Inflammatory conditions

of the heart
Pericarditis
 A. Pericarditis

´ Inflammation of the pericardium

(membranous sac enveloping
the heart)
´ Can be related to :
• primary inflammatory process
• may develop during medical
and surgical procedures
´ Could either be :
• Fibrous ( dry)
• Effusive with purulent serous fluid
 Overview
´ Pericarditis
• the membrane around the heart is red and
swollen
• the pericardium is a thin, two-layered, fluid-filled
sac that covers the outer surface of the heart.
ü Layers : visceral and parietal layers, between
this 2 layers is the pericardial space or cavity (
which holds 5- 20 ml of fluid)
• provides lubrication for the heart, shields it from
infection and malignancy, and contains the
heart in the chest wall.
• keeps the heart from overexpanding when blood
volume increases, which keeps the heart
functioning efficiently.
Types of pericarditis
a. Acute pericarditis: develops suddenly along with the sudden onset
of symptoms.
b. Chronic pericarditis: lasts for three months or longer after the initial
acute attack.
c. Constrictive pericarditis:
• the inflamed layers of the pericardium stiffen, develop scar tissue, thicken
and stick together.
• interferes with the heart’s normal function
• usually happens after multiple episodes of acute pericarditis over time.
d. Infectious pericarditis: develops as the result of a viral, bacterial,
fungal or parasitic infection.
Risk factors

´ Male ( 20-50 years old)

´ Systemic autoimmune disease
´ Viral / bacterial infection
´ Past renal and cardiac surgery
´ ( uremia ) Dialysis
´ Heart attack
Causes
• bacterial infection, including tuberculosis, causes
bacterial pericarditis.
• fungal infection causes fungal pericarditis.
• infection from a parasite causes parasitic pericarditis.
• autoimmune diseases, such as lupus, rheumatoid arthritis
• Injury to the chest, such as after a car accident, causes
traumatic pericarditis.
• Kidney failure causes uremic pericarditis.
• Tumors like lymphoma causes malignant pericarditis
 Pathophysiology of pericarditis
´ Inflammation / thickening of the pericardium, constricts the heart, causing compression

Injury of pericardial space (pericardial sac becomes inflamed)

Loss of pericardial elasticity /accumulation of fluid within the sac

Pericardial Effusion ( complication due to accumulation of fluid)

Exerts pressure

Cardiac Muscle

Cardiac dysfunction
Heart failure or cardiac tamponade may result.
Triad of symptoms
1. Chest pain
• Typical symptom, sharp more often radiating left shoulder
• Becomes worse with deep inspiration
• Worsen when in supine position
• Maybe relieved with a forward leaning or sitting position ( Tripod position)
2. Pericardial friction rub
• (scratchy, high- pitched sound)
• is heard on auscultation
• is produced by the rubbing of the inflamed pericardial layers
3. ECG changes
• ST segment elevation with the onset of inflammation, PR depression
Signs and symptoms

1. Chest pain
2. Fever and chills
3. Fatigue and malaise
4. Tripod position
5. Elevated white blood cell count
7. Signs of right sided heart failure in clients with chronic
constrictive pericarditis :
• Distended jugular veins
• Peripheral edema
Diagnostic exams
• Electrocardiogram (ECG or EKG)
• ESR ( erythrocytes sedimentation rate )
• C- reactive protein
• CBC
• Chest X-ray to see the size of your heart and any fluid in in the
lungs
´ Echocardiogram
´ MRI
´ CT scan
´ Serum Urea, troponin levels
 Complications of pericarditis

´ Cardiac tamponade
• Pericardial effusion limit cardiac filling low cardiac output
Cardiac tamponade ( life threatening circulatory shock )

´ Chronic constrictive pericarditis reduces cardiac filling blood backs up in

the body’s veins, legs leads to venous congestion ( edema, abdominal
organs ( hepatomegaly) , elevated pulmonary pressure ( dyspnea)
Medical Management

1. Analgesics and Nonsteroidal Anti- inflammatory Drugs

( NSAIDs )
• Indomethacin ( Indocin) is contraindicated it may decrease
coronary blood flow.
2. PPI’S ( proton pump inhibitors )
• Given to prevent peptic ulcer disease as a result of NSAIDs
administration
3. Corticosteroids
4. Antibiotics
Surgical interventions: pericarditis

a.Pericardial window
ü A small opening in the pericardium
ü Performed to allow continuous drainage into the
chest cavity
b. Pericardiectomy
ü Surgical removal of the tough encasing pericardium
ü To release both the ventricles from constrictive
inflammation and scarring.
Pericardial window and
pericardiectomy
Pericardiocentesis
´ Removal Pericardial fluid.
• Emergency resuscitation equipment should be available
• Elevate head of bed to 45 to 60 degrees, placing the
heart in proximity to the chest wall so that the needle
can be directly inserted into the myocardial sac.
• Slow IV infusion is started for administration of
emergency drugs/ blood products.
• Ultrasound imaging to guide placement of the needle
to pericardial space
Desired effect : pericardiocentesis

ü Decrease in CVP
ü Increase in BP
ü Withdrawal of pulsus paradoxus
• >10 mm Hg drop in BP during inspiration
ü Disappearance of prominent neck veins due to
increased venous pressure
Complications of pericardiocentesis

´ Coronary artery rupture

´ Myocardial trauma
´ Dysrhythmias
´ Pleural laceration
´ Gastric puncture
Interventions
1. Evaluate nature of pain.
2. Position the client in a high Fowler’s position, or upright
and leaning forward.
3. Administer analgesics, nonsteroidal anti- inflammatory
drugs, or corticosteroids for pain as prescribed.
4. Auscultate for a pericardial friction rub.
5. Check results of blood culture to identify causative
organism.
6. Administer antibiotics for bacterial infection as
prescribed.
7. Administer diuretics and digoxin as prescribed to the
client with chronic constrictive pericarditis;
Nursing management
´ Patients with acute pericarditis require :
• Pain management with analgesics
• Positioning
• Psychological support
• Be alert for signs of cardiac tamponade
Ø After pericardiocentesis
• Monitor patient’s : heart rhythm, Bp, venous pressure,
heart sounds
• To detect possible recurrence of cardiac tamponade
Key points
´ Pericardial friction rub : is diagnostic feature of
pericarditis and lewder at the end of exhalation.
´ Monitor for pericardial friction rub by placing the
diaphragm of the stethoscope tightly against the
thorax and intercostal space the site where the
pericardium comes in contact with the left chest wall.
´ The rub is best heard when the patient is sitting and
leaning forward.
Ø Monitor for signs of cardiac tamponade, including pulsus
paradoxus, jugular vein distention with clear lung sounds,
muffled heart sounds, narrowed pulse pressure,
tachycardia, and decreased cardiac output.
Ø Notify the physician if signs of cardiac tamponade
occur.
Cardiac Tamponade
´ A condition where the heart is
unable to pump blood due to
accumulation of fluid in the
pericardial sac ( pericardial
effusion )
´ This Condition restricts ventricular
filling resulting to decreased
cardiac output.
´ This occurs when there is sudden
accumulation of more than 50 ml
fluid in the pericardial sac.
Causes of cardiac tamponade

´ Cardiac trauma
´ Complication of MI
´ Pericarditis
Assessment findings

´ BECK’s Triad
• Jugular vein distention
• Hypotension
• Distant/ muffled heart sound
• Pulsus paradoxus
ü ( > 10 mm Hg drop in blood pressure during inspiration )
Ø Increased CVP
Ø Anxiety
Ø Dyspnea
Cardiac tamponade
Laboratory findings

´ Echocardiogram : shows accumulation of fluid in the pericardial sac

´ Chest X- ray
Nursing management

´ Client needs critical care for hemodynamic monitoring

´ Administer IV fluids as prescribed to manage decreased CO
´ Prepare client. For pericardiocentesis : to withdraw pericardial fluid
´ Monitor for recurrence of tamponade following pericardiocentesis
´ If recurrent effusions develops from chronic pericarditis
• Pericardial window / pericardiectomy may be done to remove a portion to
allow adequate ventricular filling and contraction.
Infective Endocarditis

´ is an inflammation of the endocardium

( inner lining of the heart especially the valves).
´ Occurs primarily in clients :
• IV drug abusers,
• Prosthetic valve replacements
• mitral valve prolapse or other structural defects
• Hospital acquired infective endocarditis occurs
in patients with indwelling catheters
Pathophysiology infective endocarditis

´ A deformity or injury of the

endocardium brought about by
infectious organisms leads to
accumulation of fibrin and
platelets .
´ The infection may erode through
the endocardium into underlying
structures ( valves leaflets)
causing deformity
´ Ports of entry for the infecting organism include the :
ü Oral cavity (especially if the client has had a dental
procedure in the previous 3 to 6 months),
ü cutaneous invasion, infections,
ü invasive procedures, or surgery
Types of infective endocarditis

a. Subacute bacterial endocarditis ( SBE)

• Develops gradually over several weeks or months
• Caused by Streptococcus viridians

b. Acute bacterial endocarditis

• Develops over days or weeks
• Caused by streptococcus aureus
Clinical manifestations of infective.
endocarditis
´ Cluster of petechiae : found on the
body
´ Small painful nodules ( Oslers nodes);
maybe present in pads of fingers or toes
´ Janeway lesions : irregular re, purple,
painless, flat macules present in palms,
fingers and toes.
´ Roth spots : hemorrhages with pale
centers in the eyes cause by emboli
maybe observe in the fundus of the
eyes.
´ Splinter hemorrhages : reddish brown
lines and streaks maybe sees under the
fingernails and toenails.
Prevention

´ Antibiotic prophylaxis : recommended for high – risk patients immediately

before and after the following procedures
Ø Dental procedures
Ø Tonsillectomy or adenoidectomy
Ø Bronchoscopy
Ø Cystoscopy
Ø Surgery involving infected skin or musculoskeletal tissue
Medical management

a. Antibiotics ( penicillin, Streptomycin)

Given IV , continuous IV infusion for 2 to 6 weeks
Penicillin : medication of choice
b. Fungal endocarditis :
- Antifungal agent as amphotericin B
- Fungizone : usual treatment
b. Treat fever ( fluids, rest. Cooling measures, salicylates)
c. Monitor for signs of heart failure and embolic manifestations .
Interventions

´ Provide adequate rest balanced with activity to prevent thrombus formation.

´ Maintain antiembolism stockings.
´ Monitor cardiovascular status.
´ Monitor for signs of heart failure.
´ Monitor for signs of emboli.
´ Monitor for splenic emboli, as evidenced by sudden abdominal pain radiating to the left
shoulder and the presence of rebound abdominal tenderness on palpation.
´ Monitor for renal emboli, as evidenced by flank pain radiating to the groin, hematuria,
and pyuria.
´ Monitor for confusion, aphasia, or dysphasia, which may indicate central nervous system
emboli.
´ Monitor for pulmonary emboli as evidenced by pleuritic chest pain, dyspnea, and cough. j.
Assess skin, mucous membranes, and conjunctiva for petechiae
´ Assess nail beds for splinter hemorrhages.
´ Assess for Osler’s nodes on the pads of the fingers, hands, and toes.
´ Assess for Janeway lesions on the fingers, toes, nose, or earlobes.
´ Assess for clubbing of the fingers
´ Evaluate blood culture results.
´ Administer antibiotics intravenously as pre- scribed.
´ Plan and arrange for discharge, providing resources required for the continued
administration of IV antibiotics.
Myocarditis

´ The inflammation can reduce the heart's ability to pump blood.

´ Usually diagnosed when it leads to significant cardiac dysfunction
´ Can cause considerable morbidity and mortality
´ Caused by bacteria. Protozoa, fungal, parasitic.
´ Viral myocarditis : most common type
´ Characterized by necrosis and cell injury associated with inflammation of the heart muscle
´ Myocarditis can cause chest pain, shortness of breath, and rapid or irregular heart rhythms
(arrhythmias).

Ø Severe myocarditis weakens the heart so that the rest of the body doesn't get enough blood.
Clots can form in the heart, leading to a stroke or heart attack.
 Assessment findings

Ø Fatigue, Dyspnea and palpitation

Ø Symptoms of heart failure if the disease has progressed :
ü Tachycardia
ü Pulmonary edema
ü Diaphoresis
ü Neck vein distention
ü Cardiomegaly
Ø ECG shows : Low voltage QRS complexes, ST segment elevation, heart
block
Ø S4 and systolic murmurs on auscultation
Ø May lead to sudden cardiac death or severe congestive heart failure
Medical management

´ Antibiotics : penicillin ( for hemolytic streptococci)

´ Inotropic support for cardiac function with:
ü Dopamine
ü Nitroprusside
ü Nitroglycerine ( to decrease afterload)
Ø Beta- blockers are avoided because they decrease strength of ventricular
contraction
Ø Sedation may be necessary to decrease cardiac workload.
Ø Intra- aortic balloon pulsation : improves CO