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8/10/2019 unej Carditis
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Inflammatory HeartDisease
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Pericarditis inflammation of the pericardium
Causes:
may result from bacterial, viral or fungal infection
can be assoc. w/ systemic diseases such as autoimmune
disorders, rheumatic fever, tuberculosis, cancer, leukemia,
kidney failure, HIV infection, AIDS, and hypothyroidism
Heart attack (post-MI pericarditis) and myocarditis
radiation therapy to the chest and medications that
suppress the immune system
injury (including surgery) or trauma to the chest,
esophagus, or heart.
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Pericarditis
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a
t
o
f
s
o
l
o
g
i
Inflammation of thepericardium
Ventricular filling andemptying
Intrapericardialpressure
Arterial pressure
Compression of the heart
CO Venous pressure
Pericardial effusionFluid accumulation (serous, purulent,
blood) in the pericardial sac
Bacterial, viral, fungal ; sistemicdisease ; radiation/medication ; injury
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Acute Pericarditis result to exudate formation(if severe, can lead to cardiac tamponade)
Chronic Pericarditis result to fibrosing (hardening)
of the pericardial sac
- the thick fibrous pericardium tightens
around the heart and efficiency as a pump
(Constrictive Pericarditis)
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Clinical Manifestations
Pericardial friction rub
Severe precordial chest pain caused by the inflamed pericardium
rubbing against the heart Usually relieved by sitting up and leaning forward
Pleuritis type: a sharp, stabbing pain
May radiate to the neck, left shoulder & arm, back or abdomen
Often intensify with deep breathing and lying flat, and may withcoughing and swallowing
Breathing difficulty when lying down
Need to bend over or hold the chest while breathing
Dry cough
Ankle, feet and leg swelling (occasionally)
Anxiety muffled or heart sounds
Fatigue if severe- rales, breath sounds
Fever
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Diagnostic tests Chest x-ray
Echocardiogram
Chest MRI or CT scan show enlargement of the heart from fluid collection in the
pericardium, and signs of inflammation. They may also showscarring and contracture of the pericardium (constrictivepericarditis)
ECG is abnormal in 90% of pts. w/ acute pericarditis. may mimic the ECG changes of MI. To rule out heart attack, serial cardiac
marker levels (CK -MB and troponin I) may be ordered
Blood culture
CBC, may show increased WBC count
Pericardiocentesis, with chemical analysis and pericardial fluid
culture
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Constrictive Pericarditis
a chronic form of pericarditis in w/c the pericardium is rigid,
thickened, scarred, and less elastic than normal
The pericardium cannot stretch as the heart beats, which preventsthe chambers of the heart from filling w/ blood
CO & blood backs up behind the heart
symptoms of heart failure
The inflamed pericardium may cause pain when it rubs against
the heart.
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Causes:
most common causes are conditions that induce chronic
inflammation of the pericardium: tuberculosis, radiation
therapy to the chest, and cardiac surgery.
may also result from mesothelioma (a tumor) of the pericardium
incomplete drainage of abnormal fluid accumulating in the
pericardial sac, which can occur in purulent pericarditis or in
post-surgery hemopericardium(bleeding w/in the pericardial sac).
S/Sx:
dyspnea that develops slowly and progressively worsens
Fatigue, excessive tiredness - CO
Weakness
weak heart sounds
distended neck veins
chronic swelling (edema) of the legs, ankles
hepatomegaly, ascites
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CTR (CaRdio ThoRax RaTio)
Merupakan salah satu pengukuran jantung secara kasar dan
mendekati besar jantung yang sebenarnya indeks tersebut
merupakan cara pengukuran jantung yang paling cepat, mudah
dan mendekati kebenaran ( morgan john caffey )
indeks ini patologis bila nilainya lebih dari 1/2
menurut hibbish & morgan indeks tersebut sebagai corelation
coeficient dan nilainya 0,56
RUMUS CTR : a + b = < 1/2 (< 50 %)c
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a = Diameter Transversa Dextra
Jarak terpanjang antara batas jantung kanan dengan garis
tengah yang melalui tengah-tengah c.v. thoracalis
b = Diameter Transversa Sinistra
Jarak terpanjang antara batas jantung kiri dengan garis
tengah yang melalui tengah-tengah c.v. thoracalis
c = Diameter Interna
Garis yang ditarik // dengan diameter transversa yang melalui
puncak tertinggi dari Hemiadiafragma kanan merupakan
diameter dari Cavum Thoracis.
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Jika CTR >0.5 maka dikategorikan sebagai Cardiomegaly
KK2b/Ratna.doc/'11 14
A B
C
Interventions
identify the cause, if possible
analgesics for pain, anti-pyretics, anti-inflammatory
drugs(NSAIDS) such as aspirin and ibuprofen, in some cases,
corticosteroids may be prescribed
Diuretics- to remove excess fluid
Pericardiocentesis- using a 2D-echo-guided needle aspiration or
surgically in a minor procedure
Antibiotics or antifungal agents(can be instilled directly to the sac)
Bed rest, proper positioning, low-Na+ diet
If the pericarditis is chronic, recurrent, or causes constrictive
pericarditis, cutting or removing part of the pericardium may be
recommended (Pericardiectomy)
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Cardiac Tamponade
compression of the heart caused by blood or fluid accumulation inthe space between the myocardium and the pericardium
prevents the ventricles from expanding fully,
so they cannot adequately fill or pump blood
CO & signs of CHF
Causes: Pericarditis caused by bacterial or viral infections
Heart surgery
dissecting aortic aneurysm (thoracic)
wounds to the heart
end-stage lung cancer
acute MI
Other potential causes: heart tumors, kidney failure, recent heartattack, recent open heart surgery, recent invasive heart procedures,radiation therapy to the chest, and SLE
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Clinical Manifestations
weak or absent PMI & peripheral pulses
distended neck veins
muffled or decreased heart sounds
BP, narrowing pulse presure
pulsus paradoxus (BP falls when pt. inhales deeply)
Anxiety, restlessness, tachycardia, dyspnea, RR, palpitations
Fainting, light-headedness, pallor or cyanosis
Chest pain- sharp, stabbing, worsened by deep breathing or coughing
signs of CHF
CXR, Echocardiogram pericardial effusion
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Interventions an Emergency condition !
Goal: save the patient's life, improve heart function, relieve
symptoms, and treat the tamponade
Pericardiocentesis (to drain the fluid around the heart) or by
cutting & removing part of the pericardium (pericardiectomyor
pericardial window).
IV Fluids- to maintain normal blood pressure
Dopamine, dobutamine - BP
Oxygen therapy - workload on the heart
Identify and treat cause of tamponade give antibiotics or
surgical repair of injury.
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Myocarditis inflammatory disease of the myocardium that causes infiltration
and injury to myocardial tissue
Causes:
infectious process viral, bacterial, parasitic infection
- invasion of myocardial tissue by organisms or production of
toxins (Ex. polio, influenza, rubella)cells damage & nekrose
autoimmune reaction rheumatic fever
cardiac damage is char. by thrombus formation, dilation of
ventricles, scarring (fibrosis), hypertrophy, disintegration of
cardiac muscle cells heart muscles weaken signs of heart failure
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INCIDENCE
The true incidence of myocarditis is unknown because
the majority of cases aresymptom tic
Involvement of the myocardium has been reported in
one to five percent of patients with acute viral
infections
Autopsystudies have revealed varying estimates of the
incidence of myocarditis. A five percent prevalence of
active myocarditis was reported in a high-risk group
of 186 sudden, unexpected medical deaths in children
KK2b/Ratna.doc/'11 22
RISK FACTORS
Certain groups appear to be atincreased risk of virus-inducedmyocarditis, and the course may behyperacute Young males
pregnant women
children (particularly neonates)
immunocompromised patients
KK2b/Ratna.doc/'11 23
PATHOGENESIS
Both direct viral-induced myocyte damage andpost-viral immune inflammatory reactionscontribute to myocyte damage and necrosis
Inflammatory lesions and the necrotic processmay persist for months, although the virusesonly replicate in the heart for at most two orthree weeks after infection
Evidence from experimental models hasincriminated cytokines such as interleukin-1 andTNF, oxygen free radicals and microvascularchanges as contributory pathogenic factors
thogenesis
Three phases:
Viral Replication
Autoimmune injury
Dilated cardiomyopathy
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Phase 1
Viral replication Cardiotropic RNA viruses are taken into
myocytes by receptor-mediated endocytosis.
Directly translated intracellularly to produceviral protein.
Virus infection directly contributes to cardiactissue destruction by cleaving the cytoskeletonprotein dystrophin, leading to a disruption ofthe dystrophin-glycoprotein complex.
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Phase 2Autoimmunity Phase 1 concludes with activation of the host
system.
Ideally, the immune system should down-regulate to a resting state once viralproliferation is controlled.
If host immune activation continues unabated autoimmune disease.
T cells target the hosts own tissue throughmolecular mimicry.
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Phase 3
Dilated Cardiomyopathy Re-modelling mechanisms lead to dilated
cardiomyopathy (DCM). The persistent myocyte viral gene expression progressive DCM.
Cytokines: activate matrix metalloproteinases(gelatinase, collagenase, elastases).
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Dikelompokkan menjadi :
1. Miokarditis Purulenta
- Terjadi abses yg besar/kecil dlm otot
jantung
2. Miokarditis Parenkimatosa
- Serabut otot jantung menunjukkan
kelainan degeneratif
3. Miokarditis Interstitialis
Terjadi peradangan jaringan interstitium
KK2b/Ratna.doc/'11 29
Clinical Manifestations
Most patients are asymptomatic and recoverwithout treatment
60% of pts had antecedent flulike symptoms
Large number identified by heart failuresymptoms
35% of pts with myocarditis and HF havechest pain
May mimic an acute MI with ventriculardysfunction, ischemic chest pain, ECG evidenceof injury or Q waves
S/Sx: fever, tachycardia, abnormal heart beats
abnormal heart sounds (murmurs, extra heart sounds)
pericardial friction rub
chest pain
fatigue, shortness of breath, orthopnea
fainting often related to arrhythmias
peripheral edema
other signs suggestive of infection: rashes, sore throat, itchy
eyes, swollen joints
Interventions: bed rest, low Na+ diet - cardiac workload, promote healing
Digitalis (digoxin) - myocardial contractility, HR, to
prevent heart failure
Diuretics to control pulmonary or systemic congestion
Antibiotics, anti-inflammatory drugs, steroids
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Bacterial Endocarditis Infeksi lapisan bag dalam jantung (endocardium) yg disbbkan
oleh invasi langsung dari bakteri atau organisme lain yg memicutrjadinya deformitas katup & endokardium.
Causative agents: Streptococcus viridans (found in the mouth) - 50%of cases, Staphylococcus aureusand enterococcus. Less commonorganisms include pseudomonas, serratia, and candida.
Classification:
1. Acute bacterial endocarditis rapidly progressing infection
high fever, murmurs, spleenomegaly, emboli formation
follows a rapid course and may severely damage the endocardiumearly in the disease
2. Subacute bacterial endocarditis slower progressing infection
fever, wt. loss, fatigue, joint pains, headache, malaise
has a prolonged course31KK2b/Ratna.doc/'11
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Predisposing factors: Who are at risk? congenital heart defects
damaged valves by rheumatic fever, atherosclerosis
artificial heart valves
may occur after cardiac surgery, invasive procedures (dentalprocedures, catheterization, prolonged IV therapy) minorsurgery, gynecologic examinations, dialysis
may follow after acute infection of the tonsils, gums, teeth,skin, lungs, GIT, GUT
immunocompromised patients
drug abusers (injections)
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Pathophysiology
Organism travels inthe blood stream
forms vegetations(clumps of bacteria,
fibrin, cellular debris,platelets)
growth of vegetation onheart valves
attaches to theendocardial lining of a
normal heart or an areaof defect (heart valves)
Emboli that can lodge tovarious organs (kidney,coronary artery, spleen,
lungs, brain)
deforms, thicken, stiffen,perforate the valve leaflets
infected clots may break freeand travel through the
bloodstream
Dysfunctional heart valves
obstruct blood flow and
produce organ damage 34KK2b/Ratna.doc/'11
Clinical Manifestations
Infection fever, chills, night sweats, malaise, fatigue, anorexia
wt. loss, muscle aches, joint pains
Cardiac murmurs (valve dysfunction), tachycardia
- advanced signs of CHF
Peripheral Manifestations:
Petechiae small pinpoint hemorrhages in the conjunctiva,mucous membranes, neck, ankles
Splinter hemorrhages - small, dark lines under the fingernails
Oslers nodes (red, painful nodes with a white center on thepads of fingers, toes, palms or soles) a late sign of infection
Janeway lesions (flat, painless, red to bluish-red spots on thepalms and soles) an early sign of endocardial infection
Roths spots ( boat shaped retinal hemorrhages near the opticdisc seen in fundoscopy
* result from Microemboli35
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IE: Osler Nodes
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Janeway lesions
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enlarged spleen continuous antigenic process
Embolic manifestations
Lung hemoptypis, chest pain, shortness of breath
Kidney hematuria
Heart myocardial infarction
Brain sudden blindness, paralysis, meningitis, brain abscess
Complications:
CHF - most common, due to damage to the aortic, mitral valve
Embolic episodes ischemia and necrosis of organs
arrhythmias atrial fibrillation
Glomerulonephritis
Stroke
Brain abscess
Clinical Manifestations (cont.)
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blood cultures & sensitivity to identify organism best test for detection
- obtain sample just before & during height of
fever
2D Echo valvular vegetations
CBC high ESR, high WBC, anemia ; peningkatan Cardiac iso-enzym(CPK CK-MB)
ECG
Prevention:
Prophylactic antibiotics are often given to people with predisposing
heart conditions before dental procedures or surgeries involving
the respiratory, urinary, or intestinal tract
Continued medical follow-up is advised for people with a history of
endocarditis
proper oral hygiene
Diagnostic tests
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Infectious Endocarditis
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1. Identify the infectious organism - serial blood cultures
2. Destroy the infectious org., stop the growth of valvular vegetations
IV Antibiotics 4-6 weeks (Penicillin, Aminoglycosides)
- to ensure high blood levels of medication
- to eradicate the bacteria from the chambers & valves
repeated blood cultures are done to assess effectiveness of thedrug
3. Surgical repair of valvular deformities and congenital defects
4. Provide nutritional supplementation & bed rest
5. Prevent relapse and recurrent fever & infection
- good oral hygiene, avoid invasive procedures as possibleprophylactic antibiotic therapy, aseptic technique
Medical Interventions
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1. Menurunkan beban kerja jantung yg ber>> , mencegah komplikasi2. Mengurangi ataumenghilangkannyeri.
3. Membantudlm pengobatan atau mengurangi proses infeksi utama
4. Membantuklien memahami kondisi.
Prioritas keperawatan
1. Perubahan perfusi jaringan.
2. PK : Gagal jantung kongestif atau syokkardiogenik
3. Gagguan kenyamanan : nyeri akut
4. Kecemasan
5. Perubahan pola tidur
6. Dsb
Diagnosa keperawatan
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Nursing Interventions
Provide comfort measures, fever
encourage adequate fluids & nutrition
CBR if w/ signs of valve dysfunctions (murmurs)
assess for signs of heart failure, tachycardia, embolic
manifestation
provide health teachings: cause of infection, prolonged use
of antibiotic, prophylactic antibiotics, preventing recurrence
of infection (good oral hygiene), monitor signs of recurrence
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