NOTES Mod #6 Inflammatory
Endocarditis/Myocarditis/Pericarditis
Cardiac Tamponade cmj
Inflammatory Disease affecting the Heart
Etiology/Pathophysiology (general)
A. Pathophysiology
1. Various causes of inflammatory disease affecting heart (bacteria, fungus)*
Review rheumatic fever and RHD management)
a. Endocarditis: precipitated by bacteria/fungal infection; untreated lead
to death from emboli and valvular disturbance
b. Myocarditis: virus, toxin or autoimmune response damaging heart
muscle> lead to cardiomyopathy and death!
c. Pericarditis: Bacterial, fungal or viral infection affecting visceral and
parietal pericardium; restricts heart pumping action> lead to cardiac
tamponade and death!
Endocarditis (Infective)
A. Etiology/Pathophysiology:
1. Pathogens: enter bloodstream through dental work, invasive procedures>
vegetation forms on damaged endothelium
a. Organisms colonize vegetations> become covered with platelets and fibrin
b. Friable vegetations break off> *embolize> travel through blood stream
to other organ systems
c. Emboli lodge in small vessels > hemorrhages, infarcts, abscesses**
d. *Vegetation scars, deforms valves > causes turbulent blood flow
through heart
2. Classifications (See p. 891, Tab 30-5)
a) Acute infective endocarditis
1) Abrupt onset, rapidly progressive severe disease
2) Staphylococcus aureus most common infective organism
(associated usually with IV drug use)
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b) Subacute infective endocarditis
1) Gradual onset; systemic manifestation
2) Occurs with preexisting heart disease
3) Organisms include Streptococcus viridans, enterococci, yeasts, fungi
c) Prosthetic valve endocarditis (PVE) (generally 2 mo after surgery; esp
aortic valve)
1) Early onset usually due to contamination during surgery or
preoperative bacteremia;has high mortality rate
2) Late onset similar to subacute endocarditis
3. Risk factors
a. Previous heart damage as deformed valves, valve prostheses, areas of
heart damaged by congenital or ischemic disease (left sided valves,
especially mitral); history rheumatic fever! (Subacute)
b. *Intravenous illicit drug use (right sided valves usually affected):
why? Due to IV site injection > travel to rt side of heart (Acute)
c. Invasive catheters (central venous lines, indwelling urinary catheters)
d. Dental procedures, poor dental health
e. Recent heart surgery
B. Common Manifestation/Complications
1. Temperature above 101.5o F. (39.4o C); flulike symptoms (cough,
shortness of breath, joint pain); esp acute endocarditis; blood cultures
required!
2. Acute staphylococcal endocarditis; may present with sudden onset of chills.
high fever
3. Heart murmurs occur (new or worsening)…occurs in 90% of all cases…**
4. *Embolic complications (Recall why this happens!)
a. Splenomegaly with chronic disease
b. Peripheral manifestations due to microemboli (some findings significant,
others not)
1) Petechiae
2) Splinter hemorrhages (hemorrhagic streaks under finger or toenails)
3) Osler’s nodes: small, reddened painful raised growths on finger and
toe pads
4) Janeway lesions: small nontender purplish red macular lesions on
palms of hands or soles of feet
5) Roth’s spots, small whitish spots seen on retina
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Osler’s nodes: small, reddened, painful growths, finger and
toe pads
Janeway lesion, nontender on
palms of hand, soles of feet
Splinter
hemorrhages
Roth’s spots (cotton
wool) seen on retina
5. Complications include heart failure, organ infarction
a. RT emboli (50% break off; have septic clots
1) Right sided endocarditis develop pulmonary emboli
2) Left sided emboli affect brain, spleen, heart and limbs
b. CHF
c. Arrhythmia (a-fib most common)
d. Death
e. Cardiac tamponade
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests: *Identify, eradicate infected organism with antibiotics;
minimizing valve damage and complications
a. Blood cultures: considered positive if infecting organism identified from
2 or more separate blood cultures (different sites, different times); temp
above 101 drawn from different sites, different times) (Recall how blood
cultures done!)
b. WBC, ESR for elevations; dec. HCT and HGB
c. Echocardiography: visualization of vegetations and eval. of valve function;
TEE visualization of vegetation
d. Serologic immune testing: test for circulating antigens
e. Monitor Bun, creatinine with use of antibiotics necessary in treatment
2. Medications (*understand reason why!)
a. *Antibiotic prophylaxis-for pre-existing valve damage or heart disease
prior to high risk procedures
b. *Infective endocarditis involves extended course of multiple
intravenous antibiotics (2 – 8 weeks); repeat blood cultures
c. *Prosthetic valve endocarditis includes extended treatment (6 – 8
weeks) with combination of antibiotics
3. Surgery
a. Surgery may be part of treatment
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1) replace damaged valve
2) remove large vegetation
3) remove valve if source of infection/not responding to antibiotics
b. *Surgery usually indicated for clients with valvular regurgitation
causing heart failure -not responding to antibiotic therapy; also for
fungal endocarditis
4. Nursing Diagnoses (p. 893-894)
a. Risk for Imbalanced Body Temperature
b. Risk for Ineffective Tissue Perfusion
c. Ineffective Health Maintenance
d. Knowledge deficit include: use of medications/need to complete therapy/
need to notifying health practitioners of need for *prophylaxis with all
invasive procedures (penicillin) ; need for dental care and hygiene and
follow-up with physician (understand this)
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Myocarditis
A. Etiology/Pathophysiology:
1. Inflammation of heart muscle from infectious process, immunologic
response to radiation, toxins, medications
2. Due to Coxsakie B virus** (in US)
3. More common with altered immunity (10% HIV clients develop this)
4. Dec. contractitility
5. Viral myocarditis usually self-limiting-can become chronic > lead to
*dilated cardiomyopathy
6. Myocardial cells damaged by inflammation and invading pathogens
7. Extent of damage determines outcome*
8. Risk factors: URI, toxic or chemical effects (radiation, alcohol);
autoimmune; metabolic disturbance-lupus; heat stroke or hypothermia & a
complication of pericarditis and rheumatic fever
•This is an infection in the muscles of the heart,
most commonly caused by the Coxsackie B virus
that follows upon a respiratory or viral illness,
bacteria and other infectious agents.
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View of transverse section of heart from above.
•Note area of myocardial pallor (2 arrows)
mostly to the left of the left ventricular cavity
involving less than 1/2 of the wall thickness…due
to a dense interstitial infiltrate of inflammatory
cells. •The normal appearing red myocardium
elsewhere could also show microscopic infiltrates,
which are not dense enough to see grossly
Patho (click here for more information)
B. Common Manifestation/Complications
1. Dependent on degree of myocardial damage; from asymptomatic to heart
failure
2. Non-specific: fever, fatigue, general malaise, dyspnea, palpitations,
arthralgias (may be preceded by nonspecific febrile illness or upper
respiratory infection)
3. Heart sounds: muffled S1, S3, murmur, pericardial friction rub, tachycardia
4. **Manifestations of heart failure, chest pain, maybe MI, signs CHF,
arrhythmia
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests:
a. Electrocardiography: may show ST segment and T wave changes,
dysrhythmias, possible heart block
b. Cardiac markers (Creatinine kinase, troponin T and I) may be elevated
c. Endomyocardial biopsy for definitive diagnosis-show patchy cell
necrosis and inflammatory process
2. Medications
a. To eradicate infecting organism, including interferon-alpha for virus
(antibiotics, antiviral with interferon-a)
b. Immunosuppressive therapy- corticosteroids & others
c. Other medications for symptoms:heart failure drugs including ACE
inhibitors, beta blockers, antiarrhythmics if indicated; anticoagulants, to
prevent emboli
d. Bedrest and restricted activity during the acute inflammatory process;
may be limited 3- 6 months (Very imortant!!)…why? (see p. 895)
3. Nursing diagnosis/Nursing Care
a. Nursing Care focus: dec. myocardial work; maintain cardiac output
b. Nursing Diagnoses (See p. 895)
1) Activity Intolerance
2) Decreased Cardiac Output
3) Fatigue
4) Anxiety
5) Excess Fluid Volume
6) Knowledge Deficit
a) Home Care_ teach activity restriction; recognition early
manifestations heart failure; medications, diet modifications;
follow-up with medical care
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Pericarditis and Cardic Tamponade
A. Etiology/Pathophysiology:
1. Inflammation of pericardium (may be 1st or 2nd to other cardiac/systemic
disorders
2. Types: acute (usually viral in nature, bacterial or fungal) or chronic
a. *Result from end-stage renal disease and uremia, post-MI, post open
heart surgery
b. Heart loses natural lubrication (15-50cc’s) > layers roughen and rub
c. Damage occurs to pericardial tissue > lead to inflammation
d. Increased capillary permeability and plasma proteins seep into
pericardial space forming exudates**
e. Scar tissue or adhesions may form between pericardial layers
3. Chronic inflammation > cause** pericardium to become rigid.
4. Risk factors: Post MI (Dressler’s syndrome); secondary to chemo and
cancer; secondary to uremia in renal failure-(40-50% of ESRD pts. develop
this); trauma or cardiac surgery
B. Common Manifestation/Complications (know this!)
1. **Chest pain: aggravated by respiratory movement, changes in body
position; sitting upright, leaning forward may reduce the pain (moves
the heart away from side of lung pleura)!
2. Typically has abrupt onset; sharp, steady or intermittent pain, may
radiate to back or neck! (acute)
3. Pericardial friction rub: leathery grating sound produced by inflamed layers
rubbing together; heard most clearly at left lower sternal border with
client sitting and leaning forward during expiration
Pericardial Friction Rub (Go here to auscultate a pericardial friction rub)
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Hear a typical friction rub-caused by the beating of the heart against inflamed pericardium or lung pleura; various
etiologies. Sound usually continuous, heard diffusely over chest. Typically has three components, one systolic and
two diastolic. Systolic occurs with ventricular contraction, diastolic occurs during both rapid ventricular filling and atrial
contraction; accentuated when patient sits up, leans forward, may be accentuated during inspiration. If rub
completely disappears when patient holds his breath it is more likely due to pleural, not pericardial, origin.
4. Fever (low grade) with dyspnea and tachycardia (less than 100)
5. Complications
a. Pericardial effusion
Heart huge due to fluid
in pericardial space
1) Abnormal collection of fluid in pericardial space> threatens normal
cardiac function
2) Fluid may be pus, blood, serum, lymph or combination
3) Rate at which effusion develops effects manifestations: (Why is this
significant??)
a) Slow build > no immediate effects
b) **Rapid buildup > compress heart interfer with myocardial function
(tamponade)
c) May have distant or muffled heart sounds, cough, mild dyspnea
b. Cardiac tamponade (*Important!)
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1) Medical emergency; rapid collection of fluid> interferes with
ventricular filling, pumping, reducing cardiac output
2) Manifestations (know this!)
a) Paradoxical pulse (pulsus paradoxus): pulse has marked decrease
in amplitude during inspiration
b) Paradoxical pulse indicated by drop in systolic blood pressure of
more than 10 mm HG during inspiration
c) Distant, muffled heart sounds
d) Dyspnea and tachypnea
e) Narrowed pulse pressure
f) Elevated CVP
g) Distended neck veins
c. Chronic Constrictive Pericarditis
Results from chronic
pericarditis
1) Scar tissue forms between pericardial layers >restricts heart
movement and filling
2) May follow viral infection, radiation therapy, heart surgery
3) Manifestations: dyspnea; fatigue, weakness; ascites; neck vein
distension during inspiration (Kussmaul’s sign)
C. Therapeutic Interventions/Collaborative Care (relieve symptoms; prevent
complications)
1. Diagnostic tests:
a. Differentiate from MI: CBC and ESR: Elevated WBC and ESR reflect acute
inflammation
b. Cardiac enzymes: elevation is lower than with MI
c. Electrocardiography (ECHO): diffuse ST segment elevation in all leads;
resolves more quickly than with MI; Q waves and T wave changes found
with MI not present
d. Echocardiography: assesses heart motion, pericardial effusion; any
restricted movement
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e. Hemodynamic monitoring: assesses pressures, cardiac output
f. Chest xray: cardiac enlargement if pericardial effusion is present
g. CT scan or MRI: identify effusion or constrictive pericarditis
2. Medications
a. Aspirin or acetaminophen to reduce fever
b. NSAIDS for comfort
c. Corticosteroids for severe or recurrent pericarditis
3. Surgery/Other
a. Pericardiocentesis: Removal of fluid from pericardial sac for diagnostic
or therapeutic purposes; needle insertion into pericardial sac and
withdrawal of fluid; emergency procedure for *cardiac tamponade
Cardiac monitoring during procedure; catheter to V lead
b. Surgery
1) Pericardial Window: excision of rectangular piece of pericardium to
allow fluid to drain into pleural space if recurrent pericarditis or
effusion
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A procedure in which an opening is made in the
pericardium to drain fluid that has accumulated around
the heart. A pericardial window can be made via a small
incision below the end of the breastbone (sternum) or
via a small incision between the ribs on the left side of
the chest.
2) Partial or total pericardectomy with constrictive pericarditis
4. Nursing Care/Nursing Diagnoses Pericardidits (p. 898)
a. Acute Pain
b. Ineffective Breathing Pattern
c. Risk for Decreased Cardiac Output
d. Activity Intolerance
e. Knowledge deficit: regarding anti-inflammatory medications; activity
restriction; manifestations of recurrent pericarditis and seeking treatment
Summary
Inflammatory conditions of the heart can be life threatening, cause
death
Management will depend upon etiology and disease manifestation
Surgery and in some cases, even transplant of the heart may be
required.
General nursing (during acute phase) care includes:
O2
Bedrest
Positioning
Space Activities
Prevent complications of immobility
Psychological support
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