10/6/2011

Pericarditis
inflammation of the pericardium

Inflammatory Heart
Disease

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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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P
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Bacterial, viral, fungal ; sistemic

disease ; radiation/medication ; injury

Acute Pericarditis result to exudate formation

(if severe, can lead to cardiac tamponade)

Inflammation of the
pericardium
Pericardial effusion
Fluid accumulation (serous, purulent,
blood) in the pericardial sac

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)

Intrapericardial
pressure
Compression of the heart
Ventricular filling and
emptying
Venous pressure

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CO

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Arterial pressure
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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 with
coughing 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 show
scarring and contracture of the pericardium (constrictive
pericarditis)

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 prevents

the 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 %)

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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.

Jika CTR >0.5 maka dikategorikan sebagai Cardiomegaly

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Cardiac Tamponade

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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compression of the heart caused by blood or fluid accumulation in

the 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 heart
attack, 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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Myocarditis

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 (pericardiectomy or
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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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 are asymptomatic
Involvement of the myocardium has been reported in
one to five percent of patients with acute viral
infections
Autopsy studies 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

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PATHOGENESIS
Both direct viral-induced myocyte damage and
post-viral immune inflammatory reactions
contribute to myocyte damage and necrosis
Inflammatory lesions and the necrotic process
may persist for months, although the viruses
only replicate in the heart for at most two or
three weeks after infection
Evidence from experimental models has
incriminated cytokines such as interleukin-1 and
TNF, oxygen free radicals and microvascular
changes as contributory pathogenic factors
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RISK FACTORS
Certain groups appear to be at
increased risk of virus-induced
myocarditis, and the course may be
hyperacute

Young males
pregnant women
children (particularly neonates)
immunocompromised patients
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Pathogenesis
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 produce
viral protein.
Virus infection directly contributes to cardiac
tissue destruction by cleaving the cytoskeleton
protein dystrophin, leading to a disruption of
the dystrophin-glycoprotein complex.

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Phase 2
Autoimmunity
Phase 1 concludes with activation of the host
system.
Ideally, the immune system should downregulate to a resting state once viral
proliferation is controlled.
If host immune activation continues unabated
autoimmune disease.
T cells target the hosts own tissue through
molecular mimicry.

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Dikelompokkan menjadi :

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).

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

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Clinical Manifestations

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S/Sx:

Most patients are asymptomatic and recover

without treatment
60% of pts had antecedent flulike symptoms
Large number identified by heart failure
symptoms
35% of pts with myocarditis and HF have
chest pain
May mimic an acute MI with ventricular
dysfunction, ischemic chest pain, ECG evidence
of injury or Q waves
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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 memicu
trjadinya deformitas katup & endokardium.
Causative agents: Streptococcus viridans (found in the mouth) - 50%
of cases, Staphylococcus aureus and enterococcus. Less common
organisms 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 endocardium
early in the disease
2. Subacute bacterial endocarditis slower progressing infection
fever, wt. loss, fatigue, joint pains, headache, malaise
has a prolonged course
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congenital heart defects

damaged valves by rheumatic fever, atherosclerosis
artificial heart valves
may occur after cardiac surgery, invasive procedures (dental
procedures, catheterization, prolonged IV therapy) minor
surgery, 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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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 the
pads of fingers, toes, palms or soles) a late sign of infection
Janeway lesions (flat, painless, red to bluish-red spots on the
palms and soles) an early sign of endocardial infection
Roths spots ( boat shaped retinal hemorrhages near the optic
disc seen in fundoscopy
* result from Microemboli

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Organism travels in
the blood stream

attaches to the
endocardial lining of a
normal heart or an area
of defect (heart valves)

growth of vegetation on
heart valves

infected clots may break free

and travel through the
bloodstream

deforms, thicken, stiffen,

perforate the valve leaflets

Emboli that can lodge to

various organs (kidney,
coronary artery, spleen,
lungs, brain)
obstruct blood flow and
produce organ damage

forms vegetations
(clumps of bacteria,
fibrin, cellular debris,
platelets)

Dysfunctional heart valves

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IE: Osler Nodes

Clinical Manifestations

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Pathophysiology

Predisposing factors: Who are at risk?

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Clinical Manifestations (cont.)

Janeway lesions

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

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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
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Diagnostic tests

Infectious Endocarditis

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
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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 the
drug
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 possible
prophylactic antibiotic therapy, aseptic technique

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Prioritas keperawatan

Medical Interventions

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1.
2.
3.
4.

Menurunkan beban kerja jantung yg ber>> , mencegah komplikasi

Mengurangi atau menghilangkan nyeri.
Membantu dlm pengobatan atau mengurangi proses infeksi utama
Membantu klien memahami kondisi.

Diagnosa keperawatan
1. Perubahan perfusi jaringan.
2. PK : Gagal jantung kongestif atau syok
kardiogenik
3. Gagguan kenyamanan : nyeri akut
4. Kecemasan
5. Perubahan pola tidur
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6. Dsb

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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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