION Prayer CONTENT TIME ALLOT MENT 3 mins METHOD OLOGY Song of worships RESOURCE S Human Resources: Knowledge and skills of the reporter and participatio n of the class. Knowledge and time of the Clinical Instructor References: Internet Books (See Bibliography) Material resources: Ballpens Pencils EVAL UATION

Cerebrovascular disease is a group of brain dysfunctions related to disease of the blood vessels supplying the brain. Hypertension is the most important cause; it damages the blood vessel lining, endothelium, exposing the underlying collagen where platelets aggregate to initiate a repairing process which is not always complete and perfect. Sustained hypertension permanently changes the architecture of the blood vessels making them narrow, stiff, deformed, uneven and more vulnerable to fluctuations in blood pressure. A fall in blood pressure during sleep can then lead to a marked reduction in blood flow in the narrowed blood vessels causing ischemic stroke in the morning. Conversely, a sudden rise in blood pressure due to excitation during the daytime can cause tearing of the blood vessels resulting in intracranial hemorrhage. Cerebrovascular disease primarily affects people who are elderly or have a history of diabetes, smoking, or ischemic heart disease. The results of cerebrovascular disease can include a stroke, or occasionally a hemorrhagic stroke. Ischemia or other blood vessel dysfunctions can affect the person during a cerebrovascular accident.

II. Enumerate the Clients general data.

Demographic Profile Name: Presbitero, Armingol Coliflores Age: 75 years old Case No: 20129484 Address: Poblacion, Sogod Cebu

Cellphone No: 09264022059 Gender: Male Civil Status: Married Date of Birth: April 27, 1937 Nationality: Filipino Religion: Roman Catholic Date/Time Admitted: November 26, 2012 @ 10:30PM Physician: Dr. Chela Marie T. Romero Chief Complaint: Left Sided Weakness Admitting Diagnosis: R/I Cerebrovascular Infarction, Right MCH, HCVD, DM TYPE 2 Vital Signs taken upon admission: T- 36.8 degree celsius P- 72 bpm R- 21 cpm BP- 140/80 mmHg III. Trace Clients Present Health Illness, Past medical History, family History HISTORY OF PRESENT ILLNESS Left sided weakness 6 hours prior to admission had sudden onset of left sided weakness, slurring of speech, (-) fever , persistence prompted admission. Past Medical History Patient A.C.P. is hypertensive for 2 years, diabetic with no bronchial asthma. Has been hospitalized last 2010 at Cebu Doctors Hospital. No food and drug allergies and a previous smoker, not alcoholic and with no immunizations. Family History Hypertension- Yes Diabetes Mellitus- No CAD- No Cancer- No Bronchial Asthma- No

Notebook Laptops DLP Tables Chairs Papers Flash Drives Airconditio ner Lights

IV. Learn beginning concepts about the Human Nervous System

VII. Review and trace the pathophysiology of CVD VIII. Discuss the different kinds of medical management. VIII.MEDICAL MANAGEMENT VIII.1 Diagnostic Exams Refer to Appendix A VIII. 2 Medications Refer to Appendix B VIII. 3Nursing Care Plan Refer to Appendix C IX. Formulate and rationalized the discharge plan for a client with Discharge Plan Refer to Appendix D


Glascow Coma Scale Best Eye Opening Opens eyes in response to voice = 3 Best Verbal Response Confused, disoriented = 4 Best Motor Response- Localizes painful stimuli= 12 Total: 12 FBS November 27, 2012 @ 8:00 am TEST Chemistry SI Fasting Blood H 7.37 Glucose Cholesterol, Total Triglycerides VL DL Cholesterol HDL LDL 4.65 0.54 0.25 0.99 3.41

RESULT CONV 132.77 179.81 47.24 9.67 38.28 131.86

INTERPRETATION Diabetes Mellitus, Cerebral Lesions, Infection Normal Normal Normal Normal Normal

November 27, 2012 @ 12:45 pm Clinical Microscopy Urinalysis Macroscopic Color Transparency pH Specific Gravity Glucose Protein

Yellow Clear 7.5 1.010 Negative Negative

Microscopic Pus Cells RBC Epithelial Cells Bacteria Amorphous Urates 0-3 1-5 Rare Few Rare

Hematology Complete Blood Count Result Leukocyte H 10.2 Unit x10^9/L Reference Ranges 4.0-10.0 Interpretation Acute infection, polycythemia vera, myelofibrosis Anemia after hemorrhage when blood volume has been restored Various anemia, severe or prolonged hemorrhage Normal


L 3.90




L 11.4






MCV MCH RDW Platelet Count

88 L 26.8 11.9 207

fl pg % x10^9/L

80-100 27.0-32 11.0-16 150-500

Normal Microcytic Anemia Normal Normal

Differential Count Result Neutrophil Lymphocyte Monocyte Eosinophil Basophil 11/26/12 11:49 PM Immunology Control Test % Activity INR Control Test Result 13.2 13.1 93.6 0.99 31.0 31.1 Unit secs. Secs. % secs. secs. Interpretation Normal Normal Normal Normal Normal Normal H 80.2 L 13.6 4.8 1.2 0.2 Unit % % % % % Reference Ranges 45-65 20-40 2-11 0-5 0-2 Interpretation Acute Infection, Malignant Disease Aplastic Anemia, Immunodeficiency Normal Normal Normal

Result Chemistry Potassium Glycosylated SI 3.63 H 7.1 CONV

Unit mmol/L %

Reference Ranges 3.5-5.3 4.5-6.3

Interpretation Normal Diabetes Mellitus, Cerebral Lesions and Infection Normal Normal

Sodium Creatinine

138.0 88.03


mmol/L Mmol/L

135-148 53-97


Generic/ Brand Name & Classification (10%) Generic: lactulose

Dose, strength & Formulation (10%) Ordered: .

Indication/Mechanism of Drug Action ( 15%)

Adverse/Side effects (15%)

Nursing Responsibilities (15%)

Rationale (10%)

Client teaching (20%)

Indications: *To treat constipation *To prevent and treat hepatic encephalopathy

GI: Abdominal cramps and distention, diarrhea, flatulence ENDO: Hyperglycemia

*Monitor diabetic patient for hyperglycemia *Advise patient to take lactulose with food or dilute with juice *Advise diabetic patient to check blood glucose level often *Bowel movement may not occur for 24 to 48 hrs after taking drug *Plan to replace fluids if frequent bowel movements

*Because lactulose contains galactose and lactose (Jones & Bartlett, 2011) *To reduce sweet taste (Jones & Bartlett, 2011) *To report hyperglycemia (Jones & Bartlett, 2011) *Because oral lactulose must Rreach the colon to work (Jones & Bartlett, 2011) *Hypovolemia occur (Jones & Bartlett, 2011)

*Direct patient not to use other laxatives while taking lactulose *Instruct patient to report abdominal distention or severe diarrhea. *Instruct patient to increase fluid intake if frequent bowel movements occur.

Timing: Mechanism of Action: Arrives unchanged in the colon, where it breaks down into lactic acid and small amounts of formic and acetic acid, acidifying fecal contents. Acidification leads to increased osmotic pressure in the colon, which, in turn, increases stool water content and softens stool. Also, lactulose makes intestinal contents more acidic than blood. This prevents ammonia diffusion from intestine into blood, as occurs in hepatic encephalopathy. The trapped ammonia is converted into ammonia

Other: Hypernatremia, hypokalemia, hypovolemia

Brand: Acilac Duration: Unknown

*Teach patient with chronic constipation the importance of exercising, increasing fiber in diet, and may increasing fluid intake. *Do not self-medicate with another laxative due to slow onset of drug action.

Classification: Ammonia reducer, laxative

Other forms:

ions and, by lactuloses cathartic effect, is expelled in feces with other nitrogenous wastes.

Generic/brand & classification Generic: Citicoline Brand: Zynapse Classification: Neurotonics Nootropics

Dose, strength & formulation Ordered: Citicoline 600mg IVTT Timing: Duration:

Indication & mechanism of action Indication: -cerebrovascular disease, accelerates the recovery of consciousness and overcoming motor deficits.

Adverse/ side effect & drug interaction

Nursing responsibilities 1.The supplement should not be taken in the late afternoon or at night. 2. assess allergy to warfarin.


Client teaching

Other types: Capsule IM injection

Adverse effect: -Body temperature elevation -Restlessness -Headaches -Nausea and vomiting -Diarrhea Mechanism of action: -Low or high blood Citicoline seems to increase a pressure brain chemical called phosphatidylcholine. This brain -Tachycardia chemical is important for brain -Sleeping troubles or insomnia function. Citicoline might also decrease brain tissue damage -Blurred vision -Chest pains when the brain is injured.It is usually known that Drug interaction: phospholipid, especially Levod lecithin, decreases following opa decline in brain activity with cerebral trauma. Citicoline, which is a co-enzyme, accelerates the biosynthesis of lecithin in the body. http://www.prescriptiondruginfo.com/Discuss/mechanismaction-of-citicoline-192971.htm

1.Because it can cause difficulty sleeping. (http://www.scribd.com) 2. to avoid blood coagulation. (http://www.scribd.com) 3. to avoid error. (http://www.scribd.com) 4. to aid with diagnosis of neurological disorder. (http://www.scribd.com) 5. Slurred speech may be temporary or permanent. (http://www.scribd.com)

3. verify doctors order. 4. monitor neurologic status.

Teach patient on how to take the drug. Advise patient to take citicoline as prescribed. Arrage for regular follow-ups. Tell the S.O to note adverse reaction.

5. note if there is slurring of speech.






GENERIC: mannitol


ORDERED: 100cc IV Bolus


INDICATIONS: To reduce intracranial intraocular pressure.



Exposed to low temperature, place solution in hot-water bath to redissolve crystals. Check weight and monitor BUN AND serum creatinine electrolyte levels daily. During I.V. infusion of mannitol, monitor vital signs, central venous pressure, and fluid intake and output every hour. Provide frequent mouth care.


Inform patient that he may experience dry mouth and thirst during mannitol therapy. Instruct patient to report chest pain, difficulty breathing, or pain at I.V. site.

TIMING: BRAND: Every 9 Hours


Antigalucoma, diagnostic agent, osmotic diuretic, OTHER FORMS: urinary irrigant I.V. Infusion Irrigation Solution

or CNS: Chills, dizziness, fever, headache, seizures CV: Chest pain, heart failure, hypertension, tachycardia, thrombophlebitis EENT: Blurred vision, MECHANISM OF ACTION: dry mouth, rhinitis GI: Diarrhea, nausea, Elevates plasma osmolality, thirst, vomiting causing water to flow from GU: Polyuria, urine tissues, such as brain and retention eyes, and from CSF, into RESP: Pulmonary extracellular fluid, thereby edema decreasing intracranial and SKIN: Extravasation intraocular pressure. with edema and tissue necrosis, rash, urticarial As an osmotic diuretic, Other: Dehydration, mannitol increases the hyperkalemia, osmolarity of glomerular filtrate, hypernatremia, which decreases water hypervolemia, reabsorption. This leads to hypokalemia, increased excretion of water, hyponatremia(dilutional), sodium, chloride, and toxic metabolic acidosis, substances. water intoxication. As an irrigant, mannitol DRUG INTERACTION minimizes the hemolytic effects of water used as an irrigant Digoxin: Increased risk

If crystals form in mannitol solution.

To know if the patient is experiencing electrolyte imbalance.

It may cause hypertension, tachycardia and urinary retention.

To relieve thirstand dry mouth.

and reduces the movement og of digitalis toxicity. hemolyzed blood from the urethra to the systemic circulation, which prevents hemoglobinemia and serious renal complications.

Generic / Brand

Dose, strength & Indication / Mechanism of

Adverse / Side



Client Teaching

Name & Classification Generic: Paracetanol


Drug Action




Classification: Antipyretic, nonopioid analgesic

Tell patient that tablets may be Ordered: Indications: Adverse Reactions Before and during to know drugs crushed or 500 mg PRN for To relieve mild to GI: Abdominal long-term therapy, effectiveness. swallowed whole. fever moderate pain from pain, monitor liver (Jones & Bartlett; 2011., Instruct patient to read headache, muscle ache, hepatotoxicity, function test results, 10th Ed., p. 25 ) manufacturers Timing: backache, minor nausea, including label and follow dosage guidelines PRN arthritis, common cold, vomiting AST, ALT, precisely. toothache, or HEME: Hemolytic bilirubin, and Explain that infants and childrens Duration: menstrual cramps; to reduce anemia (with long- creatinine levels, acetaminophen 3-4 hours fever term as ordered. liquid arent equal in drug use), leukopenia, concentration and arent Other forms: Mechanism of Action: neutropenia, Monitor renal interchangeable. CAPLETS, Inhibits the enzyme pancytopenia, function in patient to avoid any incident Advise patient to use CAPSULES, cyclooxygenase, blocking thrombocytopenia on longterm of drug toxicity. manufacturers dropper CHEWABLE prostaglandin production SKIN: Jaundice, therapy. Keep in (Jones & Bartlett; 2011., or dosage cup for measuring liquid TABLETS, and interfering rash, urticaria mind that blood or 10th Ed., p. 24 ) acetaminophen. ELIXIR, with pain impulse Other: albumin in urine Advise him to contact prescriber E.R. CAPLETS, generation in the Angioedema, may indicate before GELCAPS, peripheral nervous system. hypoglycemic coma nephritis; taking other prescription or OTC LIQUID, Acetaminophen decreased urine products SOLUTION, also acts directly on Interactions output may indicate because they may contain SPRINKLES, temperature-regulating DRUGS renal failure; and acetaminophen. SUSPENSION, center in the hypothalamus anticholinergics: dark brown urine Teach patient to recognize signs of TABLETS by inhibiting Decreased onset of may indicate hepatotoxicity, synthesis of prostaglandin acetaminophen presence of the such as bleeding, easy bruising, E2. action metabolite and malaise, which commonly (Jones & Bartlett; 2011., barbiturates, phenacetin. occurs with 10th Ed., p. 24 ) carbamazepine, chronic overdose. hydantoins, Expect to reduce isoniazid, dosage for patients rifampin, with

sulfinpyrazone: Decreased therapeutic effects and increased hepatotoxic effects of acetaminophen lamotrigine, loop diuretics: Possibly decreased therapeutic effects of these drugs oral contraceptives: Decreased effectiveness of acetaminophen probenecid: Possibly increased therapeutic effects of acetaminophen propranolol: Possibly increased action of acetaminophen zidovudine: Possibly decreased zidovudine effects

renal dysfunction. to avoid nehprotoxicity (Jones & Bartlett; 2011., Store suppositories 10th Ed., p. 24 ) under 80 F (26.6 C). to keep drugs effectiveness. (Jones & Bartlett; 2011., 10th Ed., p. 24 )

Generic/Brand Name & Classification Generic: Amlodipine

Dose, Strength & Formulation Ordered: Vasalat 5mg 1 tab OD Timing:

Indication/Mechanism of Drug Action Indication: -Treatment of essential hypertension and angina Mechanism of Action:

Adverse/Side Effect Drug Interaction Adverse Effect: CNS: Dizziness Lightheadedness Fatigue Lethargy CV: Peripheral edema Arhythmias Dermatologic: Flushing, rash GI: Nausea Abdominal discomfort

Nursing Responsibility 1.Assess patient for history of allergy to amlodipine, impaired hepatic or renal function, sick sinus syndrome, heart block, or CHF.

Rationale 1. Allergy reaction may occur, and may cause drug toxicity.

Client Teaching 1.Advise patient to take medication as directed, even if feeling well. Take missed doses as soon as possible unless almost time for next dose; do not double doses. May need to be discontinued gradually. 2.Advise patient to avoid large amounts (68 glasses of grapefruit juice/day) during therapy.

Brand: Vasalat Duration: Inhibits calcium ions from entering the slow channels or select voltage sensitive areas of vascular smooth muscle and myocardium during depolarization.

Classification: Other Forms: Calcium-channel blocker

2.Assess for adverse drug reactions; report irregular heartbeat, swelling of the hands and Drug Interaction: feet, shortness of In patients with severe breath, pronounced coronary artery disease, dizziness, and amlodipine can increase the constipation. frequency and severity of angina or actually cause a 3.Monitor BP and heart attack on rare cardiac occasions. This rhythm. phenomenon usually occurs when first starting 4. Take medication amlodipine, or at the time with meals. of dosage increase. Excessive lowering of blood pressure during 5.Assist patient initiation of amlodipine when ambulation treatment can occur, after drug especially in patients administration. already taking another blood pressure lowering medication. In rare instances, congestive heart failure has been associated with amlodipine, usually in patients already on a beta

2. Drug adverses reaction could cause complicatio ns.

3. Instruct patient on correct technique for monitoring pulse. 3. For baseline Instruct patient to data. contact health care professional if heart rate is <50 bpm. 4. Can cause G.I 4. Caution patient to irritation. change positions slowly to minimize 5 . To avoid orthostatic injury. hypotension. 5.May cause drowsiness or dizziness. Advise patient to avoid driving or other activities requiring alertness until response to the

Generic/ Brand Name & Classification (10%) Generic: Roswin

Dose, strength & Formulation (10%) Ordered: 10mg iTab OD P.O

Indication/Mechanism of Drug Action ( 15%)

Adverse/Side effects (15%)

Nursing Responsibilities (15%)

Rationale (10%)

Client teaching (20%)

Indications: Adjunct to diet to reduce elevated total cholesterol (total-C), LDL-cholesterol (LDL-C), apolipoprotein B (apo-B), non-HDLcholesterol (non-HDL-C) & triglycerides (TG) levels & to increase HDL-C in patients w/ primary hypercholesterole mia(excluding heterozygous familial & non-familial) & mixed dyslipidemia (Fredrickson type IIa & IIb); treatment of patients w/ elevated serum TG levels (Fredrickson type IV); reduce LDL-C, total-C & apo-B in patients w/ homozygous familialhypercholesterolemi a as an adjunct to other lipid-lowering treatments Mechanism of Action:

Timing: Brand: 8am Rosutat Duration: 3-5 hours Classification: Other forms: Cardio/ LipidRegulating Drugs/ Statins

Interactions DRUGS antacids: Decreased blood rosuvastatin level if given within 2 hours of rosuvastatin cyclosporine, gemfibrozil, lopinavir/ritonavir, niacin, other lipidlowering drugs: Increased rosuvastatin level and risk of myopathy oral contraceptives: Increased blood ethinyl estradiol and norgestrel levels warfarin: Increased INR Adverse Reactions CNS: Asthenia, depression, dizziness, headache, hypertonia, insomnia, memory loss, paresthesia CV: Chest pain, hypertension, peripheral

Use rosuvastatin cautiously in patients who consume large quantities of alcohol or have a history of liver disease Monitor serum lipoprotein level. Notify prescriber if proteinuria or hematuria appears on patients routine urinalysis

-drug is contraindicated in patients with active liver disease or unexplained persistent elevations of transaminase levels. (Jones & Bartlett, 2011) -to evaluate response to therapy. (Jones & Bartlett, 2011) -rosuvastatin dosage may need to be reduced. (Jones & Bartlett, 2011)

Encourage patient to follow a low-fat, lowcholesterol diet. Tell patient to wait at least 2 hours after taking rosuvastatin before taking antacids. Instruct patient to notify prescriber immediately about muscle pain, tenderness, or weakness, especially if accompanied by malaise or fever. Tell woman of childbearing age about the need to use reliable contraceptive method while taking drug. Instruct her to notify prescriber at once if she suspects she may be pregnant.

Cholesterol and triglycerides circulate in the blood as part of lipoprotein complexes. Rosuvastatin inhibits the enzyme 3hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase. This inhibition reduces lipid levels by increasing the number of hepatic low-densitylipoprotein (LDL) receptors on the cell surface to increase uptake and catabolism of LDL. It also inhibits hepatic synthesis of verylowdensity lipoprotein (VLDL), which decreases the total number of VLDL and LDL particles. (Jones & Bartlett, 2011)

edema EENT: Pharyngitis, rhinitis, sinusitis ENDO: Thyroid function abnormalities GI: Abdominal pain, constipation, diarrhea, elevated liver function test results, gastroenteritis, hepatic failure, hepatitis, jaundice, nausea, pancreatitis GU: Acute renal failure, proteinuria, UTI MS: Arthralgia, arthritis, back pain, myalgia, myopathy, rhabdomyolysis RESP: Bronchitis, increased cough SKIN: Rash, urticaria Other: Angioedema, flulike symptoms, generalized pain, infection





NURSING ACTIONS & NURSING ORDERS Nursing Actions: After 8 hours of Nursing intervention, patient will be able to display decrease signs of ineffective tissue perfusion as evidence by gradual improvement of vital signs. INDEPENDENT 1. Assess higher functions, including speech, if patient is alert


EVALUATION After 8 hours of Nursing intervention, patient was able to display decreased signs of ineffective tissue perfusion as evidence by gradual improvement of vital signs.

GOAL: After 8 hours of Ineffective The Cerebral presence of Nursing intervention, patient will be able to Tissue partial display decrease signs of perfusion blockage of ineffective tissue related to the blood perfusion as evidence by Interruption vessel can be gradual improvement of Objective: of blood flow: multifactorial. vital signs. Occlusive These can be Received patient disorder, due to vaso Outcome criteria: lying on bed, .. hemorrhage; constriction, Specifically the client Cerebral platelet Difficulty will: vasosasm, adherence on producing cerebral rough speech 1. Maintain edema ? surface, fat Changes in usual/improved (Friend unsa accumulation motor/ sensory jud diay ni level of and therefore responses noted specifically decreases consciousness Changes in vital iyang CVD?) elasticity of 2. Demonstrate signs especially secondary to vessel wall stable vital signs the blood 3. Absence of signs Cerebrovasc leading to pressure of increased ular disease alteration of Difficulty in intracranial blood swallowing pressure perfusion with Vital signs are as the initiation follows: 4. Display no further of the clotting deterioration/ sequence. Trecurrence of This may later deficits lead to the

1. Changes in cognition and speech content are an indicator of location/degree of cerebral involvement and may indicate deterioration/increased ICP. (Doenges;2006;p. 240) 2. Fluctuations in pressure may occur because of cerebral pressure/injury in vasomotor area of the brain. Hypertension or postural hypotension may have been a precipitating factor. Hypotension may occur

2. Monitor vital signs, i.e., note: Hypertension/hypotensio n, compare BP readings in both arms;Heart rate and rhythm

PRBP- 170/100?

development of thrombus which can be loosened and dislodged in some areas of the brain such as mid cerebral carotid artery that may lead to alteration of blood perfusion and further develop to cerebral infarct. (Ellenbogen, 2012 ; p.192)

because of shock. Increased ICP may occur because of tissue edema or clot formation. (Doenges, 2006; p.239) 3. Document changes in vision, e.g., reports of 3. Specific visual blurred vision, alterations alterations reflect area in visual field/depth of brain involved, perception. indicate safety concerns, and influence choice of interventions. (Doenges 2006; p.240) 4. Position with head slightly elevated and in neutral position.

4. Reduces arterial pressure by promoting venous drainage and may improve cerebral circulation/perfusion. (Doenges, 2006; p.240)

5. Prevent straining at stool, holding breath. 5. Valsalva maneuver increases ICP and potentiates risk of rebleeding. (Doenges,2006;p.240) 6. Maintain bedrest; provide quiet environment;

restrict visitors/activities as indicated. Provide rest 6. Continual stimulation /activity can periods between care increase ICP. Absolute activities, limit duration of rest and quiet may be procedures. needed to prevent rebleeding in the case of hemorrhage. (Doenges,2006;p.240 DEPENDENT 1. Administer supplemental oxygen as indicated 1. Reduces hypoxemia, which can cause cerebral vasodilation and increase pressure/edema formation. (Doenges,2006;p.240)

2. Administer medications as indicated: *Anticoagulants


-May be used to improve cerebral blood flow and prevent further clotting when embolus/thrombosis is the problem. Contraindicated in hypertensive patients because of increased risk of hemorrhage.Used with caution in hemorrhagic disorder to prevent lysis of formed clots and

subsequent rebleeding. (Doenges,2006;p.240 -Preexisting/chronic hypertension requires cautious treatment because aggressive management increases the risk of extension of tissue damage. Transient hypertension often occurs during acute stroke and resolves often without therapeutic intervention. (Doenges,2006;p.240 -These agents are being researched as a means to protect the brain by interrupting the destructive cascade of biochemical events (e.g., influx of calcium into cells, release of excitatory neurotransmitters, buildup of lactic acid) to limit ischemic injury. (Doenges,2006;p.240

*Neuroprotective agents, e.g., calcium channel blockers, excitatory amino acid inhibitors,


1. Monitor laboratory studies as indicated, e.g., prothrombin time (PT)/activated partial thromboplastin time (aPTT) time, Dilantin level.

1. Provides information about drug effectiveness/therape utic level. (Doenges,2006;p.240

S> dli kaayo masabtan iyang estorya maglisod siya ug litok sa iyang gustong ipasabot nako as verbalized by the patients significant others. O> received patient lying on bed, awake, afebrile, conscious, -speaks with difficulty -difficulty in forming words or sentences -difficulty in expressing his needs with the following vital signs. T: P: R: BP:

Impaired verbal communication related to cerebral impairment as evidenced by slurring of speech.

A stroke is a medical emergency that occurs when the blood flow to the brain is interrupted. This typically occurs when a blood clot blocks the flow of blood, thereby preventing the brain from getting the oxygen that it needs. Without oxygen, the brain cannot function properly and could be permanently damaged. Stroke may cause language and speech problems, abnormally slow and cautious behavior, problems judging distances, impaired judgment and behavior, short-term memory loss and other memory problems, balance problems, and more. Therefore, it is extremely important that everyone know about the symptoms of strokes. If caught early, brain damage treatment can take place and the stroke victim can live an ordinary life. (Morbys, 2006).

After 8hrs of nurse-client interventions the patient will be able to establish method of communication in which needs can be understood. OUTCOME CRITERIA: Specifically the patient will be able to: 1. Communi-cate needs in an effective manner. 2. Identify on plan appropriate alternative speech methods after healing. 3. Use resources appropriate-ly. 4. Indicate an understanding of the communication problems.

INDEPENDENT 1. Assess the functional type as the patient does not seem to understand the words or have difficulty speaking / making sense of their own. 1. To help determine the areas and degree of cerebral damage and the difficulty that occurs in several stages of the communication process. (Doenges,2006). 2. Permits patient to express needs and concern. (Doenges,2006). 2. Provide alternative means of communication appropriate to patients needs such as sign language, picture, pen and paper. 3. Encourage significant others to talk with the patient, providing information about family and daily happenings. The patient was able to establish method of communica-tion in which needs can be expressed.

3. Significant others may feel selfconscious in onesided conversation, but knowledge that he or she is assisting patient to regain or maintain contact with reality and enabling patient to feel part of family unit can reduce feelings of awkwardness. (Doenges,2006). 4. Presence of other problem influences plan for alternative communication. (Doenges,2006).

4. Determine

5. Loss of speech and stress of alternative