Inflammatory Disorders

Updated Fall 2012 by Renee Redman

From the notes of Nancy Jenkins

Overview of Todays Lecture

A & P Review
Endocarditis- infection of the endocardial

surface of the heart

Myocarditis- a focal or diffuse inflammation

of the myocardium
Pericarditis- 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

(Contd)

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 Rematik
Terjadinya 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 bilahbilah 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.

Pencegahan
Langkah 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. Menggigil
3. Sakit tenggorok
4. Kemerahan difus di tenggorok dengan eksudat
pada orofaring
5. Pembesaran dan nyeri tekan kelenjar limfe
6. Nyeri abdomen
7. 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 Organisms
Causative organism often bacterial
Streptococcus viridans
Staphylococcus aureus

Other Etiologies
Viruses- Coxsackie B
Fungi Candida alibcans

Etiology and Pathophysiology

Vegetation Fibrin, leukocytes, platelets, and microbes
Adhere to the valve or endocardium
Embolization of portions of vegetation into

circulation
50% of patients with IE will have systemic
embolization

Endocarditis
Infection of the innermost layers of the

heart
May occur in people with congenital and
valvular heart disease
May occur in people with a history of
rheumatic heart disease
May occur in people with normal valves
with increased amounts of bacteria

Etiology/Pathophysiology
Endocarditis
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. 37-2

Risk Factors- endocarditis

Hx of rheumatic fever or damaged heart valve-

less common now (20% of cases)

Prior history of endocarditis
Aging (50% associated with aortic stenosis)
Invasive procedures- (introduce bacteria into
blood stream) (surgery, dental, etc)
Permanent Central Venous Access- MRSA
IV drug users
Valve replacements
Renal dialysis

Nursing Assessment
Subjective Data
History of valvular, congenital, or syphilitic

cardiac disease
Previous endocarditis
Staph or strep infection
Immunosuppressive therapy
Recent surgeries and procedures

Nursing Assessment
Functional health patterns
IV drug abuse
Alcohol abuse

Nursing Assessment
Nonspecific Clinical Manifestations
Weight changes
Chills
Low grade fever in 90% patients
Malaise

Nursing Assessment
Diaphoresis
Bloody urine
Exercise intolerance
Generalized weakness
Fatigue
Cough
Headache

Nursing Assessment
Dyspnea on exertion
Night sweats
Chest, back, abdominal pain
Also consider s/s related to embolization to

specific organ
New or changing heart murmur

Collaborative Care

Fungal and prosthetic valve endocarditis

Responds poorly to antibiotics
Valve replacement is adjunct procedure

Assesment endocarditis
Infection and emboli
Emboli-spleen most often affected (splenectomy)
Oslers nodes- painful, red or purple pea-sized lesions on toes and
fingertips

Splinter hemorrhages- black longitudinal streaks on nail beds

Janeway lesions- flat, painless, small, red spots on palms and soles
Roth spots- hemorrhagic retinal lesions
Murmur- most have murmurs
T above 101(blood cultures) and low-grade
Chills
Anorexia
Fatigue

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

Oslers Nodes
Painful, pea-size, red or purple lesions
On finger tips or toes

Oslers nodes

Roth spots

Roths Spots

hemorrhagic retinal lesions

Clinical Manifestations
Murmur in most patients
Heart failure in up to 80% with aortic valve

endocarditis
Manifestations secondary to embolism

Past Medical History

Recent surgeries or procedures
Cardiac Cath,dental, urologocial,

gynecological (including vaginal or c-section

deliveries)
Hx of IV drug use
Central line placement
Dialysis
Infections (recent UTI, URI or skin infection)
Immunosuppression

Diagnostic Tests
Blood Cultures- most likely positive unless

recent antibiotic tx
Echocardiogram-TEE best- see vegetations
Other- WBC with differential, CBC,ESR,
serum creatinine,CXR, and EKG

Medications
Antibiotics
IV for 4-8 weeks
Monitor peaks and troughs of certain drugs
Monitor BUN and Creatinine.
Evaluate effectiveness of treatment with repeated

blood cultures.
Unclear of success of oral antibiotics

Additional Treatment
Fungal infections- poor responsive to drug

therapy
May require valve replacement
Relapses are common
Bedrest usually not indicated unless febrile,
HF or other complications

Complications
Emboli (50% incidence)
Right side- pulmonary emboli (esp. with IV drug abuse)
Left side-brain, spleen, heart, limbs, etc
CHF-check edema, rales, VS
Arrhythmias- A-fib, conduction blocks
Death

Treatment Goal
Return to baseline cardiac function
ADLs without fatigue
Prevent recurrence

Prevention
Eliminate risk factors
Patient 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/Pathophysiology
Myocarditis
Virus, toxin or autoimmune response causes necrosis

of the myocardium
Most often caused by viral infection
Frequently caused by Coxsackie A and B virus
Frequently follows an upper respiratory infection or
viral illness
Can result in decreased contractility
Can become chronic and lead to dilated
cardiomyopathy- heart transplant or death

Risk factor-myocarditis
Hx of upper respiratory infection
Toxic or chemical effects (radiation, alcohol)
Autoimmune or immunosuppresents- 10%

HIV develop it
Metabolic-lupus
Heat stroke or hypothermia

Myocarditis- Assessment
Early s/s
Fever, fatigue
Malaise, mylagias
Dyspnea, lymphadenopathy
Nausea, vomiting

Myocarditis- Assessment
Cardiac s/s 7-10 days after viral

infection
Pleuritic chest pain (pericardial friction rub)
Pericarditis frequently occurs with myocarditischeck friction rub
Tachycardia
Arrhythmias- PVCs, PACs, Atrial Tachycardias,

Signs of heart failure late cardiac s/s

S3 heart sound, crackles, JVD, syncope,

edema

Myocarditis- Assessment
Sudden DeathIn young adults Myocarditis is the cause of up

to 20% of sudden cardiac death

Diagnostic Tests
EKG- Non-specific T-wave abnormalities
CK-MB and Troponin may be elevated
Endomyocardial biopsy- there are risks and not

used for every case but is definitive for

myocarditis
Chest X-Ray- Variable (Normal to
Cardiomegaly)
Echocardiogram
Cardiovascular Magnetic Resonace

Chest X-Ray in Myocarditis

Myocarditis Treatment
Manage cardiac symptoms
Viral antibiotics for secondary
58% adults recover on own
Treatment Goal
Decrease workload of the heart so it can heal

Medications
Digoxin- use cautiously!
Improves CO but causes dysrhytmias in these

patients
HF drugs- ACE, diuretics, beta blockers etc
Immunosupressive therapy
prednisone, etc
Evidence inconclusive

AnticoagulantsReduces risks of thrombus in low EF

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

yr.
O2
Intraaortic balloon pump
Transplant

Pericarditis
Pericarditis 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 Anatomy
Composed of two layers
Visceral pericardium (inner)
Parietal layer (outer)
Pericardial space is inbetween
Contain about 10-15ml of serous fluid
Provides lubrication
Decreases friction

Etiology/Pathophysiology
Pericarditis
bacterial, fungal or viral infection
Heart loses natural lubrication(10-30ccs) and

layers roughen and rub

Inflammatory 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/pericarditis
Post MI (Dresslers syndrome)
Radiation
Infection
Trauma
Cancer
Drugs and toxins
Rheumatic diseases
Trauma or cardiac surgery
Can be chronic disorder-pericardium becomes

rigid

Assessment pericarditis
Inflammation and pain
Pericardial friction rubFever
Substernal, sharp, pleuritic chest pain
Inc. with coughing, breathing,turning,lying flat
Dec. with sitting up and leaning forward
Referred to trapezius muscle
Dyspnea

Diagnostic Tests- to R/O

EKG- 90% have ekg changes: serial ekgs
ST elevation, PR changes, differ from MI
CBC- WBC, ESR and CRP
Cardiac Enzymes elevated but not as much as with MI
Echo- for wall movement
CT or MRI- for pericardial effusion
Pericardiocentesis fluid for analysis- attempt to

determine cause

ECG in Pericarditis

Medications
Antibiotics to treat bacterial pericarditis
ASA or tylenol
NSAIDS- ibuprofen
Corticosteroids
Typically reserved for patients with

autoimmune conditions or not responding to

NSAIDS

Complications of Pericarditis
Pericardial 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 Effusion
Can occur rapidly or slowly
Pulmonary compression-cough, dyspnea,

and tachypnea
Phrenic nerve involvement- hiccups
Laryngeal nerve- hoarseness

Pericardial Effusion- EKG

Electrical 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.

PERICARDIUM
CARDIAC
TAMPONADE

Original heart
size
Excess pericardial
fluid

Nursing Diagnoses for

Pericarditis
Acute Pain
Ineffective Breathing Pattern
Risk for Decreased Cardiac Output
Activity Intolerance

Specific Nursing Assessment

Paradoxical pulse
Murmur
Pericardial friction rub
Emboli
Chest pain
CHF

Comfort Measures
O2
Bedrest
Positioning
Prevent complications of immobility
Psychological support

DIAGNOSA KEPERAWATAN
Adapun 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.