Download NOTES Mod #6 Inflammatory

NOTES Mod #6 Inflammatory
Endocarditis/Myocarditis/Pericarditis
(6/30/05)
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: may lead to cardiomyopathy and death!
c. Pericarditis: Bacterial, fungal or viral infection affecting visceral and
parietal pericardium; restricts heart pumping action, can lead to cardiac
tamponade and death!
Endocarditis (Infective)
A. Etiology/Pathophysiology:
1. Pathogens enter bloodstream through dental work, invasive procedures and
vegetation forms on damaged endothelium
a. Organisms colonize the vegetations and become covered with platelets
and fibrin
b. Friable vegetations break off and* embolize and travel through blood
stream to other organ systems
c. Emboli lodge in small vessels causing hemorrhages, infarcts, abscesses
d. *Vegetation scars and deforms valves and causes turbulent blood flow
through the heart
2. Classifications (See p. 891, Tab 30-5)
a) Acute infective endocarditis
1) Abrupt onset, rapidly progressive severe disease
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2) Staphylococcus aureus most common infective organism (associated
usually with IV drug use)
b) Subacute infective endocarditis
1) Gradual onset with 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 is usually due to contamination during surgery or
preoperative bacteremia and has high mortality rate
2) Late onset is similar to subacute endocarditis
3. Risk factors
a. Previous heart damage such as deformed valves, valve prostheses,
areas of heart damaged by congenital or ischemic disease (left sided
valves, especially mitral); history rheumatic fever!
b. *Intravenous illicit drug use (right sided valves usually affected):
why? Due to IV site injection and travel to rt side of heart)
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) with 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 and
high fever
3. Heart murmurs occur (new or worsening)
4. *Embolic complications
a. Splenomegaly with chronic disease
b. Peripheral manifestations
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 and have septic clots
1) Right sided endocarditis develop pulmonary emboli
2) Left sided emboli affect brain, spleen ,heart and limbs
b. CHF
c. Arrhythmia (afib most common)
d. Death
e. Cardiac tamponade
C. Therapeutic Interventions/Collaborative Care
1. Diagnostic tests: * Identify and eradication infected organism with
antibiotics; minimizing valve damage and complications
a. Blood cultures: considered positive if infecting organism is identified
from 2 or more separate blood cultures (different sites, different times);
temp above 101 drawn from different sites, different times)
b. WBC, ESR for elevations and decreased HCT and HGB
c. Echocardiography: visualization of vegetations and evaluation of valve
function and TEE for best visualization of vegetation
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d. Serologic immune testing: test for circulating antigens to infective
organisms
e. Monitor Bun creatinine with use of antibiotics necessary to treat infection!!
2. Medications
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
1) To replace damaged valve
2) To remove large vegetation
3) To remove valve that is source of infection not responding to
antibiotics
b. Surgery usually indicated for clients with valvular regurgitation
causing heart failure that does not respond to antibiotic therapy; also
fungal endocarditis
4. Nursing Diagnoses
a. Risk for Imbalanced Body Temperature
b. Risk for Ineffective Tissue Perfusion
c. Ineffective Health Maintenance
d. Knowledge deficit include: use of medications and 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;
Myocarditis
A. Etiology/Pathophysiology:
1. Inflammation of heart muscle from infectious process, immunologic response
to radiation, toxins, medications
2. In US most myocarditis is viral due to Coxsakie B virus
3. More common in clients with altered immunity
4. Get decreased contractitility
5. Viral myocarditis usually self-limiting, but can become chronic and lead to
*dilated cardiomyopathy
6. Myocardial cells damaged by inflammation and invading pathogens
7. Extent of damage determines outcome*
8. Risk factors include: URI, toxic or chemical effects (radiation, alcohol);
autoimmune; metabolic disturbance-lupus; heat stroke or hypothermia
132  RNSG 2331
•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.
View of transverse section of heart from
above. Anterior surface faces upwards,
thick left ventricle on the left, right ventricle
on right.
•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
B. Common Manifestation/Complications
1. Dependent on degree of myocardial damage; range 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
2. Medications
a. Medications to eradicate infecting organism, including interferon-alpha for
virus (antibiotics, antiviral with interferon-a)
b. Immunosuppressive therapy may be instituted with corticosteroids
c. Other medications may include: (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
RNSG 2331  133
3. Nursing diagnosis/Nursing Care
a. Nursing Care focus: decreasing myocardial work and maintaining cardiac
output
b. Nursing Diagnoses
1) Activity Intolerance
2) Decreased Cardiac Output
3) Fatigue
4) Anxiety
5) Excess Fluid Volume
6) Knowledge Deficit
a) Home Care teaching includes activity restriction; recognition of
early manifestations of heart failure; medications, diet
modifications; continue follow-up with medical care
Pericarditis and Cardic Tamponade
A. Etiology/Pathophysiology:
1. Inflammation of pericardium
2. Types include acute, which is usually viral in nature, can be bacterial or
fungal
3. *Can result from end-stage renal disease and uremia, post-MI, post open
heart surgery
4. Heart loses natural lubrication (15-50cc’s) and layers roughen and rub
5. Damage occurs to pericardial tissue leading to inflammation
6. Increased capillary permeability and plasma proteins seep into pericardial
space forming exudates
7. Scar tissue or adhesions may form between pericardial layers
8. Chronic inflammation may cause pericardium to become rigid: chronic
disorder* as pericardium becomes rigid
9. 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
134  RNSG 2331
B. Common Manifestation/Complications
1. Chest pain: aggravated by respiratory movement, changes in body position;
sitting upright and leaning forward may reduce the pain
2. 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 to this web site to hear a pericardial friction rub)
Go to this site to hear a typical example of a friction rub. It is caused by the beating of the heart against an inflamed pericardium or
lung pleura; various etiologies. Sound is usually continuous, and heard diffusely over the chest. It typically has three components,
one systolic and two diastolic. The systolic occurs with ventricular contraction, and the diastolic occurs during both rapid ventricular
filling and atrial contraction. It is accentuated when the patient sits up and leans forward, and may be accentuated during inspiration.
If the rub completely disappears when the patient holds his breath it is more likely due to pleural, not pericardial, origin.
3. Fever (low grade) with dyspnea and tachycardia
4. Complications
a. Pericardial effusion
1) Abnormal collection of fluid in pericardial space that threatens normal
cardiac function
2) Fluid may be pus, blood, serum, lymph or combination
3) Rate at which effusion develops effects manifestations:
a) Slow build up causes no immediate effects
RNSG 2331  135
b) Rapid buildup can compress heart interfering with myocardial
function (tamponade)
c) May have distant or muffled heart sounds, cough, mild dyspnea
b. Cardiac tamponade
1) Medical emergency; rapid collection of fluid interferes with
ventricular filling and pumping, reducing cardiac output
2) Manifestations
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) Muffled heart sounds
d) Dyspnea and tachypnea
e) Narrowed pulse pressure
f) Distended neck veins
c. Chronic Constrictive Pericarditis
1) Scar tissue forms between pericardial layers and 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
136  RNSG 2331
c. Electrocardiography: diffuse ST segment elevation in all leads which
resolves more quickly than as with MI; Q waves and T wave changes
associated with MI do not occur
d. Echocardiography: assesses heart motion, pericardial effusion and any
restricted movement
e. Hemodynamic monitoring: assesses pressures and cardiac output
f. Chest xray: cardiac enlargement if pericardial effusion is present
g. CT scan or MRI to 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; involves 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 with recurrent pericarditis or
effusion
RNSG 2331  137
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
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
Inflammatoru 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
138  RNSG 2331