CARDIAC INFECTIONS

Heart layers:

(outside to inside) Epicardium (visceral pericardium)MyocardiumEndocardium

Etiology/Pathophysiology/Clinical Manifestations of ineffective Endocarditis:

Previously known as bacterial endocarditis. The endocardium, which is the innermost

layer of the heart (lines all the hearts chambers and covers structures such as heart valves),
if contiguous with the valves of the heart, so inflammation from IE affects cardiac valves.
Penicillin as helped with prognosis. Subacute form affects those with preexisting valve
disease and has a clinical course that may extend over several months, caused by
enterococci. Acute form affects those with healthy valves and presents as a rapidly
progressive illness rapid onset), caused more by virulent. (Now classified based on cause or
site.) **Prophylactic treatment! Blood Cultures primary diagnostic tool.**

Etiology/Pathophysiology: Caused by bacteria, viruses, and fungi, treated with

penicillin, but MRSA caused IE can be a challenge to treat. Blood flow turbulence within the
heart allows the causative organism to infect previously damaged valves or other
endothelial surfaces. Principal risk factors include prior endocarditis, prosthetic valves
common due to increased use of prosthetic valves, acquired valvular disease to a once
healthy functional valve, cardiac lesions, or Rheumatic fever in past medical history. Invasive
procedures can allow large numbers of organisms to enter the bloodstream and trigger
infectious process. Primary lesions of infective endocarditis (vegetations), consist of fibrin,
leukocytes, platelets, and microbes that will adhere to the valve surface or endocardium
(abnormal growths). A portion of the vegetation can break off into the circulatory system
causing embolization (mostly in left sided vegetation, right sided will go to lungs). If the
infection spreads locally and causes damage to the valves and the supporting structures, the
end results may be dysrhythmias’s, valvular incompetence and further invasion into the
myocardium causing heart failure, sepsis, and heart block.

Left Sided (mitral valve) endocarditis is more common with bacterial

infections and a pt with an underlying heart condition.

Right Sided (tricuspid valve) endocarditis usually caused by IV drug users

(IVDA) and most commonly cocaine abusers.

Clinical Manifestations: Nonspecific, can involve multiple organ systems, a low grade
fever, weakness, malaise, arthralgias, myalgias, back pain, abdominal pain, weight loss,
headache, clubbing of fingers may occur in the subacute endocariditis. A new murmur or a
changing murmur is common, aortic valves or mitral valves are most commonly affected, HF
can occur. Vascular manifestations include splinter hemorrhages, petechiae, osler’s nodes
on finger tips or toes, Janeway’s lesions on palms or soles of feet, and roth’s spots
(hemorrhagic retinal legions) found on fundoscopic exam. (May NOT need complete bed
rest unless elevated fever or HF).

Nursing Management of Infective endocarditis:

Assess heart sounds and vital signs, assess for arthralgia-joint tenderness, decreased
ROM, and muscle tenderness, examine the oral mucosa, conjunctivae, upper chest and
lower extremities for petechiae, perform a general assessment of the body looking for
hemodynamic and embolic complications. Health promotion and education for those at risk
or have IE. Adequate home environment and hospital access plus live in companions
available, educate about s/s that indicate recurrent infection, antibiotics prophylactically,
importance of follow up care, nutrition, and early treatment of infections.

Etiology/Pathophysiology/Clinical Manifestations of Acute Pericarditis:

Inflammation of pericardial (pericardiumthin sac enclosing the heart). Pericardium

is composed of the inner serous membrane that adheres to the epicardial surface of the
heart, this space creates the cavity between the two layers and normally has 10-30mls of
serous fluid.

Etiology/Pathophysiology: Common causes include it most often being idiopathic!

Also can be from suspected viral causes, hypersensitive or autoimmune causes (rheumatoid
arthritis), uremia, bacterial infection, acute myocardial infarction, tb, neoplasm, and trauma.

MI has 2 distinct forms: First acute pericarditis may occur within the initial 48-
72 hrs after an MI. Second-Dressler syndrome (late pericarditis) appears 4-6
weeks after an MI.

Clinical Manifestations: Chest pain can be sharp, severe, pleuritic in nature. Pain is
aggravated with deep inspiration and lying supine, eased with sitting. Pain may radiate to
shoulder, neck, arms, or left shoulder. Dyspnea-related to the need to breath in rapid,
shallow breaths to avoid chest pain. Pt may have a fever and be anxious. Pericardial friction
rub hallmark finding! (Stethoscope to diaphragm at lower, left sterna border of chest. Rub
is like “sand paper”, high pitched sound believed to rise between roughened pericardial and
epicardial surfaces. Does not radiate widely or vary in timing from the heartbeat.)

Complications include pericardial effusion (accumulation of excess pericardial

fluid), compressed adjoining structures, pulmonary compression (cough, dyspnea,
tachycardia), phrenic nerve compression (hiccups), laryngeal nerve compression
(hoarseness), heart sounds distant and muffled because pericardium is filling up with fluid,
blood pressure IS maintained by compensatory mechanisms, cardiac temponade (pericardial
effusion is increasing in size, creating an increase in intrapericardial pressure = compression
of the heart), the faster the fluid accumulation, the more severity of manifestations.
Acuterupture of heart, trauma, car accident. Subacutesecondary to uremia, malignancy.

Nursing Assessment: S/S of cardiac tamponade include chest pain, (confusion,

anxious, restlessness not enough O2), heart sounds become distant and muffled,
tachycardia, decreased cardiac output, markedly JVD, pulse pressure narrows, pulsus
paradoxus (an exaggeration of the normal variation during the inspiratory phase of respiration, in
which the blood pressure declines as one inhales and increases as one exhales) , diastole bp
decreased. ECG may be normal or change, used to determine presence of pericardial
effusion or cardiac tamponade. CXR usually normal. Elevated troponin levels with the pt who
has ECG changes and acute pericarditis=myocardial damage. Pericardiocentesis or biopsy
done to determine cause.

Nursing Management of Acute Pericarditis:

Management directed towards identification and treatment of UNDERLYING cause.

Bacterialantibiotics, Inflammatory causescorticosteroids (increase glucose, bad for
diabetic, but may need), pain or inflammationnsaids, recurrent pericarditiscolchicine (an
anti-inflammatory angent). Pericardiocentesis can be performed for acute cardiac
tamponade to remove fluid and improve diastolic filling time. (DIAGNOSTICALLY it is done to
remove a sample for examination!)

PRIMARY nursing consideration is managing pts anxiety and pain. Assess amount,
quality, and location of pain to distinguish pain of an MI from pain of pericarditis (pain with
MI does not stop no matter what position). ECG monitoring, bed rest with HOB 45 degrees
and provide a table to lean on for support (pain relieved by semi-fowlers position), Anti-
inflammatory meds given with milk or food (GI upset), monitor vital signs every 15-30min for
potential increase in cardiac output.

Etiology/Pathophysiology/Clinical Manifestations of Myocarditis:

Focal or diffuse inflammation of the myocardium (middle layer of heart wall).

Etiology/Pathophysiology: Variety of factors such as viruses, bacteria, fungi, radiation

therapy, pharmacologic and chemical, autoimmune disorders (polymyositis), may have no
no causative agent (idiopathic), frequently associated with acute pericarditis-particularly
when caused by the coxsackievirus B strains, most COMMON etiologic factor is viruses. As
the myocardium becomes infected cellular damage is caused along with necrosis, immune
response is activated, cardiac dysfunction results-development of DILATED cardiomyopathy.

Clinical manifestations: Variable, begin course without any manifestations to severe

involvement or sudden death (sudden cardiac arrest).

Vital early signsFever, fatigue, malaise, myalgias, pharyngitis, dyspnea,

nausea, vomiting, lymphadenopathy.

Cardiac manifestations appear 7-10 days after viral infection. (Pleuritic chest
pain with pericardial friction rub and effusion 2nd to pericarditis).

Late cardiac signsS3 heart sound (third heart sound, ventricular filling
sound, occurs early during diastole during the rapid filling phase) abnormal
pathologic finding, crackles, JVD, syncope, peripheral edema, angina.
Nursing management of myocarditis:

Most diagnostic tool is endomyocardial biopsy (EMB), done during initial 6 week of
acute illness when lymphocytic infiltration and myocyte damage are indicative of
myocarditis. Myocarditis heart is “touchy”, careful with meds (digoxinventricular failure),
could be toxic. Manage associated cardiac decompensation. Diuretics to reduce fluid
volume, decrease preload. Nitropress, Inocor, Primocor reduce afterload and improve CO.
Anticoagulation to reduce risk of thrombus. Immunosuppressant therapy to reduce
myocardial inflammation and prevent irreversible damage. Oxygen therapy, bed rest and
restricted activity are supportive measures.

ONGOING ASSESSMENT!!! Assess s/s/ of heart failure, take measures to decrease

cardiac workload:semi-fowler’s position, rest periods, spacing of activites, quiet
environment, monitor meds, decrease anxiety with explanations, monitor complications if
pt taking immunosuppressive therapy. Encourage family to learn CPR.

Etiology/Pathophysiology/Clinical Manifestations of Rheumatic Fever:

Inflammatory disease of the heart that could involve all three layers, a chronic
condition that results from rheumatic fever that is characterized by scarring and deformity
of the heart valves.

Etiology/Pathophysiology: Acuterheumatic fever occurs over 2-3 week following a

group A streptococcal pharyngitis. ARF affects hearts, joints, CNS, and skin. 40% involve all
layers of the heart = Carditis. Mitral and aortic valves are most commonly affected. Aschoff’s
bodiesmyocardial involvement. Rheumatic pancarditisgeneralized involvement.

Chronic rheumatic carditis is changes in valvular structure that may

occur months to years after initial episode of ARF.

Mitral Valve MOST commonly involved. Other valves involved may be

aortic and tricuspid.

Clinical manifestations: Cluster s/s and laboratory results. Presence of 2 major criteria
and 1 minor, or 1 major and 2 minor criteria PLUS evidence of a preceding group A
streptococcal infection = high probability of ARF.

Major Criteria: Carditis is most important manifestation.

1. Organic heart murmur, mitral or aortic regurgitation, mitral

stenosis
2. Cardiac enlargement or HF secondary to myocarditis
3. Pericarditis resulting in muffled heart sounds, chest pain, pericardial
friction rub, or signs of effusion.

Mono or polyarthritismost common finding (larger joints more

frequently affected, knees, wrists, ankles, elbows.)
 Chorea (involuntary movement of the face and limbs), major CNS
manifestation; delayed sign occurring several months after being infected.

Erythema marginatum lesions- less common bright pink, nonpruritic, map

like, macular lesions that occur on the trunk and extremities.

Subcutaneous nodules- associated with severe carditis firm, small, hard,

painless swellings over joints like knees, wrists, and elbows.

Minor Criteria: Fever, polyarthralgia, lab findings (increased ESR, WBC, or CRP)

Third CriteriaHAVE TO HAVE! Evidence of infection!

Lab findings: increased ASO titers, positive throat culture (had strep throat),
positive rapid antigen test for group A streptococci.

Abnormal ECG findings.

Nursing Management of Rheumatic Fever:

Antibiotics will NOT modify the course of the disease, or prevent against carditis, but
does eliminate residual group A strep and prevent spread. Salicylates and NSAID’s help with
fever and joint pain, Corticosteroids if severe carditis is present, and supportive measures
such as bedrest.

Use of subjective and objective data, likely to occur in person with past history of it.

GOALS: Normal or baseline heart function, resumption of ADL;s without joint pain,
and verbalization of ability to manage disease.

PREVENTION IS KEY! This involves early detection and immediate treatment of group
A Strep pharyngitis. Educate community to seek medical attention for symptoms.

Acute intervention primary goals: Control and Eradicate the infecting organism,
prevent cardiac complications, relieve joint pain and fever, administer antibiotics as ordered,
FINISH PRESCRIPTION, promote optimal rest to reduce cardiac workload/diminish metabolic
demands but after acute symptoms subside, pt without carditis should ambulate.

Secondary prevention: Prevent recurrence, prior history makes pt more susceptible

to recur, best prevention is monthly injections of long-acting penicillin—alternate treatment
is to administer oral penicillin or erythromycin 1-2 times a day.

*Rheumatic fever WITHOUT carditis after age 18 may require 5yrs of prophylactic
antibiotic therapy. If the pt is frequently expised to group A strep, treatment will be
indefinite. Pt who has developed rheumatic heart disease, treatment will last the lifetime.
(Teach when to seek treatment!)
Describe pathophysiology, clinical manifestations, and nursing management of different
cardiomyopathies:

A group of heart muscle diseases that primarily affects structural or functional ability
of the myocardium.

Primaryetiology of the heart disease is unknown, the heart muscle is the

only portion of the heart involved, other cardiac structures are unaffected.

Secondaryetiology of the myocardial disease is known and is secondary to

another disease process. Ex., ischemia, viral infection, alcohol, drug abuse,
pregnancy, htn.

3 kinds Dilated Cardiomyopathy (most common), Hypertrophic cardiomyopathy,

and restrictive cardiomyopathy. All three can lead to cardiomegaly (hypertrophy of the
heart) and HR.

Dilated Cardiomyopathy: Usually after myocarditis. Characterized by diffuse

inflammation, rapid degeneration of myocardial fibers, cardiomegaly with ventricular
dilation, impairment of systolic function, walls of ventricles do not become hypertrophic as
in chronic HF.

Clinical manifestations: S/s may develop acutely or insidiously over time (lack
of symptoms, pt unaware of onset). Symptoms include fatigue, decreased
exercise capacity, dyspnea at rest, orthopnea.

Nursing Management: More palliative than curative- prevention/control of HF

is major goal. Control symptoms of heart failure, call dr at 1 st sign og HF (SOB,
edema, etc). Digoxin (CAUTION), Anticoagulation, Nitrates, loop diuretics,
ACE inhibitors. Nutritional therapy, cardiac rehab. If severe Dobutamine or
Primacor infusions for HF, heart transplant, and family MUST learn CPR.
Prognosis for disease poor, but good with heart transplanttakes a while to
get, could die waiting.

Hypertrophic Cardiomyopathy: Produces asymmetric LEFT ventricular hypertrophy

without ventricular dilation, can be idiopathic, ½ cases are genetic bases, thickened
intraventricular septum and ventricular wall, obstruct blood flow to left ventricle, may also
be called hypertrophic obstructive cardiomyopathy (HOCM).

Displaced apical pulse on palpation of chest, S4 sound with a murmur on

Auscultation.

Clinical manifestations: Patients may be asymptomatic. May have dyspnea on

exertion (DOE), fatigue, angina, syncope. Most common symptom is dyspnea.
Patient may experience dsyrhythmia’s.
 Nursing management: GOAL is to improve ventricular filling, decrease
obstruction in the left ventricles, and reduce the contractility of the left
ventricles. Beta Blockers are used, calcium channel blockers are used, digoxin
is CONTRAINDICATED unless for the use in treatment of the atrial fibrillation.
Pacemakers may be used. Surgery may be an option. RELEIVE symptoms,
observe pt, prevent complications, provide emotional support, and teach pt
to adjust lifestyle to avoid strenuous activity and dehydration.

Restrictive Cardiomyopathy: Least common, disease of the heart that impairs

diastolic volume and stretch (hardens). Systolic function is unaffected. Etiology is unknown.
May have signs of BOTH right and left HF.

Clinical manifestations: Fatigue, exercise intolerance, and dyspnea. Angina,

orthopnea, syncope, and palpitations can occur. There may be signs of HF
(peripheral edema, ascites, JVD).

Nursing Management: No specific treatment exists. Improve diastolic filling

and treat underlying cause. Heart transplant is an option. Teach pt to avoid
strenuous activities, and proper hygiene because pt is at risk for IE, (inform
health care provider or dentist before any invasive procedures) instruct for
prophylactic antibiotics.