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.
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