Chapter 37: Inflammatory and Structural Heart Disorders
Infective endocarditis (IE) is an infection of the endocardial surface of the heart that
affects the cardiac valves. It is treated with penicillin.
Two forms of IE include the subacute form (typically affecting those with preexisting
valve disease) and the acute form (typically affecting those with healthy valves).
The most common causative organisms of IE are Staphylococcus aureus and
The principal risk factors for IE are prior endocarditis, prosthetic valves, acquired
valvular disease, and cardiac lesions.
Vegetations, the primary lesions of IE, adhere to the valve surface or endocardium and
can embolize to various organs (particularly the lungs, brain, kidneys, and spleen) and to
the extremities, causing limb infarction.
The infection may spread locally to cause damage to the valves or to their supporting
structures resulting in dysrhythmias, valvular incompetence, and eventual invasion of the
myocardium, leading to heart failure (HF), sepsis, and heart block.
Clinical findings in IE are nonspecific and can include the following:
o Low-grade fever, chills, weakness, malaise, fatigue, and anorexia
o Arthralgias, myalgias, back pain, abdominal discomfort, weight loss, headache,
and clubbing of fingers
o Splinter hemorrhages (black longitudinal streaks) in the nail beds
o Petechiae (a result of fragmentation and microembolization of vegetative lesions)
in the conjunctivae, the lips, the buccal mucosa, and the palate and over the
ankles, the feet, and the antecubital and popliteal areas
o Osler’s nodes (painful, tender, red or purple, pea-size lesions) on the fingertips or
toes and Janeway’s lesions (flat, painless, small, red spots) on the palms and
o Hemorrhagic retinal lesions called Roth’s spots
o A new or changing murmur in the aortic or mitral valve
Definitive diagnosis of IE exists if two of the following major criteria are present:
positive blood cultures, new or changed cardiac murmur, or intracardiac mass or
vegetation noted on echocardiography.
Collaborative care consists of antibiotic prophylaxis for patients with specific cardiac
conditions before dental, respiratory tract, gastrointestinal (GI), and genitourinary (GU)
procedures and for high-risk patients who (1) are to undergo removal or drainage of
infected tissue, (2) receive renal dialysis, or (3) have ventriculoatrial shunts for management of hydrocephalus.
Drug therapy consists of long-term treatment with IV antibiotic therapy with subsequent
blood cultures to evaluate the effectiveness of antibiotic therapy.
Early valve replacement followed by prolonged (6 weeks or longer) drug therapy is
recommended for patients with fungal infection and prosthetic valve endocarditis.
Fever is treated with aspirin, acetaminophen (Tylenol), ibuprofen (Motrin), fluids, and
Complete bed rest is usually not indicated unless the temperature remains elevated or
there are signs of HF.
Overall goals for the patient with IE include (1) normal or baseline cardiac function, (2)
performance of activities of daily living (ADLs) without fatigue, and (3) knowledge of
the therapeutic regimen to prevent recurrence of endocarditis.
Patients and families must be taught to recognize signs and symptoms of life-threatening
complications of IE, such as cerebral emboli (e.g., change in mental status), pulmonary
edema (e.g., dyspnea), and HF (e.g., chest pain).
o Fever (chronic or intermittent) is a common early sign that the drug therapy is
Laboratory data and blood cultures are monitored to determine the effectiveness of the
Pericarditis is caused by inflammation of the pericardial sac (the pericardium).
Acute pericarditis most often is idiopathic but can be caused by uremia, viral or bacterial
infection, acute myocardial infarction (MI), tuberculosis, neoplasm, and trauma.
Pericarditis in the acute MI patient may be described as two distinct syndromes: (1) acute
pericarditis (occurs within the initial 48 to 72 hours after an MI), and (2) Dressler
syndrome (late pericarditis which appears 4 to 6 weeks after an MI).
Clinical manifestations include the following:
o Progressive, frequently severe chest pain that is sharp and pleuritic in nature and
worse with deep inspiration and when lying supine. The pain is relieved by
o Pain can be referred to the trapezius muscle (shoulder, upper back).
o The hallmark finding in acute pericarditis is the pericardial friction rub.
Complications include pericardial effusion and cardiac tamponade. Collaborative care includes the following:
o Corticosteroids for pericarditis secondary to systemic lupus erythematosus,
patients already taking corticosteroids for a rheumatologic or other immune
system condition, or patients who do not respond to nonsteroidal
antiinflammatory drugs (NSAIDs)
o Pain and inflammation are usually treated with NSAIDs or high-dose salicylates
o Colchicine, an antiinflammatory agent used for gout, may be considered for
patients who have recurrent pericarditis.
o Pericardiocentesis is usually performed for pericardial effusion with acute
cardiac tamponade, purulent pericarditis, and a high suspicion of a neoplasm.
Complications from pericardiocentesis include dysrhythmias, further
cardiac tamponade, pneumomediastinum, pneumothorax, myocardial
laceration, and coronary artery laceration.
The management of the patient’s pain and anxiety during acute pericarditis is a primary
ECG monitoring can aid in distinguishing ischemic pain from pericardial pain as
ischemia involves localized ST-segment changes, as compared to the diffuse ST-segment
changes present in acute pericarditis.
Pain relief measures include maintaining bed rest with the head of the bed elevated to 45
degrees and providing an overbed table for support, and antiinflammatory medications.
CHRONIC CONSTRICTIVE PERICARDITIS
Chronic constrictive pericarditis results from scarring with consequent loss of elasticity
of the pericardial sac and begins with an initial episode of acute pericarditis followed by
fibrous scarring, thickening of the pericardium from calcium deposition, and eventual
obliteration of the pericardial space.
The end result is that the fibrotic, thickened, and adherent pericardium impairs the ability
of the atria and ventricles to stretch adequately during diastole.
Clinical manifestations mimic HF and cor pulmonale and include dyspnea on exertion,
peripheral edema, ascites, fatigue, anorexia, and weight loss.
The most prominent finding is jugular venous distention.
Auscultation reveals a pericardial knock, which is a loud early diastolic sound often heard
along the left sternal border.
Treatment of choice for chronic constrictive pericarditis is a pericardiectomy.
Pericardiectomy involves complete resection of the pericardium through a median sternotomy with the use of cardiopulmonary bypass.
Myocarditis is a focal or diffuse inflammation of the myocardium caused by viruses,
bacteria, fungi, radiation therapy, and pharmacologic and chemical factors.
Myocarditis is frequently associated with acute pericarditis, particularly when it is caused
by coxsackievirus B strains.
Myocarditis results in cardiac dysfunction and has been linked to the development of
Clinical manifestations include the following:
o Fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, and
nausea and vomiting are early systemic manifestations of the viral illness.
o Early cardiac manifestations appear 7 to 10 days after viral infection and include
pleuritic chest pain with a pericardial friction rub and effusion.
o Late cardiac signs relate to the development of HF and may include an S h3art
sound, crackles, jugular venous distention, syncope, peripheral edema, and
Collaborative care includes the following:
o Managing associated cardiac decompensation with:
Digoxin (Lanoxin) to treat ventricular failure
Diuretics to reduce fluid volume and decrease preload
Nitroprusside (Nitropress), inamrinone (Inocor), and milrinone (Primacor)
to reduce afterload and improve cardiac output
The use of anticoagulation therapy may be considered in patients with a
low ejection fraction who are at risk for thrombus formation from blood
stasis in the cardiac chambers.
o Immunosuppressive therapy to reduce myocardial inflammation and to prevent
irreversible myocardial damage.
o Oxygen therapy, bed rest, and restricted activity.
o Intraaortic balloon pump therapy and ventricular assist devices.
Nursing interventions focus on assessment for the signs and symptoms of HF and include
assessing the level of anxiety, instituting measures to decrease anxiety, and keeping the
patient and family informed about therapeutic measures.
Most patients with myocarditis recover spontaneously, although some may develop
dilated cardiomyopathy. If severe HF occurs, the patient may require heart
RHEUMATIC FEVER AND HEART DISEASE
Rheumatic fever is an inflammatory disease of the heart potentially involving all layers
of the heart. Rheumatic heart disease is a chronic condition resulting from rheumatic fever that is
characterized by scarring and deformity of the heart valves.
Acute rheumatic fever (ARF) is a complication that occurs as a delayed sequela of a
group A streptococcal pharyngitis and affects the heart, joints, central nervous system
(CNS), and skin.
About 40% of ARF episodes are marked by carditis, meaning that all layers of the heart
are involved, and this is referred to as rheumatic pancarditis.
o Rheumatic endocarditis is found primarily in the valves. Vegetation forms and
valve leaflets may fuse and become thickened or even calcified, resulting in
stenosis or regurgitation.
o Myocardial involvement is characterized by Aschoff’s bodies.
o Rheumatic pericarditis affects the pericardium, which becomes thickened and
covered with a fibrinous exudate, and often involves pericardial effusion.
o The lesions of rheumatic fever are systemic, especially involving the connective
tissue, as well as the joints, skin, and CNS.
Clinical manifestations of ARF include the following:
o The presence of two major criteria or one major and two minor criteria plus
evidence of a preceding group A streptococcal infection.
Carditis results in three signs: (1) murmurs of mitral or aortic
regurgitation, or mitral stenosis; (2) cardiac enlargement and HF; (3)
Mono- or polyarthritis causes swelling, heat, redness, tenderness, and
limitation of motion.
Chorea (Sydenham’s chorea) involves involuntary movements,
especially of the face and limbs, muscle weakness, and disturbances of
speech and gait.
Erythema marginatum lesions are bright pink, nonpruritic, maplike
macular lesions that occur mainly on the trunk and proximal
Subcutaneous nodules are firm, small, hard, painless swellings
located over extensor surfaces of the joints.
Clinical findings: fever, polyarthralgia
Laboratory findings: elevated ESR, elevated WBC, elevated CRP
Complications of ARF include chronic rheumatic carditis.
Skin should be assessed for subcutaneous nodules and erythema marginatum.
The overall goals for a patient with rheumatic fever include (1) normal or baseline heart
function, (2) resumption of