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BIOC33H3 (127)
Lecture

Inflammatory and Structural Heart Disorders

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Department
Biological Sciences
Course
BIOC33H3
Professor
Stephen Reid
Semester
Fall

Description
Chapter 37: Inflammatory and Structural Heart Disorders INFECTIVE ENDOCARDITIS  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 Streptococcus viridans.  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 soles o Hemorrhagic retinal lesions called Roth’s spots o A new or changing murmur in the aortic or mitral valve o HF  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 rest.  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 ineffective.  Laboratory data and blood cultures are monitored to determine the effectiveness of the antibiotic therapy. ACUTE PERICARDITIS  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 sitting. 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 Antibiotics 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 (e.g., aspirin). 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 nursing consideration.  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  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 dilated cardiomyopathy.  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 angina.  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 transplantation. 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.  Major criteria:  Carditis results in three signs: (1) murmurs of mitral or aortic regurgitation, or mitral stenosis; (2) cardiac enlargement and HF; (3) pericarditis.  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 extremities.  Subcutaneous nodules are firm, small, hard, painless swellings located over extensor surfaces of the joints.  Minor criteria:  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
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