Chapter 40

Inflammatory and Structural Heart Disorders

KEY POINTS

INFECTIVE ENDOCARDITIS

• Infective endocarditis (IE) is an infection of the endocardial surface of the heart that

affects the heart valves.

• The most common causative organisms of IE are Staphylococcus aureus, Streptococcus

viridans or Coagulase negative staphylococci.

• Vegetation adheres to the valve surface or endocardium and can embolize to various

organs and to the extremities, causing ischemia and infarction.

• The infection may spread locally to cause damage to the valves or to their supporting

structures resulting in dysrhythmias, valve dysfunction, and eventual invasion of the

myocardium, leading to heart failure (HF), sepsis, and heart block.

• Clinical findings in IE are nonspecific and can involve multiple organ systems.

• Guidelines for the diagnosis of IE are based on Duke Criteria. The patient must have 2

major criteria and 1 minor criterion, or 1 major and 3 minor, or 5 minor criteria.

• Major criteria include: positive blood cultures, typical microorganism for IE from 2

separate blood cultures, evidence of endocardial involvement, and new valvular vegetation.

• Minor criteria include: predisposing heart condition or IV drug use, vascular phenomena,

immunologic phenomena, microbiologic evidence, or echocardiographic findings consistent

with

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IE but not meeting major criteria• Patients with specific heart conditions undergoing certain

invasive procedures (e.g., dental work that perforates the oral mucosa) need antibiotic

prophylaxis.

• Accurate identification and destruction of the infecting organism are key to successful

treatment of IE.

• Drug therapy consists of long-term treatment with IV antibiotic therapy and 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.

• The patient with IE has multiple problems that require nursing care.

• Teach patients and caregivers to recognize signs and symptoms of life-threatening

complications of IE, such as stroke, pulmonary edema, and HF.

• Fever (chronic or intermittent) is a common early sign that the drug therapy is ineffective.

ACUTE PERICARDITIS

• Pericarditis is an inflammation of the pericardial sac (the pericardium).

• Acute pericarditis most often is idiopathic. Other causes include uremia, viral or bacterial

infection, acute myocardial infarction (MI), heart surgery, tuberculosis, cancer,

inflammation from radiation to the chest, and trauma.

• Pericarditis in the acute MI patient may be described as 2 distinct syndromes: (1) acute

pericarditis (occurs within the first 48 to 72 hours after an MI) and (2) Dressler syndrome

(late pericarditis that appears 4 to 6 weeks after an MI).

• Clinical manifestations include the following:

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• Progressive, often severe chest pain that is sharp and pleuritic in nature and worse with

deep inspiration and when lying supine. The pain is relieved by sitting up and leaning

forward. It may be referred to the shoulder and upper back.

• A hallmark finding in acute pericarditis is a pericardial friction rub.

• Complications include pericardial effusion and cardiac tamponade.

• Interprofessional care includes:

• Antibiotics

• Pain and inflammation are usually treated with nonsteroidal antiinflammatory drugs

(NSAIDs) or high-dose salicylates. Corticosteroids may be an option in some patients.

• Patients who have recurrent pericarditis may receive colchicine, an antiinflammatory

agent used for gout.

• Pericardiocentesis or pericardial window is often done for acute cardiac tamponade,

purulent pericarditis, or a high suspicion of cancer.

• The management of the patient’s pain and anxiety during acute pericarditis is a key

nursing consideration. Pain relief measures include maintaining bed rest with the head of

the bed elevated to 45 degrees, providing an overbed table for support, and

antiinflammatory drugs.

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CHRONIC CONSTRICTIVE PERICARDITIS

• Chronic constrictive pericarditis results from scarring with consequent loss of elasticity

of the pericardial sac. The result is that the pericardium impairs the ability of the atria and

ventricles to stretch adequately during diastole.

• Occurs over time and mimics HF and cor pulmonale. Jugular venous distention (JVD) is

common.

• Treatment of choice for chronic constrictive pericarditis is a pericardiectomy.

MYOCARDITIS

• Myocarditis is a focal or diffuse inflammation of the myocardium caused by viruses,

bacteria, fungi, radiation therapy, and pharmacologic and chemical factors.

• Clinical manifestations include the following:

• Fever, fatigue, malaise, myalgias, pharyngitis, dyspnea, lymphadenopathy, and nausea

and vomiting are early systemic manifestations of the viral illness.

• Early cardiac signs appear 7 to 10 days after viral infection and include pleuritic chest

pain with a pericardial friction rub and effusion.

• Late cardiac signs relate to the development of HF and may include an S3 heart sound,

crackles, jugular venous distention, syncope, peripheral edema, and angina.

• Treatment for myocarditis consists of managing the associated heart symptoms.

• Drug therapy includes the use of angiotensin-converting enzyme (ACE) inhibitors,

blockers, digoxin, and diuretics.

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 • Vasodilators may be used if hypotension is not present.
• Those at risk for thrombus formation receive anticoagulation therapy.

• Immunosuppressive therapy to reduce myocardial inflammation and prevent

irreversible myocardial damage may be considered.

• Other therapy includes oxygen and bed rest or restricted activity.

• Intraaortic balloon pump therapy and/or ventricular assist devices reduce the workload

of the heart.

• Nursing interventions focus on managing the signs and symptoms of HF. These

include instituting measures to decrease anxiety and keeping the patient and caregiver

informed about the therapeutic plan.

• Most patients with myocarditis recover spontaneously, although some may develop

dilated cardiomyopathy (CMP). If severe HF occurs, the patient may need a heart

transplant.

RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE

• Rheumatic fever (RF) is an inflammatory disease of the heart that occurs as a

complication following group A streptococcal pharyngitis.

• Rheumatic heart disease is a chronic condition resulting from RF. It is characterized by

scarring and deformity of the heart valves.

• About 40% of RF episodes are marked by rheumatic pancarditis, meaning that all layers

of the heart are involved.

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 • 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.

• Clinical manifestations of RF include the presence of 2 major criteria or 1 major and 2

minor criteria plus evidence of a preceding group A streptococcal infection.

• Major criteria include the following:

• Carditis results in 3 signs: murmurs of mitral or aortic regurgitation, or mitral stenosis;

cardiac enlargement and HF; pericarditis

• Monoarthritis or polyarthritis • Sydenham’s chorea

• Erythema marginatum lesions

• Minor criteria include the clinical findings of fever and polyarthralgia and laboratory

findings of increased erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).

• The main goals of managing a patient with RF are to control and eradicate the infecting

organism; prevent heart complications; and relieve joint pain, fever, and other symptoms

with antibiotics, optimal rest, and antipyretics, NSAIDs, and steroids.

• Health promotion emphasizes prevention of RF by early detection and treatment of group

A streptococcal pharyngitis with antibiotics, specifically penicillin. Successful treatment

requires strict adherence to the full course of antibiotic therapy

.• Secondary prevention aims at stopping the recurrence of RF with prophylactic antibiotics.

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Patients with RF without carditis need prophylaxis until age 20 and for a minimum of 5 years.

Patients with rheumatic carditis and residual heart disease (e.g., persistent valve disease) will

need longer-term and even life-long prophylaxis.

VALVULAR HEART DISEASE

• Valvular stenosis refers to a constriction or narrowing of the valve opening.

• Valvular regurgitation, also called insufficiency, occurs with incomplete closure of the

valve leaflets and results in the backward flow of blood.

MITRAL VALVE STENOSIS

• Most adult mitral valve stenosis results from rheumatic heart disease. Less often, it can

occur congenitally, from rheumatoid arthritis, or from systemic lupus erythematosus.

• Clinical manifestations of mitral stenosis include exertional dyspnea, fatigue, palpitations

from atrial fibrillation, and a loud first heart sound and a low-pitched, diastolic murmur.

MITRAL VALVE REGURGITATION

• Mitral regurgitation (MR) is caused by MI, chronic rheumatic heart disease, mitral valve

prolapse, ischemic papillary muscle dysfunction, and IE.

• In chronic MR, the added volume load results in atrial enlargement (placing the patient at

risk for atrial fibrillation), ventricular dilation, and eventual ventricular hypertrophy.

• In acute MR, there is a sudden increase in pressure and volume that is transmitted to the

pulmonary bed, resulting in pulmonary edema and life-threatening cardiogenic shock.

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 • Clinical manifestations of acute MR include thready peripheral pulses; cool, clammy

extremities; and a new systolic murmur.

• Patients with asymptomatic MR should be monitored carefully, and surgery should be

considered before significant left ventricular failure or pulmonary hypertension develops.

MITRAL VALVE PROLAPSE

• Mitral valve prolapse (MVP) is an abnormality of the mitral valve leaflets and the

papillary muscles or chordae that allows the leaflets to prolapse, or buckle, back into the

left atrium during systole. The cause of MVP is unknown.

• In many patients, MVP found by echocardiography is not accompanied by any other

clinical manifestations of heart disease, and the significance of the finding is unclear.

AORTIC VALVE STENOSIS

• In older patients, aortic stenosis (AS) is a result of rheumatic fever or fibrocalcific

degeneration.

• AS results in left ventricular hypertrophy and increased myocardial oxygen consumption.

As the disease progresses, cardiac output (CO) decreases, leading to decreased tissue

perfusion, pulmonary hypertension, and HF.

• Clinical manifestations include a systolic murmur and the classic triad of angina,

syncope, and exertional dyspnea.

AORTIC VALVE REGURGITATION

• Acute aortic regurgitation (AR) is caused by IE, trauma, or aortic dissection.

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 • Clinical manifestations of acute AR include severe dyspnea, chest pain, and hypotension

indicating left ventricular failure and cardiogenic shock that constitute a medical

emergency.

• Chronic AR is often the result of rheumatic heart disease, a congenital bicuspid aortic

valve, syphilis, or chronic rheumatic conditions.

• Clinical manifestations of chronic AR include exertional dyspnea, orthopnea, and

paroxysmal nocturnal dyspnea after considerable myocardial dysfunction has occurred.

TRICUSPID AND PULMONIC VALVE DISEASE

• Diseases of the tricuspid and pulmonic valves are uncommon, with stenosis occurring

more often than regurgitation. Pulmonary stenosis is almost always congenital.

• Tricuspid stenosis occurs almost exclusively in patients with RF or who are IV drug

users. It results in right atrial enlargement and increased systemic venous pressures.

INTERPROFESSIONAL CARE OF VALVULAR HEART DISEASE

• Interprofessional care of valvular heart disease includes the prevention of recurrent RF

and IE and the prevention of exacerbations of HF, acute pulmonary edema, and

thromboembolism.

• Anticoagulant therapy prevents and treats systemic or pulmonary embolization.

• Percutaneous transluminal balloon valvuloplasty to split open the fused commissures is

an alternative treatment for stenotic valvular heart disease.

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 • Surgical intervention is based on the valves involved, the pathology and severity of the

disease, and the patient’s clinical condition.

• Valve repair, including a valvulotomy, valvuloplasty, or annuloplasty, is typically the

surgical procedure of choice.

• Valve replacement may be needed. A wide variety of valves, both mechanical and

biologic, are available.

• The overall goals for a patient with valve disease include normal heart function,

improved activity intolerance, and an understanding of health maintenance measures.

• Prophylactic antibiotic therapy is needed to prevent IE.

• The patient needs ongoing antibiotic prophylaxis if RF caused valve disease.

• Patients on anticoagulation therapy (warfarin [Coumadin]) after valve replacement

surgery must have the international normalized ratio (INR) checked regularly.

• Teach the patient to seek medical care if any manifestations of infection, HF, or bleeding

occur, and any invasive or dental procedures are planned.

CARDIOMYOPATHY

• Cardiomyopathy (CMP) is a group of diseases that directly affect the structure or function

of the myocardium.

• CMP is classified as primary (conditions in which the cause of the heart disease is

unknown) or secondary (the cause of the myocardial disease is known and is a result of

another disease process).

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DILATED CARDIOMYOPATHY

• A diffuse inflammation and rapid degeneration of myocardial fibers characterize dilated

CMP. This results in ventricular dilation, impairment of systolic function, atrial

enlargement, and stasis of blood in the left ventricle.

• Clinical manifestations develop acutely after an infectious process or slowly over a

period of time. Most patients eventually develop HF.

• Interventions focus on controlling HF by enhancing myocardial contractility and

decreasing preload and afterload. The goals of therapy are to keep the patient at an

optimal level of functioning and out of the hospital.

• Drug therapy is the mainstay of treatment.

• Nutritional therapy and cardiac rehabilitation may help lessen symptoms and improve

quality of life.

• Cardiac resynchronization therapy, implantable cardioverter defibrillators (ICD), and

ventricular assist devices are options.

HYPERTROPHIC CARDIOMYOPATHY

• Hypertrophic CMP is asymmetric left ventricular hypertrophy without ventricular

dilation. The result is impaired ventricular filling as the ventricle becomes noncompliant

and unable to relax.

• Patients with hypertrophic CMP may be asymptomatic or may have exertional dyspnea,

fatigue, angina, syncope, and dysrhythmias.

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 • Goals of intervention are to improve ventricular filling by reducing ventricular

contractility and relieving left ventricular outflow obstruction.

• Drug therapy for hypertrophic CMP includes -blockers or calcium channel blockers.

Digitalis preparations are contraindicated unless the patient has atrial fibrillation.

Dysrhythmias are treated with the appropriate antidysrhythmic.

• Patients at risk for sudden cardiac death (SCD) need an ICD• Atrioventricular pacing can

be beneficial for patients with hypertrophic CMP and outflow obstruction.

• Some patients may be candidates for a ventriculomyotomy and myectomy.

• Nursing interventions for hypertrophic CMP focus on relieving symptoms, observing for

and preventing complications, and providing emotional support.

RESTRICTIVE CARDIOMYOPATHY

• Restrictive CMP, the least common CMP, impairs diastolic filling and stretch, although

systolic function is unaffected.

• Clinical manifestations include fatigue, exercise intolerance, and dyspnea. No specific

treatment for restrictive CMP exists. Interventions are aimed at improving diastolic filling

and the underlying disease process.

• Treatment includes conventional therapy for HF and dysrhythmias. vHeart transplant may be

an option.

• Nursing care is similar to the care of a patient with HF.

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