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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

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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


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.


Jika CTR >0.5 maka dikategorikan sebagai Cardiomegaly


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)


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




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.


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



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


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


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.


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.


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



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


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)


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


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


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.)


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


Infectious Endocarditis


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


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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