i. AKAL LOBENYO MORRIS 21-2668
ii. CALEB WANYONYI 21-2220
iii. TONY BARAKA 21-2114
iv. ASNATH MAKORI 21-2853
v. SOFIA MURIUNGI 21-2755
vi. TRACY MURANDE 22-0173
vii. NEDDY CHELANGAT 21-2315
viii.VINCENT KIBUNGEI 21-2435
ix. MACHUKA DAVID 21-22325
x. HADEN NYAMIAKA 21-2340
Names Reg No
• The heart is a vital organ which pumps bloods all through the body.
• The heart is made of three layers; endocardium, pericardium and
• Endocardium – lined by simple epithelium
◊Endocarditis is an inflammation of inner layer of the heart;
◊It usually involves the valves and other structures like intraventricular
CLASSIFICATION OF ENDOCARDITIS
There are several ways to classify endocarditis:
i. Based on the duration of symptoms:
Acute endocarditis: develops rapidly and can be severe.
Subacute endocarditis: develops more slowly and may be less severe.
ii. Based on the location of the infection:
Native valve endocarditis: infection occurs on heart valves that are not artificial.
Prosthetic valve endocarditis: infection occurs on artificial heart valves.
Intravenous drug use-associated endocarditis: infection occurs on heart valves due to
injection drug use.
iii. Based on the causative organism:
Infective endocarditis: caused by bacteria, fungi, or other microorganisms.
Non-infective endocarditis: caused by non-infectious factors such as autoimmune
disorders, tumors, or certain medications.
iv. Based on the clinical features:
Typical endocarditis: presents with the classic symptoms of fever, new onset of
heart murmur, and positive blood cultures.
Atypical endocarditis: presents with non-specific symptoms, such as fatigue or
weight loss, and may not have positive blood cultures.
• Infective endocarditis is a microbial infection of the endothelial surface of the
• A deformity or injury of the endocardium leads to accumulation on the
endocardium of fibrin and platelets (clot formation).
• Infectious organisms, usually staphylococci, streptococci, enterococci,
pneumococci, or chlamydiae invade the clot and endocardial lesion.
• Other causative microorganisms include fungi (eg, Candida, Aspergillus) and
• Prosthetic heart valves or structural cardiac defects
• Age: More common in older people, who are more likely to have
degenerative or calcific valve lesions, reduced immunologic response to
infection, and the metabolic alterations associated with aging.
• Intravenous (IV) drug use: There is a high incidence of staphylococcal
endocarditis among IV drug users.
• Hospitalization: patients with debilitating disease or. indwelling catheters
• Immunosuppression: Patients taking immunosuppressive or corticosteroids
• Reproductive conditions e.g abortions, PID( Pelvic Inflammatory Diseases).
- The bacteria and any other causing agents enter the bloodstream through invasive procedures like dental
procedures surgery, urinary, catheterization.
i. Damage to the endocardium:
The causing agents accumulate on the valves of the heart or the endocardium, damaging the
endocardium. The damage is facilitated by factors such as turbulent blood flow, mechanical damage from
a prosthetic heart valve or catheter, or trauma to the heart.
ii. Colonization of bacteria:
Once the endocardium is damaged, bacteria can enter the bloodstream and adhere to the damaged
surface. The most common bacteria causing endocarditis are Staphylococcus aureus and Streptococcus
iii. Formation of vegetation:
As the bacteria colonize the damaged endocardium, they can form a biofilm called vegetation. Vegetation
consists of bacteria, fibrin, and platelets, and it can grow in size and interfere with the function of the
iv. Destruction of heart valves:
• Over time, the vegetation can erode the heart valves, causing them to leak or become
• Also can cause tearing which means there’s poor flow of blood and lead into accumulation
of blood in the chambers of the heart hence endocarditis.
• This can lead to heart failure, stroke, or other serious complications.
v. Can cause Systemic effects:
• In addition to the local effects on the heart, endocarditis can cause systemic effects such
as fever, fatigue, and muscle aches. The bacteria can also spread to other parts of the body,
causing secondary infections.
• Primary presenting symptoms are fever and a heart murmur.
• Vague complaints of malaise, anorexia, weight loss, cough, and back and
• Cardiomegaly, heart failure, tachycardia, or splenomegaly may occur.
• Central nervous system manifestations include headache, temporary or
transient cerebral ischemia, and strokes.
• Embolization may present-clot
• Hemorrhages with pale centers (Roth spots) caused by emboli.
• Irregular, red or purple, painless, flat macules may be present on the
palms, fingers, hands, soles, and toes.
• Blood Culture-to test presence of micro-organisms
• Urinalysis-to see microscopic hematuria
• CT Scan- to rule out heart damage
• Review of BUN, Creatinine, WBC Levels to evaluate renal
function and course of infection
• •Provide psychosocial support while patient is confined to hospital or home
with restrictive IV therapy.
• Monitor patient’s temperature; a fever may be present for weeks.
• Assess heart sounds for new or worsening murmur.
• Monitor for signs and symptoms of systemic embolization, or, for patients
with right heart endocarditis, signs and symptoms of pulmonary infarction
• Assess for signs and symptoms of organ damage such as stroke
(cerebrovascular accident, brain attack), meningitis, heart failure, myocardial
infarction, glomerulonephritis, and splenomegaly.
• Instruct patient and family about activity restrictions, medications, and signs and
symptoms of infection.
• Reinforce that antibiotic prophylaxis is recommended for patients who have had
infective endocarditis and who are undergoing invasive procedures.
• If patient received surgical treatment, provide postsurgical care and instruction.
• Refer to home care nurse to supervise and monitor IV antibiotic therapy in the
home. For additional nursing interventions.
• Infective breathing pattern related to inflammation of heart muscle as evidenced
by use of accessory muscles and dyspnea
• Impaired gaseous exchange related to fluid accumulation in lungs as evidenced by
shortness of breath
• Decreased C.O related to damaged muscles
• Objectives of treatment are to eradicate the invading organism through adequate
doses of an appropriate antimicrobial agent (continuous IV infusion for 2 to 6
weeks at home).
• Treatment measures include the following:
Isolating causative organism through serial blood cultures, which are taken to
monitor the course of therapy.
Monitoring patient’s temperature for effectiveness of the treatment.
After recovery from the infectious process, seriously damaged valves may require
debridement or replacement.