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Inflammatory Disorders
TISSUES SURROUNDING THE HEART
Layers of the Heart Muscle
Etiology/Pathophysiology
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Endocarditis
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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
Classifications of Endocarditis
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Acute Infective Endocarditis
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Subacute Infective Endocarditis SBE
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Abrupt onset
Rapid course
Staph Aureus
Gradual onset
Systemic manifestations
Prosthetic Valve Endocarditis
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Occurs within 2 months after OR
Risk Factors- endocarditis
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Hx of rheumatic fever or damaged heart
valve
Invasive procedures- dental,gyne, etc.
IV drug users
Valve replacements
Assesment endocarditis
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Infection and emboli
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Emboli-spleen most often affected
Osler’s nodes
Splinter hemorrhages
Janeway lesions
Murmur
T above 101(blood cultures),chills
Anorexia
Fatigue
Roth spots
Osler’s nodes
Janeway lesions
Splinter hemmorrhages
Roth spots
Diagnostic Tests
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Blood Cultures- for temp >101
Echocardiogram-TEE best- see vegetations
Other- CBC,ESR, serum creatinine,CXR,
and EKG
Medications
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Antibiotics
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IV for 2-8 weeks
Monitor peaks and troughs of certain drugs
Monitor BUN and Creat.
Nursing Diagnoses
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Risk for Imbalanced Body Temperature
Risk for Ineffective Tissue Perfusionemboli
Ineffective Health Maintenance
Complications
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Emboli(50% incidence)
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Right side- pulmonary emboli
Left side-brain, spleen, heart, limbs,etc
CHF-check edema, rales, VS
Arrhythmias-Afib most common
Death
Cardiac Tamponade
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Prevention
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Eliminate risk factors
Patient teaching
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Penicillin prophylaxis
Etiology/Pathophysiology
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Myocarditis
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Virus, toxin or autoimmune response causes
necrosis of the myocardium
Frequently caused by Coxsackie B virus
Get dec. contractility
Can become chronic and lead to dilated
cardiomyopathy
•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.
Risk factor-myocarditis
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Hx of URI
Toxic or chemical effects(radiation,
alcohol)
Autoimmune
Metabolic-lupus
Heat stroke or hypothermia
Assessment myocarditis
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Infection and CHF
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Fatigue,DOE
Tachycardia
Arrhythmias
Chest pain- maybe an MI
Signs of CHF
Diagnostic Tests
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EKG- ST segment and T wave changes
CK-MB and Troponin may be elevated
Endomyocardial biopsy
Medications
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Antibiotics
Antiviral with interferon-a
Corticosteroids or immunosuppressents
HF drugs-ACE, diuretics, beta blockers etc
Antiarrhythmics
Anticoagulants
Other Treatments
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Bedrest and activity restrictions
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**Activities may be limited for 6 months1 yr.
GOAL- Decrease workload of the
heart
Nursing Diagnoses
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Activity Intolerance
Decreased CO
Anxiety
Excess fluid Volume
A 42 year old West African man was admitted unconscious
to the intensive care unit, after an out of hospital cardiac
arrest and resuscitation by a friend. He had little medical
history of note other than that he had had a recent upper
respiratory tract infection. There were no risk factors for
HIV infection. While on intensive care he had recurrent
episodes of ventricular fibrillation requiring multiple dc
shocks, but ultimately settled on treatment with intravenous
lignocaine (lidocaine), amiodarone, and overdrive pacing.
His resting ECG showed non-specific T wave changes (fig 1)
and he intermittently had non-sustained episodes of a broad
complex, irregular tachycardia (fig 2). Full blood count,
urea and electrolytes, and liver function tests were normal.
Transthoracic echocardiography showed normal left
ventricular function and size. He gradually recovered
without any sequelae. Electrophysiological testing revealed
inducible non-sustained polymorphic ventricular
tachycardia. Coronary angiography was entirely normal. A
right ventricular biopsy was taken which subsequently
showed healing myocarditis (fig 3). The patient declined to
have an implantable cardioverter/defibrillator and was
discharged on oral amiodarone.
Normal Pericardium
Pericarditis
 slit
like opening between two layers
 contains pericardial fluid
 film of serous fluid
 lubricant that reduces friction between
the beating heart and pericardial sac
Etiology/Pathophysiology
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Pericarditis
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bacterial, fungal or viral infection
Heart loses natural lubrication(15-50cc’s)and
layers roughen and rub
Inflammatory process causes lymphatic fluid
build-up
Pericardial Effusion- usually 250 cc’s before
show up on x-ray
PERICARDIUM
CARDIAC
TAMPONADE
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Original heart size
Excess pericardial fluid
Cardiac tamponade
Paradoxical pulse is a pulse that markedly decreases in
amplitude during inspiration. On inspiration, more blood is
pooled in the lungs and so decreases the return to the left
side of the heart; this affects the consequent stroke volume.
Determination of Pulsus
Paradoxus
1.Place the patient in a position of comfort and take their systolic blood
pressure during baseline respiration.
2.Raise sphygmomanometer pressure until Korotkoff sounds disappear.
3.Lower pressure slowly until first Korotkoff sounds are heard during early
expiration with their disappearance during inspiration
4.Record this pressure.
5.Very slowly lower pressure (1mm at atime) until Korotkoff sounds are
heard throughout the respiratory cycle with even intensity.
6.Record this pressure.
7.The difference between the two recorded pressures is the Pulsus
Paradox.
8.Hemodynamically significant pulsus paradox is greater than or equal to
10% of the pressure at which all Korotkoff sounds are heard with even
intensity.
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Risk Factors/pericarditis
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Post MI (Dressler’s syndrome)
Secondary to chemo and cancer
Secondary to uremia in renal failure-4050% of ESRD Pts. Develop this
Trauma or cardiac surgery
Can be chronic disorder-pericardium
becomes rigid
Assessment pericarditis
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Inflammation and pain
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Friction rub-LLsternal border in knee chest
position Cardiac Resources
Fever
Substernal, pleuritic chest pain
Inc. with coughing, breathing,turning,lying flat
 Dec. with sitting up and leaning forward
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Diagnostic Tests- to R/O
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CBC-inc. WBC and ESR
Cardiac Enzymes- inc. but not as much as
with MI
EKG
Echo- for wall movement
CXR
CT or MRI- for pericardial effusion
Medications
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ASA or tylenol
NSAIDS
Corticosteroids
Surgical/invasive Interventions
for all
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Pericardiocentesis
Hook needle to V lead
 Look for ST elevation
 Withdraw fluid
 Afterward watch for cardiac tamponade(PP)
Valve Replacement
Heart Transplant
Pericardial window
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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.
Nursing Diagnoses for
Pericarditis
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Acute Pain
Ineffective Breathing Pattern
Risk for Decreased Cardiac Output
Activity Intolerance
Specific Nursing Assessment
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Paradoxical pulse
Murmurhttp://www.music.mcgill.ca/auscult
ation/heart_tables.html
Pericardial rub
Emboli
Chest pain
CHF
Comfort Measures
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O2
Bedrest
Positioning
Space Activities
Prevent complications of immobility
Psychological support
Case Studies
http://www.indegene.com/Car/ClinRound/i
ndCarCase2.html myocarditis
 Vascular Infections Case 7-endocarditis
 http://www.med.unsw.edu.au/pathology/Pat
hmus/m1004089.htm-endocarditis
http://intmedweb.wfubmc.edu/grand_rounds/1
999/tamponade.html CASE%20PRESENTATION
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Johns Hopkins Arthritis Case report on rheumatoid
pericarditis