CHAPTER III
NURSING CARE
 
3.1 Assessment
Assessment is the first step in the nursing process and basic overall
a. The main complaint
• Fever
• Chest pain similar to angina pectoris and pericarditis
• Palpitations
• Shortness of breath
b. Important Signs
• Tachycardia
• Kardomegali (rapidly occurring)
• weakened heart sound
• Rhythm gallopTanda signs of heart failure, especially right heart failure.
Assessment of patients myocarditis (Marilynn E. Doenges, 1999) include:
Activity / rest
Symptoms: fatigue, weakness.
Signs: tachycardia, decreased blood pressure, dyspnea with activity.
Breathing
Symptoms: shortness of breath (chronic shortness of breath worse at night).
Signs: DNP (paroxismal nocturnal dyspnea), coughing, wheezing inspiration; tachypnea, krekels, and ronkhi; breathing shallow.
Circulation
Symptoms: a history of rheumatic fever, congenital heart disease, cardiac surgery, heart palpitations, fainting.
Signs: tachycardia, dysrhythmias, perpindaha point of maximal impulse, cardiomegaly, frivtion rub, murmur, gallop rhythm (S3 and S4), edema, DVJ, petechiae, splinter hemorrhage, Osler nodes, Janeway lesions.
Elimination
Symptoms: a history of renal disease / renal failure; decreased frequency / jumlsh urine.
Signs: dark concentrated urine.
 
Painful
Symptoms such as pain struck and burned bert load
Signs: distraction behavior, such as anxiety.
 Security
Symptoms: a history of viral, bacterial, fungal (myocarditis; chest trauma; malignancy / irradiation thorakal; handling gear; sitem endoscopic examination of the GI / GU), decreased immune system, SLE or other collagen diseases.
Signs: fever.
 
3.2 Special Examination
a. Examination of ECG: Not a typical
• inferior ST-T changes
• cardiac conduction disorders
1. Thoracic Photo: Not your typical
• Enlarged heart or pleural effusion perikard.
1. Echocardiography:
• Enlargement of the left heart
• Can be confused with hypertrophic cardiomyopathy and mitral stenosis.
 
3.3 Nursing Diagnosis
Nursing diagnosis is a unification of the problem of real or potential patients based on data that has been collected.
Nursing diagnoses that appear in patients with myocarditis (Doenges, 1999) is
1. Pain associated with myocardial inflammation, systemic effects of infection, tissue ischemia.
2. High risk for decreased cardiac output associated with heart muscle degeneration, decreased / kontriksi ventricular function.
3. Infection associated with the spread of infectious agents
4. Impaired peripheral tissue perfusion related to penrunan cardiac output.
5. Activity intolerance related to inflammation and degeneration of myocardial muscle cells, decreased cardiac output.
6. Lack of knowledge (learning need) regarding condition, treatment plan related to lack of knowledge / memory, mis-interpretation of information, cognitive limitations, deny the diagnosis.
 
3.4 Intervention
Intervention is planning nursing actions that will be implemented to address the problem in accordance with the nursing diagnoses.
Nursing interventions and implementation occur in patients with myocarditis (Doenges, 1999).
1. Painful
Purpose: Pain is lost or controlled.
Results Criteria: - Pain is reduced or lost
  - Clients look cool.
Intervention:
• Collaboration of drugs as indicated (nonsteroidal agents: aspirin, indocin; antipyretic; steroids).
R: to relieve pain, reduce inflammation response, reduce fever; steroids given for more severe symptoms.
• Collaboration of oxygen supplementation as indicated.
R: maximizing the availability of oxygen to reduce the workload of the heart
• Provide a quiet environment and comfort measures eg change of position, rub your back, use a warm compress / cold, emotional support.
R: This action can reduce the physical and emotional discomfort of patients.
• Provide appropriate distraction techniques
R: redirect attention, provide distraction in individual activity levels.
• Menitoring complaints of chest pain and a weighting factor or lowering. Note the nonverbal cues of discomfort, for example; lay silent / anxiety, muscle tension, crying.
R: the pain is worse in the inspirations, move or lie down and disappear by sitting upright / bent.
 
2. High risk for decreased cardiac output
Objective: Identify the behavior to decrease the heart's workload.
Criteria Results -Melaporkan/menunjukkan period decreased dyspnea, angina, and dysrhythmias.
  -Shows stable cardiac rhythm and frequency.
Intervention:
• Maintain bed rest in a semi-Fowler position.
R: decrease the heart's workload, maximize cardiac output.
• Provide comfort measures eg change of position, rub his back, and entertainment activities in tolerransi heart.
R: increase relaxation and redirect the attention.
• Collaboration of drugs as indicated, such as digitalis, diuretics.
R: can be provided to increase myocardial contractility and cardiac workload meurunkan.
• Collaboration of antibiotic / antimicrobial intervena
R: is given to address the identified pathogens and prevent further heart damage.
• Monitor frequency / heart rhythm, blood pressure, and respiratory rate before and after the activity and as long as necessary.
R: help determine the degree of cardiac decompensation and pulmonary. Decrease TD, tachycardia, dysrhythmias, and tachypnea are indicative of the damage tolerance of the heart to the activity.
• Auscultation of heart sounds. Note the distance / muffled tone heart murmur, S3 and S4 gallops.
R: provide early detection of serious complications such as: GJK, cardiac tamponade.
3. The risk of the spread of infectious agents b.d infection
Objective: Do not spread the infection occurs
Expected outcomes are:-normal body temperature, 36.5 to 37 C
Normal WBC values ​​3800-9800/mcl
Intervention:
• Collaboration of antibiotics
R / antibiotics to reduce infectious agents
• Perform complete blood tests to monitor the value of granulocytes and WBC
R / to find out the value of WBC and granlosit as an indicator of infection
• Observation of vital signs
R / Monitor the patient's condition and progress further action
4. Activity intolerance
Objective: the patient has enough energy to move.
Criteria results: - Behavior reveal the ability to provide for ourselves.
 - Patients expressed able to do some activities without assistance.
 -Coordination of muscle, bone and other limbs either.
Intervention:
• Assist patients in gradually progressive exercise program as soon as possible to get out of bed, take vital signs and responses of patients at increased activity tolerance.
R: when inflammation / basic condition is resolved, the patient may be able to perform the desired activity, except for permanent myocardial damage / complications occur.
• Assess the patient's response to the activity. Watch for changes and complaints of weakness, keletiahan, and dyspnea with respect to activity.
R: myocarditis causing inflammation and possible damage to the function of myocardial cells.
• Maintain bed rest during periods of fever, and as indicated.
R: improving the resolution of inflammation during the acute phase.
• Collaboration of oxygen supplementation as indicated.
R: menmgimbangi maximize the availability of oxygen to oxygen consumption that occurs with activity
• Meantau frequency / heart rhythm, blood pressure, and respiratory rate before and after the activity and as long as necessary.
R: help determine the degree of cardiac decompensation and pulmonal.Penurunan TD, tachycardia, dysrhythmias, and tachypnea are indicative of the damage tolerance of the heart to the activity.
5. Impaired tissue perfusion bd decreased cardiac output.
Objective: Impaired tissue perfusion resolved within 3x24 hours.
Results Criteria: - RR 30-60 x / mnt
-Nadi 120-140 x / mnt.
-Temperature 36.5 to 37 C
-Cyanosis (-)
Warm-Extremity
Intervention:
• Give oxygen as needed
R / Help increase cardiac output
• Observation frequency and heart sounds
R / frequency heart sounds were normal and indicates the blood flow smoothly, which means back to normal tissue perfusion.
• Observe for cyanosis.
R / presence of cyanosis or bluish indicate impaired tissue perfusion.
• Observation TTV.
R / Monitor development of the condition of patients
• Collaboration with physicians for the provision of therapy.
R / Increase cardiac output
6. Lack of knowledge
Objective: To express understanding of the disease process and treatment regimen.
Expected outcomes:-Identify the side effects and possible complications to consider.
-Memperlihatan behavior change to prevent complications.
Intervention:
• Assess readiness and barriers to learning, including people nearby.
R: A feeling of well-being has long enjoyed affect the interests of patients / significant other to study the disease.
• Explain the effects of inflammation on the heart, the patient individually. Ajarakkn to pay attention to the symptoms associated with complication / recurrence and symptoms reported immediately to the caregiver, for example fever, increased chest pain that is not normal, weight gain, increased tolerance to activity.
R: to take responsibility for their own health, patients need to understand the specific causes, treatment and long-term effects are expected from inflammatory conditions, according to the signs / symptoms that indicate recurrence / complications.
• Instruct the patient / significant other about the dosage, purpose and side effects of medication; dietary needs; special considerations; activity is allowed / restricted.
R: the information necessary to improve self-care, increased involvement in the therapeutic program, prevent complications.
• Review the need for long-term antibiotic / antimicrobial terapy.
R: length of hospitalization / giving IV antibiotic / antimicrobial necessary until blood culture negative / other blood results showed no infection.
3.5 Evaluation
Evaluation addalah stadium on the nursing process in which the degree of success in achieving the goals of nursing assessed and the need to modify or nursing intervention defined purpose.
The evaluation is expected in patients with myocarditis (Doenges, 1999) are:
1. Lost or uncontrolled pain
2. Identify behaviors to reduce the heart's workload.
3. No systemic infection
4. Peripheral tissue perfusion returns to normal
5. Patients have enough energy to move.
6. Stating understanding of the disease process and treatment regimen.
 
 
CHAPTER IV
CLOSING
 
4.1 Conclusion
            Myocarditis is rarely obtained at the peak of the infection because the disease will be covered by the systemic manifestations of the disease and new infections clear on the recovery phase. This form is generally heal by itself, but most continue to be a form of cardiomyopathy, and there is also a cause of arrhythmias, conduction disorders or heart trouble which is structurally considered normal.
Most of the clients are not the typical complaints, may be obtained weakness, palpitations, shortness of breath, and chest discomfort. Chest pain is usually there when accompanied by pericarditis. Sometimes resembling obtained pain of angina pectoris. The most common symptoms are tachycardia that does not conform to the temperature rise. Sometimes hypotension obtained with a small pulse or the pulse interference.
 
4.2 Suggestion
            As a nurse should always alert in the management of myocarditis as it would be fatal if too late to handle it. Besides nurses also provide health education to clients and their families to understand with myocarditis and how its treatment.
 
REFERENCES
 
Anonim.2008.Inefective Endocarditis. Retrieved from: www.satriaperwira.wordpress.com On: December 6, 2010. Time: 11:00 pm.
Baswin, Ade.2009.Endokarditis. Retrieved from: www.one.indoskripsi.com On: December 5, 2010. Time: 19:00 pm.
Doenges, E. Marilynn. 1999. Nursing care plan. Jakarta: EGC.
Wulandari, Veni.2009.Endokarditis. Retrieved from: www.veniwulandari.blogspot.com On: December 5, 2010. Time: 20.00 pm.
Medika, Yasir.2009.Askep endocarditis. Retrieved from: www.yasirblogspotcom.blogspot.com On: December 8, 2010. Hours: 19:30 pm.
Muttaqin, Arif. , 2009. Nursing Clients with Cardiovascular System Disorders. Jakarta: Salemba Medika.
Patriani.2008.Askep Miokasrditis. Retrieved from: www.asuhan-nursing-patriani.blogspot.com On: December 6, 2010. At 18:30 pm.
Udjianti, Wok June. , 2010. Cardiovascular Nursing. Jakarta: Salemba.
Yuflihul-khair.2010.Endokarditis. Retrieved from: www.yuflihul-khair.blogspot.com On: December 8, 2010. Time: 19:00 pm.
Nonik.2010.All About Nursing. Retrieved from: www.nerstitis.blogspot.com On: December 13, 2010. Time: 16:15 pm

NURSING CARE (nursing) Myocarditis
CHAPTER I
INTRODUCTION
1.1 Background
Myocarditis is an inflammation of the heart muscle or myocardium. generally caused by infectious diseases, but it can be as a result of allergic reactions to drugs and toxins effects of chemicals and radiation
There is a change in the epidemiology of infective endocarditis at the present time due to the good level of general health, level of good dental health, early treatment and the use of antibiotics. The incidence of endocarditis 10-60 cases per 1,000,000 people per year worldwide and is likely to increase in the elderly.
This disease needs proper handling and treatment, and as soon as possible because if not disegerkan will result in a fatal impact.
 
1.2 Formulation of the problem
1. What is myocarditis?
2. What is the etiology of myocarditis?
3. What are the risk factors in patients with myocarditis?
4. What are the clinical manifestations of myocarditis myocarditis?
5. What are the diagnostic tests in myocarditis?
6. How nursing care myocarditis?
 
1.3 Objectives
1. To menegetahui definition of myocarditis?
2. To determine the etiology of myocarditis?
3. To determine the risk factors in clients with myocarditis?
4. To determine the clinical manifestations of myocarditis?
5. For the kind of diagnostic checks on myocarditis?
6. To know the nursing care of myocarditis?
 
1.4 Benefits
The benefits to be obtained in the preparation of this paper are:
1.4.1 Gaining knowledge of Myocarditis?
 1.4.2 Gaining knowledge about nursing care Myocarditis?
 
CHAPTER II
LITERATURE REVIEW
 
2.1 Definition
Myocarditis is an inflammation of the heart muscle or myocardium. From the above it can be concluded that myocarditis is an inflammation of the heart muscle by a variety of causes, especially infectious agents.
Myocarditis is an inflammation of the heart muscle or myocardium. In general myocarditis caused infectious diseases but can be as a result of allergic reactions to drugs and toxic effects of chemicals radiation. Myocarditis can be caused by infection, allergic reaction, and toxic reactions. In myocarditis, myocardial damage caused by toxins released basil myocytes. Toxin would inhibit protein synthesis and myocyte be obtained microscopically by infiltration entry, hyaline necrosis of muscle fibers. Some organisms can invade the walls of small arteries, especially the arteries koronaintramuskular which will provide myocardial perivascular inflammatory reaction. This condition can be caused by pseudomonas and some types of fungi such as aspergillus and candida. A small percentage of microorganisms invade cells directly myocardium arrives menyebaban inflammatory reaction. It can happen to Toxoplasmosis gondii. In trikinosis, inflammatory cells are found mainly eusinofil (Elly Nurachmach, 2009).
Medial layer of the heart wall myocardium consists of cardiac muscle tissue highly specialized (Brooker, 2001). Myocarditis is an inflammation of the heart muscle or myocardium. generally caused by infectious diseases, but it can be as a result of allergic reactions to drugs and toxins effects of chemicals and radiation (Faculty of Medicine, 1999). Myocarditis is an inflammation of the heart muscle walls caused by infection or other causes to an unknown (idiopathic) (Dorland, 2002).
Myocarditis is a focal or diffuse inflammation of the heart muscle (myocardium) (Doenges, 1999). From the above it can be concluded that pebgertian myocarditis is an inflammation / inflammation of the heart muscle by a variety of causes, especially infectious agents.
 
2.2 Etiology and Classification
1) Acute isolated myocarditis is acute interstitial myocarditis of unknown aetiology.
2) Bacterial myocarditis myocarditis is caused by a bacterial infection.
3) Chronic myocarditis is an inflammatory disease of chronic myocardial infarction.
4) Diphtheritic mikarditis myocarditis is caused by a bacterial toxin produced in diphtheria: the primary lesion is degeneratiff and necrotic with secondary inflammatory response.
5) Fibras myocarditis was focal fibrosis / diffuse mikardial caused by chronic inflammation.
6) Giant cell myocarditis is a subtype of acute isolated myocarditis characterized by multinukleus giant cells and other inflammatory cells, including lymphocytes, plasma cells and macrophages and by ventikel dilatation, mural thrombi and necrotic areas were widespread.
7) hypersensitivity myocarditis is mikarditis caused an allergic reaction caused by hypersensitivity to various drugs, especially sulfonamides, penicillin, and methyldopa.
8) myocarditis Infection is caused by an infectious agent; including bacterial, viral, rickettsial, protozoal, spirochaeta, and fungus. The agent can damage the myocardium through direct infection, toxin production, or intermediate response immunologist.
9) interstitial myocarditis is mikarditis that the interstitial connective tissue.
10) Parenchymatus myocarditis myocarditis is mainly about the substance of the muscle itself.
11) Protozoa myocarditis myocarditis is caused by a protozoan, especially happening on Chagas disease and toxoplasmosis.
12) rheumatic myocarditis is a common sequelae of rheumatic fever.
13) mikarditis Rickettsial myocarditis is associated with rickettsial infection.
14) Toxic myocarditis is a degeneration of fibers and focal myocardial necrosis caused by drugs, chemicals, physical materials, such as radiation of animal / insect toxins or materials / other circumstances that cause trauma to the myocardium.
15) Tuberculosis granulumatosa myocarditis is inflammation of the myocardium in tuberculosis.
16) Viral myocarditis caused by a viral infection mainly by enteroviruses; most common in infants, pregnant women, and in patients with low immune response (Dorland, 2002).
 
2.3 Pathophysiology
Myocardial damage by infectious germs can go through three basic mechanisms:
1) direct invasion to the infarction.
2) Process immunologically against infarction.
3) Remove the toxins that damage the myocardium.
The process of viral myocarditis two phases, the first phase (acute) berangsung approximately 1 week (in mice) in which the invasion of the virus into the myocardium, viral replication and cell lysis. Then formed neutralizing antibody and virus will be cleared or reduced in number with the help of macrophages and neutral killer cells (NK cells).
The second phase would myocardium infiltrated by inflammatory cells and the immune system is activated for example by the formation of antibodies to the myocardium, due to changes in cell surface exposed to the virus. This phase lasts a few weeks to several months and followed myocardial damage and minimal to severe.
Enterovirus as the cause of viral myocarditis also damage endothelial cells and endothelial antibody, is suspected as the cause of microvascular spasm. Although the etiology of microvascular abnormalities is uncertain, but it may have come from an immune response or endothelial damage due to virus infection.
So basically there is spasm microcirculation causing iterative process between obstruction and reperfusion myocardium resulting in dissolution of the matrix and the exhaustion of the heart muscle causing focal muscle fibers collapse, cardiac dilatation and hypertrophy of the remaining myocytes. Finally, this process resulted in endless mechanical and biochemical compensation ended with heart trouble (Elly Nurachmach, 2009).
2.4 Clinical Symptoms
1. Weary
2. Shortness of breath
3. Irregular heartbeat
4. Fever
Other symptoms due to interference yangmendasarinya (Griffith, 1994).
a) Shivering
b) Fever
c) Anorexia
d) Chest pain
e) Dyspnea and dysrhythmias.
f) tamponade
g) ferikardial / compression (in the pericardial effusion)
 
2.5 Complications
1. Congestive cardiomyopathy / dilated.
2. Congestive heart trouble.
3. Pericardial effusion.
4. Total AV block.
5. Thrombi Kardiac
2.6 Diagnostic Examination
1. Laboratory: leukocytes, LED, lymphocytes, LDH.
2. Electrocardiography.
3. Rontgen thorax.
4. Echocardiography.
5. Biopsy endomiokardial.
2.7 Management
1. Treatment for action observation.
2. Bed rest / activity restrictions.
3. Antibiotic or chemotherapeutic.
4. Treatment is aimed at supportive systemic defect systemic infection.
5. Antibiotics.
6. Corticosteroid drugs.
7. If developed into congestive heart failure: diuretics for retention mnegurangi ciaran; digitalis to stimulate the heart rate; drugs antifreeze to prevent clot formation.
8. Therapeutic complications: a pacemaker (total blocks)
 
2.8 Prognosis
• Some recover quickly, sometimes become chronic.
• Prognosis is poor if:
1) Age youth, often die suddenly
2) The form of acute fulminant viral or diphtheria
3) a very progressive Myocarditis
4) The chronic form that persists into cardiomyopathy
5) Disease chaga.
DOWNLOAD: WOC nursing myocarditis

NURSING CARE (nursing) syncope
I.1 Background
The term comes from the Greek syncope consists of the words "syn" and "koptein" which means to decide. Medically, the definition of syncope is a loss of consciousness and postural body strength and ability to stand up for the reduction of blood flow to the brain. The prognosis of syncope vary widely depending on diagnosis and etiology. Individuals who experience syncope include syncope of unknown origin have a higher mortality rate than those who did not have syncope.
    In the U.S. an estimated 3% of the patient visits the emergency digawat syncope caused by 6% and is one reason for coming to the hospital. Recurrence rate in 3 years is estimated to 34%. Syncope often occurs in adults, the incidence of syncope increases with increasing age. Hamilton get frequent syncope at the age of 15-19 years, more often in women than in men, whereas the Framingham study the incidence of syncope getting 3% in men and 3.5% in women, there was no difference between men and women.
1.2 Formulation of the problem
What is syncope?
What is the etiology of syncope?
What are the clinical manifestations of syncope?
What are the diagnostic tests in syncope?
How algorithms and WOC at syncope?
1.3 Objectives
For the definition of syncope menegetahui
To determine the etiology of syncope
To determine the risk factors in the client with syncope
To determine the clinical manifestations of syncope
For the kind of diagnostic checks on syncope
To determine the management of the syncope
 
1.4 Benefits
The benefits to be obtained in the preparation of this paper are:
1.4.1 Gaining knowledge of syncope
 1.4.2 Gaining knowledge on the management of the syncope
 
CHAPTER II
LITERATURE REVIEW
 
2.1 Definition
The term comes from the Greek syncope consists of the words "syn" and "koptein" which means to decide. Medically, the definition of syncope is a loss of consciousness and postural body strength and ability to stand up for the reduction of blood flow to the brain (Padmosantjojo, 2000). The prognosis of syncope vary widely depending on diagnosis and etiology. Individuals who experience syncope include syncope of unknown origin have a higher mortality rate than those who did not have syncope.
Cardiac syncope is the second most common cause of syncope include 10-20% or one-fifth of the entire event. Syncope kardiakini will cause higher mortality than cases that do not have basic cardiac abnormalities. Patients with cardiac syncope have the highest risk of death within 1 to 6 months. Mortality rate of 18-33% in the first year, compared with non-syncope caused by cardiac disorders is 0-12%, even without apparent cause syncope only approximately 6%.
 
2.2 Etiology of Syncope
     a) syncope FOR HEART RHYTHM DISORDERS
In general, cardiac syncope cardiac syncope can be divided up as abnormal heart rhythms and cardiac syncope due to structural abnormalities. Syncope due to heart rhythm abnormalities most often caused by circumstances tachycardia (ventricular or supraventricular), or bradyarrhythmias.
     b) syncope FOR CARDIAC DISORDERS structure
Cardiac structural abnormalities that can cause syncope include valvular stenosis
(Aortic, mitral, pulmonary) valve prosthesis dysfunction or thrombosis, hypertrophic cardiomyopathy,
pulmonary embolism, pulmonary hypertension, cardiac tamponade, and anomalies of the coronary arteries.
 
2.3 Pathophysiology
The loss on any type of syncope is caused by a decrease in oxygenation of the parts of the brain that is part of consciousness. There was a reduction of blood flow, cerebral oxygen utilization, cerebrovascular resistance that can be shown. If ischemia only ended a few minutes, there is no brain effects. Ischemia long jaringn necrosis in the border area of ​​the brain perfusion of the vascular area anatara serebralis major arteries.
In patients with marked weakness or syncope with bradycardia, one must distinguish reflex caused by kegagagalan neurologenaik of seranagn kardiogenaik (Stokes-adam). ECG is decisive, but even without ECG, seranagn stokes. Adam can be detected clinically by a longer duration, and nature of persistent slow heartbeat, the sound can be heard view of synchronous atrial contraction, the contraction wave antrial (A) in the jugular venous pulse, and with different intensity of the first heart sound real despite regular rhythm
 
2.4 Clinical manifestations Syncope
1. As for the signs and symptoms of fainting are:
2. Decreased awareness / missing
3. Face pale, moist skin, sweating, and restlessness
4. Shallow breathing, rapid pulse
5. Complained of nausea, sometimes vomiting, dizziness, thirst and lip numbness
2.5 Diagnostic
1. Laboratory: leukocytes, LED, lymphocytes, LDH.
2. Electrocardiography.
3. Electroencephalography examination.
4. Echocardiography.
 
Nursing Diagnosis and Intervention
1. Decreased cardiac output b / d the disturbance of blood flow to the heart muscle
Purpose:
Expected outcomes:
Rational Intervention
• Check the ABC and if necessary release of the airway, and Massage Heart
• Monitor pulse, RR, TD regularly
 
• Check the state of the client dg EKG heart
• Assess changes in skin color to pale or cyanotic.
 
• Monitor intake and output every 24 hours.
 
• Limit activities adequately.
 
 
• Provide a quiet psychological condition.
• Knowing kepatenan airway and blood circulation
o Monitoring the change of heart circulation as early as possible.
o Knowing the changes in heart rhythm.
• Pale shows a decrease in peripheral perfusion to inadequate cardiac output. Cyanosis occurs as a result of the obstruction of blood flow to the ventricles.
• The kidneys respond to lower cardiac output by holding the production fluid and sodium.
• Adequate rest is needed to improve the efficiency of cardiac contraction and lower O2 consumption and excessive work.
• Stress the emotions produce vasoconstriction that increases TD and increase cardiac work.
2. Impaired tissue perfusion b / d decrease in peripheral blood circulation; cessation of the flow of arterial-venous
Purpose:
Criteria results:
 
Rational Intervention
• Monitor changes abrupt or continuous mental disorders (camas, confusion, lethargy, pinsan).
 
• Observe for pallor, cyanosis, blemishes, skin cold / humid, my peripheral pulse strength.
 
• Assess Homan's sign (pain in the calf with dorsiflexion position), erythema, edema.
• Encourage leg exercises active / passive.
 
 
 
• Monitor breathing.
 
 
 
 
• Assess GI function, noted anorexia, decreased bowel sounds, nausea / vomiting, abdominal distension, constipation.
 
• Monitor urine input and output changes.
 • Cerebral perfusion is directly related to cardiac output, affected by the electrolyte / acid-base variations, hypoxia or systemic embolism.
• systemic vasoconstriction caused by decreased cardiac output may be evidenced by a decrease in skin perfusion and decreased pulse.
• The presence of deep venous thrombosis.
 
• Reduce venous stasis, increasing venous return and lowers risk tromboplebitis.
• cardiac pump failure can trigger respiratory distress. However, dyspnea tiba-tiba/berlanjut showed pulmonary thromboembolic complications.
• Decreased blood flow can lead to mesentrika GI dysfunction, eg loss of peristalsis.
 
• Reduction of income / constant nausea can result in decreased circulating volume, which impacts negatively on perfusion and organ.
 
 
3. impaired cerebral tissue perfusion bd decreased oxygen flow to the cerebral
Objectives: After the action keperawatn 2 × 24 hour client is expected to show effective tissue perfusion
Criteria Results: Systolic and diastolic blood pressure is stable
                                Communicate clearly and in accordance with the age and ability
Rational Intervention
• Monitor TTV
• Position the patient in shock position dg feet up 45 degrees
• Monitor the level of awareness
 
• Monitor SpO2
 
• Monitor symmetry and pupillary reaction
• Collaboration: to facilitate the circulation of the brain •
 
• The level of consciousness is also
influenced by the perfusion of oxygen to the brain
• Prevent the occurrence of hypoxia in the brain
 
 DOWNLOAD: WOC nursing syncope
CHAPTER III
CONCLUSIONS AND RECOMMENDATIONS
 
3.1. CONCLUSION
1. The incidence of cardiac syncope vasovagal syncope is smaller than, but the death rate is higher than cardiac syncope.
2. The cause of cardiac syncope can be divided into two abnormal heart rhythms and cardiac structural abnormalities.
3. The diagnosis of cardiac syncope is a bit difficult because there is no examination is the gold standard.
4. Management of patients with cardiac syncope consists of pharmacological treatment, installation of pacemakers and surgical therapy.
 
3.2. ADVICE
Required a precise diagnosis of the causes of cardiac syncope be optimized in order management, so that the death rate can be reduced.
 
REFERENCES
 
1. Padmosantjojo. Neurosurgery Nursing. New York: The FKUI Neurosurgery. 2000
2. Lumbantobing. Clinical Neurology and Mental Physical Examination. Jakarta: Faculty of medicine. , 2008. p.7
3. Rasjidi K, Nasution SA. Syncope. In: Sudoyo AW, Setiyohadi B, Alwi I, K MS, Setiati S, editors. Textbook of Medicine Volume I. Edition 5. New York: Publishing Center Department of Medicine Faculty of Medicine; 2009. h. 210-212
4. HB Brown, Ropper AH. Adams & Victor's Principles of Neurology. Edition 8. Mc-Graw Hill. , 2006. p.321-328
5. Morag R. Syncope. October 2010. http://emedicine.medscape.com/article/811669-overview Downloaded on December 2, 2010. 6. Darrof RB. Carlson MD. Dizziness, syncope, And Vertigo. In Harrison's Neurology in Clinical Medicine. McGraw-Hill. , 2006. p.115-119