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Inflammatory Disorders of the Heart
Endocarditis
Pericarditis
Myocarditis
infection of endocardial surface of
heart
focal or diffuse inflammation of
myocardium
inflammation of pericardial
sac (pericardium)
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Endocarditis: precipitated by bacteria/fungal infection; potential
death from emboli and valvular disturbance
Myocarditis: virus, toxin or autoimmune response damage heart
muscle > lead to cardiomyopathy and death!
Pericarditis: Bacterial, fungal or viral infection affect visceral and
parietal pericardium; restrict heart pumping action> lead to
cardiac tamponade and death!
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Layers of the Heart
Layers of heart muscle and
pericardium; section of heart
wall shows fibrous pericardium,
parietal and visceral layers of
serous pericardium (with
pericardial sac between them),
myocardium, and endocardium-
Fig. 37-1
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Layers of the Heart Muscle
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TISSUES SURROUNDING THE HEART
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Infective Endocarditis
(Click to access YOUTube video)
 Infection of inner layer of heartusually affects cardiac valves
 Was almost always fatal until
development of penicillin
 15,000 cases diagnosed in US each
year
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A- Aortic Valve
B- Mitral Valve
C- Tricuspid
Valve
- Pulmonary
Valve
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A&P ReviewBlood enters right atrium and moves through _______ into
right ventricle.
Blood then moves from right ventricle into pulmonary
artery via _________.
A- Aortic Valve
B- Mitral Valve
C- Pulmonary Valve
D- Tricuspid Valve
 After entering left atrium via pulmonary veins, blood moves
through the _____ into left ventricle.
 Finally, it travels through the _____ and out of heart
A- Aortic Valve
B- Mitral Valve
C- Pulmonary Valve
D- Tricuspid Valve
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Risk Factors- endocarditis
 Hx of rheumatic fever or damaged heart
valve
 Prior history of endocarditis
 Invasive procedures- (introduce bacteria into
blood stream) dental,gyne, etc.
 Recent Dental Surgery
 Permanent Central Venous Access
 IV drug users
 Valve replacements
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Classification
 Subacute form (subacute bacterial endocarditis-SBE)
 Gradual onset; longer clinical course
 Caused by enterococci
 Usually those with damaged valves
 Acute form
 Shorter clinical course
 Abrupt onset
 Usually those with healthy valves
 Usually caused by staph aureus
 *Classify by cause as IVBA; prosthetic valve endocarditis
(PVE), fungal endocarditis
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Causative Organisms
 Most common causative organism
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Streptococcus viridans
Staphylococcus aureus
Viruses
Fungi
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Etiology and Pathophysiology
 Key -Blood turbulence within heart
allows causative agent to infect
previously damaged valves or other
endothelial surfaces
 Principal risk factors
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Prior endocarditis
Prosthetic valves
Acquired valvular disease
Cardiac lesions
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 When valve damaged, blood > slowed
down > forms clot.
 Bacteria > into blood stream
 Bacterial or fungal vegetative growths
deposit on normal or abnormal heart
valves
 Infection of innermost layers of heart may
occur in people with:
 congenital and valvular heart disease
 history of rheumatic heart disease
 normal valves with increased amounts of bacteria
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Endocarditis
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Bacterial Endocarditis of Mitral Valve
Bacterial endocarditis
of mitral valve. Valve
covered with large,
irregular vegetations
(note arrow). From
text
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Any valve can be
affected!
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Etiology and Pathophysiology
 Vegetation
 Fibrin, leukocytes, platelets, and
microbes
 Adhere to valve or endocardium
 Embolization of portions of vegetation
into circulation
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Sequence of Events in
Infective Endocarditis (view carefully)
Fig. 37-3
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Clinical Manifestations
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Nonspecific
*Fever in 90% of patients
Chills
Weakness
Malaise
Fatigue
Anorexia
*Murmur
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Clinical Manifestations
 Subacute form
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Arthralgias
Myalgias
Back pain
Abdominal discomfort
Weight loss
Headache
Clubbing of fingers
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Clinical Manifestations
 Vascular manifestations
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Splinter hemorrhages in nail beds
Petechiae * most common
Osler’s nodes on fingers or toes *painful
Janeway’s lesions on palms or soles
Roth’s spots
 *Murmur in most patients
 Heart failure in up to 80% with aortic valve
endocarditis
 *Manifestations secondary to embolism
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Sites of emboli due to
infective endocarditis (AKA
metastic infections)-site
determined by location of
original lesion
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Osler’s nodes
Splinter hemorrhages
Janeway lesions
Roth spots
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•Osler’s nodes- painful, red or purple peasized 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
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Diagnostic Studies
 History
 Recent dental, urologic, surgical, or gynecological
procedures
 Heart disease; onset *new heart murmur
 Recent cardiac catheterization
 Skin, respiratory, or urinary tract infection
 Laboratory tests
 Blood cultures (if temp above 101, typically do 2 sets)
 WBC with differential
 ESR, CRP
 Echocardiography- TEE best- see vegetations
1) Vegetations on mitral valve
 Chest x-ray
2) Vegetations on aortic Valce
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Collaborative Care
 Prophylactic treatment for patients having
(see prevention)
 Removal or drainage of infected tissue
 Renal dialysis
 Ventriculoatrial shunts
 Antibiotic administration
 Monitor antibiotic serum levels (peak &
trough)
 Subsequent blood cultures
 Renal function monitored
 BUN, Creatinine
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Collaborative Care
 Antibiotic therapy cont
 IV for 2-8 weeks
 *Maybe oral meds if not good candidate for
IV and can identify and treat specific
causative organism
 Fungal and prosthetic valve endocarditis
 Responds poorly to antibiotics
 Valve replacement- adjunct procedure
 Fever
 Comfort with ASA, Ibuprofen etc
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Collaborative Care
 Surgical/Therapeutic/Nursing
 Early valve replacement.
 Complete bed rest –only if temp remains
elevated or signs HF
 Overall goals
 normal or baseline cardiac function
 performance of activities of daily living
(ADLs) without fatigue
 Antibiotic therapy cont
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Nursing Diagnoses
 Risk for Imbalanced Body
Temperature-Hyperthermia
 Risk for Ineffective Tissue Perfusionemboli
 Risk for decreased cardiac output
 Ineffective Health Maintenance
 Deficient knowledge
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Complications
 Emboli (50% incidence)
 Right side- pulmonary emboli (esp. with IV drug
abuse- Why??)
 Left side-brain, spleen, heart, limbs,etc
 CHF-check edema, rales, VS
 Arrhythmias- A-fib
 Death
.
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Collaborative Care
 Priority Teaching
 Signs/symptoms of life-threatening complications
of IE, as cerebral emboli, HF etc.
 Monitor fever (chronic or intermittent)- sign that
drug therapy ineffective
 Monitor lab data, blood cultures- determine
effectiveness of antibiotic therapy
 *Critical-prophylactic antibiotic therapy prior to
ANY invasive procedure - see later slide)
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Collaborative Care
 Priority Teaching/nursing care
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Stress need to avoid infectious people
Avoidance of stress and fatigue
Manage rest, hygiene, nutrition
Assessment of nonspecific manifestations
Monitor laboratory data
Monitor patency of IV
Teach reduction measures dec risk infection
Stress follow-up care
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Collaborative Care
•Eliminate risk factors
•Patient teaching
•Penicillin prophylaxis
Recent change Guidelines (not all
require prophylaxis)
• if prosthetic valve
• History of endocarditis
• Certain congenital heart defects
• Heart transplant recipients• Removal/drainageinfected tissue
• Renal dialysis
• Ventriculoatrial shunts
•*see tab 37-3&4
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TABLE 37-3 SITUATIONS
SeeREQUIRING ANTIBIOTIC
PROPHYLAXIS TO PREVENT
ENDOCARDITIS
Oral
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Dental manipulation
involving or periapical
region of teeth
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Dental manipulation
involving perforation of
oral mucosa
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Dental
extractions/dental
implants
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Prophylactic teeth
cleaning with
anticipated bleeding
Respiratory
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Respiratory tract
incisions (e.g., biopsy)

Tonsillectomy/adenoide
ct
GI/GU

Presence wound
infection

Presence UTI
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Risk Stratisfication for IE
High Risk
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Mechanical prosthetic heart valve
Natural prosthetic heart valve
Prior infective endocardititis
Valve repair with prosthetic material
Most congenital heart diseases
Moderate Risk
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Valve repair without prosthetic material
Hypertrophic cardiomyopathy
Mitral valve prolapse with regurgitation
Acquired valvular dysfunction
• Prophylactic antibiotics
are generally
recommended only for
people in the “High Risk”
category
Low Risk
Innocent heart murmurs
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Mitral valve prolapse without
regurgitation
Coronary artery disease
People with pacemakers/ defibrillators
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
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Pericarditis
(Click to access YouTube video)
 Pericarditis
 inflammation of pericardium, thin,
fluid-filled sac surrounding heart.
 Can cause severe chest pain especially
upon taking a deep breath)
 Shortness of breath; hear pericardial
friction rub.
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Etiology/Pathophysiology
 Pericarditis due to
 Bacterial, fungal or viral infection infectious)
 Non-infectious as uremia
 Hypersensitive/autoimmune as Dresslers
syndrome
 Heart loses natural lubrication(10-15 ml
serous fluid); layers roughen and rub
 Inflammatory response>lymphatic fluid build-up if sudden > cardiac tamponade Pericardial Effusion- usually 250ml before show
on x-ray-Can have 1000ml (danger!)
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Pericardial Sac Anatomy-video
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Fig. 37-4
Acute pericarditis. Note
shaggy coat of fibers
covering surface of heart.
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Risk Factors/pericarditis
 Be Acute or Chronic
 Infectious, non-infections or
hypersensitive/autoimmune causes
 Acute-48=72 hrs post Mi or late-post MI
(Dressler’s syndrome)-4-6 wks
 Secondary to chemo and cancer
 Secondary to uremia in renal failure-4050% of pts will develop
 Trauma or cardiac surgery
 If chronic disorder-pericardium >rigid
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Clinical Manifestations
 Inflammation and pain
 Pericardial friction rub-(click to hear)
diaphragm at LL sternal, lean forward, listen
at inspiration
 Fever
 Substernal, sharp, pleuritic chest pain
 Inc. with coughing, breathing, turning,
lying flat
 Dec. with sitting up and leaning forward
 Referred to trapezius muscle
 Dyspnea
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Complications of Pericarditis
 Pericardial Effusion
 Cardiac Tamponade
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Pericardial Effusion
(YouTubeVideo)
 Can occur rapidly or slowly
 Pulmonary compression-cough,
dyspnea, and tachypnea
 Phrenic nerve art sounds distant,
muffled
 *Slow build-up; no immediate
effects; if rapid>compression of heart
>tamponade!
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Cardiac Tamponade
 Compression of heart
 Occur acutely (trauma) or sub-acutely
(malignancy)
 Symptoms- chest pain, confusion, anxious,
^ CVP, restless, muffled heart sounds
 Later- tachypnea, tachycardia, and dec.
CO, NVD and pulsus paradoxus
 With slow onset dyspnea may be only
symptom
 If rapid compression-Medical Emergency
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PERICARDIUM
CARDIAC
TAMPONADE

Original heart size
Excess pericardial fluid
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Cardiac tamponade
Definition- a decrease in
systolic BP with
inspirations that is
exaggerated in cardiac
tamponade
Physiology- 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
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Collaborative Care
-Pericarditis, Pericardial Effusion,
Cardiac Tamponde
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Diagnostic Tests
Medications
Surgical/Therapeutic Interventions
Nursing Diagnosis/Interventions
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Diagnostic Tests- to R/O
 CBC-inc. WBC, ESR, and CRP
 Cardiac Enzymes- inc. but not as much as
with MI
 *EKG- diffuse St elevation *important to
different from MI changes (acute
pericarditis)
 Echo- for wall movement
 CXR; Doppler imaginga
 CT or MRI- for pericardial effusion
 Pericardiocentesis fluid- determine cause;
treat cardiac tamponade
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MedicationsASA or tylenol
NSAIDS
*Corticosteroids
Pain relief-HOB to 45 degrees, lean
forward
 Anti-anxiety meds; maybe proton
pump inhibitors
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
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Surgical/invasive Interventions
(remove fluid-treat tamponade)
 Pericardiocentesis
 Hook needle to V lead- guided by EKG and
echo
 Look for ST elevation
 Withdraw fluid
 Afterward watch for cardiac tamponade
(PP), dysrhythmias, pneumothorax
 Pericardial window
 Percutaneous balloon pericardiotomy
 Sclerosing agent- tetracycline (Bonds layers
together)
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Pericardiocentesis
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Pericardial
Window
Procedure in which opening is made in pericardium to
drain fluid that has accumulated around heart-ericardial
window can be made via a small incision below end of the
breastbone (sternum) or via a small incision between the
ribs on the left side of chest.
See also Thoracoscopic Assisted Pericardial Window
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Cardiac Tamponade and
treatment
Live Search Videos: cardiac tamponade
Single-balloon percutaneous balloon
pericardiotomy
Technique used in managing
patient with large pericardial
effusions typically due to
malignancy
Balloon creates a tear in wall of
pericardium to insert a drain and
instill local anesthesia
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Nursing Diagnoses for
Pericarditis
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Acute Pain
Ineffective Breathing Pattern
Risk for Decreased Cardiac Output
Activity Intolerance
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Nursing Management
 O2 (if indicated-as cardiac
tamponade)
 Recognize complications
 Bedrest
 Positioning/sit up/lean forward
 Space Activities
 Prevent complications of immobility
 Psychological support
 Appropriate medication selection
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Chronic Constrictive Pericarditis
 Starts with acute then scarring and
fibrosis occur
 See signs of HF and cor pulmonale;
most relate to dec. CO
 Most prominent finding is JVD and
pericardial knock (click to hear)
 Treatment of choice pericardectomywith use of cardiopulmonary bypass
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Case Studies
John Hopkins- Rheumatoid ArthritisPericarditis Case study
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Myocarditis
Myocarditis-uncommon inflammation of
heart muscle (myocardium) .
 Can be caused by infectious agents,
toxins, drugs or for unknown reasons
 May be localized to one area of heart,
or affect entire heart.
 *Myocarditis (Click for YouTube video)
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Etiology/Pathophysiology
 Virus, toxin or autoimmune response
causes necrosis of myocardium
 *Frequently caused by Coxsackie B virus
 Usually follows URI or viral illness-7-10
days
 Leads to dec cardiac contractility
 May become chronic
 *Lead to dilated cardiomyopathy and
require heart transplant or death
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Myocarditis- infection in muscles of heart; most commonly caused by Coxsackie B
virus that follows a respiratory or viral illness, bacteria and other infectious
agents
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Risk factor-myocarditis
 Hx of URI
 Toxic or chemical effects(radiation,
alcohol)
 Autoimmune disorders
 Post pericarditis
 Metabolic-lupus
 Heat stroke or hypothermia
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Clinical Findings
 Infection and CHF
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Fatigue, DOE
Tachycardia, pleuritc chest pain
Dysrhythmias- esp A fib
Chest pain- maybe an MI
Signs of HF *other late signs
*Pericarditis frequently occurs with
myocarditis- check friction rub
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Collaborative Care Diagnostic Tests
 Diagnostic Tests
 EKG- ST segment and T wave changesWhy??
 Leukocytosis, inc ESR, CRP troponin
levels
 CK-MB and Troponin may be elevated
 Endomyocardial biopsy- has risks; not
used for every case; is definitive
 Echo
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Endomyocardial biopsy
(Click for YouTube Heart Biopsy)
*also helpful to understand cardiac tamponade
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Medications
Antibiotics
Antiviral with interferon-a
IVIG- experimental trials
Corticosteroids or immunosuppressents
*HF drugs- ACE, diuretics, beta
blockers etc
 Antiarrhythmics
 Anticoagulants- Why??
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

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Other Treatments
 Bedrest and activity restrictions- Why
important??
 **Activities may be limited for 6
months- 1 yr.
 O2
*GOAL- Decrease workload of
heart to allow healing!
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Nursing Diagnoses
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Activity Intolerance
Decreased CO
Anxiety
Excess fluid Volume
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Priority Question # 23
 You have just received change of shift report
about these clients on coronary step-down unit.
Who will you assess first?
 A. 26 year old with heart failure caused by
congenital mitral stenosis who is scheduled for
balloon valvuloplasty later today.
 B. 45 year old with constrictive cardiomyopathy
who developed acute dyspnea and agitation about
1 hour before shift change.
 C. 56 year old who had a coronary angioplasty and
stent placement yesterday and has complained of
occasional chest pain since the procedure.
 D. 77 year old who transferred from intensive care
2 days ago after coronary artery bypass grafting
and has a temperature of 100.6F.
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Priority Question # 23
 You have just received change of shift report
about these clients on coronary step-down unit.
Who will you assess first?
 A. 26 year old with heart failure caused by
congenital mitral stenosis who is scheduled for
balloon valvuloplasty later today.
 B. 45 year old with constrictive cardiomyopathy
who developed acute dyspnea and agitation about
1 hour before shift change.
 C. 56 year old who had a coronary angioplasty and
stent placement yesterday and has complained of
occasional chest pain since the procedure.
 D. 77 year old who transferred from intensive care
2 days ago after coronary artery bypass grafting
and has a temperature of 100.6F.
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Priority Question # 19
 While working on the cardiac step-down unit, a nurse is
precepting a new graduate RN who has been in a 6
week orientation program. Which client will be best to
assign to the new GN?
 A. 19 year old with rheumatic fever who needs
discharge teaching prior to going home with a roommate
today.
 B. 33 year old admitted a week ago with endocarditis
who will be receiving Ancef 2 gm IV.
 C. 50 year old with newly diagnosed stable angina who
has many questions about medications and nursing
care.
 D. 75 year old who has just been transferred to the unit
after having coronary artery bypass grafting yesterday.
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Priority Question # 19
 While working on the cardiac step-down unit, a nurse is
precepting a new graduate RN who has been in a 6
week orientation program. Which client will be best to
assign to the new GN?
 A. 19 year old with rheumatic fever who needs
discharge teaching prior to going home with a roommate
today.
 B. 33 year old admitted a week ago with endocarditis
who will be receiving Ancef 2 gm IV.
 C. 50 year old with newly diagnosed stable angina who
has many questions about medications and nursing
care.
 D. 75 year old who has just been transferred to the unit
after having coronary artery bypass grafting yesterday.
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