penyakit infeksi jantung
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penyakit infeksi jantungTRANSCRIPT
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Updated Fall 2012 by Renee Redman From the notes of Nancy Jenkins
Inflammatory Disorders
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Overview of Today’s LectureA & P ReviewEndocarditis- infection of the endocardial
surface of the heartMyocarditis- a focal or diffuse inflammation
of the myocardiumPericarditis- inflammation of the pericardial
sac (the pericardium)
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Anatomy and Physiology review
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Anatomy and Physiology review
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A- Aortic Valve
B- Mitral Valve
D- Tricuspid Valve
- Pulmonary Valve
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Anatomy and Physiology Review
Blood enters the right atrium and moves through the _______ into the right ventricle.
Blood then moves from the right ventricle into the pulmonary artery via the _________.
A- Aortic Valve
B- Mitral Valve
C- Pulmonary Valve
D- Tricuspid Valve
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Anatamy and Physiology Review (Cont’d)
After entering the left atrium via the pulmonary veins, blood moves through the _____ into the left ventricle.
Finally, it travels through the _____ and out of the heart.
A- Aortic Valve
B- Mitral Valve
C- Pulmonary Valve
D- Tricuspid Valve
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Layers of the Heart Muscle
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TISSUES SURROUNDING THE HEART
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Endokarditis RematikTerjadinya endokarditis rematik disebabkan langsung oleh demam rematik, suatu penyakit sistemik yang disebabkan oleh infeksi streptococcus grup A. Demam rematik merupakan mempengaruhi semua persendian, menyebabkan poliartritis. Jantung juga merupakan organ sasaran dan merupakan bagian yang kerusakannya paling serius
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• Endokarditis rematik secara anatomis dimanifestasikan dengan adanya tumbuhan kecil yang transparan, yang menyerupai manik dengan ukuran sebesar kepala jarum pentul, tersusun dalam deretan sepanjang bilah katup
• Mereka menjadi awal terjadinya suatu proses yang secara bertahap menebalkan bilah-bilah katup, menyebabkannya memendek dan menebal dibanding yang normal. Sehingga tidak dapat menutup dengan sempurna. Sehingga timbullah regurgitasi katup
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• Bilah katup yang meradang juga dapat menempel satu sama lain, mengakibatkan stenosis katup. Yaitu penyempitan lumen katup
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Manifestasi Klinis
Gejala jantung yang muncul tergantung pada bagian jantung yang terkena, katup mitral adalah yang paling sering terkena. Menimbulkan gejala gagal jantung kiri seperti sesak nafas dengan krekel dan wheezing
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Penatalaksanaan
Tujuan penatalaksanaan medis adalah membunuh organismen penyebab dan mencegah komplikais yang terjadi. Terapi antobiotik jangka panjang dan penisilin parenteral adalah pengobatan terpilih.
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PencegahanLangkah awal :• Mendeteksi adanya infeksi streptokokus, Setiap perawat
harus mampu mengenal dengan baik tanda dan gejala faringitis streptokokus, sebagai berikut :
1. Demam (38,9 sampai 40 derajat celcius)2. Menggigil3. Sakit tenggorok4. Kemerahan difus di tenggorok dengan eksudat pada
orofaring5. Pembesaran dan nyeri tekan kelenjar limfe6. Nyeri abdomen7. Sinusitis akut dan otitis media akut
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Infective Endocarditis
• Infection of the inner layer of the heart
• Usually affects the cardiac valves
• Was almost always fatal until
development of penicillin
• Around 15,000 cases diagnosed
annually in the U.S.
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Causative OrganismsCausative organism –often bacterial
Streptococcus viridansStaphylococcus aureus
Other EtiologiesViruses- Coxsackie BFungi – Candida alibcans
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Etiology and PathophysiologyVegetation -
Fibrin, leukocytes, platelets, and microbesAdhere to the valve or endocardium Embolization of portions of vegetation into
circulation 50% of patients with IE will have systemic
embolization
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EndocarditisInfection of the innermost layers of the
heartMay occur in people with congenital and
valvular heart diseaseMay occur in people with a history of
rheumatic heart diseaseMay occur in people with normal valves
with increased amounts of bacteria
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Etiology/PathophysiologyEndocarditis
When valve damaged, blood is slowed down and forms a clot.
Bacteria get into blood stream Bacterial or fungal vegetative growths
deposit on normal or abnormal heart valves
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Bacterial Endocarditis of the Mitral Value
Fig. 37-2Fig. 37-2
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Risk Factors- endocarditisHx of rheumatic fever or damaged heart valve-
less common now (20% of cases)Prior history of endocarditisAging (50% associated with aortic stenosis)Invasive procedures- (introduce bacteria into
blood stream) (surgery, dental, etc)Permanent Central Venous Access- MRSAIV drug usersValve replacementsRenal dialysis
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Nursing AssessmentSubjective Data
History of valvular, congenital, or syphilitic cardiac disease
Previous endocarditis Staph or strep infectionImmunosuppressive therapyRecent surgeries and procedures
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Nursing AssessmentFunctional health patterns
IV drug abuseAlcohol abuse
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Nursing AssessmentNonspecific Clinical Manifestations
Weight changesChillsLow grade fever in 90% patientsMalaise
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Nursing AssessmentDiaphoresisBloody urineExercise intolerance Generalized weaknessFatigue CoughHeadache
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Nursing AssessmentDyspnea on exertion Night sweats Chest, back, abdominal painAlso consider s/s related to embolization to
specific organ New or changing heart murmur
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Collaborative Care
Fungal and prosthetic valve endocarditisResponds poorly to antibioticsValve replacement is adjunct procedure
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Assesment endocarditisInfection and emboli
Emboli-spleen most often affected (splenectomy)Osler’s nodes- painful, red or purple pea-sized lesions on toes and
fingertipsSplinter hemorrhages- black longitudinal streaks on nail bedsJaneway lesions- flat, painless, small, red spots on palms and soles
Roth spots- hemorrhagic retinal lesionsMurmur- most have murmursT above 101(blood cultures) and low-gradeChillsAnorexiaFatigue
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Splinter hemorrhage
• small areas of bleeding under the fingernails or toenails.
• due to damage to capillaries by small clots
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Janeway Lesions
• flat, painless red spots on palms and soles
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Osler’s Nodes
Painful, pea-size, red or purple lesionsOn finger tips or toes
Roth spotsOsler’s nodes
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Roth’s Spots
• hemorrhagic retinal lesions
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Clinical ManifestationsMurmur in most patientsHeart failure in up to 80% with aortic valve
endocarditis Manifestations secondary to embolism
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Past Medical HistoryRecent surgeries or procedures
Cardiac Cath,dental, urologocial, gynecological (including vaginal or c-section deliveries)
Hx of IV drug useCentral line placementDialysisInfections (recent UTI, URI or skin infection)Immunosuppression
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Diagnostic TestsBlood Cultures- most likely positive unless
recent antibiotic txEchocardiogram-TEE best- see vegetationsOther- WBC with differential, CBC,ESR,
serum creatinine,CXR, and EKG
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MedicationsAntibiotics
IV for 4-8 weeks Monitor peaks and troughs of certain drugsMonitor BUN and Creatinine.Evaluate effectiveness of treatment with repeated
blood cultures.Unclear of success of oral antibiotics
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Additional TreatmentFungal infections- poor responsive to drug
therapyMay require valve replacementRelapses are commonBedrest usually not indicated unless febrile,
HF or other complications
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ComplicationsEmboli (50% incidence)
Right side- pulmonary emboli (esp. with IV drug abuse)Left side-brain, spleen, heart, limbs, etc
CHF-check edema, rales, VSArrhythmias- A-fib, conduction blocksDeath
.
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Treatment GoalReturn to baseline cardiac functionADL’s without fatiguePrevent recurrence
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PreventionEliminate risk factorsPatient teaching
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Layers of the Heart Muscle
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Myocarditis
Myocarditis is an uncommon inflammation of the heart muscle (myocardium). This inflammation can be caused by infectious agents, toxins, drugs or for unknown reasons. It may be localized to one area of the heart, or it may affect the entire heart.
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Etiology/PathophysiologyMyocarditis
Virus, toxin or autoimmune response causes necrosis of the myocardium
Most often caused by viral infectionFrequently caused by Coxsackie A and B virusFrequently follows an upper respiratory infection or
viral illnessCan result in decreased contractilityCan become chronic and lead to dilated
cardiomyopathy- heart transplant or death
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Risk factor-myocarditisHx of upper respiratory infectionToxic or chemical effects (radiation, alcohol)Autoimmune or immunosuppresents- 10%
HIV develop itMetabolic-lupusHeat stroke or hypothermia
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Myocarditis- AssessmentEarly s/s
Fever, fatigue Malaise, mylagiasDyspnea, lymphadenopathyNausea, vomiting
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Myocarditis- AssessmentCardiac s/s 7-10 days after viral
infectionPleuritic chest pain (pericardial friction rub)
Pericarditis frequently occurs with myocarditis- check friction rub
TachycardiaArrhythmias- PVCs, PACs, Atrial Tachycardias,
Signs of heart failure –late cardiac s/sS3 heart sound, crackles, JVD, syncope,
edema
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Myocarditis- AssessmentSudden Death-
In young adults Myocarditis is the cause of up to 20% of sudden cardiac death
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Diagnostic TestsEKG- Non-specific T-wave abnormalities CK-MB and Troponin may be elevatedEndomyocardial biopsy- there are risks and not
used for every case but is definitive for myocarditis
Chest X-Ray- Variable (Normal to Cardiomegaly)
EchocardiogramCardiovascular Magnetic Resonace
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Chest X-Ray in Myocarditis
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Myocarditis TreatmentManage cardiac symptomsViral – antibiotics for secondary58% adults recover on ownTreatment Goal
Decrease workload of the heart so it can heal
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MedicationsDigoxin- use cautiously!
Improves CO but causes dysrhytmias in these patients
HF drugs- ACE, diuretics, beta blockers etcImmunosupressive therapy
prednisone, etcEvidence inconclusive
Anticoagulants- Reduces risks of thrombus in low EF
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Other TreatmentsBedrest and activity restrictions-**Activities may be limited for 6 months- 1
yr. O2Intraaortic balloon pumpTransplant
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PericarditisPericarditis is an inflammation of the
pericardium, the thin, fluid-filled sac surrounding the heart. It can cause severe chest pain (especially upon taking a deep breath) and shortness of breath.
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Pericardium AnatomyComposed of two layersVisceral pericardium (inner)Parietal layer (outer)Pericardial space is inbetween
Contain about 10-15ml of serous fluidProvides lubricationDecreases friction
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Etiology/PathophysiologyPericarditis
bacterial, fungal or viral infectionHeart loses natural lubrication(10-30cc’s) and
layers roughen and rubInflammatory process causes lymphatic fluid
build-up- if sudden may have cardiac tamponade
Pericardial Effusion- usually 250 mls before show up on x-ray. Can have 1000 mls.
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Risk Factors/pericarditisPost MI (Dressler’s syndrome)Radiation InfectionTraumaCancerDrugs and toxinsRheumatic diseasesTrauma or cardiac surgeryCan be chronic disorder-pericardium becomes
rigid
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Assessment pericarditisInflammation and pain
Pericardial friction rub-FeverSubsternal, sharp, pleuritic chest pain
Inc. with coughing, breathing,turning,lying flatDec. with sitting up and leaning forwardReferred to trapezius muscleDyspnea
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Diagnostic Tests- to R/OEKG- 90% have ekg changes: serial ekg’s
ST elevation, PR changes, differ from MICBC- WBC, ESR and CRPCardiac Enzymes-
elevated but not as much as with MIEcho- for wall movementCT or MRI- for pericardial effusion Pericardiocentesis fluid for analysis- attempt to
determine cause
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ECG in Pericarditis
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MedicationsAntibiotics to treat bacterial pericarditisASA or tylenolNSAIDS- ibuprofenCorticosteroids
Typically reserved for patients with autoimmune conditions or not responding to NSAIDS
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Complications of PericarditisPericardial Effusion- an accumulation of
excess fluid in the pericardium
Cardiac Tamponade- as the pericardial effusion increases in volume it causes increased intrapericardial pressure resulting in compression of the heart
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Pericardial EffusionCan occur rapidly or slowlyPulmonary compression-cough, dyspnea,
and tachypneaPhrenic nerve involvement- hiccupsLaryngeal nerve- hoarseness
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Pericardial Effusion- EKGElectrical Alternans
Pericardial effusion with electrical alternans
•The QRS axis alternates between beats. In this example it is best seen in the chest leads where the QRS points in different directions!
•This is rarely seen and is due to the heart moving in the effusion.
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PERICARDIUMCARDIAC TAMPONADE
Original heart size
Excess pericardial fluid
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Nursing Diagnoses for Pericarditis
Acute PainIneffective Breathing PatternRisk for Decreased Cardiac OutputActivity Intolerance
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Specific Nursing AssessmentParadoxical pulseMurmurPericardial friction rubEmboliChest painCHF
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Comfort MeasuresO2BedrestPositioningPrevent complications of immobilityPsychological support
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DIAGNOSA KEPERAWATANAdapun diagnosa keperawatan yang mucul pada infeksi
jantung (perikarditis, endokarditis dan miokarditis) yaitu :
Nyeri berhubungan dengan inflamasi miokardium atau perikardium.
Intolerasi aktifitas berhubungan dengan inflamasi dan degenerasi sel-sel otot miokard.
Penurunan curah jantung berhubungan dengn akumulasi cairan dalam kantung perikardia (perikarditis)
Perubahan perfusi jaringan berhubungan dengan embolisasi trombus/vegetasi katub sekunder terhadap endokarditis.
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Kriteria hasil : Rencana tindakan : Mengidentifikasi metode yang
memberi penghilangan Melaporkan nyeri hilang/terkontrol Mendemonstrasikan penggunaan
ketrampilan relaksasi dan aktifitas pengalih sesuai indikasi untuk situasi individual
Kaji keluhan nyeri dada, perhatikan awitan dan faktor pemberat atau penurun. Perhatikan petunjuk non-verbal dari ketidaknyamanan
Berikan lingkungan yang tenang dan tindakan kenyamanan, misalnya perubahan posisi, masase punggung, dukungan emosional
Berikan aktifitas hiburan yang tepat
Berikan obat-obatan sesuai indikasi
Berikan oksigen suplemen sesuai indikasi
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Kriteria hasil : Rencana tindakan :
Klien melaporkan/menunjukkan peningkatan yang dapat diukur dalam toleransi aktifitas
Klien mendemonstrasikan penurunan tanda fisiologis intolerans
Klien mengungkapkan pemahaman tentang pembatasan terapeutik yang diperlukan
Kaji respon klien terhadap aktifitas
Pantau frekwensi/irama jantung, tekanan darah dan frekwensi pernafasan sebelum/setelah aktifitas dan selama diperlukan
Pertahankan tirah baring selama periode demam dan sesuai indikasi
Rencanakan perawatan dengan periode istirahat/tidur tanpa gangguan
Bantu klien dalam program latihan progresif bertahap sesegera mungkin untuk turun dari tempat tidur, mencatat respon dan tanda vital serta toleransi klien pada peningkatan aktifitas
Evaluasi respon emosional terhadap situasi dan berikan dukungan
Berikan oksigen suplemen
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Kriteria hasil : Rencana tindakan :
Klien melaporkan atau menunjukkan penurunan episode dispnea, angina dan disritmia
Klien mengidentifikasi perilaku untuk menurunkan beban kerja jantung
Pantau frekwensi dan irama jantung
Dorong tirah baring dalam posisi semi fowler
Berikan tindakan kenyamanan Anjurkan penggunaan teknik
manajemen stress Pantau vital sign Evaluasi keluhan yang dialami
klien Berikan oksigenasi supplemen Berikan obat-obatan sesuai
dengan indikasi Bantu dalam perikardiosentesis
darurat Siapkan klien untuk
pembedahan, bila diindikasikan
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Kriteria hasil : Rencana tindakan :
o Klien mempertahankan atau mendemonstrasikan perfusi jaringan adekuat secara individual, misalnya mental normal, tanda vital stabil, kulit hangat dan kering, nadi perifer adekuat, masukan dan haluaran seimbang
o Evaluasi status mental klien dan keluarga
o Kaji nyeri dada yang timbul o Observasi ekstremitas te rhadap
edema, eritema, nyeri tekan o Observasi hematuria disertai
dengan nyeri punggung/ pinggang dan oliguria
o Tingkatkan tirah baring o Anjurkan latihan aktif dan bantu
dengan rentang gerak sesuai toleransi
o Berikan/lepaskan stoking antiembolisme sesuai indikasi
o Berikan antikoagulan.