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1 . Anatomy and fisiology 1.

1 Anatomy

1.2 Fisiology Brain blood obtained through the two systems the carotid system (internal carotid artery right and left) and vertebral systems. Koritis internal artery, after the split from the common carotid artery, up and into the carnial cavity through a canal karotikus, walking in the sinus cavernosum, artery ramify oftalmika optic nerve and retina for, finally a two pronged: the anterior cerebral artery and middle cerebral artery. To the brain, this system gives blood to the frontal lobe, parietal and temporal lobe sections. Vertebral system formed by the right and left vertebral arteries that originate in the subclavian artery, toward the base of the skull through tranversalis canal in the cervical vertebral column, enter the cavity of the cranium through the foramen magnum, and then each pair of branch arteries serebeli inferior. In the limit of the medulla oblongata and pons, both united basilaris artery, and after removing the 3 groups of arterial branches, at the level of mensensefalon, ended up as a pair basilaris artery branches: posterior cerebral artery, the blood service for the occipital lobe, and the medial temporal lobe.

To 3 pairs of these cerebral artery branches skimmed the surface of the brain, and other parts of the anastomoses. Branches smller penetrate into the brain tissue an is also interconnected with the cerebral arterial branches other. To ensure the delivery of blood to the brain, there are at least there collateral system between the carotid and vertebral systems, namely: Circle of willis, the vascular environment composed of the right middle cerebral artery and left anterior communicating artery (which connects the two anterior cerebral arteries), a pair of middle cerebral artery and posrerior communicating artery posterior (which connect the middle cerebral artery and posterior) and right the left. Matting artery is located at the base of the brain Middle cerebral artery anastomosis between the internal and external carotid artery in the orbit, respectively through the arteries to the facial artery oftalmika and external maxillary artery. The relationship between carotid arterial system with external vertebral (extracranial arteries). In additional there are more relationships between the branches of these arteries, so that by the end of the artery Buskrik no (true end arteriges) in brain tissue. Venous blood drained from the brain through two systems: the internal veins, which collect the blood into the vein of Galen and sinus rectus, and the external veins are located on the surface of the brain hemispheres, and bled into the superior sagittal sinus and basal sinuses laterals, and so on through jugular veins to the heart shed. Carotid system mainly serves the two hemispheres of the brain, and especially to give blood vetebrabasilaris system for brain stem, cerebellum and the posterior cerebral hemispheres. Blood flow in the brain (ADO) is influenced mainly there factors. Two of the most important factor is the pressure to pump blood from the capillaries into the arterial system, venous system, and resistance (peripheral) blood vessels of the brain. The third factor, the factors own blood is the blood viscosity and its kongulabilitas (ability to clot). From the first factor, the most important is the systemic blood pressure (cardiac factors, blood, blood vessels, etc) and factor specific capabilities of the brain blood vessels (arterioles) to contract when the systemic blood pressure rises and dilates when the systemic blood pressure decreases. The accommodation system is called the brain arterioles otoregulasi brain blood vessels (the normal functioning when the systolic pressure between 50-150 mmHg). Blood factors, in addition to blood viscosity and freezing power,as well as among such content / CO2 and O2 partial pressure effect on arteriolar diameter. levels / increased CO2 partial pressure, PO2 is decreased, and the network environment acidic (low PH), causing vasodilation, whereas when the CO2 partial pressure drop of blood, PO2 rose, or a high pH environment, then there is vasoconstriction. Viscosity / high blood viscosity reducing ADO. While a large koagulobilitas also facilitate, blood flow is slow, due to decreased ADO.

. Review the theory of stroke non hemorrhagic

2.1 Definition Stroke or cerebrovascular injury is loss of brain function caused by the cessation of blood supply to the brain often is the culmination of cerebrovascular disease for serval years. (Suzanne C. smeltzer , 2002) Circulatory disorder in the brain (GPDO), known as CVA ( cerebral Vascular Accident) is a neurodegenerative disorder caused by impaired blood flow in the brain that can occur suddenly (within seconds) or rapidly (within hours) with symptoms or sign corresponding to the affected area. (harson, 1996). 2.2 Etiology That causes include : 1 . Thrombosis (clot of fluid in the brain blood vessels) 2 . Cerebral embolism (blood clot or other material) 3 . Ischemia (decrease blood flow to areas of the brain) ( smeltzer c. Suzanne, 2002, hal 2131) Risk factor in stroke: 1 . Hypertension 2 . Cardiovascular disease 3 . High idesterol 4 . Obesity 5 . Increased hematocrit 6 . Diabetes mellitus 7 . Drug abuse 8 . conception of alcohol 2.3 Pathophysiology Cerebral infarction is the reduction of blood supply to a particular area in the brain. The extent of infarction depends on factors such as the location and size of the blood vessels and inadequate collateral circulation to the area supplied by the blocked artery. The blood supply to the brain can be changed (the slower or faster) on a local disturbance (thrombus, embolism, hemorrhage, and spasm of the heart). Atherosclerosis is often a contributing factor in brain infarction. Thrombus may originate from the plaque arterosklerotik, or blood can be frozen in the stenosis area, where blood flow is slowed or turbulence. Thrombus could rupture of the blood vessel walls carried as emboli in the blood stream. Thrombus resulting in ischemia brain tissue supplied by blood vessels in question and edema and congestion in the surrounding area. Areas of edema is caused greater dysfunction than the infarct area itself. Edema can be reduced in a few hours or sometimes after a few days. With the reduction of edema clients began to show improvement. Because thrombosis is usually not fatal, if not massive bleeding. Occlusion of the blood vessel by an embolus causing cerebral edema and necrosis followed by thrombosis. If there is a septic infection will spread to the blood vessel wall, there will be an abscess or encephalitis, or if the rest of the infection are the

blood vessels that tersubbat causes dilation of blood vessels aneuresma. This will lead to cerebral hemorrhage, if aneuresma rupture or rupture. Bleeding in the brain caused by ruptured blood vessels arteriosklerotik and hypertension. vast intracerebral hemorrhage will often cause death compared to overall vascular cerebrovascular disease, because of extensive bleeding occurs destruction of brain mass, increased intracranial pressure and may cause more severe brain herniation or cerebral Falk through the foramen magnum. Death can be caused by compression of the brain stem, cerebral hemispheres, and secondary brain stem hemorrhage or bleeding into the brain stem extension. Permeation of blood into the ventricles of the brain occurs in a third of cases of brain hemorrhage in the caudate, thalamus, and pons. If the cerebral circulation is blocked, can develop cerebral anoxia. Changes desebabkan by cerebral anoxia can be reversible to within 4-6 minutes. Anoxia irreversible changes if more than 10 minutes. Cerebral anoxia can result from a variety of disorders one cardiac arrest. Other than brain parenchymal damage, due to the relative volume of bleeding will only lead to increased intracranial pressure and decreased cerebral perfusion pressure and drainage of brain disorders. Vasoactive elements of blood loss and ischemic cascade due to decreased perfusion pressure, causing the nerves in the affected area and surrounding blood pressure again.

Risk factor stroke

atherosclerosis hiperkogulasi artesis

damaged heart valve, myocardial, infarction, fibrillation, endocarditis

aneurysm malformations arteriovenous

blockage of a brain blood vessel by a blood clot, fat, and air Bleeding intracerebral permeation of blood to the brain perenkim suppression of brain tissue

cerebral thrombosis blockage of a brain blood vessel by a blood clot, fat, and air blood vessel occlusion cerebral embolism ischemic brain tissue Stroke (cerebro vascular accident)

tissue edema and congestion around

infrak brain edema and brain herniation

Deficit neurological

cerebral infarction

loss of control voluntary

1.Risk for enhancement TIK

2. decreased tissue perfusion cerebral

herniplegi and hemiparesis 4. Impaired physical mobility

Falk cerebral herniation and the foram en magrum Compression brainstem

damage to the frontal lobe capacity, memory, or intellectual functioning cortical

dysfunction, language and communication

cognitive impairment and psychological effects

disartia, dysphasia / aphasia, apraxia 9. impaired verbal communication

coma

Falk cerebral herniation and the foram en magrum Compression brainstem Depression nerve cardiovascular and respiratory

Intake nutrient Inadequate

general physical weakness

field limited attention, difficulties in understanding, forgetfulness, and lack of motivation, frustration, emotional lability, hostility, resentment, and lack of cooperation; decreased sexual desire 10. ineffective individual coping 11. change the thought process 12. decreased sexual desire 13. risk for waywardness the management

5. changes in nutrition

general physical weakness

Failure cardiovascular and respiratory

decreased level of consciousness

dysfunction, visualspatial perception and loss sensory

death 14. disturbance psychological 15. change role family 16. anxiety client and family 17. risk for decreased implementation of worship decreased ability to cough, lack of physical mobility, and production of secretions Dysfunction bladder and digestive tract

8. risk for trauma 12. disturbed sensory perception

The emphasis local network emphasis

6. Risk for impaired skin integrity

3. risk for ineffective airway clearance

7. disturbance elimination uri and avi

2.4 SIGNS AND SYMPTOMS In the non hemorrhagic stroke (ischemia), the main symptom is sudden onset of neurological deficit / subacute, preceded by prodnormal symptoms, occording at rest or get up early. And awareness is usually not decreased, except when the embolus is large enough. It usually occurs at age > 50 years (mansjoer, 2000) According to smelzer (2001), clinical manifestation of non hemorrhagic stroke consist of : 1 . field vision deficit 2 . motor deficit 3 . verbal deficit 4 . cognitive deficit 5 . emotional deficit 2.7 Treatment 1 . Diuretic : to reduce cerebral edema 2 . Anti coagulants : preventing weight / increase of thrombosis and embolization (smeltzer c Suzanne, 2002) 2.8 Diagnostic Examination 1 . CT scan show the presence of edema, hematoma, and the presence of myocardial ischemia. 2 . Cerebral angiography to help determine the specific causes of stoke such as bleeding or obstruction of the arteries. 3 . Lumbar puncture * indicates a normal pressure. * pressure increase and fluids containing blood showed the bleeding 4 . MRI : Indicates areas of infraction, hemorrhagic 5 . Ultra sound dopler : identify arteriovena disease 6 . Skull X-rays : Describes changes in the paneal gland plates. (Doengese, Marilynn, 2000) 2.9 Prognosis According Harson, influed by several factor : 1 . level of consciousness = conscious 16% die, samnolance 39% die, 71% die of salpor 2 . Age = at age 70 years or more, the rate mortality rate increased sharply. 3 . Blood pressure. 2.10 Complication According to smeltzer (2001) 1 . Cerebral hypoxia 2 . Decrease in cerebral blood 3 . Cerebral embolism

3 . Nursing Care Plan Of Non Hemorrhagic 3.1 Assessment 3.1.1 Primary Assessment Airway Blockage / obstruction of the airway caused by the buildup of secretions, cough reflex weaknes Breathing Weakness swallow / cough / protect the airway, the onset of difficult breathing and / or irregular breathing sounds heard ronchi / aspiration Circulation BP may be normal or increased, hypotension occurred in stages, tachycardia, abnormal heart sounds at an early stage, dysrhythmias, skin and mucous membranes pale, cold, cyanosis at an advanced stage 3.1.2 Secondary assessment 1. Activity and rest Subjective Data: - Difficulties in the move; weakness, loss of sensation or paralysis. - Tiredness, trouble breaks (pain or muscle spasms) Objective data: - Changes in the level of consciousness - Changes in muscle tone (flaccid or spastic), paraliysis (hemiplegia), general weakness. - Impaired vision 2. circulation Subjective Data: - History of heart disease (heart valve disease, dysrhythmias, heart failure, bacterial endocarditis), polycythemia. Objective data: - Arterial Hypertension - Dysrhythmias, ECG changes - Pulsation: the possibility of varying - Pulse carotid, femoral and iliac artery or abdominal aorta 3. ego integrity Subjective Data: - Feelings of helplessness, despair Objective data: - Emotions are unstable and improper angry, sadness, joy - Difficulties to express themselves 4. elimination Subjective Data: - Incontinence, anuria - Abdominal distension (bladder is very full), the absence of bowel sounds (paralytic ileus)

5. Eating / drinking Subjective Data: - Appetite lost - Nausea / vomiting indicates PTIK - Loss of sensation of the tongue, cheeks, throat, dysphagia - History of DM, Increased fat in the blood Objective data: - Problems in chewing (decreased reflexes palate and pharynx) - Obesity (risk factors) 6. Sensory neural Subjective Data: - Dizziness / syncope (prior CVA / TIA while over) - Headache: the intra-cerebral hemorrhage or sub arachnoid hemorrhage. - Weakness, tingling / numbness, affected side looks like a lame / off - Vision is reduced - Touch: loss of sensors on the collateral in the extremities and the face ipsilateral (same side) - Impaired sense of taste and smell Objective data: - Mental status; coma stage is usually marked bleeding, behavioral disturbances (such as: letergi, apathy, attack) and impaired cognitive function - Extremity: weakness / paraliysis (contralateral to all types of stroke, uneven hand grip, reduced deep tendon reflexes (contralateral) - Face: paralysis / parese (ipsilateral) - Aphasia (damage to or loss of the function of language, expressive possibility / difficulty saying the word, receptive / difficulty saying the word comprehensive, global / combination of both. - Loss of the ability to know or see, auditory, tactile stimuli - Apraxia: lose the ability to use motor - Reaction and pupil size: not dilated and did not react on the lateral side of the IPSI 7. Pain / comfort Subjective Data: - Headache varying intensity Objective data: - Unstable behavior, anxiety, muscle tension / facial 8. Respiration Subjective Data: - Smokers (risk factors) 9.security Objective data: - Motor / sensory: problems with vision - Changes in the perception of the body, difficulty seeing objects,

missing vigilance to the sick body - Not being able to recognize objects, colors, words, and faces never recognized - Disturbance respond to heat, cold and / disturbances in body temperature regulation - Disturbance in deciding, little attention to security, reduced selfawareness 10. Social interactions Objective data: - Problem speech, inability to communicate (E Doenges, Marilynn, 2000 case 292) 3.2 Nursing diagnosis 1. Risk for decreased TIK related to increase in intracranial volume, compressing brain tissue, and edema 2. change tissue perfusion brain related to intracerebral hemorrhage, brain occlusion, vasospasm, and cerebral edema 3. ineffective airway clearance related to artificial airway in the trachea, increased secretion of secretions and inability to cough / cough effectively secondary to pain and fatigue 4. deficit self care related to neuromuscular weakness, decrease of strength and awareness, loss of muscle control / coordination 5. impaired verbal communication related to neuromuscular weakness, decrease of strength and awareness, loss of muscle control / coordination 6. . Risk for impaired skin integrity related to long bed rest 3.3 nursing intervention Risk for decreased TIK related to increase in intracranial volume, compressing brain tissue, and edema goal: within 3x24 hours there was no increase of ICT on the client. criteria: client not agitated, the client did not complain of headache, nausea and vomiting, GCS E4, V5, M6. there is no papilledema. Viatal Sign within normal limits. Intervention Examine the causes of the situation / circumstances of the individual / cause coma / decreased tissue perfusion and possible causes of increased ICP. Monitor Vital Signs every 4 hours Rational Early detention for prioritizing interventions, reviewing neurology / signs of failure to determine the severity of treatment and surgery. normal unit cerebral circulation could be well maintained or marked fluctuations in systemic blood pressure, a decrease of outregulator mostly a sign of lowering the diffusion of local cerebral blood vasculature, with increased blood pressure (diatolik) then

coupled with increased intracranial blood pressure. An increase in blood pressure, bradycardia, dysrhythmias, dyspnea is a sign of increased ICP. Keep the head / neck in a neutral position, try to have a little cushion. Avoid using pillows that are high on the head. Observation of level of consciousness with GCS change head on one side can cause pressure on the jugular veins and impede blood flow the brain (cerebral venous drainage inhibit) for it can increase intracranial pressure. The change indicates an increase ICT awareness and is useful to determine the location and progression of the disease. 1. Reduce hypoxemia, which can increase blood volume and cerebral vasodilation and increase ICT. 2. fluid administration may be desirable to reduce cerebral edema, an increase in the minimum of the blood vessels, blood pressure, and ICT. 3. Diuretics may be used in acute pase for the water to drain from the brain cells, reducing cerebral edema, and ICT.

Collaboration: 1. Administration of oxygen as indicated 2. Giving intravenous fluids according to indicated. 3. Give an osmotic diuretic, such as mannitol, furosid

change tissue perfusion brain related to intracerebral hemorrhage, brain occlusion, vasospasm, and cerebral edema
Goal: 2x24 hours in brain tissue perfusion can be achieved optimally. criteria: the client is not anxious, not Aada complaints of headache, nausea and seizures. GCS E4, V5, M6. isokor pupil, light reflex, normal vital signs

intervention Provide a description of the client's family about the causes and consequences of increased ICP. Lay the client (bed rest) total with supine sleeping position without a pillow. monitor signs of neurological status with the GCS . Create an environment that is quiet and limit visitors.

rational family better participate in the healing process

changes in intracranial pressure could cause risk for the occurrence of brain herniation. Can reduce further brain damage Stimulus increasing activity can improve ICT increases. Rest and tranquility may be required to prevention against bleeding in cases of hemorrhagic stroke / other bleeding.

Collaboration: . provide appropriate therapy doctor's instructions, such as 1. staroid 2. aminofel 3. Antibintika

1.decrease capillary permeability 2.decrease cerebral edema 3.lower metabolic cells / consumption and seizures.

ineffective airway clearance related to artificial airway in the trachea, increased secretion of secretions and inability to cough / cough effectively secondary to pain and fatigue
goal: within 2x24 hours clients can improve and maintain the effectiveness of the airway to keep it clean and prevent aspiration. Expected outcomes: wheezing sounds clean. Does not sound crackles. Trackeal free tube blockage. Demonstrate effective cough. No Longer buildup of secretions in the respiratory tract. Respiratory rate 16-24 beats / min.

intervention
Assess the state of the airway

Rational
Obstruction may be caused by the accumulation of secretions, mucus remaining liquid, bleeding, brokospasme, and or position of the tracheostomy / endotracheal tube changing set spending segment secretions and lung ventilation, reducing the risk of atelectasis. Helps thinning secretions, secretions facilitate expenditure. oral hygine increase sense of well being and prevent bad breath. regulate ventilation and release secretions for muscle relaxation / bronchospasme.

Set / change position regularly every 2 hours.

Give drink warm if at all possible push or give good oral care after coughing. collaboration bronchodilator administration of drugs as indicated, such aminiphilin, metaproterenol sulfate (alupent), adoethaine hydrochloride (bronkosol).

deficit self care related to neuromuscular weakness, decrease of strength and awareness, loss of muscle control / coordination goal: 3x within 24 hours increased self-care behaviors. criteria: the client can indicate changes in lifestyle to take care of the needs of self, clients are able to do self-care activities in accordance with the level of skills, identify personal / community that can help. intervention
examine the rate of decline in the ability to perform ADL scale of 0-4 avoid what not to do clients and help if necessary

rational
helps to anticipate and plan for meeting the needs of individual client in a state of anxiety and subject it to prevent frustration and self-esteem client

place the furniture to the wall, away from the road

maintain security client move around the bed and lower the risk of falling furniture

. identification chapters habits, encourage drinking and increase activity kalaborasi: providing lubricants suppositories and stool / laxative

increased training and helps constipation

The main relief against bowel function or bowel

impaired verbal communication related to neuromuscular weakness, decrease of strength and awareness, loss of muscle control / coordination goal: within 2x24 hours the client can demonstrate an understanding of the problems of communication, capable of expressing feelings, being able to use the language isarat criteria: the creation of a communication in which the client's needs can be met, the client is able to respond to any cues to communicate verbally and intervantion
examine the types of dysfunction, such as the client does not understand the words or speech problems or do not understand the problem yourself

Rational
to help determine the area of the brain damage and determine the client's difficulties with most or all of the communication process, the client may have a problem in interpreting the words (aphasia, Wernicke, area and keruskan the area brocalk to determine the choice of intervention according to the type of disorder to comfort associated with the inability to communicate

distinguish aphasia with disartia give warning that in this space impaired speech, provide special bell when necessary

speak in a normal tone and avoid words that are too fast. Give the client time to respond

The client is not forced to hear, does not cause red client, and does not cause frustration

calaboration: consult a speech therapist

Traffic assess individual verbal and motor sensory and cognitive functions to identify deficits and needs therapy

Risk for impaired skin integrity related to long bed rest

goal: within 3 x 24 hour client is able to maintain skin integrity Criteria: clients want to participate against pencegahn wound, find the cause and how to prevent injuries, no signs of redness or sores

intervention
encourage you to do the exercise ROM (range of motion) and mobilization if possible change position every 2 hours

Rational
increases blood flow to all areas avoid pressure and improves blood flow

use a booster cushion or soft water under areas that stand out do massage in a prominent area of the new pressure when changing positions

avoid excessive pressure on the prominent areas

avoid damage to the capillaries

eritemia and paleness observation and palpation warm and softening is a sign of tissue damage area around the warmth and softening of the tissue by changing the position of

REFERENCE Long C,Barbara, perawatan Medikal Bedah, Jilid 2, Bandung, Yayasan Ikatan Alumni pendidikan Keperawatan Pajajaran, 1996 Tuti pahria, dkk, Asuhan Keperawatan pada Pasien dengan gangguan system persarafan, Jakarta, EGC, 1993 Pusat pendidikan tenaga kesehatan departemen kesehatan, Asuhan Keperawatan Klien Dengan Gangguan Sistem Persarafan, Jakarta, Depkes, 1996 Smeltzer C. Suzanne, Brunner & Suddarth, Buku Ajar Keperawatan Medikal Bedah, Jakarta, EGC, 2002 Marilynn E, Doengoes, 2000, rencana asuhan keperawatan, Edisi 3, Jakarta, EGC, 2000 Harson, Buku ajar : Neurologi klinis, Yogyakarta, Gajah Mada university press, 1996

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