Updated Fall 2012 by Renee Redman From the notes of Nancy Jenkins

Inflammatory Disorders

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)

Anatomy and Physiology review

Anatomy and Physiology review

A- Aortic Valve

B- Mitral Valve

D- Tricuspid Valve

- Pulmonary Valve

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

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

Layers of the Heart Muscle

TISSUES SURROUNDING THE HEART

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

• 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

• Bilah katup yang meradang juga dapat menempel satu sama lain, mengakibatkan stenosis katup. Yaitu penyempitan lumen katup

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

Penatalaksanaan

Tujuan penatalaksanaan medis adalah membunuh organismen penyebab dan mencegah komplikais yang terjadi. Terapi antobiotik jangka panjang dan penisilin parenteral adalah pengobatan terpilih.

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

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.

Causative OrganismsCausative organism –often bacterial

Streptococcus viridansStaphylococcus aureus

Other EtiologiesViruses- Coxsackie BFungi – Candida alibcans

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

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

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

Bacterial Endocarditis of the Mitral Value

Fig. 37-2Fig. 37-2

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

Nursing AssessmentSubjective Data

History of valvular, congenital, or syphilitic cardiac disease

Previous endocarditis Staph or strep infectionImmunosuppressive therapyRecent surgeries and procedures

Nursing AssessmentFunctional health patterns

IV drug abuseAlcohol abuse

Nursing AssessmentNonspecific Clinical Manifestations

Weight changesChillsLow grade fever in 90% patientsMalaise

Nursing AssessmentDiaphoresisBloody urineExercise intolerance Generalized weaknessFatigue CoughHeadache

Nursing AssessmentDyspnea on exertion Night sweats Chest, back, abdominal painAlso consider s/s related to embolization to

specific organ New or changing heart murmur

Collaborative Care

Fungal and prosthetic valve endocarditisResponds poorly to antibioticsValve replacement is adjunct procedure

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

Splinter hemorrhage

• small areas of bleeding under the fingernails or toenails.

• due to damage to capillaries by small clots

Janeway Lesions

• flat, painless red spots on palms and soles

Osler’s Nodes

Painful, pea-size, red or purple lesionsOn finger tips or toes

Roth spotsOsler’s nodes

Roth’s Spots

• hemorrhagic retinal lesions

Clinical ManifestationsMurmur in most patientsHeart failure in up to 80% with aortic valve

endocarditis Manifestations secondary to embolism

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

Diagnostic TestsBlood Cultures- most likely positive unless

recent antibiotic txEchocardiogram-TEE best- see vegetationsOther- WBC with differential, CBC,ESR,

serum creatinine,CXR, and EKG

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

Additional TreatmentFungal infections- poor responsive to drug

therapyMay require valve replacementRelapses are commonBedrest usually not indicated unless febrile,

HF or other complications

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

.

Treatment GoalReturn to baseline cardiac functionADL’s without fatiguePrevent recurrence

PreventionEliminate risk factorsPatient teaching

Layers of the Heart Muscle

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.

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

Risk factor-myocarditisHx of upper respiratory infectionToxic or chemical effects (radiation, alcohol)Autoimmune or immunosuppresents- 10%

HIV develop itMetabolic-lupusHeat stroke or hypothermia

Myocarditis- AssessmentEarly s/s

Fever, fatigue Malaise, mylagiasDyspnea, lymphadenopathyNausea, vomiting

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

Myocarditis- AssessmentSudden Death-

In young adults Myocarditis is the cause of up to 20% of sudden cardiac death

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

Chest X-Ray in Myocarditis

Myocarditis TreatmentManage cardiac symptomsViral – antibiotics for secondary58% adults recover on ownTreatment Goal

Decrease workload of the heart so it can heal

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

Other TreatmentsBedrest and activity restrictions-**Activities may be limited for 6 months- 1

yr. O2Intraaortic balloon pumpTransplant

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.

Pericardium AnatomyComposed of two layersVisceral pericardium (inner)Parietal layer (outer)Pericardial space is inbetween

Contain about 10-15ml of serous fluidProvides lubricationDecreases friction

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.

Risk Factors/pericarditisPost MI (Dressler’s syndrome)Radiation InfectionTraumaCancerDrugs and toxinsRheumatic diseasesTrauma or cardiac surgeryCan be chronic disorder-pericardium becomes

rigid

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

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

ECG in Pericarditis

MedicationsAntibiotics to treat bacterial pericarditisASA or tylenolNSAIDS- ibuprofenCorticosteroids

Typically reserved for patients with autoimmune conditions or not responding to NSAIDS

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

Pericardial EffusionCan occur rapidly or slowlyPulmonary compression-cough, dyspnea,

and tachypneaPhrenic nerve involvement- hiccupsLaryngeal nerve- hoarseness

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.

PERICARDIUMCARDIAC TAMPONADE

Original heart size

Excess pericardial fluid

Nursing Diagnoses for Pericarditis

Acute PainIneffective Breathing PatternRisk for Decreased Cardiac OutputActivity Intolerance

Specific Nursing AssessmentParadoxical pulseMurmurPericardial friction rubEmboliChest painCHF

Comfort MeasuresO2BedrestPositioningPrevent complications of immobilityPsychological support

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.

 

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

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

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

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.