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
